According to the conclusions made in the SIDS Initial Assessment Report (SIAR), benzyl 

alcohol, benzoic acid and its sodium and potassium salts can be considered as a single category 

regarding human health, as they are all rapidly metabolized and excreted via a common pathway 

within 24-hours. 

In addition, sodium benzoate and benzoic acid, both considered by US Food and Drug 

Administration (FDA) as Generally Recognized as Safe (GRAS) chemicals were included since 

potassium benzoate would react identically. In addition, the US FDA has approved potassium 

benzoate as a food additive based on its similarity to sodium benzoate 

Executive Summary 

Landis International, on behalf of Whitmire Micro-Gen, submitted two petitions (7E7241 and 

8E7333) requesting exemptions from tolerance for residues of potassium benzoate when used as 

an inert ingredient (preservative) in pesticide formulations applied pre- and post-harvest under 

40 CFR 180.910 and applied to animals under 40 CFR 180.930. A Notice of Filing for each 

petition was published in the Federal Register. 

Potassium benzoate is an approved food preservative similar in structure and reactivity to the 

more widely used and classified by US FDA as GRAS, sodium benzoate. Both are salts of 

benzoic acid. Perhaps as a result of potassium benzoate’s similarity to sodium benzoate, few 

toxicological studies on it were found. Because all benzoates, and in particular benzoic acid and 

sodium benzoate, react similarly, they were used as surrogates in the development of this profile. 

Available data suggest that the acute toxicity of potassium benzoate is negligible, having an oral 

median lethal dose (LD50) of >10,000 milligrams per kilogram body weight (mg/kg bw). Acute 

dermal and inhalation toxicity is low as indicated by the >2000 mg/kg bw LD50 and >12.2 

milligrams per liter (mg/L) median lethal concentration (LC50) of benzoic acid. Sodium 

benzoate was not irritating to the skin and induced only slight eye irritation in rabbits. Sodium 

benzoate and benzoic acid were non-sensitizing in animal tests but showed a very low incidence 

of sensitization in humans patch tested. Both sodium benzoate and benzoic acid are known to 

induce non-immunogenic contact reactions, and that is the likely explanation for the low positive 

response. 

Sub-acute, sub-chronic and chronic toxicity data also indicate that potassium benzoate should be 

relatively nontoxic. Oral and dermal studies had a no observed adverse effect level (NOAEL) 

≥2000 mg/kg bw and the inhalation study had a NOAEL > 25 milligrams per cubic meter 

(mg/m3

). Sodium benzoate was not carcinogenic in a lifetime mouse feeding study and there is 

no indication that potassium benzoate should be neurotoxic. Genotoxicity studies indicate the 

benzoates are not mutagenic; however chromosomal aberration studies gave ambiguous results. 

Benzoic acid did not induce reproductive toxicity in a four-generation study. In the human body 

under normal physiological conditions, potassium benzoate changes from the ionized form to the 

undissociated benzoic acid. Benzoic acid and its salts are rapidly absorbed by mammals, 

conjugated with glycine, and rapidly excreted in the urine as hippuric acid. There is no reported 

accumulation of benzoate in the body. However, the ability to conjugate benzoic acid depends 

upon adequate liver function and nutritional supply of glycine. All data indicates that potassium 
benzoate is relatively non-toxic as are the other benzoates. No toxicity would be expected from 

potassium benzoate when used at low concentrations in pesticides.

No developmental toxicity studies are available in the database. However, no systemic toxicity 

was observed at doses up to 750 mg/kg/day in a four-generation reproductive study with benzoic 

acid. In addition, no systemic toxicity was observed in the laboratory animals at high doses 

(>2000 mg/kg/day) of potassium benzoate and benzoates indicating relatively low hazard 

potential. In terms of hazard, there are low concerns and no residual uncertainties regarding 

prenatal and/or postnatal toxicity. Based on this information, there is no concern at this time for 

increased sensitivity to infants and children to potassium benzoate when used as an inert 

ingredient in pesticide formulations and a safety factor analysis has not been used to assess risk. 

For the same reason, EPA has determined that an additional safety factor is not needed to protect 

the safety of infants and children. 

Residues of concern are not anticipated for dietary exposure (food and drinking water) or for 

residential exposure from the use of potassium benzoate for the proposed use pattern as an inert 

ingredient in pesticide products. EPA expects aggregate exposure to potassium benzoate to pose 

no appreciable dietary risk given that the data on potassium benzoate show a lack of any 

systemic toxicity and a lack of any apparent reproductive or developmental effects. 

There is limited environmental fate and ecotoxicity data available for potassium benzoate, but 

the fate and occurrence of benzoic acid have been well studied. The available data indicate that 

these compounds are expected to be readily biodegradable in the environment and of low toxicity 

to fish, aquatic organisms, mammals and birds. The Agency believes that benozoic acid and the 

benzoate salts will not cause unreasonable adverse effects on the environment. 

