
[Federal Register: August 5, 2009 (Volume 74, Number 149)]
[Rules and Regulations]               
[Page 38924-38935]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr05au09-16]                         

=======================================================================
-----------------------------------------------------------------------

ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 180

[EPA-HQ-OPP-2008-0889; FRL-8430-2]

 
Amine Salts of Alkyl (C8-C24) 
Benzenesulfonic Acid (Dimethylaminopropylamine, Isopropylamine, Mono-, 
Di-, and Triethanolamine); Exemption from the Requirement of a 
Tolerance

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

-----------------------------------------------------------------------

SUMMARY:  This regulation establishes an exemption from the requirement 
of a tolerance for residues of amine salts of alkyl (C8-
C24) benzenesulfonic acid (dimethylaminopropylamine, 
isopropylamine, mono-, di-, and triethanolamine) when used as an inert 
ingredient in pesticide formulations applied to growing crops and 
applied to animals. The Joint Inerts Task Force, Cluster Support Team 
Number 8, submitted a petition to EPA under the Federal Food, Drug, and 
Cosmetic Act (FFDCA), requesting an exemption from the requirement of a 
tolerance. This regulation eliminates the need to establish a maximum 
permissible level for residues of amine salts of alkyl (C8-
C24) benzenesulfonic acid (dimethylaminopropylamine, 
isopropylamine, mono-, di-, and triethanolamine).

DATES: This regulation is effective August 5, 2009. Objections and 
requests for hearings must be received on or before October 5, 2009, 
and must be filed in accordance with the instructions provided in 40 
CFR part 178 (see also Unit I.C. of the SUPPLEMENTARY INFORMATION).

ADDRESSES: EPA has established a docket for this action under docket 
identification (ID) number EPA-HQ-OPP-2008-0889. All documents in the 
docket are listed in the docket index available at http://
www.regulations.gov. Although listed in the index, some information is 
not publicly available, e.g., Confidential Business Information (CBI) 
or other information whose disclosure is restricted by statute. Certain 
other material, such as copyrighted material, is not placed on the 
Internet and will be publicly available only in hard copy form. 
Publicly available docket materials are available in the electronic 
docket at http://www.regulations.gov, or, if only available in hard 
copy, at the OPP Regulatory Public Docket in Rm. S-4400, One Potomac 
Yard (South Bldg.), 2777 S. Crystal Dr., Arlington, VA. The Docket 
Facility is open from 8:30 a.m. to 4 p.m., Monday through Friday, 
excluding legal holidays. The Docket Facility telephone number is (703) 
305-5805.

FOR FURTHER INFORMATION CONTACT: Kerry Leifer, Registration Division 
(7505P), Office of Pesticide Programs, Environmental Protection Agency, 
1200 Pennsylvania Ave., NW., Washington, DC 20460-0001; telephone 
number: (703) 308-8811; e-mail address: leifer.kerry@epa.gov.

SUPPLEMENTARY INFORMATION:

I. General Information

A. Does this Action Apply to Me?

    You may be potentially affected by this action if you are an 
agricultural

[[Page 38925]]

producer, food manufacturer, or pesticide manufacturer. Potentially 
affected entities may include, but are not limited to those engaged in 
the following activities:
     Crop production (NAICS code 111).
     Animal production (NAICS code 112).
     Food manufacturing (NAICS code 311).
     Pesticide manufacturing (NAICS code 32532).
    This listing is not intended to be exhaustive, but rather to 
provide a guide for readers regarding entities likely to be affected by 
this action. Other types of entities not listed in this unit could also 
be affected. The North American Industrial Classification System 
(NAICS) codes have been provided to assist you and others in 
determining whether this action might apply to certain entities. If you 
have any questions regarding the applicability of this action to a 
particular entity, consult the person listed under FOR FURTHER 
INFORMATION CONTACT.

B. How Can I Access Electronic Copies of this Document?

    In addition to accessing electronically available documents at 
http://www.regulations.gov, you may access this Federal Register 
document electronically through the EPA Internet under the ``Federal 
Register'' listings at http://www.epa.gov/fedrgstr. You may also access 
a frequently updated electronic version of EPA's tolerance regulations 
at 40 CFR part 180 through the Government Printing Office's e-CFR cite 
at http://www.gpoaccess.gov/ecfr. To access the OPPTS Harmonized 
Guidelines referenced in this document, go directly to the guidelines 
at http://www.epa.gov/opptsfrs/home/guidelin.htm.

