Page 2 of 14

principally on the Agency’s 2006 analysis. No new data have been received by the Agency which

might alter the conclusions presented in the 2006 Re-Registration Eligibility Document. 

Propylene glycol has an extensive database of acute, subchronic, chronic, developmental, and 

reproductive toxicity, carcinogenicity, mutagenicity, metabolism/pharmacokinetics and dermal

toxicity studies.

EPA (2006) concluded that there are no toxicity endpoints of concern for oral, dermal, or 

inhalation exposure to propylene glycol. This conclusion is based on the results of toxicity testing 

of propylene glycol at dose levels near or above testing limits (as established in the OPPTS 870 

series harmonized test guidelines).

The acute oral and dermal toxicity of propylene glycol is low (toxicity category IV). The LD50

was >8000 mg/kg in the rat, mouse, rabbit and guinea pig (oral). Propylene glycol is non-irritating 

to the eyes and skin in rabbits. It is not a dermal sensitizer. 

In a 15-week and 2 year oral toxicity studies, rats were fed a diet containing up to 50,000 ppm 

(approximately 2,500 mg/kg bw/day) propylene glycol. Treatment related effects were not 

observed in either study. Also, systemic toxicity was not observed in dogs treated with up to 5000 

mg/kg bw/day propylene glycol for 2 years. An increased incidence of tumor formation was not 

observed in either 2 year carcinogenicity study in rats or dogs.

Propylene glycol was evaluated in an In Vivo teratology screening study and continuous breeding 

study in mice. Propylene glycol was administered by oral gavage and drinking water at a dose rate 

up to 10,100 mg/kg bw/day. Neither maternal, developmental nor reproduction effects were seen 

at doses as high as 10,100 mg/kg bw/day, a dose that is 10 times higher than the limit dose of 

1,000 mg/kg bw/day.

In a 12 week, repeat dose, dermal toxicity study on female Swiss mice were tested at 100 %, 50 % 

and 10 % (approximately 100,000; 50,000 and 10,000 mg/kg/day) concentration propylene glycol. 

Neither systemic toxicity nor a statistically significant increase in skin tumor incidence was 

observed. 

Propylene glycol was not mutagenic or genotoxic on the basis of a battery of studies that 

included the bacterial gene mutation assay using Salmonella typhimurium (AMES) in vitro 

assay, in vitro Chinese hamster ovary (CHO) mutation assay, Chinese hamster ovary (CHO) 

chromosomal aberration assays, and an in vitro sister chromatid exchange assay. 

EPA concluded that propylene glycol was negative for carcinogenicity in studies conducted up to 

the testing limit doses established by the Agency; therefore no further carcinogenic analysis was 

required.

Neurotoxicity and Immunotoxicity studies were not available in the database. However, no 

evidence of neurotoxicity or immunotoxicity was present in the submitted studies.

Propylene glycol should be readily metabolized to lactic acid at the typical low-level exposures 

associated with the already approved pesticide inert ingredient registrations under 40 CFR 

§180.910 and 40 CFR §180.930 uses, and the intended 40 CFR §180.940(a) use in antimicrobial 
Page 3 of 14

formulations. At higher concentrations (absorbed doses), propylene glycol is primarily excreted 

unchanged in the urine.

EPA concluded that the FQPA Safety Factor should be removed (i.e., reduced to 1X) for propylene 

glycol, because there is no pre- or post-natal evidence for increased susceptibility following 

exposure.

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

risk assessment purposes, was not identified. Therefore, a quantitative dietary exposure risk 

assessment for propylene glycol is not necessary.

An aggregate assessment was not conducted for exposures through food, drinking water and 

residential exposure since toxicological endpoints for risk assessment were not identified based on 

the available data. In reaching this determination, EPA considered the available information on 

the special sensitivity of infants and children, as well as aggregate exposure. The inclusion of the 

uses supported by expanding the current 40 CFR §180.910 and §180.930 tolerance exemptions to 

include uses cited at 40 CFR §180.940(a) should not change this determination.

