2

Table of Contents

EXECUTIVE SUMMARY ................................................................................................... 3

I. BACKGROUND ................................................................................................................... 6

II. INERT INGREDIENT PROFILE ......................................................................................... 6

A. Summary of Uses....................................................................................................... 6

B. Physical Chemical Properties .................................................................................... 7

III. HUMAN HEALTH ASSESSMENT..................................................................................... 8

A. Summary of Toxicity Data......................................................................................... 8

B. Toxicity Endpoint Selection .................................................................................... 12

C. Special Considerations for Infants and Children ..................................................... 13

IV. EXPOSURE ASSESSMENT .............................................................................................. 13

A. Dietary Exposure: .................................................................................................... 13

i. Acute exposure ..................................................................................................... 16

ii. Chronic exposure................................................................................................. 16

iii. Cancer exposure ................................................................................................. 16

iv. Dietary exposure from drinking water................................................................ 16

B. Residential (Non-Occupational) Exposure: ............................................................. 16

i. From non-dietary exposure................................................................................... 16

V. AGGREGATE RISK ASSESSMENT ................................................................................ 16

i. Acute Dietary Risk................................................................................................ 16

ii. Chronic Dietary Risk. .......................................................................................... 17

iii. Aggregate Cancer Risk for U.S. Population....................................................... 17

iv. Short-term Aggregate Risk. ................................................................................ 17

v. Intermediate-Term Aggregate Risk. .................................................................... 17

VI. OCCUPATIONAL EXPOSURE/RISK PATHWAY.......................................................... 17

VII. CUMULATIVE EXPSOURE ............................................................................................. 17

VIII. ENVIRONMENTAL JUSTICE STATEMENT.................................................................. 18

IX. ENVIRONMENTAL FATE CONSIDERATIONS ............................................................ 18

X. ECOTOXICITY................................................................................................................... 19

XI. RISK CHARACTERIZATION........................................................................................... 19

REFERENCES ................................................................................................................................ 21

APPENDIX...................................................................................................................................... 22
3

EXECUTIVE SUMMARY

Exponent on behalf of Ecolab, Inc. (370 N. Wabasha Street, St. Paul, MN 55102) is 

requesting that EPA expand the current sodium bisulfate tolerance exemption. Sodium bisulfate 

also referred to as sodium acid sulfate (CAS Reg. No. 7681-38-1) has an existing inert ingredient 

tolerance exemption listed in 40 CFR 180.920 for pre-harvest use. Ecolab requested that EPA 

expand the tolerance exemption to include use as an inert ingredient in antimicrobial formulations 

in accordance with 40 CFR 180.940(a), which includes use on food contact surfaces in public 

eating places, dairy processing equipment, and food processing equipment and utensils at no more 

than 2000 ppm in formulation. 

Sodium bisulfate has a long history of use in pesticides as an antimicrobial disinfectant 

active ingredient, in pre-harvest pesticide formulations as an inert ingredient and in food 

applications as a food additive, pH control, and a leavening agent in cake mixes. All of these uses 

involve direct exposure and ingestion by humans. EPA re-registered sodium bisulfate for indoor 

antimicrobial residential use as a toilet bowl cleaner to control household and odor causing 

bacteria, Staphylococcus spp. (EPA, 1993). In 1993, sodium bisulfate was granted a exemption 

from the requirement of a tolerance when used as an acidifying/buffering agent in pesticide 

formulations to growing crops in accordance with 40 CFR 180.1001(d), which was revised in 2004 

to 40 CFR 180.920. 

Sodium bisulfate when used as a general acidifier or general food additive was a subject of

Generally Recognized as Safe (GRAS) notification for which the Food and Drug Administration 

(FDA) found no objections with. The subject meets the FDA definition of a natural product (FDA 

1998). The Joint FAO/WHO Expert Committee on Food Additives (JECFA) (JECFA, 2000, 

2010a) has approved the use of sodium bisulfate as a food additive (an acidifier) in a broad range 

of beverage, confectionary, and general food uses at levels ranging from 500 to 4000 mg/kg. 

JECFA assigned an acceptable daily intake (ADI) of “not specified” because the parent sulfate 

anion is a natural constituent of food and a product of sulfur metabolism. 

Sodium bisulfate readily dissociates to the bilsulfate anion and the sodium cation. 

Bisulfate/sulfate anion is a naturally-occurring constituent in many food substances as well as an 

essential component in a large number of mammalian (human) metabolic processes. The 

bisulfate/sulfate anion is present in all human tissue, with blood plasma sulfate concentrations of 2-

3 mmol/L. Since the bisulfate anion is converted to sulfate in aqueous solution, toxicology studies 

for sodium sulfate are generally considered as relevant for sodium bisulfate. 

The information presented in this document is summarized from the EPA Reregistration 

Eligibility Document, Mineral Acids dated September 1993, Joint FAO/WHO Expert Committee 

on Food Additives (JECFA) 2010, United Nation Envionment Programme (UNEP) SIDS Initial 

Assessment Report on sodium sulfate (2005), Institute of Medicine of the National Academies 

(2005) Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate and Food 

and Drug Administration (FDA) Generally Recognized as Safe (GRAS) Notice 1998 and Letter 

2011.
4

The acute oral toxicity of sodium bisulfate is low (Toxicity category III). The acute oral 

LD50 in male rats was 2800 mg/kg. It was minimally irritating to the rabbit’s skin (Toxicity 

category IV) and mildly irritating to the eyes (Toxicity category III). An acute inhalation study was 

available with sodium sulfate. Inhalation toxicity was not observed at 0.01 mg/l (the only dose 

tested). No dermal toxicity or dermal sanitization studies were available in the database.

Due to the data for sodium bisulfate, both human metabolic processes and toxicity data for 

sodium sulfate were used for the risk characterization. Both sodium bisulfate and sodium sulfate 

readily undergo hydrolysis and dissociate to sodium ions and sulfate ions in the body. Although 

there are no subchronic oral toxicity studies were available in the database for sodium bisulfate, 

studies are available for sodium sulfate. 

No mutagenicity or genotoxicity studies were available in the database.