C. Can I File an Objection or Hearing Request?

    Under section 408(g) of FFDCA, 21 U.S.C. 346a, any person may file 
an objection to any aspect of this regulation and may also request a 
hearing on those objections. You must file your objection or request a 
hearing on this regulation in accordance with the instructions provided 
in 40 CFR part 178. To ensure proper receipt by EPA, you must identify 
docket ID number EPA-HQ-OPP-2008-0889 in the subject line on the first 
page of your submission. All requests must be in writing, and must be 
mailed or delivered to the Hearing Clerk as required by 40 CFR part 178 
on or before October 5, 2009.
    In addition to filing an objection or hearing request with the 
Hearing Clerk as described in 40 CFR part 178, please submit a copy of 
the filing that does not contain any CBI for inclusion in the public 
docket that is described in ADDRESSES. Information not marked 
confidential pursuant to 40 CFR part 2 may be disclosed publicly by EPA 
without prior notice. Submit this copy, identified by docket ID number 
EPA-HQ-OPP-2008-0889, by one of the following methods:
     Federal eRulemaking Portal: http://www.regulations.gov. 
Follow the on-line instructions for submitting comments.
     Mail: Office of Pesticide Programs (OPP) Regulatory Public 
Docket (7502P), Environmental Protection Agency, 1200 Pennsylvania 
Ave., NW., Washington, DC 20460-0001.
     Delivery: OPP Regulatory Public Docket (7502P), 
Environmental Protection Agency, Rm. S-4400, One Potomac Yard (South 
Bldg.), 2777 S. Crystal Dr., Arlington, VA. Deliveries are only 
accepted during the Docket Facility's normal hours of operation (8:30 
a.m. to 4 p.m., Monday through Friday, excluding legal holidays). 
Special arrangements should be made for deliveries of boxed 
information. The Docket Facility telephone number is (703) 305-5805.

II. Background

    In the Federal Register of March 25, 2009 (74 FR 12856) (FRL-8399-
4), EPA issued a notice pursuant to section 408(d)(3) of FFDCA, 21 
U.S.C. 346a(d)(3), announcing the filing of a pesticide petition (PP 
8E7472) by The Joint Inerts Task Force (JITF), Cluster Support Team 8 
(CST 8), c/o CropLife America, 1156 15th Street, NW., Suite 400, 
Washington, DC 20005. The petition requested that 40 CFR 180.920 and 40 
CFR 180.930 be amended by establishing exemptions from the requirement 
of a tolerance for residues of the inert ingredient amine salts of 
alkyl (C8-C24) benzenesulfonic acid 
(dimethylaminopro-pylamine, isopropylamine, mono-, di-, and 
triethanolamine) (herein referred to in this document as ASABSA) 
including CAS Reg. Nos. 68953-97-9, 26545-53-9, 877677-48-0, 319926-68-
6, 90194-53-9, 55470-69-4, 68910-32-7, 26264-05-1, 157966-96-6, 68584-
24-7, 68648-81-7, 68649-00-3, 68953-93-5, 90218-35-2, 27323-41-7, 
68584-25-8, 68648-96-4, 68411-31-4, 90194-42-6, and 1093628-27-3, when 
used as an inert ingredient in pesticide formulations applied to 
growing crops under 40 CFR 180.920 and applied to animals under 40 CFR 
180.930. That notice referenced a summary of the petition prepared by 
The JITF, CST 8, the petitioner, which is available to the public in 
the docket, http://www.regulations.gov. There were no comments received 
in response to the notice of filing.
    Based upon review of the data supporting the petition, EPA has 
modified the exemption requested by limiting the diethanolamine salt of 
alkyl (C8-C24) benzenesulfonic acid (CAS Reg. 
Nos. 26545-53-9 and 68953-97-9) to a maximum of 7% by weight in 
pesticide formulations intended for application to growing crops and to 
animals. This limitation is based on the Agency's risk assessment which 
can be found at http://www.regulations.gov in documents 
``Dimethylaminopropylamine, Isopropylamine, Ethanolamine and 
Triethanolamine Salts of Alkyl (C8-C24) 
Benzenesulfonic Acid (JITF CST 8 Inert Ingredients). Human Health Risk 
Assessment to Support Proposed Exemption from the Requirement of a 
Tolerance When Used as Inert Ingredients in Pesticide Formulations and 
Diethanolamine Salt of Alkyl (C8-C24) 
Benzenesulfonic Acid (DEA - JITF CST 8 Inert Ingredient). Human Health 
Risk Assessment to Support Proposed Exemption from the Requirement of a 
Tolerance When Used as Inert Ingredients in Pesticide Formulations,'' 
in docket ID number EPA-HQ-OPP-2008-0889.
    This petition was submitted in response to a final rule that was 
published in the Federal Register of August 9, 2006 (71 FR 45415) (FRL-
8084-1) in which the Agency revoked, under section 408(e)(1) of FFDCA, 
the existing exemptions from the requirement of a tolerance for 
residues of certain inert ingredients because of insufficient data to 
make the determination of safety required by section 408(b)(2) of 
FFDCA. The expiration date for the tolerance exemptions subject to 
revocation was August 9, 2008, which was later extended to August 9, 
2009 in the Federal Register of August 4, 2008 (73 FR 45317) (FRL-8373-
6) to allow for data to be submitted to support the establishment of 
tolerance exemptions for these inert ingredients prior to the effective 
date of the tolerance exemption revocation.