The Agency believes that amending the existing 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 propylene glycol, i.e., 

approved use under 40 CFR § 180.910 and § 180.930 and no new toxicological information to 

indicate otherwise, it is not necessary to quantitatively assess occupational exposure.

UNEP (2001) has summarized propylene glycol’s environmental fate characteristics and its 

toxicity to aquatic organisms:

• Propylene glycol is not volatile and it is miscible with water. 

• The concentrations of propylene glycol in the atmosphere are expected to be extremely low 

because of its low vapor pressure and high water solubility. 

• Propylene glycol is readily biodegraded in water or soil. Four studies reported >60% 

biodegradation in water in 10 days. 

• Propylene glycol is not expected to bioaccumulate. The calculated Bio-Concentration Factor 

(BCF) is <1. 

• Propylene glycol is not acutely toxic to aquatic organisms except at very high concentrations 

that would exceed the intended use as a pesticide inert ingredient according to the current 40 

measured freshwater aquatic toxicity data of propylene glycol to fish, daphnia, and algae, have 

LC/EC50’s that exceed values of >18,000 mg/l (18,000 ppm). Additionally, using an 

assessment factor of 100 and the Ceriodaphnia data (48-hour EC50 = 18,340 mg/l), the 

Predicted No Effect Concentration (PNEC) is 183 mg/l.

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

human health risk assessment, in accordance with U.W. 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.
Page 4 of 14

Based on the information summarized above the Agency approves of the use of Propylene Glycol 

without limitation as an inert ingredient in antimicrobial pesticide formulations applied to “food 

contact surfaces in public eating places, dairy processing equipment, and food processing 

equipment and utensils” as described in 40 CFR § 180.940(a).

II. BACKGROUND

This is the Decision Document for the proposed use of Propylene Glycol (CASRN 57-55-6; PC 

Code 868603) as an inert ingredient in antimicrobial pesticide products applied to food contact 

surfaces and food processing equipment. Specifically, Ecolab, Inc. (370 N. Wabasha Street, St. 

Paul, MN 55102) is requesting the Environmental Protection Agency approve of the use of 

Propylene Glycol under 40 CFR § 180.940(a) as an inert ingredient in antimicrobial pesticide 

products which may be applied to “food contact surfaces in public eating places, dairy processing 

equipment, and food processing equipment and utensils.”

Currently, Propylene Glycol is exempt from the requirements of a tolerance under 40 CFR 

§180.910 (pre- and post-harvest crop uses) and 40 CFR § 180.930 (direct application to animals). 

It is approved by the Food and Drug Administration under 21 CFR § 184 for Direct Food 

Substances Affirmed as Generally Recognized as Safe (GRAS).

In September, 2006, the EPA published the “Reregistration Eligibility Decision for Propylene 

Glycol and Dipropylene Glycol” (EPA Publication EPA-739-R-06-002; U.S. EPA Office of 

Prevention, Pesticides and Toxic Substances). The toxicological database for propylene glycol is 

extensive and is complete. 

Much of the discussion of propylene glycol is taken from the Agency’s 2006 publication and 

portions are taken from the Registrant’s petition.

III. PHYSICAL/CHEMICAL PROPERTIES

Propylene glycol belongs to a class of organic compounds called diols, which includes compounds 

with two hydroxy groups as part of their chemical functionality. Propylene glycol is a colorless, 

nearly odorless, clear, viscous, hydroscopic liquid with a faintly sweet taste. The compound 

referred to herein as propylene glycol is specifically the α-propylene glycol (1,2 diol) isomer in 

which the two hydroxy (diol) moieties are adjacent, or 1,2. The less common congeneric 1,3-diol 

isomer, called β-propylene glycol, is a different compound. 

Chemical Structure of Propylene Glycol

 CH3

 

HO—CH—CH2—OH
Page 5 of 14

Based on information provided in the US EPA RED (2006), the UNEP SIDs (2001), and 

EPISuiteTM 4.0 modeling, the following summary of the physicochemical data for propylene 

glycol are relevant to consider in the assessment of environmental and mammalian safety. 