Taking into consideration all available information on potassium benzoate, EPA has determined 

that there is a reasonable certainty that no harm to any population subgroup will result from 

aggregate exposure to potassium benzoate when used as an inert ingredient in pesticide 

formulations applied pre-and post-harvest and applied to animals, when considering dietary 

exposure and all other non-occupational sources of pesticide exposure for which there is reliable 

information. Therefore, the establishment of an exemption from tolerance under 40 CFR 

180.910 and 40 CFR 180.930 for residues of potassium benzoate (CAS Reg. No. 582-25-2) when 

used as an inert ingredient in pre- and post-harvest and animal applications in pesticide 

formulations, can be considered assessed as safe under section 408(q) of the FFDCA. 

I. Background 

Landis International, on behalf of Whitmire Micro-Gen, submitted a petition (7E7241) 

requesting an exemption from tolerance for residues of potassium benzoate when used as an 

inert ingredient (preservative) in pesticide formulations applied pre- and post-harvest under 40 

CFR 180.910. EPA published the Notice of Filing for this petition in the Federal Register on 

February 6, 2008 (73 FR 6964). Landis International, on behalf of Whitmire Micro-Gen, 

submitted at second petition (8E7333) requesting and exemption from tolerance for residues of 

potassium benzoate when used as an inert ingredient (preservative) in pesticide formulations 
applied to animals under 40 CFR 180.930. EPA published a Notice of Filing for this petition in 

the Federal Register on June 4, 2008 (73 FR 31862). Two comments were received in the docket 

for Petition #7E7241, however they are unrelated to potassium benzoate and the Agency believes 

they were placed in this docket in error by the commenters. There were no comments received 

in response to the notice of filing for Petition #8E7333. 

This document provides an assessment of the risk to human health and the environment for 

potassium benzoate when used as an inert ingredient in pesticide formulations and was based on 

information provided by the submitter and information available in the public literature. It was 

also based on the OECD/SIDS Assessment for benzoates. According the conclusions made in 

the SIDS Initial Assessment Report (SIAR), benzyl alcohol, benzoic acid and its sodium and 

potassium salts can be considered as a single category regarding human health, as they are all 

rapidly metabolized and excreted via a common pathway within 24-hours. 

II. Substance Identity 

A. Potassium Benzoate 

TABLE 1. Substance identity POTASSIUM BENZOATE 

Chemical abstracts service registry number 

(CAS RN) 

582-25-2 

Other names Benzoic acid, potassium salt 

DP # 

PC Code 

Chemical formula C7H6O2·K 

SMILES (ChemIDplus Lite) c1(ccccc1)C(=O)[O-].[K+] 

Chemical structure 

 
B. Surrogate Chemicals for Potassium Benzoate 

TABLE 2. Substance Identity for Potassium Benzoate Surrogate Chemicals(*)

Chemical Name Chemical Formula CAS No. Structure 

Benzoic Acid C7-H6-O2 65-85-0 

Sodium Benzoate C7-H5-Na-O2 532-32-1

Calcium Benzoate C7-H6-O2.1/2Ca 2090-05-3
Ammonium Benzoate C7-H6-O2.H3-N 1863-63-4

• ChemIDplus Lite 

III. Use Information 

A. Pesticide Uses 

Potassium benzoate is currently approved for use as an inert ingredient in nonfood use pesticide 

products. 

B. Other Uses 

Potassium benzoate is currently used as a preservative in pharmaceutical and cosmetic products. 

It is also used as a preservative in human foods such as syrups, jams, jellies, prepared salads, 

tomato based products, margarine, olives, pickles, condiments and carbonated and 

noncarbonated beverages. (MRID 47180107) It is also listed as generally recognized as safe 

(GRAS) by the U.S. Food and Drug Administration (FDA). (MRID 47180106) 

 

IV. Physical and Chemical Properties 

Table 3 contains the physical and chemical properties of potassium benzoate. Since suitable data 

for potassium benzoate were often lacking, data for sodium benzoate, which is expected to be 

similar, were substituted when insufficient data were found.
TABLE 3. Physical and chemical properties 

Parameter Potassium benzoate Source 

Appearance White powder MRID 47180104 

Molecular wt. 160.12 ChemID 

Melting point (oC)* 330.6 EPI Suite 4.0 

Boiling pt. (1013hPa, 

oC) 

464.9 EPI Suite 4.0 

Density 0.72/0.73 g/cm3 MRID 47180107 

Vapor pressure (hPa)* <0.001 EPI Suite 4.0 

Log Kow* -2.269 EPI Suite 4.0 

Water solubility (mg/L) 5.56E5 EPI Suite 4.0 

* No data available for potassium benzoate, but expected to be similar to sodium 

benzoate 

V. Human Health Assessment 

Toxicological Discussion

Few studies on the acute, sub-acute, sub-chronic, chronic, developmental and mutagenicity of 

potassium benzoate were available for review. Because of potassium benzoate’s similarity to 

sodium benzoate and benzoic acid, these studies have been included to build any data gaps for 

toxicological assessment. 