 III. Inert Ingredient Definition

    Inert ingredients are all ingredients that are not active 
ingredients as defined in 40 CFR 153.125 and include, but are not 
limited to, the following types of ingredients (except when they have a 
pesticidal efficacy of their own): Solvents such as alcohols and 
hydrocarbons; surfactants such as polyoxyethylene polymers and fatty 
acids; carriers such as clay and diatomaceous earth; thickeners such as 
carrageenan and modified cellulose;

[[Page 38926]]

wetting, spreading, and dispersing agents; propellants in aerosol 
dispensers; microencapsulating agents; and emulsifiers. The term 
``inert'' is not intended to imply nontoxicity; the ingredient may or 
may not be chemically active. Generally, EPA has exempted inert 
ingredients from the requirement of a tolerance based on the low 
toxicity of the individual inert ingredients.

IV. Aggregate Risk Assessment and Determination of Safety

    Section 408(b)(2)(A)(i) of FFDCA allows EPA to establish an 
exemption from the requirement of a tolerance (the legal limit for a 
pesticide chemical residue in or on a food) only if EPA determines that 
the tolerance is ``safe.'' Section 408(b)(2)(A)(ii) of FFDCA defines 
``safe'' to mean that ``there is a reasonable certainty that no harm 
will result from aggregate exposure to the pesticide chemical residue, 
including all anticipated dietary exposures and all other exposures for 
which there is reliable information.'' This includes exposure through 
drinking water and in residential settings, but does not include 
occupational exposure. Section 408(b)(2)(C) of FFDCA requires EPA to 
give special consideration to exposure of infants and children to the 
pesticide chemical residue in establishing a tolerance and to ``ensure 
that there is a reasonable certainty that no harm will result to 
infants and children from aggregate exposure to the pesticide chemical 
residue. * * *''
    EPA performs a number of analyses to determine the risks from 
aggregate exposure to pesticide residues. First, EPA determines the 
toxicity of pesticides. Second, EPA examines exposure to the pesticide 
through food, drinking water, and through other exposures that occur as 
a result of pesticide use in residential settings.
    Consistent with section 408(b)(2)(D) of FFDCA, and the factors 
specified in section 408(b)(2)(D) of FFDCA, EPA has reviewed the 
available scientific data and other relevant information in support of 
this action. EPA has sufficient data to assess the hazards of and to 
make a determination on aggregate exposure for the petitioned-for 
exemption from the requirement of a tolerance for residues of ASABSA 
when used as inert ingredients in pesticide formulations applied to 
growing crops and to animals. EPA's assessment of exposures and risks 
associated with establishing tolerances follows.

