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EPA BIOPESTICIDES AND POLLUTION PREVENTION DIVISION 

COMPANY NOTICE OF FILING FOR PESTICIDE PETITIONS PUBLISHED IN 

THE FEDERAL REGISTER 

EPA Biopesticides and Pollution Prevention Division contact: Linda Hollis #17 (703-

308-8367)

INSTRUCTIONS: Please utilize this outline in preparing the pesticide petition. In 

cases where the outline element does not apply, please insert “NA-Remove” and 

maintain the outline. Please do not change the margins, font, or format in your 

pesticide petition. Simply replace the instructions that appear in green, i.e., “[insert 

company name],” with the information specific to your action.

SUBMISSION: E-mail the completed template to: hollis.linda@epa.gov.

TEMPLATE:

Arkion Life Sciences

[Insert petition number]

EPA has received a pesticide petition ([insert petition number]) from 

Interregional Research Project Number 4(IR-4) 500 College Road East, Suite 

201W Princeton, New Jersey on behalf of Arkion Life Sciences, 551 Mews Drive 

Suite J, New Castle DE 19720 proposing, pursuant to section 408(d) of the 

Federal Food, Drug, and Cosmetic Act (FFDCA), 21 U.S.C. 346a(d), to amend 40 

CFR part 180.

(Options (pick one)

1. by establishing a tolerance for residues of

2. to establish an exemption from the requirement of a tolerance for

3. to establish an amendment/expansion of an existing tolerance exemption for the

(Options (pick one)

1. microbial pesticide [insert name of active ingredient]

2. biochemical pesticide 9,10 anthraquinone
2

3. plant-pesticide [insert name of active ingredient] in or on [insert 

commodity].

Pursuant to section 408(d)(2)(A)(i) of FFDCA, as amended, Interregional 

Research Project Number 4(IR-4) on behalf of Arkion Life Sciences has submitted the 

following summary of information, data, and arguments in support of their pesticide 

petition. This summary was prepared by Interregional Research Project Number 4(IR-4) 

on behalf of Arkion Life Sciences and EPA has not fully evaluated the merits of the 

pesticide petition. The summary may have been edited by EPA if the terminology used 

was unclear, the summary contained extraneous material, or the summary unintentionally

made the reader conclude that the findings reflected EPA’s position and not the position 

of the petitioner.

I. Arkion Life Sciences Petition Summary

[Insert petition number]

A. Product Name and Proposed Use Practices

Avipel liquid corn seed treatment. Avipel will be used for the protection of 

planted field and sweet corn seed against consumption by blackbirds, cranes, grackles 

and pheasants. Application will be performed to corn seed either by commercial seed 

treatment businesses or on farm as a planter box seed treatment.

B. Product Identity/Chemistry

1. Identity of the pesticide and corresponding residues.

The active ingredient in Avipel is 9,10 anthraquinone (CAS 84-65-1). Residues 

of 9,10 anthraquinone, 1-hydroxy anthraquinone and 2-hydroxy anthraquinone have been 

quantitatively and qualitatively measured using a GLP Magnitude of Residue study

conducted under the auspices of IR-4 and included in this filing.

2. Magnitude of residues at the time of harvest and method used to determine the 

residue.

Anthraquinone, the active ingredient in Avipel liquid formulation and Avitec

dry powder formulation, is a pesticide used on field corn for control of sandhill crane. To 

provide the sponsor with residue chemistry data to support the establishment of a 

tolerance for anthraquinone in or on field corn, 15 field trials were conducted for this 

study during the 2006 and 2007 growing seasons, two each in Michigan (EPA Region 5) 

and New York (Region 1); three in North Dakota (one Region 5, two Region 7); one each 

in Ohio (Region 5), South Dakota (Region 5), and Texas (Region 6); and five in 

Wisconsin (Region 5). Six varieties of field corn seed were treated with Avipel liquid 

formulation at targeted rates of approximately 0.005 lb ai/lb seed (1X), and at 0.025 lb 

ai/lb seed (5X)(2006 trials), or 0.05 lb ai/lb seed (10X) (2007 trials). In addition, at the 
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Wisconsin 06-WI07 and North Dakota 06-ND04 trials, seed was treated with Avitec

dry powder formulation at rates of approximately 0.005 lb ai/lb seed (1X) and 0.025 lb 

ai/lb seed (5X). The seed was planted and samples of kernels plus cob with husks

removed (K+CWHR) and samples of forage were collected at the milk stage. Samples of 

grain and stover were collected at crop maturity.