Non-volatile viscous liquid; estimated vapor pressure 0.11mm Hg at 25°C; Boiling Point, 

155.2o C at 760 mm Hg; Specific Gravity, 1.040 mg/ml at 20o C

Polar/non-lipophilic unlikely to bioaccumulate: log Kow -0.78

Solubility: Miscible in water; solubility estimated at 8.11 e+005 (mg/L) at 25o C; soluble 

in acetone and chloroform.

Log Koc (Kow method) of -0.407 indicates a low potential to bind to soil.

EPISuite 4.0 Estimated Atmospheric Oxidation indicates potentially rapid oxidation and 

degradation in air, Half-Life 10.12 hours.

Low potential to bioaccumulate. Log BCF = 0.5

Not persistent in the environment. EPI SuiteTM 4.0 Primary Level Three Fugacity Model 

indicated a preference for the water (34.5%; half-life 208 hours) and soil compartments 

(65%; 416 hours half-life).

 Common Name: Propylene glycol

CAS Chemical Name: 1, 2-Propanediol

CAS Reg Number: 57-55-6

OPP Chem Code: 868603

Synonyms: 2,3-Propanediol: 1, 2-Dihydroxypropane;

Methylethylene Glycol; Trimethyl Glycol; 1,2-

 Propylene Glycol; Monopropylene Glycol; Propane

 -1, 2-diol; α –Propylene Glycol; Propanediol; 1,2-

 Dihydroxypropane; 2-Hydroxypropanol;

Methyethyl Glycol; Methyl Glycol

Commercial Names: Dowfrost; GR12; Sirlene; Solar Winter Ban

Chemical Formula: C3H8O2

Molecular Weight: 76.00 g/mol

IV. CURRENT USE

Due to its low toxicity, propylene glycol is widely used as an inert ingredient in agrochemical, 

industrial chemical, pharmaceutical, food, and personal care formulations. The intended purposes 

include that of a solvent, emulsifier, humectant, wetting agent, de-icer, antifreeze, fragrance 

carrying agent, and sanitizer. 
Page 6 of 14

Propylene glycol is already exempt from the requirement of a tolerance when used as a diluent 

(solvent, cosolvent) in pesticide formulations as described below: 

40 CFR §180.910. Propylene glycol is exempt from the requirement of a tolerance when used as a 

diluent (solvent, cosolvent) in accordance with good agricultural practice as an inert ingredient in 

pesticide formulations when applied to growing crops or to raw agricultural commodities after 

harvest. This includes use in food and feed handling establishments for products other than 

antimicrobials. 

40 CFR §180.930. Propylene glycol is exempt from the requirement of a tolerance when used as a 

defoaming agent (solvent, cosolvent) in accordance with good agricultural practice as an inert 

ingredient in pesticide formulations applied to animals. 

FDA has also approved propylene glycol as a preservative in food products as listed in 21 CFR, 

Part 184-Direct Food Substances Affirmed as Generally Recognized as Safe (GRAS): 

184.1666(d). The ingredient is used in foods at levels not to exceed current good manufacturing 

practice in accordance with Sec. 184.1(b)(1) which includes the following:

Current good manufacturing practice results in maximum levels, as served, of:

− 5 percent for alcoholic beverages, as defined in Sec. 170.3(n)(2) of this chapter;

− 24 percent for confections and frostings as defined in Sec. 170.3(n)(9) of this 

chapter;

− 2.5 percent for frozen dairy products as defined in Sec. 170.3(n)(20) of this 

chapter; 

− 97 percent for seasonings and flavorings as defined in Sec. 170.3(n)(26) of this 

chapter;

− 5 percent for nuts and nut products as defined in Sec. 170.3(n)(32) of this 

chapter; and

- 2 percent for all other food.