A. Toxicological Profile

    EPA has evaluated the available toxicity data and considered its 
validity, completeness, and reliability as well as the relationship of 
the results of the studies to human risk. EPA has also considered 
available information concerning the variability of the sensitivities 
of major identifiable subgroups of consumers, including infants and 
children.
    Amine salts of alkyl (C8-C24) benzenesulfonic 
acid readily and fully dissociate to the corresponding amine and alkyl 
(C8-C24) benzenesulfonic acid constituents, 
therefore the hazard assessment conducted to support the requested 
exemption from the requirement of a tolerance for ASABSA is primarily 
based on the hazard assessment for each of the constituents, 
specifically each associated amine (i.e., dimethylaminopropylamine, 
isopropylamine, ethanolamine, diethanol-amine and triethanolamine) and 
alkyl (C8-C24) benzenesulfonic acid.
    The hazard profile and endpoints for risk assessment for 
alkylbenzene sulfonic acid have previously been addressed as part of 
the tolerance reassessment for tolerance exemptions for alkyl 
(C8-C24) benzenesulfonic acid and its ammonium, 
calcium, magnesium, potassium, sodium, and zinc salts http://
www.epa.gov/opprd001/inerts/alkylc8.pdf. The toxicology database for 
these alkylbenzene sulfonates consists almost entirely of published 
literature, and is essentially complete and of acceptable quality to 
assess the potential hazard to humans. The alkylbenzene sulfonates are 
readily absorbed following oral ingestion, but not following dermal 
exposure. Following oral exposure, they are readily metabolized, 
excreted fairly rapidly, and do not accumulate in any tissues. 
Available acute toxicity data show that alkylbenzene sulfonates are not 
highly acutely toxic, are irritating to the eye and skin, and are not 
skin sensitizers. Subchronic and chronic exposures show that the liver, 
kidney and intestinal tract (following oral exposures) are the major 
target organs of toxicity. Both in vitro and in vivo genotoxicity data 
show that alkylbenzene sulfonates are not genotoxic. The alkylbenzene 
sulfonates did not cause reproductive or developmental toxicity in 
acceptable studies. Early (pre Good Laboratory Practice standards) 
carcinogenicity studies indicate that alkylbenzene sulfonates do not 
cause an increase in tumor incidence.
    The existing toxicology database for the dimethylaminopropylamine, 
isopropylamine, ethanolamine and triethanolamine salt of alkyl 
(C8-C24) benzenesulfonic acid consists of an 
OPPTS Harmonized Test Guideline 870.3550 study and acute, subchronic, 
chronic, carcinogenicity, developmental, and mutagenicity studies on 
the individual amines. In addition, the petitioner submitted an OPPTS 
Harmonized Test Guideline 870.3650 combined repeated dose toxicity 
study with the reproduction/developmental toxicity screening tests on 
isopropylamine dodecylbenzene sulfonate. The Agency considered these 
data in its evaluation of amine toxicity. While the test compound for 
the study is effectively a mixture of the amine and the acid, the study 
findings do provide some insight into the potential toxicity of the 
amine constituent.
    A summary of the toxicological data considered as part of this 
action is given below:
    1. Isopropylamine dodecylbenzene sulfonate (CAS No. 26264-05-1). In 
an oral gavage OPPTS Harmonized Test Guideline 870.3650 combined 
repeated dose toxicity study with the reproduction/developmental 
toxicity screening tests, the parental LOAEL was 320 milligrams/
kilograms/day (mg/kg/day) (highest dose tested, (HDT)) based on 
excessive salivation (both sexes), soft/liquid feces (males), lesions 
of the forestomach (both sexes). No reproductive or developmental 
toxicity or neurotoxicity was observed. The NOAEL was 80 mg/kg/day.
    2. Ethanolamine (CAS No. 141-43-5). Ethanolamine is not acutely 
toxic in rats by the oral route of exposure but appears to be very 
acutely toxic by the dermal route of exposure, although this may be a 
species-specific effect in the rabbit. It is a skin sensitizer and is 
corrosive to the eye and skin. There is no evidence of mutagenicity in 
the Ames, Saccharomyces cerevisiae gene conversion, mouse micronucleus, 
cell transformation, and SCE human lymphocytes tests. In a dermal rat 
developmental toxicity study conducted with ethanolamine, no maternal 
or developmental toxicity was observed at 225 mg/kg/day (HDT). Also in 
a dermal rabbit developmental toxicity study, no maternal or 
developmental toxicity was observed at 75 mg/kg/day (HDT). In an oral 
rat developmental toxicity study, the maternal LOAEL was 450 mg/kg/day 
(HDT) based on decreased body weights during the latter part of 
gestation and throughout lactation. The developmental LOAEL was 450 mg/
kg/day based on decrease body weights in female fetuses on postnatal 
day (PND) 1 and 4. The maternal/developmental NOAEL was 120 mg/kg/day.
    3. Triethanolamine (CAS No. 102-71-6). In acute toxicity studies, 
triethanolamine is mildly to moderately toxic by the oral and dermal 
routes of