Sample analysis for residues of anthraquinone, 1-hydroxyanthraquinone, and 

2-hydroxyanthraquinone was conducted by Cornell Analytical Laboratories, Geneva, 

NY. The procedure used was “Residue Analysis of Anthraquinone on Corn (field) 

including Kernels plus Cob with Husks Removed (K+CWHR), Forage, Grain, and Stover 

by LC/MS Detection”, Version #1

The results from the 15 trials show that no residues above the LLMV of 0.10 ppm 

of anthraquinone, 1-hydroxyanthraquinone, and 2-hydroxyanthraquinone were observed 

in any of the samples following seed treatment at rates of approximately 0.025 lb ai/lb 

seed (5X), or 0.05 lb ai/lb seed (10X) in any grain sample. Residues of 0.12 ppm 

1-hydroxyanthraquinone were observed in one stover sample treated with Avipel liquid 

formulation at the 10X rate from the Texas trial. The sample was reanalyzed at a later 

date and no residues above the LLMV were observed. 

3. A statement of why an analytical method of detecting and measuring the levels 

of the pesticide residue are not needed.

An analytical method is available. Sample analysis for residues of anthraquinone, 

1-hydroxyanthraquinone, and 2-hydroxyanthraquinone was conducted by Cornell 

Analytical Laboratories, Geneva, NY. The procedure used was “Residue Analysis of 

Anthraquinone on Corn (field) including Kernels plus Cob with Husks Removed 

(K+CWHR), Forage, Grain, and Stover by LC/MS Detection”, Version #1.

C. Mammalian Toxicological Profile

The information submitted on this formulation as Flight Control for outdoor 

nonfood use was previously reviewed by BPPD and states: Adequate mammalian 

toxicology data are available and support registration of the active ingredient 9,10 –

anthraquinone. The registrant, (Arkion Life Sciences), submitted acceptable acute 

toxicity studies for both the Technical Grade Active Ingredient (TGAI) and the end-use 

product. 

For the TGAI: (i) acute oral LD50 in rats was >5000 mg/kg (Tox category IV); (ii) acute

dermal LD50 in rabbits was >5000 mg/kg (Tox category IV); (iii) acute inhalation LC50 

in rats was >2.11 mg/L (Tox category IV); and (iv) the EP caused mild ocular irritation 

symptoms in rabbits which cleared in 72 hours post-instillation (Tox category III). 

For the EP: (i) acute oral LD50 in rats was >5000 mg/kg (Tox category IV); (ii) acute 

dermal LD50 in rats was >5000 mg/kg (Tox category IV); (iii) acute inhalation LD50 in 

rats was > 2.04 mg/L (Tox category IV); (iv) the EP caused mild ocular irritation 
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symptoms in rabbits which cleared by 72 hours post instillation (Tox category III); (v) the 

EP caused slight dermal irritation symptoms in rabbits which cleared by 24 hours post 

dosing (Tox category III); and (vi) the EP was shown to be a contact sensitizer in guinea 

pigs using the Buehler Method.

The National Toxicology Program (NTP) has conducted a series of studies on 

anthraquinone. All these studies were conducted with anthraquinone samples produced 

from a process based on anthracene. The current process does not give rise to this 

impurity. The sample of anthraquinone used in the NTP studies were contaminated with 

up to 0.11% 9-nitroanthracene (9-NA) and 0.6% of mutagenic impurities. The sample 

was produced using an anthracene-derived process. This process has not been used for 

decades and is not used in any of the Arkion Life Sciences material. 

The level of 9-nitroanthracene in the studies were calculated at roughly 4 ppm in the diet 

at 3750 ppm anthraquinone The high dose tested in the rat study was 7500 ppm 

anthraquinone. The contamination of the anthraquinone sample with the potent mutagen 

9-nitroanthracene was well documented in both the NTP report and the open literature. 

Estimates based on mutagenic potency indicate it is plausible that the 9-NA and other 

contaminants could have been responsible for a portion, if not all, of the tumor induction 

observed in the NTP study.