No carcinogenicity studies were available in the database. National Toxicology Program 

(NTP), International Agency for Research on Cancer (IARC), and Occupational Safety & Health 

Administration (OSHA) have not listed sodium bisulfate as a carcinogen. A DEREK analysis was 

performed on sodium bisulfate and no structural alerts were detected.

In two teratogenicity studies in mice, sodium sulfate was administered via subcutaneous 

injection and gavage at doses of 60 and 2800 mg/kg bw, respectively. Neither maternal nor 

developmental toxicity was observed ≤ 2800 mg/kg bw. This exceeds the limit dose of 1,000 

mg/kg/day.

No immunotoxicity or neurotoxicity studies were available in the database.

Sodium bisulfate metabolism is essentially that of sodium cation and sulfate anion. When 

sodium bisulfate is added to food products containing water or after ingestion of sodium bisulfate 

it ionizes to sodium ions, hydrogen ions and sulfate ions. Following ingestion, sulfate anions are 

predominantly not absorbed from the gastrointestinal tract and are excreted unchanged in urine. 

However, the sulfate anion is normal constituent in the body, predominantly resulting from the 

body’s metabolism of sulfur-containing food sources such as foods containing the essential amino 

acids cysteine and methionine. Sulfate anions are a vital component in a number of human

biosynthetic pathways such as cartilage production and the formation of pancreatic digestive 

enzymes. 

Based on the metabolism of sodium bisulfate to sulfate and sodium ions, both of which are 

essential components in the human metabolic processes, there is a lack of toxicological concern. 

Additionally, there is no indication of toxicity at the limit dose and a toxicological endpoint of 

concern for risk assessment purposes was not identified. Since no endpoint of concern was 

identified for the acute and chronic dietary exposure assessment and short and intermediate dermal 

and inhalation exposure, a quantitative risk assessment for sodium bisulfate is not necessary.

The Agency believes that amending the tolerance exemption to include 40 CFR § 

180.940(a) will not significantly/measurably increase occupational exposure. The change in use 

pattern would be expanded to include food contact surfaces such as tableware, utensils, dairies and 
5

beverage and food processing plants. In view of the regulatory history of sodium bisulfate, i.e., 

approved use under 40 CFR §180.920 and no new toxicological information to indicate otherwise, 

it is not necessary to quantitatively assess occupational exposure.

Based on the ecotoxicity data available on sodium sulfate, sodium bisulfate is not expected 

to be toxic to aquatic and sediment dwelling organisms. Toxicity to terrestrial plants is also 

expected to be low.

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.

Taking into consideration all available information on sodium bisulfate, EPA concludes 

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

aggregate exposure to sodium bisulfate when considering occupation, dietary exposure and all 

other nonoccupational sources of pesticide exposure for which there is reliable information. 

Therefore, the establishment of an exemption from tolerance under 40 CFR 180.940(a) for residues 

of sodium bisulfate (CAS Reg. No. 7681-38-1) when used as a pesticide inert ingredient at no 

more than 2000 ppm in antimicrobial formulations on food-contact surfaces in public eating 

places, dairy processing equipment, food processing equipment and utensils can be considered 

assessed as safe under section 408(q) of the FFDCA.
6

I. BACKGROUND

Exponent on behalf of Ecolab, Inc. (370 N. Wabasha Street, St. Paul, MN 55102) is 

requesting that EPA expand the current sodium bisulfate tolerance exemption. Sodium bisulfate 

also referred to as sodium acid sulfate (CAS Reg. No. 7681-38-1) is already approved for inert 

ingredient tolerance exemption listed in 40 CFR 180.920 for pre-harvest use. Ecolab request that 

EPA expand it to include use as an inert ingredient at no more than 2000 ppm in antimicrobial 

formulations in accordance with 40 CFR 180.940(a), which includes use on food contact surfaces 

in public eating places, dairy processing equipment, and food processing equipment and utensils. 

The information presented in this document is summarized primarily from the EPA 

Reregistration Eligibility Document, Mineral Acids dated September 1993, Joint FAO/WHO 

Expert Committee on Food Additives (JECFA) 2010, United Nation Envionment Programme 

(UNEP) SIDS Initial Assessment Report on sodium sulfate (2005) and Food and Drug 

Administration (FDA) Generally Recognized as Safe (GRAS) Notice 1998 and Letter 2011. 

Sodium bisulfate has a long history of use in pesticides as an antimicrobial disinfectant 

active ingredient, as a pre-harvest pesticide inert formulation ingredient and in food applications as 

a food additive, pH control, and a leavening agent in cake mixes. All of these uses involve direct 

exposure and ingestion by humans. EPA re-registered sodium bisulfate for indoor antimicrobial 

residential use as a toilet bowl cleaner to control household and odor causing bacteria, 

Staphylococcus spp. (EPA, 1993). In 1993, sodium bisulfate was granted a exemption from the 

requirement of a tolerance when used as an acidifying/buffering agent in pesticide formulations to 

growing crops in accordance with 40 CFR 180.1001(d), which was revised in 2004 to 40 CFR 

180.920. 

USDA also cleared the use of sodium bisulfate as a cooling and retort water treatment 

agent to inhibit corrosion on the exteriors of canned goods. Sodium bisulfate is also used in the 

poultry industry and dairies, to acidify animal waste for the reduction of ammonia emission and as 

a browning inhibitor for granny smith apple slices while reducing microbial growth (Fan et al., 

2009). Sodium bisulfate is Generally Recognized as Safe (GRAS) by FDA (1998) and meets the 

FDA definition of a natural product. JECFA (FECFA, 2000, 2010a) has approved the use of 

sodium bisulfate as a food additive (an acidifier) in a broad range of beverage, confectionary, and 

general food uses at levels ranging from 500 to 4000 mg/kg. JECFA assigned an ADI of “not 

specified” because the parent sulfate anion is a natural constituent of food and a product of sulfur 

metabolism. 

II. INERT INGREDIENT PROFILE

A. Summary of Uses

In accordance with 40 CFR 180.920, sodium bisulfate is currently exempt from the 

requirement of a tolerance when used as an acidifying/buffering agent in pesticide 

formulations applied to growing crops. EPA has re-registered sodium bisulfate in solid and 

liquid (solutions), for indoor antimicrobial residential use as a toilet bowl cleaner to control 

household and odor causing bacteria, Staphylococcus spp. EPA (1993) specified the rate of 
7

application as 30,400 ppm up to 49, 248 ppm a.i. by weight. Sodium bisulfate is used as a 

food additive with FDA (1998 approving sodium bisulfate as a Generally Recognized As 

Safe (GRAS) food additive with sulfate salts cited safe in 21 CFR 184.111; 184.1230; 

184.1643; and 186.1797. 