V. TOXICOLOGICAL PROFILE

Propylene glycol has an extensive database of acute oral toxicity in the rat, mouse, rabbit and 

Guinea pig; acute eye irritation in the rabbit, acute skin irritation in the rabbit, subchronic, chronic, 

developmental, and reproductive toxicity, carcinogenicity, mutagenicity, 

metabolism/pharmacokinetics and dermal toxicity studies. These data have been summarized in 

the UNEP SIDs (2001) and EPA RED (2006) reports. The Antimicrobials Division Toxicology 

Endpoint Selection Committee (ADTC) memorandum and the toxicology chapter are available in 

EPA’s Pesticide Docket, EPA-HQ-OPP-2006-0831 at www.regulations.gov. The remainder of the 

toxicological profile is taken directly from the Agency’s 2006 RED document.

A. Hazard Assessment
Page 7 of 14

EPA (2006) concluded that there are no toxicity endpoints of concern for oral, dermal, or 

inhalation exposure to propylene glycol. This conclusion is based on the results of toxicity testing 

of propylene glycol at dose levels near or above testing limits (as established in the OPPTS 870 

series harmonized test guidelines).

1. Acute Toxicity 

EPA concluded that no significant acute toxicity was observed. There were no endpoints of 

concern for oral, dermal, or inhalation exposure to propylene glycol. 

Table 1. Acute Toxicity of Propylene Glycol 

Guideline Study Type Results

(mg/kg)

Toxicity 

Category

870.1100 Acute Oral - Rat LD50 range = 8,000 – 46,000 IV 

870.1100 Acute Oral - Mouse LD50 range = 23,000 – 24,900 IV 

870.1100 Acute Oral - Rabbit, Guinea pig LD50 range = 18,000 – 20,000 IV 

870.2400 Acute Eye Irritation - Rabbit Non-irritant IV 

870.2500 Acute Skin Irritation - Rabbit Non-irritant IV

870.2600 Skin Sensitization Non-sensitizer NA

2. Repeat Dose Dermal Toxicity and Carcinogenicity Study

Mice

In 1973, Stenback and Shubik conducted a 12 week, repeat dose, dermal toxicity study on female 

Swiss mice from the Eppley colony. Seven compounds were evaluated, propylene glycol was one 

of the compounds tested. The results for propylene glycol are reported here.

Seven week old female Swiss mice from the Eppley colony were used. Animals were randomized

and littermates were separated. There were 50 animals per concentration group. Propylene glycol 

was tested at 100 %, 50 % and 10 % (~500,000, 100,000, 50,000, mg/kg bw/day) concentration. 

Animals were housed in plastic cages, 10 per group. Commercial bedding was used and the 

animals fed a commercial diet. 135 untreated animals served as a control group. 

The application consisted of 0.02 ml dropped on the dorsal skin between the flanks, twice a week 

on a 1-inch square area which was shaved regularly. Animals were checked weekly and all lesions 

as well as tumors were recorded. Animals were allowed to die spontaneously or were sacrificed 

when moribund. Complete autopsies were performed on all animals. The skin from all animals, 

all grossly observed tumors and other lesions in the lungs, livers kidneys, etc from treated as well 

as control groups were evaluated histologically.

None of chemicals studied (including propylene glycol) produced a statistically significant 

increase in skin tumor incidence as compared to the controls. The treatments did not produce 

lesions in other organs related to the treatment. The authors cited a study by Gaunt et al. (1972) 

did not report any pathological findings or carcinogenic potential after feeding propylene glycol in 
Page 8 of 14

concentrations up to 50,000 ppm (~2,500 mg/kg bw/day) in rats. Stenback and Shubick state that 

the findings of Gaunt et al. are similar to what they reported. 

Rats

As noted earlier, Gaunt et al. (1972) conducted a long-term toxicity study of propylene glycol in 

rats. In the study, groups of 30 male and female weanling rats (strain not specified) were fed diets 

containing 0, 6,250, 12,500, 25,000, or 50,000 ppm (approximately 312.5, 625, 1,250, 2,500 mg/kg 

bw/day respectively) propylene glycol for 2 years. Animals were observed daily for signs of illhealth or death.