In a subchronic oral toxicity study in rats conducted by the NTP, groups of 10 male and 

10 female F344/N rats were fed diets containing 0, 1,875, 3,750, 7,500, 15,000, or 30,000 

ppm anthraquinone (equivalent to average daily doses of approximately 135, 275, 555, 

1,130, or 2,350 mg anthraquinone/kg body weight) for 14 weeks. All rats survived until 

the end of the study. Mean body weights of females were significantly less in the exposed 

groups than in the control group. Feed consumption by the exposed and control groups 

was similar at the end of the study. Liver and kidney weights of exposed groups were 

greater than those of the controls, as were testis weights of males exposed to 7,500 ppm 

or greater. A minimal, responsive anemia was apparent in groups of male and female rats 

exposed to 3,750 ppm or greater by day 26 of the study. The anemia persisted and 

involved all exposed groups of rats at the end of the study but the response was weak and 

the dose response curve was flat across all treated groups. Renal function was also 

affected by anthraquinone exposure as demonstrated by increases in urine protein and 

glucose concentrations and aspartate aminotransferase and N-acetyl-β-D-glucosaminidase

activities. Estrous cycles were longer in 15,000 and 30,000 ppm females than in the 

controls. Groups of exposed rats had liver hypertrophy; eosinophilic hyaline droplets in 

the kidney; congestion, hematopoietic cell proliferation, and pigmentation of the spleen; 

and bone marrow hyperplasia. The incidences of nephropathy in 15,000 and 30,000 ppm 

females were significantly greater than that in the controls, and the severities of 

nephropathy were increased in exposed groups of males and in 30,000 ppm females. The 

concentrations of α-2u-globulin in the kidneys were significantly greater in all exposed 

groups of males. Thyroid gland follicular cell hypertrophy was present in all males and

females exposed to 3,750 ppm or greater. Incidences of inflammation and transitional cell 

hyperplasia in the urinary bladder of 30,000 ppm females were greater than those in the 

controls. This study was performed with samples of anthraquinone containing the 
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impurity 9-aminoanthracene, a known toxicant. The US EPA Guideline sets the limit 

dose for 90-day studies at 1000 mg/kg. The high dose in this study exceeded the limit 

dose.

The NTP has conducted a subchronic oral toxicity study in mice. Groups of 10 male and 

10 female B6C3F1 mice were fed diets containing 0, 1,875, 3,750, 7,500, 15,000, or

30,000 ppm anthraquinone (equivalent to average daily doses of approximately 250, 500, 

1,050, 2,150, or 4,300 mg/kg to males and 300, 640, 1,260, 2,600, or 5,300 mg/kg to 

females) for 14 weeks. All mice survived until the end of the study. Mean body weights

and feed consumption were similar among exposed and control groups. A responsive 

anemia occurred in exposed mice at week 14 but a clear dose response was not evident 

and the response was weak. Liver weights of exposed groups of mice were significantly

greater than those of the control groups. The incidences of centrilobular hypertrophy in 

the liver of mice exposed to 3,750 ppm or greater were significantly greater than those in 

the controls, and the severities increased with increasing exposure concentration.

Cytoplasmic alteration of the urinary bladder was observed in all exposed mice, and the 

severities increased with increasing exposure concentration. The incidences of 

hematopoietic cell proliferation were increased in all exposed groups of males and 

females, and pigmentation was observed in the spleen of all exposed mice (except one 

male and one female in the 30,000 ppm groups). This study was performed with samples 

of anthraquinone containing the impurity 9-aminoanthracene, a known toxicant. The US 

EPA Guideline sets the limit dose for 90-day studies at 1000 mg/kg. The high dose in 

this study exceeded the limit dose.

In an NTP study for oncogenicity in rats, groups of 50 male and 50 female F344/N rats 

were fed diets containing 469, 938, or 1,875 ppm anthraquinone for 105 weeks. Groups 

of 60 male and 60 female F344/N rats received 0 or 3,750 ppm anthraquinone for the 

same period. Five males and five females receiving 0 or 3,750 ppm were evaluated for 

histopathology and α2u-globulin concentrations at 3 months and for organ weights and 

histopathology at 12 months. These dietary anthraquinone concentrations resulted in

average daily doses of approximately 20, 45, 90, and180 mg/kg to males and 25, 50, 100, 

and 200 mg/kg to females. Additional groups of 18 males given 469, 938, 1,875, or 3,750 

ppm for 8 days and 10 males and 10 females given 469, 938, or 1,875 ppm for 3, 6, 12, or 

18 months were designated for toxicokinetic studies. Survival of all groups of males was 

similar, and survival of exposed groups of females was greater than that of the controls. 

Mean body weights of exposed groups of males during the latter part of the study and 

mean body weights of exposed females throughout most of the study were less than those 

of the controls. Feed consumption by exposed groups was similar to that by the controls.