Toxicological Data 

A. Acute Toxicity 

Acute toxicological data on potassium and sodium benzoate and on benzoic acid are summarized 

in Table 4. 

TABLE 4. Acute toxicity studies 

Study Type 

Potassium Benzoate 

(CAS No. 582-25-2)

Chemic

al 

Species/ 

strain Results Tox. Category Reference 

Acute oral Benzoic 

acid Rat LD50 = 2565 mg/kg III IRDC #163-282, 1974 

Acute oral Benzoic 

acid Mouse LD50 = 2250 mg/kg III BRL#9348, 1979 

Acute oral Sodium 

benzoate Rat LD50 = 3140 mg/kg III 

Loeser, 1977-

A; Deuel et 

al., 1954 
TABLE 4. Acute toxicity studies 

Study Type 

Potassium Benzoate 

(CAS No. 582-25-2)

Chemic

al 

Species/ 

strain Results Tox. Category Reference 

Acute oral Sodium 

benzoate Rat LD50 = 4070 mg/kg III 

Smyth & 

Carpenter, 

1948 

Acute oral 

Potassiu

m 

benzoate 

Rat 

Mouse 

Guinea pig 

LD50 ≥ 10,000 mg/kg 

LD50 ≥ 10,000 mg/kg 

LD50 ≥ 10,000 mg/kg 

IV 

KravetsBekkerIvanov

a, 1970 

Acute 

dermal 

Benzoic 

acid Rabbit LD50> 2000 mg/kg III IRDC#163-

282 1974 

Acute 

inhalation 

Benzoic 

acid Rat LC50 >12.2 mg/L/4hours IV IRDC#163-

282, 1974 

Skin 

irritation 

Benzoic 

acid Rabbit Not irritating IV IRDC#163-282, 1974 

Skin 

irritation 

Sodium 

benzoate Rabbit Not irritating IV 

RCC 

NOTOX 

Study No. 

014658 

Eye 

irritation 

Benzoic 

acid Rabbit Highly irritating I 

RCC 

NOTOX 

Study No. 

0847/10864, 

1988 

Eye 

irritation 

Sodium 

benzoate Rabbit Not irritating IV Loeser, E., 1977-B 

Eye 

irritation 

Sodium 

benzoate Rabbit Slightly irritating III 

RCC 

NOTOX 

Study No. 

014669, 1988

Skin 

Sensitizatio

n 

Benzoic 

acid Guinea pig Draize method – not sensitizing 

BRL #9347, 

1979 

Skin 

Sensitizatio

n 

Benzoic 

acid Guinea pig Maximization test – not sensitizing Gad, 1986 

Skin 

Sensitizatio

n 

Benzoic 

acid Human Patch test – occasionally positive 

Rademaker& 

Forsyth, 

1989; 

Forsbek & 

Skog, 1977 
TABLE 4. Acute toxicity studies 

Study Type 

Potassium Benzoate 

(CAS No. 582-25-2)

Chemic

al 

Species/ 

strain Results Tox. Category Reference 

Skin 

Sensitizatio

n 

Sodium 

benzoate Human Patch test 5/2045 patients positive 

Brasch, J., et 

al., 1993 

Skin 

Sensitizatio

n 

Sodium 

benzoate Human Nonimmunologic contact urticaria 

Nethercott, 

J.R. 1984 

The acute toxicity studies of sodium benzoate and benzoic acid suggest the toxicity of potassium 

benzoate would be low. No firm conclusion can be made on the sensitizing potential of potassium benzoate. Sodium benzoate and benzoic acid were non-sensitizing in animal tests but 

showed a very low incidence in humans patch tests. Both sodium benzoate and benzoic acid are 

known to induce non-immunogenic contact reactions, and this maybe the likely explanation for 

the low positive responses shown above. No additional acute toxicity data or study reports were 

available for review other than those described in Table 4 supplied by the applicant or by 

OECD/SIDS 2001. 

B. 28-Day Oral Toxicity

In a 28-day feeding study, groups of ten rats/sex/dose were fed diets containing 0, 760, 3800, or 

7600 ppm benzoic acid (equivalent to 0, 65, 324.1, and 647.5 mg/kg bw/day, respectively)(BioFax, 1973). No clinical signs of toxicity were observed during the study and no grossly 

observable lesions were noted at necropsy. Under the study conditions utilized, it is concluded 

that the NOAEL is 647.5 mg/kg/day, the highest dose tested (HDT). 

C. 21-Day Dermal Toxicity

In a 21-day dermal toxicity study, groups of four male and four female New Zealand white 

rabbits were treated with 0, 100, 500, or 2500 mg benzoic acid/kg bw/day (IRDC #163-675, 

1981). Very slight dermal irritation was noted on one high-dose rabbit. No other treatmentrelated effects were noted on behavior, appearance, body weight, body weight gain, hematology, 

clinical chemistry, organ weights or survival. The NOAEL for the study was the high-dose, 

2500 mg/kg bw/day. A lowest observed adverse effect level (LOAEL) was not identified. 