JECFA (2010b) has established an ADI for sodium bisulfate of “not specified”. The term 

ADI “not specified” is established by JECFA to indicate a food component of very low 

toxicity and hazard to human health. JECFA (2010) reported that: “Sodium hydrogen 

sulfate [sodium bisulfate] is typically added to beverages, confectionery, fillings, syrups, 

processed cheeses, salad dressings, sauces, jams and jellies, and processed vegetable 

products at levels ranging from 500 to 4000 mg/kg for beverages. Sodium hydrogen 

sulfate is generally used in non-citrus-flavoured soft drinks, tea, and chocolate-flavoured 

and coffee-flavoured drinks, as it does not impart a sour or citric taste, as do other 

acidifiers.”

B. Physical Chemical Properties

Some of the physical and chemical characteristics of sodium bisulfate, along with its 

structure and nomenclature, are found in Table 1.

Table 1. Physical and Chemical Properties of Sodium Bisulfate

Parameter Value Source

Structure ChemIDplus

CAS # 7681-38-1

Molecular Weight (g/mol) 120.06 Sigma-Aldrich MSDS

Common Names Acid Sulfate, Sodium Pyrosulfate, 

Sodium Hydrogen Sulfate Sigma-Aldrich MSDS

Physical State Powder Sigma-Aldrich MSDS

Melting Point (°C) 315 Chemicalbook

Boiling Point (°C) @ 19 hPa N/A

Density (g/cm3 @ 20°C) 2.1 Chemicalbook

Vapor Pressure (mmHg @ 

25°C) N/A

Partition Coefficient (Log P) N/A

Water Solubility (g/L) 120.06 g/L at 20°C 

(Completely soluble) Sigma-Aldrich MSDS
8

pH 1.0 Sigma-Aldrich MSDS

Henry's Law Constant N/A EPI Suite 4.0 (registrant)

III. HUMAN HEALTH ASSESSMENT

A. Summary of Toxicity Data 

Sodium bisulfate readily dissociates into the sodium cation and the bilsulfate anion. The 

bisulfate/sulfate anion is a naturally-occurring constituent in many food substances and a 

mammalian (human) metabolite therefore the existing toxicology database is limited. Since 

the bisulfate anion is converted to sulfate in solution, toxicology studies for sodium sulfate 

are generally considered as also being relevant to the toxicity of sodium bisulfate. 

Acute Oral Toxicity

In an acute oral toxicity study, five Sprague-Dawley rats/sex/dose (except for 3000 mg/kg 

females: 10 rats), were administered by gavage, a single dose of 1750 (female only), 2000, 

2250, 2500, 3000 and 3500 (male only) mg/kg of body weight of sodium bisulfate. Control 

rats were similarly dosed with deionized water. Surviving animals were killed after 14 

days. Clinical signs (dose not specified) included weight loss, dehydration, scruffy coats, 

lethargy and death. Necropsy showed gross abnormalities observed in the animals that died 

included mottled red lungs and livers mottled with pale areas. Several of these animals 

were also observed to have either lesions on their stomachs or stomachs ruptured with 

contents emptied into the peritoneal cavity. The LD50 (Male) was 2800 (2393-3276) mg/kg.

The study failed to establish a dose response for the females. (CAL DPR, 2002) (WHO 

2010a)

Dermal Toxicity

No studies available in the database.

Inhalation Toxicity

The United Nations Environmental Programme (UNEP) in a 2005 SIDS Document on 

sodium sulfate references an inhalation study with an aerosol showed no adverse effects at 

10 mg/m3or 0.01 mg/L, however the typical limit concentration testing is 2 mg/L. 

Primary Eye Irritation

In a study using sodium sulfate was performed on rabbits with endpoint determination 

based on the DRAIZE scoring system. Sodium sulfate had no adverse effect on the iris and 

cornea. The substance was instilled into the conjunctival sac of the eye. The positive effects 

were primarily based on the conjunctvea (redness) observed in the test. The effects were 

reversible within 7 days. It is considered as mildly irritating to the eyes (Bayer, 1991 

unpublished) (UNEP 1995).

Primary Skin Irritation

A 0.5 g portion of sodium bisulfate (moistened with deionized water) was applied to two 

sites, one intact and one abraded, on the back of each rabbit (sex not specified), applied 
9

under two layer thick cotton gauze patches measuring one inch square. The entire trunks of 

the animals were wrapped in a non-occlusive manner for twenty-four hours. Observations

showed that the intact sites had an erythema score of 1 in 3/6 rabbits at 24 hours with 

clearing by 72 hours. Edema score of 1 was seen in 2/6 rabbits at 24 hours and cleared by 

72 hours. It is minimally irritating to the skin of rabbits.

Dermal Sensitization

No studies available in the database.

The results of the available acute toxicity studies are summarized in Table 2.

Acute Toxicity

Table 2. Acute Toxicity Profile of Sodium Bisulfate

Study Type Results

Toxicity 

Category MRIDs # /Reference

Acute Oral - rat LD50 (male) = 2800 mg/kg 

bw

LD50 (female) = N/A

(sodium bisulfate)

III CAL DPR 2002

WHO 2010a

Acute Dermal - N/A N/A N/A N/A

Acute Inhalation -

N/A

LD50 > 0.01 mg/L 

(sodium sulfate) 

N/A UNEP SIDS Sodium 

Sulfate 2005

Primary Eye 

Irritation - rabbit

Slightly irritating clearing 

within 7 days

(sodium sulfate)

III UNEP SIDS Sodium 

Sulfate 2005

Primary Skin 

Irritation - rabbit

Minimal irritation clearing 

by 72 hours

(sodium bisulfate)

IV CAL DPR 2002

Dermal Sensitization N/A N/A N/A

Subchronic Toxicity -

No subchronic studies were available in the database for sodium bisulfate. However there 

are studies available for sodium sulfate.