The incidences of renal tubule adenoma and renal tubule adenoma or carcinoma 

(combined) occurred with positive trends and were increased in all exposed groups of 

female rats. The incidences of renal tubule adenoma in all exposed groups of male rats 

exceeded the historical control range, but the incidence was significantly increased in the 

938 ppm group only. Increased incidences of nonneoplastic lesions of the kidney 

associated with anthraquinone exposure included hyaline droplet accumulation, 

pigmentation, and mineralization in the renal medulla and transitional epithelial 
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hyperplasia in males and females and renal tubule hyperplasia in females. Incidences of 

nephropathy were increased in females, and severities of nephropathy were increased in 

males. At 3 months, the concentration of α2u-globulin in the kidney of 3,750 ppm males 

was greater than that in the control group. 

The incidence of urinary bladder transitional epithelial papilloma was significantly

greater in 1,875 ppm males than in the control group, and the incidences in groups of 

males exposed to 938 ppm or greater exceeded the historical control range. There were 

positive trends in the incidences of transitional epithelial hyperplasia and papilloma or 

carcinoma (combined) of the urinary bladder in females. The incidences of hepatocellular 

adenoma or carcinoma (combined) were slightly increased in exposed males and females; 

the incidences in groups of females exposed to 938 ppm or greater exceeded the historical 

control range. The incidences of several nonneoplastic liver lesions of minimal severity 

were also increased. The incidences of congestion, pigmentation, and hematopoietic cell 

proliferation of the spleen were greater in exposed males and females than in the controls. 

The incidences of bone marrow hyperplasia were increased in most groups of exposed 

rats, and the incidences of bone marrow atrophy were increased in exposed females. The 

incidences of mononuclear cell leukemia were significantly less in all exposed groups 

than in the controls at 2 years, and the incidences were less than the historical control 

ranges. The NOEL was 469 ppm (20 mg/kg males, 25 mg/kg females) based on 

pathological findings in the liver, kidney and bladder at 938 ppm (45 and 50 mg/kg males 

and females, respectively).

In an NTP study for oncogenicity in mice, groups of 50 male and 50 female B6C3F1 

mice were fed diets containing 0, 833, 2,500, or 7,500 ppm anthraquinone (equivalent to 

average daily doses of approximately 90, 265, or 825 mg/kg to males and 80, 235, or 745 

mg/kg to females) for 105 weeks. Additional groups of 36 males given 833, 2,500, or 

7,500 ppm for 8 days and 10 males and 10 females given 833, 2,500, or 7,500 ppm for 12 

months were designated for toxicokinetic studies. Survival was decreased for 7,500 ppm 

males than for the control group. Mean body weights of 7,500 ppm males during the last 

6 months of the study and mean body weights of 7,500 ppm females at the end of the 

study were less than those of the control groups. Feed consumption was similar in all 

groups of males and females.

Incidences of hepatocellular neoplasms (including multiple neoplasms) increased with a 

positive trend in male and female mice, and the incidences were increased in all exposed 

groups. Incidences of hepatoblastoma were significantly increased in males exposed to 

2,500 or 7,500 ppm. The incidences of several nonneoplastic lesions of the liver were 

increased in exposed mice. There was a marginal increase in the incidences of neoplasms 

of thyroid gland follicular cells in males and females. Incidences of intracytoplasmic 

inclusion body of the urinary bladder and hematopoietic cell proliferation of the spleen in 

males and females and thyroid gland follicular cell hyperplasia and kidney pigmentation 

in males were greater in exposed groups than in the controls.

The NOEL was 833ppm (90 mg/kg and 80 mg/kg males and females, respectively) based 

on pathological findings in the liver, kidney, thyroid and spleen at 2500 ppm (265 and 
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235 mg/kg males and females, respectively).

For developmental and reproductive toxicity, no studies have been conducted for 

anthraquinone. However, a structural analog, emodin (1, 3, 8-trihydroxy-6-methylanthraquinone), has been tested for developmental toxicity by the NTP in rats and mice. 

Emodin is a naturally occurring and pharmacologically active anthraquinone found in the 

roots and bark of certain plant species.