D. Four-week Inhalation Toxicity

In an inhalation toxicity study, groups of 10 Sprague-Dawley rats/sex/dose were exposed to an 

aerosol dust of benzoic acid at concentrations of 0, 25, 250, or 1200 mg/m3

 six hours/day, five 

days/week, for four weeks (IRDC 163-676, 1981). Average particle size for the study was 4.7 

μm. During the study, one high-dose male and one high-dose female died. The body weight of 

high-dose rats was decreased at the end of the study. The absolute and relative liver weight of 

high-dose males and the absolute and relative lung/trachea weight of high-dose females were 
decreased. No treatment-related effects on body weight in mid-dose rats were found, although 

the absolute and relative kidney weight of female rats was decreased. The upper respiratory tract 

of mid- and high-dose male and female animals showed an increased incidence of interstitial cell 

infiltration and fibrosis, although the incidence was unrelated to dose. No treatment-related 

effects were noted in low-dose rats. Based on decreased kidney weight and upper respiratory 

tract irritation, the LOAEL for the study was 250 mg/m3. The NOAEL was 25 mg/m3. 

E. Sub-chronic Toxicity

In sub-chronic oral toxicity studies of sodium benzoate and benzoic acid on rats and mice, no 

treatment-related effects were found when the test materials were administered at concentrations 

≤1% (Collier et al., 2007). At higher concentrations, treatment decreased food intake, and 

growth. The same authors reported in another study there was a significant decrease in weight 

gain in mice treated with 80 mg benzoic acid/kg bw/day for three months and in rats treated with 

8% sodium benzoate for 90 days. No other details were provided. 

F. Chronic Toxicity

In a 72 week study, 20 male and 30 female Wistar rats were fed a diet containing 1.5% benzoate 

for 72 weeks (equivalent to 1125 mg/kg bw/day, Marquardt 1960). A reduced food intake, 

growth retardation, and increased mortality were noted (15/50 treated vs. 3/25 control). No 

further details were provided. 

In another 72-week study, groups of 10 male and 10 female Wistar rats were fed a diet 

containing 40 mg sodium benzoate/kg bw/day (Shtenberg and Ignat’ev, 1970). Other than an 

increase in mortality of 25%, no other treatment-related effects were reported. No other details 

were provided. 

OECD/SIDS 2001 reported the effects of sodium benzoate in a 90-day study with male and 

female Sherman rats given diets containing 0, 640, 1280, 3145, or 6290 mg/kg bw/day in a study 

reported by Deuel (1954). No treatment-related effects were found at ≤3145 mg/kg bw/day. 

Pathological lesions (not otherwise described) were found in the liver and kidneys of high-dose 

rats. The NOAEL for the study was 3145 mg/kg bw/day. 

G. Carcinogenicity 

Groups of 50 male and 50 female five-week old Swiss Albino mice were provided drinking 

water containing 2% sodium benzoate for life (Toth, 1984). Based on an average daily consumption of 6.2 mL and 5.9 mL for males and females, respectively, the dose of sodium 

benzoate was equivalent to 6200 mg/kg bw/day and 5960 mg/kg bw/day, respectively. These 

mice were compared to a control group of 100 male and 100 female mice that received distilled 

water. Both treated and control mice were monitored daily, body weights were recorded weekly, 

and gross pathological changes recorded. The mice were either allowed to die or were sacrificed 

moribund. Complete necropsies were done and the liver, spleen, kidneys, bladder, thyroid, heart, 

pancreas, testes, ovaries, brain, nasal turbinates, lungs, and other organs with grossly observable 

pathological changes were examined microscopically. Treatment with sodium benzoate had no 
effect on survival or the incidence of tumors. The study author concluded “To date sodium 

benzoate has been generally recognized as safe (GRAS) as a food additive, although its lifelong 

action has not been investigated. The present experiment is apparently the first to fill the gap and 

supply needed proof that the compound is harmless in so far as its long-term tumorigenic effect 

is concerned.” 

H. Neurotoxicity 

No neurotoxicity studies were located. Acute, sub-chronic and chronic toxicity studies do not 

indicate a neurotoxic effect would occur. 

I. Genotoxicity 

Benzoic acid was not mutagenic in Ames tests both with and without metabolic activation 

(EGG# 580-192-1-78, 1978) and was negative without metabolic activation in a Sister Chromatid Exchange assay with human lymphocytes (Jansson, 1988; Tohda, 1980). A chromosomal 

aberration study using CHL cells and without metabolic activation gave ambiguous results 

(Ishidate, et al., 1984). A recombination assay with Bacillus sublilusH17 and M45 was positive 

(reported with minimal documentation in an abstract, Nonaka, 1989). Sodium benzoate was not 

mutagenic in Ames tests, either with or without metabolic activation (Ishidate, et al., 1984) and 

was negative in a cytogenetic assay using anaphase preparations of cultured human embryonic 

lung cells without metabolic activation (FDA PB 245453, 1974). An Escherichia coli reverse 

mutation assay was also negative both with and without metabolic activation (Prival, 1991). 