At weeks 13, 21, 52 and 80 of the study, blood was collected from male and female animals from 

each group that had been fed on diets containing 0 (control), 25,000 and 50,000 ppm (~ 1,250 and 

2,500 mg/kg bw/day) propylene glycol. All samples were examined for hemoglobin content, 

packed cell volume and counts of erythrocytes, total leucocytes and the individual types of 

leucocytes. Counts of reticulocytes were also conducted on samples obtained after weeks 52, 54 

and 80. At week 104, hematological studies were limited to measurements of hemoglobin 

concentration and stained blood smears from all surviving rats. 

At weeks 13, 30 and 52, urinary concentration tests were conducted on selected individual rats 

from the control group and the two highest dose groups (25,000 and 50,000 ppm; ~1,250 and 

2,500 mg/kg bw/day). Measurements were taken of specific gravity and volume of urine produced 

during a 6 hr period of water deprivation, during a 2-hour period of water load of 25 ml/kg and 

during a 4-hour period commencing 16-hr after the water load. Urinary cell counts were taken on 

the 6-hr. samples. 

After week 104, all surviving animals were sacrificed by exsanguination under barbiturate 

anesthesia. Autopsies were conducted and any macroscopic abnormalities noted for the brain, 

heart, liver, spleen, kidneys, adrenals, gonads, stomach, small intestine and caecum. Samples of 

these organs and of salivary gland, trachea, aorta, thymus, lymph nodes, pituitary, urinary bladder, 

colon, rectum, pancreas, uterus, muscle and any tissue that appeared to be abnormal.

During the long-term study, a short-term study was conducted concurrently. Groups of 15 male 

and female rats (strain not specified) of similar age and body weight to those in the long-term 

study were used. Concurrent with the long-term study these rats were fed diets containing 0 

(control) and 50,000 ppm (2,500 mg/kg bw/day) propylene glycol for 15 weeks. Body weights 

and food consumption were not recorded as the dietary level was the same as for the long-term 

study. During the last week of the study, renal concentration tests were conducted as described 

earlier. Additionally, the activity of glutamic-oxalacetic transaminase was estimated I the 6-hr 

urine samples. Blood was collected from the aorta at autopsy and hematological examinations 

were conducted as described above. Serum was separated and measurements were made of urea 

concentration and of the activities of glutamic-oxalacetic and glutamic-pyruvic transaminases. 

The brain, heart, liver, spleen, kidneys, adrenals, gonads and pituitary were weighted at autopsy. 

The results were: At over two times the limit dose (1,000 mg/kg bw/day) no abnormalities were 

seen in the appearance or behavior of the rats. There were no statistically significant differences 
Page 9 of 14

between treated and control rats in cumulative death rates, body weight gain or food consumption. 

The mean daily intakes of propylene glycol were approximately 0-2, 0-45, 0-9 and 1-7 g/kg for 

males and 0-3, 0-5, 1-0 and 2-1 g/kg in females at the four dietary levels. There were no 

significant differences between treated and control rats in the results of hematological studies or in 

the urinary cell excretion or renal concentration tests. Values of absolute organ weights and 

weights or organs relative to the terminal body weight were similar in all treated and control 

groups. 

In the short-term study there were no differences between the controls group and those fed a diet 

containing 50,000 ppm (2,500 mg/kg bw/day) propylene glycol in the analyses of serum and urine, 

hematological indices or organ weighs. Nor abnormalities were seen at autopsy.

There were no statistically significant differences between the control animals (0 ppm) and the test 

animals (doses up to and including 50,000 ppm (2,500 mg/kg bw/day). There was no evidence of 

any dose-related effects. Thus no carcinogenic potential has been detected with dietary levels up 

to an including 50,000 ppm (2,500 mg/kg bw/day) propylene glycol administered over most of the 

life-span of rats. The no observed adverse effect level is considered to be 50,000 ppm

(2,500mg/kg bw/day) in these two studies. 

Dogs

In an oral toxicity study by Weil et al. (1971) beagle dogs were fed 0, 2,000 or 5,000 mg/kg 

bw/day propylene glycol for 2-years. No treatment related effects were observed

EPA concluded that propylene glycol was negative for carcinogenicity in studies conducted up to 

the testing limit doses established by the Agency; therefore no further carcinogenic analysis was 

required. The Antimicrobial Division’s Toxicology Committee stated that public literature sources 

which examined the carcinogenic potential of propylene glycol have shown that it is negative for 

carcinogenicity. 