[[Page 38927]]

exposure. It is not irritating in eye and skin irritation studies, and 
it is not a skin sensitizer. There is no evidence of mutagenicity in 
the Ames, mouse micronucleus, sex-linked recessive lethal, and Chinese 
hamster ovary (CHO) cell cytogenetics tests. In a 14-day inhalation 
study in rat, the NOAEL was 0.25 milligram/liter (mg/L) (approximate 
oral equivalent dose of 75 mg/kg/day) and the LOAEL was 0.5 mg/L based 
on increased kidney weights of males and females. In an oral mouse 
developmental toxicity study (Chernoff-Kavlock screening test), no 
maternal or developmental toxicity was observed at 1,125 mg/kg/day 
(only dose tested). In a 13-week dermal study in rat, the NOAEL was 
1,000 mg/kg/day and the LOAEL was 2,000 mg/kg/day (HDT) based on 
reduced body gain and clinical observations (irritation, scaliness, and 
crustiness of the skin at the site of application). In a 13-week dermal 
study in mouse, the NOAEL was 2,000 mg/kg/day and the LOAEL was 4,000 
mg/kg/day (HDT) based on clinical observations (irritation, scaliness, 
and discoloration of the skin at the site of application).
    4. Isopropylamine (CAS No. 75-31-0). In acute toxicity studies, 
isopropylamine is moderately acutely toxic in rats by the oral route of 
exposure, but is less toxic by the dermal route and is not toxic by the 
inhalation route of exposure. Rabbits appear to be more sensitive than 
rats showing significantly greater acute toxicity by the dermal route. 
Isopropylamine is not a skin sensitizer. There is no evidence of 
mutagenicity in the Ames, chromosomal aberrations in human lymphocytes 
and unscheduled DNA synthesis in rat hepatocytes tests. In a 28-day 
inhalation study, Sprague-Dawley rats were exposed to inhalation dosage 
levels of 0, 0.1, 0.5, and 1.35 mg/L for 6 hours/day for 5 days/week. 
The NOAEL was 0.1 mg/L and the LOAEL was 0.5 mg/L based on microscopic 
ocular and nasal lesions. In a developmental study, Sprague-Dawley rats 
were exposed to inhalation dosage levels of 0, 0.1, 0.5, and 1.0 mg/L 
for 6 hours/day from gestation day (GD) 6 through 15. The maternal 
toxicity was observed at 1.0 mg/L (HDT) based on decreased body weight 
and body weight gain. At this dose, no developmental toxicity was 
observed.
    5. Dimethylaminopropylamine (CAS No. 109-55-7). 
Dimethylaminopropylamine is mild to moderately toxic by the oral and 
inhalation routes of exposure, but it is not a skin sensitizer. There 
is no evidence of mutagenicity in the Ames and mouse micronucleus 
tests. Following a 28-day gavage study in Wistar rats, mortality (4/5 
females) and clinical signs (males: irregular respiration and 
respiratory sounds; females: decreased spontaneous activity, stilted 
gait, swollen abdomen, and impaired respiration) were observed at 250 
mg/kg/day (HDT). In an OPPTS Harmonized Test Guideline 870.3550 
reproduction and developmental toxicity screening test in Sprague-
Dawley rats, parental toxicity was observed at 200 mg/kg/day (HDT) 
based on decreased body weight gain and clinical signs (respiratory 
sounds and piloerection). Reproductive and developmental toxicity were 
not observed at any dose level.
    6. Diethanolamine (CAS No. 11-42-2). The existing toxicology 
database for diethanolamine (DEA) consists of several subchronic oral 
and dermal toxicity studies in rats and mice, carcinogenicity studies 
in rats and mice, oral and dermal developmental toxicity studies in 
rats and rabbits, and acute and mutagenicity data. Following repeat 
oral exposure to DEA, the kidney, liver, and blood are the major target 
organs. Repeat oral exposure via drinking water resulted in a 
microcytic anemia that does not involve the bone marrow in rats at 97 