According to the OECD SIDS 2005 assessment on sodium sulfate, 5 male Sprague-Dawley 

rats were given 0.84% of sodium sulfate in diet (320-400 mg/kg/day) for 27 and 44 weeks.

There was no mortality, tumors, body weight change or significant changes in food and/or 

water consumption. The NOAEL was ~320-400 mg/kg/day. (Blunck & Crowther 1975) 

(UNEP 2005)

In 30-day oral toxicity study cited in the OECD SIDS 2005 assessment on sodium sulfate, 

24 male Sprague-dawley rats were given in diet 0.0, 0.125, 0.250, 0.5, 1 and 2% sodium 

sulfate (estimated 125, 250, 500, 1000 and 2000 mg/kg/day) for 4 weeks. No changes in 

food and water consumption, body weight gain, food conversion efficiency, urine 

production or diarrhea. Blood hemoglobin, white blood count, serum alkaline phosphatase, 
10

inorganic phosphate and gross organ pathology were also unaffected. The NOAEL was 

2000 mg/kg/day. The LOAEL was not observed in this study (Moinuddinand Wing-Tsit 

Lee) (UNEP 2005)

Chronic Oral Toxicity -

No chronic studies were available in the database for sodium bisulfate.

Mutagenicity and Genotoxicity

No mutagenicity or genotoxicity studies were available in the database for sodium 

bisulfate. However there is one study available for sodium sulfate.

In a study cited in OECD SIDS 2005 on sodium sulfate. Sodium sulfate showed no effect 

in the Ames test using various strains of S. typhimurium (TA1535, TA1537, TA100, TA98) 

both with and without S9 activation in a GLP standardized test. 

Carcinogenicity

No carcinogenicity studies were available in the database. National Toxicology Program 

(NTP), International Agency for Research on Cancer (IARC), and Occupational Safety & 

Health Administration (OSHA) has not listed sodium bisulfate as a carcinogen. Also a 

DEREK analysis was run on sodium bisulfate and no structural alerts for carcinogenicity 

were detected. See the Appendix for the full DEREK report.

Teratogenicity

Sodium sulfate was included in a test of a method for rapid assessment of teratogenicity. 

Pregnant ICR/SIM mice were given a saturated aqueous solution of sodium sulfate orally 

by gavage to deliver a dose of 2800 mg/kg bw per day on days 8-12 of gestation. No 

maternal deaths occurred and the average maternal weight gain during the treatment period 

was not significantly different from that of water-treated controls. Twenty-four litters were 

delivered alive, and none were resorbed. The mean numbers of neonates delivered alive 

and dead in each litter and the survival of neonates on day 3 were not statistically 

significantly different from those of controls. Neonatal body weights on days 1 and 3 and 

body-weight gain were recorded. Only body weight on day 1 was statistically significantly

greater than that of controls. The maternal and developmental NOAEL = 2800 mg/kg bw, 

the only dose tested. The maternal and developmental LOAEL was not established 

(Seidenberg et al., 1986) from WHO (2000).

No reproductive studies were available in the database for sodium bisulfate.

Immunotoxicity

No immunotoxicity studies were available in the database for sodium bisulfate.

Neurotoxicity

No neurotoxicity studies were available in the database sodium bisulfate.

Metabolism and Pharmacokinetics
11

Sodium bisulfate mammalian metabolism is essentially that of the sodium cation and 

sulfate anion. As previously noted, when sodium bisulfate is added to food products 

containing water or after ingestion of sodium bisulfate it ionizes to sodium ions, hydrogen 

ions and sulfate ions. 

Following ingestion, sulfate anions are predominantly not absorbed from the 

gastrointestinal tract and are excreted unchanged in urine. However, the sulfate anion is a 

normal constituent in the body, predominantly resulting from the body’s metabolism of 

sulfur-containing food sources such as foods containing the essential amino acids cysteine 

and methionine. Sulfate anions are vital components in a number of human biosynthetic 

pathways such as cartilage production and the formation of pancreatic digestive enzymes. 

Additionally, the sulfate anion is also an important conjugate in the Phase II conjugation/ 

elimination of oxidized (OH) aromatic ring metabolites and for hydroxyl steroid hormones, 

such as estrogen, where it acts as a transport agent to target organ tissue receptors.

The following paragraph was taken from Institute of Medicine of the National Academies 

“Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate.” (2005) :

“The nutrient is required by the body for synthesis of 3’-phosphoadenosine-5’-

phosphosulfate (PAPS), which in turn is used for synthesis of many important 

sulfur-containing compounds such as chondroitin sulfate and cerebroside sulfate. 

While substantial levels of sulfate are found in foods and various sources of 

drinking water, the major source of inorganic sulfate for humans is from body 

protein turnover of the sulfur amino acids, methionine and cysteine. Dietary 

inorganic sulfate in food and water, together with sulfate derived from methionine 

and cysteine found in dietary protein, as well as the cysteine component of 

glutathione, provide sulfate for use in PAPS biosynthesis. Sulfate requirements are 

thus met when intakes include recommended levels of sulfur amino acids. For this 

reason, neither an Estimated Average Requirement (and thus a Recommended 

Dietary Allowance) nor an Adequate Intake of sulfate is established.”

Table 3. Toxicology Profile for Sodium Bisulfate

Guideline No./ 

Study Type

Doses 

Levels

MRID No. 

(year)/References

Results

27 and 44 week 

oral toxicity –

rats (diet)

0.84% in 

diet (320-

400 

mg/kg/day) 

(sodium 

sulfate)

Blunch and 

Crowther 1975 

(UNEP 2005)

NOAEL ~320-400 mg/kg/day

No mortality, tumors, changes in body 

weight, or food/water consumption.
12

Table 3. Toxicology Profile for Sodium Bisulfate

Guideline No./ 

Study Type

Doses 

Levels

MRID No. 

(year)/References

Results

4 week oral 

toxicity – rats 

(diet)

0.0, 0.01, 

0.125, 

0.250, 0.5, 

1 and 2% 

(estimated 

2000 

mg/kg/day) 

(sodium 

sulfate)

Moinuddinand 

Wing-Tsit Lee 

(UNEP 2005)

NOAEL 2000 mg/kg/day

No changes in food/water consumption, body 

weight gain, food conversion efficiency, urine 

production or diarrhea. Also no changes in 

blood hemoglobin, white blood count, serum 

alkaline phosphatase, inorganic phosphate or 

gross organ pathology. 