Immunotoxicity and neurotoxicity studies were not available in the database. However, there was 

no evidence of immunotoxicity or neurotoxicity in the studies that were submitted.

3. Mutagenicity Potential 

EPA concluded that propylene glycol was not mutagenic or genotoxic on the basis of a battery 

of studies that included the bacterial gene mutation assay using Salmonella typhimurium 

(AMES) in vitro assay, in vitro Chinese hamster ovary (CHO) mutation assay, Chinese hamster 

ovary (CHO) chromosomal aberration assays, and an in vitro sister chromatid exchange assay. 

4. Reproductive and Developmental Toxicity

Kavlock, Short and Chernoff (1987) conducted an In Vivo teratology screening study. Propylene 

glycol was one of the compounds evaluated. Sixty-day old time pregnant female CD-1 mice from 

Charles River Laboratory were used in the study. Propylene glycol was administered by oral 

gavage at a dose rate of 10,000 mg/kg bw/day. Administration was for 5 days. Pregnant females 

were then dosed on day 8-12 of gestation. Compared to the control group which was administered 
Page 10 of 14

0 mg/kg bw/day propylene glycol, there were essentially no differences in maternal effects of 

neonatal effects. Those data were from treatment levels 10 times higher than the limit dose of 

1,000 mg/kg bw/day. 

The National Toxicology Program (NTP) conducted a continuous breeding study on COBScrl:CD1(ICR)BR outbred albino mice. Mice were exposed to 0, 1, 2.5 or 5 % (approximately 1,820, 

4,800, 10,100 mg/kg bw/day) propylene glycol in the drinking water for 18 weeks. Maternal, 

offspring and reproductive toxicity were not observed (MRID46892207).

Moreover as already noted, UNEP (2001) concluded that propylene glycol is not a reproductive or 

developmental toxicant with NOELs in rats, mice, rabbits, or hamsters ranging from 1.2 to 1.6 

g/kg bw/day (all four species). These doses vastly exceed the expected propylene glycol exposure 

associated with the already approved pesticide ingredient approvals under 40 CFR §180.910 and 

40 CFR §180.930 uses, and the intended 40 CFR §180.910(a) use in antimicrobial formulations. 

5. Metabolism

The World Health Organization (WHO, 2001) has summarized the metabolism of propylene glycol 

in mammals. Propylene glycol should be readily metabolized to lactic acid at the typical low-level 

exposures associated with the already approved pesticide inert ingredient registrations under 40 

CFR §180.910 and 40 CFR §180.930 uses, and the intended 40 CFR §180.940(a) use in 

antimicrobial formulations. At higher concentrations (absorbed doses), propylene glycol is 

primarily excreted unchanged in the urine.

• “In studies of the minor pathways of metabolism of propylene glycol, administration to rats 

in drinking-water resulted in excretion unchanged in the urine ...Propylene glycol given 

orally to rabbits was conjugated with glucuronic acid and excreted in the urine...”

Propylene glycol is oxidized to lactic acid via two biochemical pathways. If phosphorylated, 

propylene glycol is converted to acetol phosphate, lactaldehyde phosphate, lactyl phosphate, and 

then lactic acid. If propylene glycol is not phosphorylated, it is successively oxidized to 

lactaldehyde, methylgloyoxal, and lactic acid. In both cases, lactate is subsequently converted to 

pyruvate, which enters the citric acid cycle and/or the gluconeogenesis pathway.

D. Toxicity Endpoint Selection

The available toxicity studies indicate that propylene glycol exhibits very low toxicity over-all. 

The No Observed Adverse Effect Levels (NOAELs) were > 2,500 mg/kg bw/day (above the limit 

dose of 1,000 mg/kg bw/day). Since signs of toxicity were not observed, a toxicological endpoint 

of concern for use in risk assessment, was not identified. Therefore, a quantitative risk assessment 

for propylene glycol is not necessary. 