mg/kg/day in males and 57 mg/kg/day in females. Increased kidney 
weights were associated with renal tubular cell necrosis, decreased 
renal function, increased incidences or severity of nephropathy, and/or 
mineralization in rats at 97 mg/kg/day (males) and 57 mg/kg/day 
(females) and in mice at 104 mg/kg/day (lowest dose tested, (LDT)) in 
males and 142 mg/kg/day (LDT) in females. Increased liver weights were 
associated with cytoplasmic vacuolization and degeneration of 
centrilobular hepatocytes in rats and hypertrophy, individual cell 
necrosis or foci of necrotic hepatocytes in mice. Dose-related 
decreases in testis and epididymis weights were associated with 
testicular degeneration, decreased sperm motility, and decreased sperm 
count in male rats at 97 mg/kg/day. Similar kidney and liver effects 
were observed following repeat dermal exposure at dose levels of 32/mg/
kg/day in rats and 80 mg/kg/day in mice. Demyelination in the brain 
(medulla oblongata) and spinal cord was observed in rats of both sexes 
following oral and dermal exposure at dose levels as low as 250 mg/kg/
day, with the female being more sensitive. Mortality and neurological 
symptoms (tremors, stiffness, and ataxia progressing to paresis and 
paralysis) have been reported following exposure via over-the-counter 
oral flea treatment (53% DEA) of dogs and cats, however, there are no 
registered pet care use products containing the DEA salt form of 
ASABSA.
    Developmental toxicity was observed in rats following both oral and 
dermal exposure to the maternal animal during gestation days (GD) 6-15. 
Maternal toxicity, as evidenced by decreased body weight/gain and food 
consumption and/or increased kidney weight, was observed at the same 
dose levels (125 mg/kg/day) as the developmental effects [an increase 
in postnatal mortality (PND 0 through 4), an increase in 
postimplantation loss, and reduced pup body weight following oral 
exposure. An increased incidence of skeletal variations was observed 
following dermal exposure at 1500 mg/kg/day (HDT) ]. Developmental 
toxicity was not observed in rabbits following oral or dermal exposure 
of the maternal animal during GD 6 through 18.
    7. Metabolism. The alkyl (C8-C24) 
benzenesulfonic acid amine salts undergo rapid dissociation in vivo to 
form an alkyl (C8-C24) benzenesulfonic acid and 
an amine. The two entities would be absorbed and metabolized 
independently. The alkyl (C8-C24) benzenesulfonic 
acid should be readily conjugated and rapidly excreted with little 
alkyl aromatic chain degradation (JITF Submission, 2008, pages 11 and 
21). Primary, secondary or tertiary amines should undergo oxidative 
amine metabolism followed by excretion. Primary aliphatic amines 
(ethanolamine, isopropylamine) are oxidized to aldehydes/ketones and or 
acid (glycolic acid or acetone) with release of ammonia. The glycolic 
acid may further oxidized and or conjugated and excreted. The acetone 
could be excreted through respiration or further oxidized to 
methylglyoxyl and then excreted. Secondary aliphatic amines 
(dimethylaminopropylamine and diethanolamine) may follow various 
oxidative patterns and some are excreted unchanged. Small molecular 
weight amines may be exhaled via respiration. Tertiary aliphatic amines 
(triethanolamine) may be oxidized to amine oxides, which may be 
excreted in the urine or deaminated with the eventual resultant being 
release of glycolic acid which may be further oxidized and or 
conjugated and excreted.
    Specific information on the studies received and the nature of the 
adverse effects caused by ASABSA and its constituents as well as the 
no-observed-adverse-effect-level (NOAEL) and the lowest-observed-
adverse-effect-level (LOAEL) from the toxicity studies can