Developmental 

Toxicity - rats

2800 

mg/kg 

bw/day

(sodium 

sulfate)

Seidengerb et al. 

1986

Developmental NOAEL = 2800 mg/kg bw. 

Developmental LOAEL was not established.

Ames Test – S. 

typhimurium

312-5000 

μg with 

and 

without 

activation

Bayer AG 1988 

(UNEP 2005)

Negative

B. Toxicity Endpoint Selection

Sodium bisulfate readily dissociates to the bilsulfate anion and the sodium cation. 

Bisulfate/sulfate anion is a naturally-occurring constituent in many food substances as well 

as an essential component in a large number of mammalian (human) metabolic processes. 

The sulfate anion is a normal constituent in the body, predominantly resulting from the 

body’s metabolism of sulfur-containing food sources such as foods containing the essential 

amino acids cysteine and methionine. Sulfate anions are vital components in a number of 

human biosynthetic pathways such as cartilage production and the formation of pancreatic

digestive enzymes. Additionally, the sulfate anion is also an important conjugate in the 

Phase II conjugation/ elimination of oxidized (OH) aromatic ring metabolites and for 

hydroxyl steroid hormones. The available toxicity studies indicate that sodium bisulfate

has a very low overall toxicity. A developmental toxicity study showed neither maternal 

nor developmental effects at 2800 mg/kg/day which is above the limit dose of 1000 

mg/kg/day. Since signs of toxicity were not observed at the limit dose and sodium and 

bisulfate ions are present ubiquitously in the human body, an endpoint of concern for risk 

assessment purposes was not identified. Therefore, since no endpoint of concern was 

identified for the acute and chronic dietary exposure assessment and short and intermediate 

dermal and inhalation exposure, a quantitative risk assessment for sodium bisulfate is not 

necessary.
13

C. Special Considerations for Infants and Children

FFDCA, as amended by FQPA, directs the Agency to use an additional 10X safety factor 

(SF), to account for potential pre- and postnatal toxicity and completeness of the data with 

respect to exposure and toxicity to infants and children. FQPA authorizes the Agency to 

modify the 10X FQPA SF only if reliable data demonstrate that the resulting level of 

exposure would be safe for infants and children.There was no hazard identified in a repeat 

dose rat developmental toxicity study at or above the limit dose of 1,000 mg/kg/day to 

either parental animals or their offspring. There is no concern for neurotoxicity, 

immunotoxicity or carcinogenicity for sodium bisulfate. There is no evidence to suggest 

susceptibility in infants and children. Since sodium and sulfate ions are found naturally in 

the human body as an essential component of human biosynthetic processes, endpoints to 

quantitatively assess dietary risk were not selected. EPA has low concentrations and no 

residual uncertainties with regard to pre- or postnatal toxicity from sodium bisulfate 

exposures. Since a qualitative assessment was conducted for potential human health 

exposure to copper, the 10X FQPA SF was not retained.

IV. EXPOSURE ASSESSMENT

A. Dietary Exposure:

In evaluating dietary exposure to the sodium bisulfate, EPA considered exposure under the 

petitioned for exemptions from the requirement of a tolerance. EPA assessed dietary exposures 

from sodium bisulfate in food as follows:

In conducting the dietary exposure assessment using the Dietary Exposure Evaluation 

Model DEEM-FCIDTM, Version 3.16, EPA used food consumption information from the 

U.S. Department of Agriculture’s National Health and Nutrition Examination Survey, What 

We Eat In America, (NHANES/WWEIA). This dietary survey was conducted from 2003 to 

2008. As to residue levels in food, no residue data were submitted for sodium bisulfate. In 

the absence of specific residue data, EPA has developed an approach which uses surrogate 

information to derive upper bound exposure estimates for the subject inert ingredient. 

Upper bound exposure estimates are based on the highest tolerance for a given commodity 

from a list of high-use insecticides, herbicides, and fungicides. A complete description of 

the general approach taken to assess inert ingredient risks in the absence of residue data is 

contained in the memorandum entitled “Alkyl Amines Polyalkoxylates (Cluster 4): Acute 

and Chronic Aggregate (Food and Drinking Water) Dietary Exposure and Risk 

Assessments for the Inerts.” (D361707, S. Piper, 2/25/09) and can be found at 

http://www.regulations.gov in docket ID number EPA-HQ-OPP-2008-0738.

In the dietary exposure assessment, the Agency assumed that the residue level of the inert 

ingredient would be no higher than the highest tolerance for a given commodity. Implicit 

in this assumption is that there would be similar rates of degradation (if any) between the 

active and inert ingredient and that the concentration of inert ingredient in the scenarios 
14

leading to these highest of tolerances would be no higher than the concentration of the 

active ingredient.

The Agency believes the assumptions used to estimate dietary exposures lead to an 

extremely conservative assessment of dietary risk due to a series of compounded 

conservatisms. First, assuming that the level of residue for an inert ingredient is equal to 

the level of residue for the active ingredient will overstate exposure. The concentration of 

active ingredients in agricultural products is generally at least 50 percent of the product and 

often can be much higher. Further, pesticide products rarely have a single inert ingredient; 

rather there is generally a combination of different inert ingredients used which 

additionally reduces the concentration of any single inert ingredient in the pesticide product 

in relation to that of the active ingredient.

Second, the conservatism of this methodology is compounded by EPA’s decision to assume 

that, for each commodity, the active ingredient which will serve as a guide to the potential 

level of inert ingredient residues is the active ingredient with the highest tolerance level. 

This assumption overstates residue values because it would be highly unlikely, given the 

high number of inert ingredients, that a single inert ingredient or class of ingredients would 

be present at the level of the active ingredient in the highest tolerance for every commodity. 

Finally, a third compounding conservatism is EPA’s assumption that all foods contain the 

inert ingredient at the highest tolerance level. In other words, EPA assumed 100 percent of 

all foods are treated with the inert ingredient at the rate and manner necessary to produce 

the highest residue legally possible for an active ingredient. In summary, EPA chose a very 

conservative method for estimating what level of inert residue could be on food, and then 

use this methodology to choose the highest possible residue that could be found on food 

and assumed that all food contained this residue. No consideration was given to potential 

degradation between harvest and consumption even though monitoring data shows that 

tolerance level residues are typically one to two orders of magnitude higher than actual 

residues in food when distributed in commerce. 