However a cytogenetic assay using CHL cells was positive without metabolic activation 

(Ishidate, et al, 1984; Ishidate & Odashirna, 1977) and Sister Chromatid Exchange assays using 

Chinese hamster cells or human lymphocytes were positive without metabolic activation (Abe & 

Saski, 1977; Xing & Zhang, 1990). Sodium and potassium benzoate were positive in a recombination assay with Bacillus sublitusHI7 and M45 (reported with minimal documentation Nonaka, 

1989, Ishizaki & Ueno, 1989). The genotoxicity data suggest that sodium and potassium 

benzoate and benzoic acid are negative in Ames point mutation assays but that these chemicals 

may induce adverse effects on chromosomes since the data were equivocal. It should be noted 

that benzaldehyde and benzyl acetate were negative in chromosomal studies. 

J. Reproductive Toxicity

In a four-generation study, groups of 20 rats/sex/dose were fed diets containing 0% 0.5%, or 1% 

benzoic acid (equivalent to 0, 375, or 750 mg/kg bw/day (Kieckebusch & Lang, 1960). No 

treatment-related effects on growth, body weight, body weight gain, food consumption or feed 

efficiency were found. No treatment-related effects were found on reproduction or lactation, and 

no effects were found on organ weight. No treatment-related histopathological effects were 

identified. The NOAEL for the study was the high-dose, 750 mg/kg bw/day. A LOAEL was not 

identified. 
K. Developmental Toxicity 

No developmental toxicity studies were located, although the four-generation reproductive study 

indicates developmental effects are unlikely. 

L Human Studies 

Other than the patch testing studies, no human studies were identified. 

M. Metabolism and Pharmacokinetics

The metabolic scheme for potassium benzoate is shown below (JECFA 1997). In the human 

body under normal physiological conditions, potassium benzoate changes from the ionized form 

to the undissociated benzoic acid. The major elimination pathway involves the rapid conjugation 

of benzoic acid with glycine to form hippuric acid which is then excreted in the urine. Some 

benzoic acid is glucuronidated and also eliminated in the urine. 

In studies of male with male B6C3F1 mice and Fischer 344 rats treated orally with 14C-benzyl 

acetate, the compound was readily absorbed from the gastrointestinal tract of both species, and 

about 90% of the total dose was recovered as urinary metabolites within 24 hours. A small proportion (0.3-1.3%) of the total dose was excreted in the feces. None of the benzyl acetate was 

eliminated via the lungs. Analysis of tissues of animals sacrificed 24 hours after oral administration of labeled compound showed no radioactivity, indicating that elimination was virtually 

complete. The relative amount of benzyl acetate absorbed, metabolized, and excreted was 

unaffected by the size or number of the doses. Repeated treatment of rats with benzyl acetate at 

500 mg/kg bw/day for 14 days followed by a single dose of radiolabeled compound did not 

change the clearance pattern. More than 90% of the radiolabel in the urine was present as 

hippuric acid, with minor amounts as benzyl alcohol and benzylmercapturic acid (up to 4%); no 

unchanged benzyl acetate was found (benzoyl glucuronide was not measured). No evidence of 

saturation or reduction of metabolic capacity in either species was found. 

In one human study, a man given 6, 9, 13.9 34.7 and 69.3 mM sodium benzoate showed 

complete elimination of the compound within 10-14 hours. No accumulation was apparent 

(WHO, 1974) 
Benzoate Metabolism 

N. Toxicity Endpoint Selection and Levels of Concern 

Potassium benzoate is not toxic by the oral, dermal, or inhalation routes. Once absorbed, it is 

readily metabolized and excreted. No toxicity endpoint of concern was identified in the 

available toxicity studies. Lung irritation in the inhalation study was likely due to an irritation 

effect of the high-dose used while decreased kidney weights in the same study, without 

microscopic correlates, were not considered treatment-related. No toxicity was observed in subchronic studies in rats and mice at doses of 1% (equivalent to 1000 mg/kg/day) and or above. No 

adverse effects in rats in a chronic study at 1125 mg/kg/day, no tumors in mice at 5900 

mg/kg/day, and no reproductive effects at 750 mg/kg/day, the highest dose tested. No systemic 

toxicity was observed via dermal route at doses up to 2500 mg/kg/day in rabbits. The 

quantitative risk assessment for the dietary and residential exposure is not necessary since no 

endpoint of concern was identified in the available database. 

VI. Special Considerations for Infants and Children 

In general, Section 408(b)(2)(c) of FFDCA provides that EPA shall apply an additional tenfold 

(10x) margin of safety for infants and children in the case of threshold effects to account for 

prenatal and postnatal toxicity and the completeness of the database on toxicity and exposure 

unless EPA determines based on reliable data that a different margin of safety will be safe for 

infants and children. This additional margin of safety is commonly referred to as the Food 

Quality Protection Act (FQPA) safety factor (SF). In applying this provision, EPA either retains 
the default value of 10x or uses a different additional safety factor when reliable data available to 

EPA support the choice of a different factor. 