Time mated Sprague Dawley (CD®) rats (25/group) were exposed to emodin at nominal 

concentrations of 0, 425, 850, and 1700 ppm in NIH-07 ground rodent diet from 

gestational day (gd) 6 to 20. Average daily intake was 0, 31, and 57 mg emodin/kg of 

body weight/day for the control, low- and mid-dose groups. Average daily intake for the 

1700 ppm group was 80-144 mg emodin/kg of body weight/day. There were no 

differences among groups for the number of corpora lutea/dam, number of implantation 

sites/litter, or percent preimplantation loss/litter. Postimplantation loss (resorptions or late 

fetal deaths), live litter size, percent male fetuses/litter, and average fetal body

weight/litter (males, females or both) were likewise unaffected. Emodin did not affect the 

incidence of fetal malformations or variations. The maternal LOAEL was considered to 

be 1700 ppm (80-144 mg/kg/day) based on maternal body weight and weight gain, and 

the NOAEL was 850 ppm (57 mg/kg/day). The developmental toxicity NOAEL was 

greater than or equal to 1700 ppm (80-144 mg/kg/day). A LOAEL for developmental 

toxicity was not established in this study.

In an NTP study, time-mated Swiss albino (CD-1®) mice (25/group) were exposed to 

emodin at concentrations of 0, 600, 2500 or 6000 ppm in NIH-07 rodent diet from 

gestational day (gd) 6 to 17. Average daily intake was 0, 94, 391, and 1005 mg 

emodin/kg/day. Nominal concentrations of emodin (ppm in feed) and calculated intake of 

emodin (mg/kg/day) are expressed as the bulk test article (96.2% purity) unless otherwise 

noted. There were no differences among groups for the number of corpora lutea/dam, 

number of implantation sites/litter, or percent preimplantation loss/litter. Postimplantation 

loss (resorptions or late fetal deaths), live litter size, and percent male fetuses/litter were 

likewise unaffected. At 6000 ppm, average fetal body weight/litter (males, females or 

both) was reduced by 10-11%, and this effect was statistically significant.

Ingested emodin failed to significantly affect the incidences of fetal malformations or 

variations. At 2500 ppm, external malformations included exencephaly (3 fetuses in 3 

litters) and cleft palate (2 fetuses in 2 litters). However, this increase in external 

malformations was not considered to be treatment related due to the clear absence of a 

dose-response relationship. At 6000 ppm, no external malformations were found among 

302 fetuses (24 litters), nor had any been observed among 161 fetuses (13 litters) at 6000 

ppm in the screening study (NTP, 2000).

The maternal toxicity LOAEL was considered to be 6000 ppm (1005 mg/kg/day) based 

on reduction of maternal body weight and weight gain, and the NOAEL was 2500 ppm 

(391 mg/kg/day). The developmental toxicity LOAEL was 6000 ppm (1005 mg/kg/day) 

based on reduction of fetal body weight, and the NOAEL was 2500 ppm (391 

mg/kg/day).
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Emodin was not a developmental toxin. It is not anticipated that anthraquinone will be a 

developmental toxin.

Several mutagenicity studies were conducted by NTP on anthraquinone using S. 

typhimurium, and mouse peripherial blood micronuclei Statistically significant increases 

in the frequencies of micronucleated normochromatic erythrocytes were observed in 

peripheral blood samples from male and female mice exposed to anthraquinone (99.8% 

pure) in feed for 14 weeks but the frequency was low. However, results of an acute 

exposure mouse bone marrow micronucleus test, with anthraquinone administered by 

intraperitoneal injection, was negative. The NTP concluded that there was evidence of 

increased erythropoiesis in the 14-week treated mice and concluded that the increased 

rate of erythropoiesis may have contributed to the micronucleus responses seen in the 

high exposure concentration groups. (Increased cell proliferation can produce increased 

levels of mitotic errors.) Overall, NTP concluded that anthraquinone was negative for 

genotoxicity.

In EPA Guideline studies, anthraquinone was negative in bacterial mutation tests using 

Salmonella and E. coli with and without activation. Anthraquinone was also negative in a 

mouse lymphoma gene mutation test with and without metabolic activation. 

Anthraquinone did not induce chromosomal aberrations in Chinese hamster ovary (CHO) 

cells in the presence or absence of activation. Additionally, another mouse micronucleus 

bone marrow study was also negative following an acute exposure.

In studies conducted as part of the NTP studies, the metabolism and disposition of 

anthraquinone in male F344/N rats were examined. Animals were administered 

uniformly labeled 14C-anthraquinone by intravenous injection at 0.35 mg/kg body 

weight or by gavage at doses ranging from 0.35 to 350 mg/kg.

Following oral administration, anthraquinone was absorbed from the gastrointestinal tract 

and distributed to tissues. No indication of bioaccumulation was apparent in any tissue. 