Accordingly, although sufficient information to quantify actual residue levels in food is not 

available, the compounding of these conservative assumptions will lead to a significant 

exaggeration of actual exposures. EPA does not believe that this approach underestimates 

exposure in the absence of residue data.

The dietary assessment for food contact sanitizer solutions calculated the Daily Dietary Dose 

(DDD) and the Estimated Daily Intake (EDI). The assessment considered: application rates, 

residual solution or quantity of solution remaining on the treated surface without rinsing with 

potable water, surface area of the treated surface which comes into contact with food, pesticide 

migration fraction, and body weight. These assumptions are based on FDA guidelines (FDA, 

2003). 

FDA Food Contact Surface Sanitizing Solution Dietary Exposure Assessment Model

EDI (mg/p/day) = AR x RS x SA x F x 10-6(1)

DDD (mg/kg/day) = AR x RS x SA x F x 10-6/BW (2)
15

Where: 

AR = Application rate (ppm)

RS = Residual solution (mg/cm2)

SA = Surface area of the treated surface which comes into contact with 

food (cm2)

F = Fraction of the pesticide transferred or migrated to food (unitless)

BW = Body weight (kg)

The input parameters listed in Table 4 below and equations 1 and 2 above are used to 

calculate EDI, DDD and %PAD for the three population subgroups (adult males, adult 

females, and infants/children).

Table 4: Input Parameters for Food Contact Surface Sanitizing Solution Dietary Exposure 

Assessment 

Parameter

Value

Rationale

Residual Solution on 

Surface 1 mg/cm2 FDA assumption

Area of Treated 

Surface 4,000 cm2 FDA assumption for food utensils/surfaces

concentration in 

diluted solution 500 ppm 

Diluted Solution concentration, 

based on maximum 

concentration (expressed in 

ppm).

Fraction Transferred 100% FDA assumption

Body Weight (kg) 

Adult man =

Adult woman =

Child =

70

60

 15

EPA, 1997

EDI (mg/p/day) = AR x RS x SA x F x 10-6

500 ppm * 1 mg/cm2* 4000 cm2* 100% * 10-6 = 20 mg/p/day

DDD (mg/kg/day) = AR x RS x SA x F x 10-6/BW therefore,

for adult males 20 mg/p/day/70 kg bw/p = 0.28 mg/kg/day

for adult female 20 mg/p/day/60 kg bw/p = 0.33 mg/kg/day

for 3 year old child 20 mg/p/day/15 kg bw/p = 1.33 mg/kg/day

In estimating total dietary (food and drinking water) exposures, the exposures estimated using the 

FDA model for components of food contact sanitizing solutions and the estimated dietary 
16

exposures (food and drinking water) resulting from the use of the inert ingredient in pesticide 

formulations are combined. The exposure estimates for the inert ingredient in pesticide 

formulations were derived using the Agency’s DEEM-FCID model for chronic dietary exposures. 

 i. Acute exposure. No adverse effects attributable to a single exposure of sodium bisulfate

were seen in the toxicity databases. Therefore, acute dietary exposure assessment for 

sodium bisulfate is not required.

 ii. Chronic exposure. No adverse effects attributable to chronic exposure of sodium

bisulfate were seen in the toxicity database and sodium bisulfate is a normal body 

constituent. Therefore, a chronic dietary exposure assessment for sodium bisulfate is not 

required.

iii. Cancer exposure.

The National Toxicology Program (NTP), International Agency for Research on Cancer 

(IARC), and Occupational Safety & Health Administration (OSHA) have not listed sodium 

bisulfate as a carcinogen. Sodium bisulfate is not mutagenic in the Ames test. A DEREK 

analysis was run on sodium bisulfate and no structural alerts for carcinogenicity were 

detected. Therefore, based on the lack of concern for carcinogenicity of sodium bisulfate a 

cancer dietary exposure assessment is not necessary to assess cancer risk.

iv. Dietary exposure from drinking water. No adverse effects attributable to acute or 

chronic exposure of sodium bisulfate were seen in the toxicity database and sodium 

bisulfate is a normal body constituent. Therefore, a dietary exposure assessment from 

drinking water for sodium bisulfate is not required.

B. Residential (Non-Occupational) Exposure:

i. From non-dietary exposure. The term ‘‘residential exposure’’ is used in this document 

to refer to non-occupational, non-dietary exposure (e.g., for lawn and garden pest control, 

indoor pest control, termiticides, and flea and tick control on pets). In the case of sodium 

bisulfate, the request is for use as an inert ingredient in antimicrobial formulations for use 

on food contact surfaces. Sodium bisulfate may also be used in products that are registered 

for specific uses that may result in residential exposure. However, based on the lack of 

toxicity, an exposure assessment from “residential exposures” was not performed.

V. AGGREGATE RISK ASSESSMENT

i. Acute Dietary Risk. 

An acute aggregate risk assessment takes into account exposure estimates from acute 

dietary consumption of food and drinking water using the exposure assumptions discussed 

in section IV for acute exposure. However there was no hazard attributable to a single 

exposure seen in the toxicity database for sodium bisulfate; therefore there is no concern 
17

for an acute dietary risk and an acute aggregate risk assessment was not conducted for 

sodium bisulfate.

ii. Chronic Dietary Risk. 

A chronic aggregate risk assessment takes into account exposure estimates from chronic 

dietary consumption of food and drinking water using the exposure assumptions discussed 

in section IV from chronic exposure. However because no toxicological endpoint of 

concern was identified for chronic dietary exposure, there is no concern for a chronic 

dietary risk and a chronic aggregate risk assessment was not conducted for sodium 

bisulfate. 

iii. Aggregate Cancer Risk for U.S. Population. 

The Agency has not identified any concerns for carcinogenicity relating to sodium 

bisulfate; therefore, an aggregate cancer risk assessment was not conducted for sodium 

bisulfate.

iv. Short-term Aggregate Risk. 

Short-term aggregate exposure takes into account short-term residential exposure plus 

chronic exposure to food and water (considered to be a background exposure level). 