No developmental toxicity studies are available in the database. However, no systemic toxicity 

was observed at doses up to 750 mg/kg/day in a four-generation reproductive study. In addition, 

no systemic toxicity was observed in the laboratory animals at high doses (>2000 mg/kg/day) of 

potassium benzoate and benzoates indicating relatively low hazard potential. There was no 

evidence of clinical signs of neurotoxicity, therefore a developmental neurotoxicity study is not 

required. In addition, no evidence of immunotoxicity is available in the database; therefore an 

immunotoxicity study is not required. In terms of hazard, there are low concerns and no residual 

uncertainties regarding prenatal and/or postnatal toxicity. Based on this information, there is no 

concern at this time for increased sensitivity to infants and children to potassium benzoate when 

used as an inert ingredient in pesticide formulations and a safety factor analysis has not been 

used to assess risk. For the same reason, EPA has determined that an additional safety factor is 

not needed to protect the safety of infants and children. 

VII. Endocrine Disruptors 

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Potassium benzoate was not among the group of 58 pesticide active ingredients on the initial list 

to be screened under the EDSP. Under FFDCA sec. 408(p) the Agency must screen all pesticide 

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

pesticide active ingredients. 

For further information on the status of the EDSP, the policies and procedures, the list of 67 

chemicals, the test guidelines and the Tier 1 screening battery, please visit our website: 

http://www.epa.gov/endo/.
VIII. Exposure Assessment 

A. Aggregate Exposure 

In examining aggregate exposure, the Federal Food, Drug, and Cosmetic Act (FFDCA) section 

408 directs EPA to consider available information concerning exposures from pesticide residue 

in food and all other non-occupational exposures, including drinking water from ground water or 

surface water and exposure through pesticide use in gardens, lawns, or buildings (residential and 

other indoor uses). 

The primary route of exposure to potassium benzoate from its use as an inert ingredient in 

pesticide products would most likely be through consumption of food to which pesticide 

products containing it have been applied, and possibly through drinking water (from runoff). 

Residential (dermal and inhalation) exposures from home garden uses are possible. Metabolism 

data indicates that potassium benzoate would be rapidly absorbed, metabolized, and excreted. It 

should also be noted that US FDA has approved potassium benzoate as a food preservative. 

No hazard was identified for the acute and chronic dietary assessment (food and drinking water), 

or for the short, intermediate, and long term residential assessments, and therefore no aggregate 

risk assessments were performed. 

B. Cumulative Exposure 

Cumulative effects from substances with a common mechanism of toxicity. Section 

408(b)(2)(D)(v) of FFDCA requires that, when considering whether to establish, modify, or 

revoke a tolerance, the Agency consider “available information” concerning the cumulative 

effects of a particular pesticide's residues and “other substances that have a common mechanism 

of toxicity.” 

EPA has not found potassium benzoate to share a common mechanism of toxicity with any other 

substances, and does not appear to produce a toxic metabolite produced by other substances. For 

the purposes of this tolerance action, therefore, EPA has assumed that potassium benzoate does 

not 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 EPA's website at 

http://www.epa.gov/pesticides/cumulative. 

IX. Environmental Justice Statement 

Potential areas of environmental justice concerns, to the extent possible, were considered in this 

human health risk assessment, in accordance with U.S. Executive Order 12898, "Federal Actions 

to Address Environmental Justice in Minority Populations and Low-Income Populations," 

http://www.eh.doe.gov/oepa/guidance/justice/eo12898.pdf. 

As a part of every pesticide risk assessment, OPP considers a large variety of consumer 

subgroups according to well-established procedures when applicable. In line with OPP policy, 
ARIA/HED estimates risks to population subgroups from pesticide exposures that are based on 

patterns of that subgroup’s food and water consumption, and activities in and around the home 

that involve pesticide use in a residential setting. Extensive data on food consumption patterns 

are compiled by the USDA under the Continuing Survey of Food Intakes by Individuals (CSFII) 

and are used in pesticide risk assessments for all registered food uses of a pesticide. These data 

are analyzed and categorized by subgroups based on age, season of the year, ethnic group, and 

region of the country. Additionally, OPP is able to assess dietary exposure to smaller, 

specialized subgroups and exposure assessments are performed when conditions or 

circumstances warrant. Whenever appropriate, non-dietary exposures based on home use of 

pesticide products and associated risks for adult applicators and for children (three to less than 

six years old), youths, and adults entering or playing on treated areas post-application are 

evaluated. Further considerations are currently in development as OPP has committed resources 

and expertise to the development of specialized software and models that consider exposure to 

bystanders and farm workers as well as lifestyle and traditional dietary patterns among specific 

subgroups. 