VI. Special Consideration for Infants and Children and Rationale that the FQPA Safety 

Factor is not Required

The FQPA Safety Factor (as required by the Food Quality Protection Act of 1996) is intended to 

provide an additional 10-fold safety factor (10X), to protect for special sensitivity in infants and 
Page 11 of 14

children to specific pesticide residues in food, drinking water, or residential exposures, or to 

compensate for an incomplete database. EPA concluded there are no toxicity endpoints of concern 

for oral, dermal, or inhalation exposure to propylene glycol based on the low toxicity observed in 

studies conducted near or above testing limit doses as established in the OPPTS 870 series 

harmonized test guidelines. This decision is supported by the lack of genotoxic, reproductive, and 

developmental toxicity reported by UNEP (2001). Therefore, EPA has removed the FQPA Safety 

Factor (i.e., reduced to 1X) for propylene glycol, because there is no pre- or post-natal evidence for 

increased susceptibility following exposure. 

VII. Exposure Assessment 

On the basis of the data summarized earlier, no acute or chronic toxicity endpoints were proposed 

by EPA for an acute or chronic risk assessment and therefore no acute or chronic dietary exposure 

assessments are warranted.

VIII. Aggregate Exposure and Risk

1. Potential Dietary and Residential Exposures 

EPA stated in the 2006 RED:

Dietary exposure (food and drinking water) could potentially occur from the use of 

propylene glycol as a food additive, from food packaging, and from its use as an 

inert ingredient in pesticide formulations. Residential exposure could also 

potentially occur as a result of the use of propylene glycol in and around the home 

as a sanitizer, disinfectant and pet treatment. However, risk estimates have not been 

calculated by EPA for potential exposures to propylene glycol on food, in drinking 

water, or as a result of use in residential settings because there are no toxicological 

endpoints of concern according to a review of the available toxicity data. 

Since the 2006 RED, no new data have been submitted to alter the conclusions about the toxicity 

of propylene glycol. The Agency still has not identified an endpoint for risk assessment purposes; 

therefore, the exposure assessment for this action is qualitative, much like the assessment done in 

the 2006 RED. This action may result in additional exposures to the propylene glycol from its use 

on food contact surfaces and on dairy or other food-processing equipment and utensils. 

2. Aggregate Exposure

EPA stated in the 2006 RED: 

The Food Quality Protection Act amendments to the Federal Food, Drug, and 

Cosmetic Act (FFDCA, Section 408(b)(2)(A)(ii)) require “that there is a reasonable 

certainty that no harm will result from aggregate exposure to pesticide chemical 

residue, including all anticipated dietary exposures and other exposures for which 

there are reliable information.” Aggregate exposure will typically include exposures 

from food, drinking water, residential uses of a pesticide and other nonoccupational sources of exposure. Since toxicological endpoints for risk assessment 

were not identified based on the available data, an aggregate risk assessment was 

not conducted by EPA for propylene glycol.
Page 12 of 14

Similarly, for this action, EPA did not conduct a quantitative aggregate risk assessment 

since hazard endpoints were not identified. 

IX. Occupational Exposure/Risk Pathway

The Agency believes that amending the existing 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 propylene glycol, i.e., 

approved use under 40 CFR §180.910 and §180.930 and no new toxicological information to 

indicated otherwise, it is not necessary to quantitatively assess occupational exposure.

X. CUMULATIVE EFFECTS

Section 408(b)(2)(D)(9v) 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.” Unlike pesticides for which EPA has followed a cumulative risk approach based on a 

common mechanism of toxicity, EPA has not conducted a common mechanism of toxicity 

evaluation for propylene glycol. 

JECFA (2001) has reported that propylene glycol does not produce a toxic metabolite. Thus, the 

Agency has assumed that propylene glycol does not have a common mechanism of toxicity with 

other substances. As a result, any potential human health risks would be those that result only 

from the use of propylene glycol as a pesticide active ingredient (bacteriostat and fungistat) and as 

an inert ingredient in food use and non-food use pesticide formulations. 