Sodium bisulfate could be as an inert ingredient in pesticide products that could result in 

short-term residential exposure. However, since there are no toxicological endpoints of 

concern for residential exposure or food and water, EPA has concluded that the combined

short-term aggregate risk assessment is not required.

v. Intermediate-Term Aggregate Risk. 

Intermediate-term aggregate exposure takes into account intermediate-term residential 

exposure plus chronic exposure to food and water (considered to be a background exposure 

level). Sodium bisulfate is not expected to be used as an inert ingredient in pesticide 

products that could result in intermediate-term residential exposure. Since there are also no 

toxicological endpoints of concern for residential exposure or food and water, EPA has 

concluded that the combined intermediate-term aggregate risk assessment is not required.

VI. OCCUPATIONAL EXPOSURE/RISK PATHWAY

The Agency believes that amending the tolerance exemption to include 40 CFR § 180.940(a) 

will not significantly/measurably increase occupational exposure. The change in use pattern would 

be expanded to include food contact surfaces such as tableware, utensils, dairies and beverage and 

food processing plants. In view of the regulatory history of sodium bisulfate, i.e., approved use 

under 40 CFR §180.920 and no new toxicological information to indicate otherwise, it is not 

necessary to quantitatively assess occupational exposure. 

VII. CUMULATIVE EXPSOURE 
18

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 sodium bisulfate to share a common mechanism of toxicity with any 

other substances, and that sodium bisulfate does not appear to produce a toxic metabolite produced 

by other substances. For the purposes of this tolerance action, therefore, EPA has assumed that 

sodium bisulfate 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.

VIII. 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. In line with OPP policy, RD 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 

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 toddlers, 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

IX. ENVIRONMENTAL FATE CONSIDERATIONS

The environmental fate and risk information available for sodium sulfate reported by 

UNEP (2005) states:

“In water sodium sulfate completely dissociates into sodium and sulfate ions. The ions 

cannot hydrolyze. In anaerobic environments sulfate is biologically reduced to (hydrogen) 
19

sulphide by sulfate reducing bacteria, or incorporated into living organisms as a source of 

sulphur, and thereby included in the sulphur cycle. Sodium sulfate is not reactive in 

aqueous solution at room temperature. Sodium sulfate will completely dissolve, ionize and 

distribute across the entire planetary “aquasphere”. Some sulfates may eventually be 

deposited, the majority of sulfates participate in the sulphur cycle in which natural and 

industrial sodium sulfates are not distinguishable.”

X. ECOTOXICITY

The environmental fate and risk information available for sodium sulfate reported by 

UNEP (2005) states:

“The BCF of sodium sulfate is very low and therefore significant bioconcentration is not 

expected. Sodium and sulfate ions are essential to all living organisms and their 

intracellular and extracellular concentrations are actively regulated. However, some plants 

(e.g. corn and Kochia Scoparia), are capable of accumulating sulfate to concentrations that 

are potentially toxic to ruminants. Algae were shown to be the most sensitive to sodium 

sulfate with an EC50 120h – 1,900 g/l. For invertebrates, (Daphnia magna), the EC50 48h = 

4,580 mg/l and fish appeared to be the least sensitive with a LC50 96h – 7,960 mg/l for 

Pimephales promelas. Activated sludge showed a very low sensitivity to sodium sulfate. 

There was no effect up to 8 g/l. Sodium sulfate is not very toxic to terrestrial plants. Picea 

banksiana was the most sensitive species, an effect was seen at 1.4 g/l. Sediment dwelling 

organisms were not very sensitive either, with an LC50 96h = 600 mg/l for Trycorythus sp. 

Overall, it can be concluded that sodium sulfate has no acute adverse effect on aquatic and 

sediment dwelling organisms. Toxicity to terrestrial plants is also low.”

XI. RISK CHARACTERIZATION 

Sodium bisulfate metabolism is essentially that of sodium cation and sulfate anion. When 

sodium bisulfate is added to food products containing water or after ingestion of sodium bisulfate 

it ionizes to sodium ions, hydrogen ions and sulfate ions. Following ingestion, sulfate anions are 

predominantly not absorbed from the gastrointestinal tract and are excreted unchanged in urine. 

However, the sulfate anion is normal constituent in the body, predominantly resulting from the 

body’s metabolism of sulfur containing food sources such as foods containing the essential amino 

acids cysteine and methionine. Sulfate anions are a vital component in a number of human 

biosynthetic pathways such as cartilage production and the formation of pancreatic digestive 

enzymes. 

Since there is no indication of toxicity at the limit dose a toxicological endpoint of concern 

for risk assessment purposes was not identified. Since no endpoint of concern was identified for 

the acute and chronic dietary exposure assessment and short and intermediate dermal and 

inhalation exposure, a quantitative risk assessment for sodium bisulfate is not necessary.
20

The Agency believes that amending the tolerance exemption to include 40 CFR § 

180.940(a) will not significantly/measurably increase occupational exposure. The change in use 

pattern would be expanded to include food contact surfaces such as tableware, utensils, dairies and 

beverage and food processing plants. In view of the regulatory history of sodium bisulfate, i.e., 

approved use under 40 CFR §180.920 and no new toxicological information to indicate otherwise, 

it is not necessary to quantitatively assess occupational exposure.

Taking into consideration all available information on sodium bisulfate, EPA concludes 

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

aggregate exposure to sodium bisulfate when considering occupation, dietary exposure and all 

other nonoccupational sources of pesticide exposure for which there is reliable information. 

Therefore, the establishment of an exemption from tolerance under 40 CFR 180.940(a) for residues 

of sodium bisulfate (CAS Reg. No. 7681-38-1) when used as a pesticide inert ingredient at no 

more than 2000 ppm in antimicrobial formulations on food-contact surfaces in public eating 

places, dairy processing equipment, food processing equipment and utensils can be considered 

assessed as safe under section 408(q) of the FFDCA.
21

REFERENCES

Alan M. Rulis, FDA Director Office of Premarket Approval, Letter to Ms. Betty J. Pendleton 

Jones-Hamilton Co., dated June 5, 1998, GRAS Notice No. GRN 000003, Docket No. 98S-0104

California Environmental protection Agency Department of Pesticide Regulation Medical 

Toxicology Branch Summary of Toxicology Data Sodium Bisulfate, 2002. Chemical Code # 905, 

Tolerance #50263.