X. Environmental Fate 

There is limited environmental fate data available for potassium benzoate, but the fate and 

occurrence of benzoic acid have been well studied. For this assessment, sodium, potassium, 

calcium and magnesium salts were considered equivalent with respect to their environmental fate 

and ecotoxicity. The physical and chemical properties for these salts varied slightly, but are not 

expected to impact their behavior or toxicity in the environment. The benzoate salts are highly 

water soluble and readily dissociate into the anion (benzoic acid) and cation (sodium, potassium, 

calcium, magnesium and ammonium ion). Therefore, the environmental fate and effects of 

benzoic acid salts are closely related to that of benzoic acid and the free cation. Table 4 provides 

environmental fate and chemical properties for benzoic acid and representative molecules of the 

salts. (US EPA, 2003) 

TABLE 5. Properties and Environmental Fate of Benzoic Acid and Selected Salts(**)

Property Benzoic Acid Sodium Benzoate Benzoic Acid, 

Ammonium Salt 

Water Solubility 

(mg/L @ 25 C) 

3400 (M) 5.56E05 (M) >1.0E06 (E) 

Vapor Pressure 

(mm Hg 25 C) 

7E-04 (M) 3.67E-09 (E) 2.65E-07 (E) 

Henry’s Law 

Coefficient (atmm3/mole) 

3.8E-08 (M) 1.09E-07 (E) 5.2E-16 (E) 

Biodegradation Primary: hours-days 

Ultimate: days-weeks 

Primary: hours-days 

Ultimate: days-weeks 

Primary: hours-days 

Ultimate: days-weeks 

Log Kow 1.87 (M) -2.27 (E) -1.33 (E) 

Koc (mL/g) 14 (E) 14 (E) 99 

Hydrolysis Halflife @ pH 7 (days) No hydrolizable 

functional groups 

No hydrolizable 

functional groups 

52 days 
** Table 5 adopted from US EPA Memorandum: “Benzoic Acid and Benzoate Salts: Health Effects Division Science Assessment Document for 

Tolerance Reassessment.” 

Estimates performed with EPI Suite 4.0 show potassium benzoate would biodegrade quickly. 

Most partitioning, based on Fugacity Level III, would occur with water (27.7%) and soil (72.2%) 

with none into air or sediment. 

XI. Ecotoxicity 

According to EPA’s 2003 document, “Benzoic Acid and Benzoate Salts: Health Effects Division 

Science Assessment Document for Tolerance Reassessment:” 

“Estimated toxicity indicates that benzoic acid is the most toxic of the substances 

reviewed in this assessment. Table 6 lists the estimated toxicity for several species based 

on predictive modeling for acute and chronic endpoints for all compounds. Based on the 

environmental fate profile of benzoic acid and its salts, exposures from label uses are 

unlikely to reach concentrations necessary to elicit effects in aquatic organisms. Using 

laboratory rat data as a surrogate for terrestrial wild mammals and birds, benzoic acid 

and its salts do not appear to be very toxic and adverse effects from labeled uses is not 

expected. “ 

Table 6: Ecotoxicity of Benzoic Acid and Selected Salts 

Property Benzoic Acid Sodium Benzoate Benzoic Acid, 

Ammonium Salt 

Fish (96-h LC50; mg/L) 1200 >1.0E06 1.4E05 

Daphnid (48-h LC50; mg/L) 1274 8.8E05 1.2E05 

Green Algae (96-h EC50; mg/L) 790 4.3E05 61172 

Fish (30-day Chronic, mg/L) 151 71380 10486 

Fish (SE)(96-h LC50, mg/L) 258 32047 6374 

Mysid Shrimp (96h LC50, mg/L) 380 >1.0E06 4.3E05 

Green Algae (96-h Chronic; 

mg/L) 

73 3646 893 

Earthworm (14-day LC50; mg/kg 

dry weight) 

8238 18317 9081 

** Table 6 adopted from US EPA Memorandum: “Benzoic Acid and Benzoate Salts: Health Effects Division Science Assessment Document for 

Tolerance Reassessment.” 

Estimated ecotoxicity data were provided by running the EPI Suite 4.0 model and obtaining 

values for acute fish LC50s, acute daphnid LC50s and acute algae EC50s. Most values for 

potassium benzoate are derived from sodium benzoate since they behave similarly. Overall, 

potassium benzoate is non-toxic to aquatic organisms and the octanol/water partition coefficient 

indicates a low potential for bioaccumulation. Values derived from EPI Suite 4.0 are provided in 

Table 7. 
TABLE 7. Ecotoxicity of Potassium benzoate 

Organism Duration/Endpoint Potassium benzoate MRID

Fish 96 Hours LC50 7.05 E5 mg/L EPI Suite 4.0 

Fish 14-day LC50 6.65 E5 mg/L EPI Suite 4.0 

Daphnid 48 Hours LC50 2.11 E5 mg/L EPI Suite 4.0 

Green Algae 96 Hour EC50 15,716 mg/L EPI Suite 4.0 

Fish 30-day ChV 55,150 mg/L EPI Suite 4.0 

Daphnid ChV 12,462 mg/L EPI Suite 4.0 

Green Algae ChV 2947 mg/L EPI Suite 4.0 

XII. Risk Characterization 

Landis International, on behalf of Whitmire Micro-Gen, submitted two petitions requesting 

exemptions from tolerance for residues of potassium benzoate when used as an inert ingredient 