The majority of the radiolabel was eliminated in the feces and the urine by 24 hours after 

dosing at all four concentrations. At 96 hours after dosing, less than 5% of the 

administered dose remained in major tissues. 

Elimination of over 50% of the administered radioactivity in the feces and there was

substantial excretion of parent and/or metabolites in the bile. Analysis of the bile samples 

indicated that less than 3% of the radioactivity collected was present as the parent 

compound, suggesting extensive hepatic metabolism. Analysis of urine from dosed rats 

revealed the presence of as many as 11 metabolites. Two of the metabolites identified 

were 1-hydroxyanthraquinone and 2-hydroxyanthraquinone.

The plasma half-life in mice was determined to be 4 hours, and in rats it was between 10-

12 hours. 
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D. Aggregate Exposure

1. Dietary exposure.

No exposure is expected based on the lack of measurable residues in the crop. A 

theoretical estimation of dietary risk was conducted using LifeLineTM version 5.0 with 

very conservative assumptions. Values of 0.1 ppm were used based on the LODs of the 

analytical method for the parent and three presumptive metabolites. No residues at a 10x 

use rate were detected which represents a 10-fold higher residue. A 100% crop treatment 

was also assumed. All LifeLine default processing values were used. The NOEL for the 

chronic study was assumed to be 7 mg/kg, based on a 3X reduction in the NOEL of the 

NTP study. A 10X FQPA safety factor was assumed as a conservative default.

Using exaggerated assumptions of residue and hazard, chronic dietary risks did not 

exceed 5% of the Reference Dose (RfD) with the most sensitive subpopulation, children 

ages 3- 5 with an estimate of 4.5% of the RfD. Taking the 95th percentile of the chronic

assessment for the acute dietary risk, the highest subpopulation was 7.9% of the chronic 

RfD.

Neither acute or chronic exposures are of dietary concern. 

i. Food.

No exposure is expected based on the lack of measurable residues in the crop.

ii. Drinking water.

No exposure is expected in drinking water.

2. Non-dietary exposure.

Based on its low toxicity and use practice (repellent of a vertebrate pest), 

anthraquinone is not subject to the Worker Protection Standards (WPS). Moreover, the 

possibility for dermal, eye and inhalation exposure is mitigated as long as the product is 

used according to label directions which recommends use of gloves, long sleeved shirts, 

long sleeved pants and NIOSH filters to prevent inhalation. It is anticipated that a 

majority of the treated corn seed will occur within a commercial seed treatment facility.

E. Cumulative Effects

Anthraquinone is not toxic and therefore there would be no expected cumulative 

effects from common mechanisms of toxicity.

F. Safety Determination
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1. U.S. population.

Aggregate exposure would primarily occur in the mixer/loader/applicator 

subpopulations via dermal and inhalation routes. Risks associated with dermal and 

inhalation aggregate exposures are measured via the acute toxicity studies previously

reviewed by the EPA as part of the Flight Control (66969-1) registration process. 

Because the inhalation toxicity studies for anthraquinone showed no toxicity (Toxicity

Category IV), the risks anticipated for this route of exposure are considered minimal. 

Results of the acute dermal study indicated low toxicity (Toxicity Category IV), and no 

significant dermal irritation (Toxicity Category IV). Based on these results, the 

anticipated risks from dermal and inhalation exposures are also considered minimal. 

Therefore, the risks from aggregate exposure via dermal and inhalation exposure are a 

compilation of two low risk exposure scenarios and are considered negligible. Exposure 

is further mitigated by use of worker protection equipment on the label.

2. Infants and children.

There is no anticipated residue associated with the proposed use of the 

anthraquinone. Therefore, the acute dietary risks should be negligible based on the lack 

of exposure.

G. Effects on the Immune and Endocrine Systems

There are no anticipated residues, therefore there is no exposure to the population 

to trigger concern for immune and endocrine effects in the general population or in the 

high risk population of infants and children.

H. Existing Tolerances

There is no established direct food tolerance in food for anthraquinone. There is 

an indirect food tolerance issued by FDA for anthraquinone in paper products used in 

contact with food. The established tolerance in this case for paper products is 2 ppm.

I. International Tolerances

There is no established direct food tolerance in food for anthraquinone. There is 

an indirect food tolerance issued by FDA for anthraquinone in paper products used in 

contact with food. The established tolerance in this case for paper products is 2 ppm.