XI. ENVIRONMENTAL RISK

UNEP (2001) has summarized propylene glycol’s environmental fate characteristics and its 

toxicity to aquatic organisms:

• Propylene glycol is not volatile and it is miscible with water. 

• The concentrations of propylene glycol in the atmosphere are expected to be extremely low 

because of its low vapor pressure and high water solubility. 

• Propylene glycol is readily biodegraded in water or soil. Four studies reported >60% 

biodegradation in water in 10 days. 

• Propylene glycol is not expected to bioaccumulate. The calculated BCF is <1. 

• Propylene glycol is not acutely toxic to aquatic organisms except at very high concentrations 

that would exceed the intended use as a pesticide inert ingredient according to the current 40 

CFR §180.910 and §180.930 uses and the proposed 40 CFR §180.940(a) applications. The 

measured freshwater aquatic toxicity data of propylene glycol to fish, daphnia, and algae, have 

LC/EC50’s that exceed values of >18,000 mg/l (18,000 ppm). Additionally, using an 

assessment factor of 100 and the Ceriodaphnia data (48-hour EC50 = 18,340 mg/l), the PNEC 

is 183 mg/l.
Page 13 of 14

XII. ENVIRONMENTAL JUSTICE

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

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, HED and 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 

the Continuing Survey of Food Intake 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, 

the 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 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 under 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.

XIII. CONCLUSIONS

In 2006, based on the available data, EPA concluded that propylene glycol exhibits low toxicity 

and that exposure to propylene glycol used both as a pesticide active ingredient and/or as a 

pesticide formulation inert ingredient does not present risks of concern. JECFA has also reported 

that propylene glycol is either readily excreted unchanged or not metabolized to toxic metabolites. 

FDA has also categorized propylene glycol as generally recognized as safe and approved its use in 

all food categories, ranging from 2% to 97% in a variety of foods. 

Furthermore, in determining whether or not infants and children are particularly susceptible to 

toxic effects from propylene glycol residues, EPA has considered the completeness of the database 

for developmental and reproductive effects. The FQPA Safety Factor has been removed (i.e., 

reduced to 1X) because there is no pre- or post-natal evidence for increased susceptibility 

following exposure.

Based on the information presented above and upon the information in the EPA Reregistration 

Eligibility Decision For Propylene Glycol and Dipropylene Glycol (2006), the Agency approves of 

the use of Propylene Glycol without limitation as an inert ingredient in antimicrobial pesticide 

formulations applied to “food contact surfaces in public eating places, dairy processing 

equipment, and food processing equipment and utensils” as described in 40 CFR § 180.940(a).
Page 14 of 14

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Gaunt, I., F. Carpanini, P. Grasso and A. Lansown. 1972. Long-term Toxicity of Propylene 

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JECFA. Propylene Glycol. 2002. Joint FAO/WHO Expert Committee on Food Additives

www.inchem.org/documents/jecfa/jeceval/jec_2031.htm.

Kavlock, R., R. Short Jr. and N. Chernoff. 1987. Further Evaluation of an In Vivo Teratology 

Screen. Teratogenesis, Carcinogenesis and Mutagenesis. 7: 7-16.

National Toxicology Program. 2003. Center for the Evaluation of Risks to Human Reproduction. 

NTP-CERHRExpert Panel Report on the Reproductive and Developmental Toxicity of Propylene 

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Stenback, F. and P. Shubik. 1974. Lack of Toxicity and Carcinogenicity of Some Commonly 

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UNEP SIDS, 2001, Initial Assessment Report for the 11th SIAM, 1,2-Dihyroxypropane (CAS 57-

55-6), www.chem.unep.ch/irptc/sids/oecdsids/57-55-6.pdf. United Nations Environment 

Programme Screening Information Dataset.

US EPA Registration Eligibility Document for Propylene Glycol and Dipropylene Glycol dated 

September 2006 (available in EPA Docket, EPA-HQ-OPP-2006-0831). 

Weil, C., M. Woodside, H. Smyth Jr. and C. Carpenter. 1971. Results of feeding propylene glycol 

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