(preservative) in pesticide formulations applied pre- and post-harvest and applied to animals. A 

Notice of Filing for each petition was published in the Federal Register 

Potassium benzoate is an approved food preservative similar in structure and reactivity to the 

more widely used and classified by US FDA as GRAS, sodium benzoate. Both are salts of 

benzoic acid. Perhaps as a result of potassium benzoate’s similarity to sodium benzoate, few 

toxicological studies on it were found. Because all benzoates, and in particular benzoic acid and 

sodium benzoate, react similarly, they were used as surrogates in the development of this profile. 

Available data suggest that the acute toxicity of potassium benzoate is negligible, having an oral 

LD50 of >10,000 mg/kg bw. Acute dermal and inhalation toxicity is low as indicated by the 

>2000 mg/kg bw LD50 and >12.2 mg/L LC50 of benzoic acid. Sodium benzoate was not irritating to the skin and induced only slight eye irritation in rabbits. Sodium benzoate and benzoic 

acid were non-sensitizing in animal tests but showed a very low incidence of sensitization in 

humans patch tested. Both sodium benzoate and benzoic acid are known to induce nonimmunogenic contact reactions, and that is the likely explanation for the low positive response. 

Sub-acute, sub-chronic and chronic toxicity data also indicate that potassium benzoate should be 

relatively nontoxic. Oral and dermal studies had a NOAEL ≥2000 mg/kg bw and the inhalation 

study had a NOAEL > 25 mg/m3

. Sodium benzoate was not carcinogenic in a lifetime mouse 

feeding study and there is no indication that potassium benzoate should be neurotoxic. 

Genotoxicity studies indicate the benzoates are not mutagenic; however chromosomal aberration 

studies gave ambiguous results. Benzoic acid did not induce reproductive toxicity in a fourgeneration study. In the human body under normal physiological conditions, potassium benzoate 

changes from the ionized form to the undissociated benzoic acid. Benzoic acid and its salts are 

rapidly absorbed by mammals, conjugated with glycine, and rapidly excreted in the urine as 

hippuric acid. There is no reported accumulation of benzoate in the body. However, the ability to 

conjugate benzoic acid depends upon adequate liver function and nutritional supply of glycine.
All data indicates that potassium benzoate is relatively non-toxic as are the other benzoates. No 

toxicity would be expected from potassium benzoate when used at low concentrations in 

pesticides. 

No developmental toxicity studies are available in the database. However, no systemic toxicity 

was observed at doses up to 750 mg/kg/day in a four-generation reproductive study. In addition, 

no systemic toxicity were observed in the laboratory animals at high doses (>2000 mg/kg/day) 

of potassium benzoate and benzoates indicating relatively low hazard potential. In terms of 

hazard, there are low concerns and no residual uncertainties regarding prenatal and/or postnatal 

toxicity. Based on this information, there is no concern at this time for increased sensitivity to 

infants and children to potassium benzoate when used as an inert ingredient in pesticide 

formulations and a safety factor analysis has not been used to assess risk. For the same reason, 

EPA has determined that an additional safety factor is not needed to protect the safety of infants 

and children. 

Residues of concern are not anticipated for dietary exposure (food and drinking water) or for 

residential exposure from the use of potassium benzoate for the proposed use pattern as an inert 

ingredient in pesticide products. EPA expects aggregate exposure to potassium benzoate to pose 

no appreciable dietary risk given that the data on potassium benzoate show a lack of any 

systemic toxicity and a lack of any apparent developmental effects. 

There is limited environmental fate and ecotoxicity data available for potassium benzoate, but 

the fate and occurrence of benzoic acid have been well studied. The available data indicate that 

these compounds are expected to be readily biodegradable in the environment and of low toxicity 

to fish, aquatic organisms, mammals and birds. The Agency believes that benozoic acid and the 

benzoate salts will not cause unreasonable adverse effects on the environment. 

Taking into consideration all available information on potassium benzoate, EPA has determined 

that there is a reasonable certainty that no harm to any population subgroup will result from 

aggregate exposure to potassium benzoate when used as an inert ingredient in pesticide 

formulations applied pre-and post-harvest and applied to animals when considering dietary 

exposure and all other non-occupational sources of pesticide exposure for which there is reliable 

information. Therefore, the establishment of an exemption from tolerance under 40 CFR 

180.910 and 40 CFR 180.930 for residues of potassium benzoate (CAS Reg. No. 582-25-2) when 

used as an inert ingredient in pre- and post-harvest and animal applications in pesticide 

formulations, can be considered assessed as safe under section 408(q) of the FFDCA. 

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