Fan X, Sokorai KJ, L iao CH, Cooke P, Zhang HQ., 2009 . Antibrowning and antimicrobial 

properties of sodium acid sulfate in apple slices. J Food Sci.; 74: 485-92.

FDA. 2003. “Sanitizing Solutions: Chemistry Guidelines for Food Additive Petitions.” 

http://www.cfsan.fda.gov/~dms/opa-cg3a.html. Last accessed June 9, 2003.

Institute of Medicine of the National Academies, Dietary Reference Intakes for Water, Potassium, 

Sodium, Chloride, and Sulfate. The National Academies Press (2005)

Stephen Mixon, Director of Operations, Advanced Food Technologies, LLC., Letter to Antonia 

Mattia Office of Food Additive Safety, FDA dated October 12, 2011, “GRAS Notification for 

sulfuric acid and sodium sulfate blend used as an antimicrobial in meat and poultry processing.”

UNEP 1995 SIDS Sodium Sulfate

US EPA Registration Eligibility Document, 1993. Mineral Acids Case 6064.

World Health Organization (WHO) Food Additives Series: 44 Safety Evaluation of Certain Food 

Additives And Contaminants, 2000.

World Health Organization (WHO) Food Additives Series: 62 Safety Evaluation of Certain Food 

Additives And Contaminants, 2010a. Pages 237-247.

WHO Technical Report Series 956 71st Report of the Joint FAO/WHO Expert Committee on Food 

Additives, 2010b Page 43-46.
22

APPENDIX

Derek Nexus Report

Author

HED

Report date

18 September 2013 13:27:47

Prediction date

18 September 2013 13:27:11

Program version

Derek Nexus: 3.0.1, Nexus: 1.5.0

Compound name

Structure-2

Species

bacterium, mammal

Endpoints

alpha-2-mu-Globulin nephropathy, Anaphylaxis, Bladder urothelial hyperplasia, Carcinogenicity, 

Cardiotoxicity, Cerebral oedema, Chloracne, Cholinesterase inhibition, Chromosome damage in vitro, 

Chromosome damage in vivo, Cumulative effect on white cell count and immunology, Cyanide-type 

effects, Developmental toxicity, Genotoxicity in vitro, Genotoxicity in vivo, Hepatotoxicity, HERG 

channel inhibition in vitro, High acute toxicity, Irritation (of the eye), Irritation (of the gastrointestinal 

tract), Irritation (of the respiratory tract), Irritation (of the skin), Lachrymation, Methaemoglobinaemia

Mutagenicity in vitro, Mutagenicity in vivo, Nephrotoxicity, Neurotoxicity, Occupational asthma, Ocu

toxicity, Oestrogenicity, Peroxisome proliferation, Phospholipidosis, Photo-induced chromosome dam

in vitro, Photoallergenicity, Photocarcinogenicity, Photogenotoxicity in vitro, Photogenotoxicity in viv

Photomutagenicity in vitro, Phototoxicity, Pulmonary toxicity, Rapid prototypes: adrenal gland toxicit

Rapid prototypes: bladder disorders, Rapid prototypes: blood in urine, Rapid prototypes: bone marrow 

toxicity, Rapid prototypes: bradycardia, Rapid prototypes: cardiotoxicity, Rapid prototypes: chromoso

damage in vitro, Rapid prototypes: hepatotoxicity, Rapid prototypes: kidney disorders, Rapid prototyp

mitochondrial dysfunction, Rapid prototypes: nephrotoxicity, Rapid prototypes: splenotoxicity, Rapid 

prototypes: testicular toxicity, Rapid prototypes: thyroid toxicity, Respiratory sensitisation, Skin 

sensitisation, Teratogenicity, Testicular toxicity, Thyroid toxicity, Uncoupler of oxidative phosphoryla

Superendpoints

Carcinogenicity (SUPER), Chromosome damage (SUPER), Genotoxicity (SUPER), Hepatotoxicity 

(SUPER), HERG channel inhibition (SUPER), Irritation (SUPER), Miscellaneous endpoints (SUPER

Mutagenicity (SUPER), Ocular toxicity (SUPER), Rapid prototypes: adrenal gland toxicity (SUPER), 

Rapid prototypes: bladder disorders (SUPER), Rapid prototypes: blood in urine (SUPER), Rapid 

prototypes: bone marrow toxicity (SUPER), Rapid prototypes: bradycardia (SUPER), Rapid prototype

cardiotoxicity (SUPER), Rapid prototypes: chromosome damage in vitro (SUPER), Rapid prototypes: 

hepatotoxicity (SUPER), Rapid prototypes: kidney disorders (SUPER), Rapid prototypes: mitochondr

dysfunction (SUPER), Rapid prototypes: nephrotoxicity (SUPER), Rapid prototypes: splenotoxicity 

(SUPER), Rapid prototypes: testicular toxicity (SUPER), Rapid prototypes: thyroid toxicity (SUPER)
23

Reproductive toxicity (SUPER), Respiratory sensitisation (SUPER), Skin sensitisation (SUPER), Thy

toxicity (SUPER)

Constraints

Perceive tautomers true

Perceive mixtures true

Perceive alerts without rules false

Average molecular mass

120.06 (Lhasa Limited, version 1.0)

Exact molecular mass

119.9493 (Lhasa Limited, version 1.0)

Log Kp

-4.99 (Potts & Guy, version 1.0 (LogP: BioByte Corp., version 5.3; Average Molecular Mass: Lhasa 

Limited, version 1.0))

Log P

-2.17 (BioByte Corp., version 5.3)

Submitted compound

Predictions

Derek KB 2012 1.0

KnowledgeBase name

Derek KB 2012 1.0

KnowledgeBase version

1.0

KnowledgeBase last modified

29 November 2012 11:56:30

KnowledgeBase location

C:/Program Files/Lhasa Limited/Lhasa Knowledge Suite - Nexus 

1.5/KnowledgeBases/org.lhasalimited.pluto.knowledge.derek_1.0.7
24

KnowledgeBase certified by

Lhasa Limited, Leeds, Yorkshire, UK

Nothing to report

Reasoning glossary:

Certain