[[Page 38928]]

be found at http://www.regulations.gov in documents 
``Dimethylaminopropylamine, Isopropylamine, Ethanolamine and 
Triethanolamine Salts of Alkyl (C8-C24) 
Benzenesulfonic Acid (JITF CST 8 Inert Ingredients). Human Health Risk 
Assessment to Support Proposed Exemption from the Requirement of a 
Tolerance When Used as Inert Ingredients in Pesticide Formulations and 
Diethanolamine Salt of Alkyl (C8-C24) 
Benzenesulfonic Acid (DEA - JITF CST 8 Inert Ingredient). Human Health 
Risk Assessment to Support Proposed Exemption from the Requirement of a 
Tolerance When Used as Inert Ingredients in Pesticide Formulations,'' 
in docket ID number EPA-HQ-OPP-2008-0889 and at http://www.epa.gov/
opprd001/inerts/alkylc8.pdf.

B. Toxicological Endpoints

    For hazards that have a threshold below which there is no 
appreciable risk, a toxicological point of departure (POD) is 
identified as the basis for derivation of reference values for risk 
assessment. The POD may be defined as the highest dose at which no 
adverse effects are observed (the NOAEL) in the toxicology study 
identified as appropriate for use in risk assessment. However, if a 
NOAEL cannot be determined, the lowest dose at which adverse effects of 
concern are identified (the LOAEL) or a Benchmark Dose (BMD) approach 
is sometimes used for risk assessment. Uncertainty/safety factors (UFs) 
are used in conjunction with the POD to take into account uncertainties 
inherent in the extrapolation from laboratory animal data to humans and 
in the variations in sensitivity among members of the human population 
as well as other unknowns. Safety is assessed for acute and chronic 
dietary risks by comparing aggregate food and water exposure to the 
pesticide to the acute population adjusted dose (aPAD) and chronic 
population adjusted dose (cPAD). The aPAD and cPAD are calculated by 
dividing the POD by all applicable UFs. Aggregate short-, intermediate-
, and chronic-term risks are evaluated by comparing food, water, and 
residential exposure to the POD to ensure that the margin of exposure 
(MOE) called for by the product of all applicable UFs is not exceeded. 
This latter value is referred to as the Level of Concern (LOC).
    For non-threshold risks, the Agency assumes that any amount of 
exposure will lead to some degree of risk. Thus, the Agency estimates 
risk in terms of the probability of an occurrence of the adverse effect 
greater than that expected in a lifetime. For more information on the 
general principles EPA uses in risk characterization and a complete 
description of the risk assessment process, see http://www.epa.gov/
pesticides/factsheets/riskassess.htm.
    A summary of the toxicological endpoints for ASABSA used for human 
health risk is shown in the following Table 1.

    Table 1.--Summary of Toxicological Doses and Endpoints for ASABSA for Use in Human Health Risk Assessment
----------------------------------------------------------------------------------------------------------------
                                     Point of Departure and
         Exposure/Scenario             Uncertainty/Safety    RfD, PAD, LOC for Risk    Study and Toxicological
                                             Factors               Assessment                  Effects
----------------------------------------------------------------------------------------------------------------
Acute dietary (all populations)            An effect attributable to a single exposure was not identified.
----------------------------------------------------------------------------------------------------------------
Chronic dietary (all populations)    NOAEL = 50 mg/kg/day    Chronic RfD = 0.5 mg/   28-day oral (gavage)
 dimethylaminopropylamine,           UFA = 10x.............   kg/day                  toxicity study in rats
 isopropylamine, ethanolamine, and   UFH = 10x.............  cPAD = 0.5 mg/kg/day..   with
 triethanolamine salts of alkyl (C8- FQPA SF = 1x..........                           dimethylaminopropylamine
 C24) benzenesulfonic acid.                                                          NOAEL = 50 mg/kg
                                                                                     LOAEL = 250 mg/kg based on
                                                                                      mortality (4/5 females)
                                                                                      and clinical signs (males:
                                                                                      irregular respiration and
                                                                                      respiratory sounds;
                                                                                      females: decreased
                                                                                      spontaneous activity,
                                                                                      stilted gait, swollen
                                                                                      abdomen, impaired
                                                                                      respiration) OECD SIDS.
                                                                                      UNEP Publication and BUA
                                                                                      Report, October 1996 plus
                                                                                      weight of evidence of
                                                                                      three studies with
                                                                                      alkylbenzene sulfonates:
                                                                                     1) Rat reproduction study
                                                                                      LOAEL = 250 mg/kg/day
                                                                                      based on decreased Day 21
                                                                                      female pup body weight
                                                                                      (Buehler, E. et al. 1971.
                                                                                      Tox. Appl. Pharmacol.18:83-
                                                                                      91)
                                                                                     2) 9-month drinking water
                                                                                      rat study
                                                                                     LOAEL = 145 mg/kg/day based
                                                                                      on decreased body weight
                                                                                      gain, and serum/
                                                                                      biochemical and enzymatic
                                                                                      changes in the liver
                                                                                      andkidney (Yoneyama et al.
                                                                                      1976 Ann. Rep. Tokyo
                                                                                      Metrop. Res.Lab. Public
                                                                                      Health 27(2):105-112)
                                                                                     3) 6-month rat dietary
                                                                                      study
                                                                                     LOAEL = 114 mg/kg/day
                                                                                      (0.2%) based on increased
                                                                                      caecum weight and slight
                                                                                      kidney damage (Yoneyama et
                                                                                      al 1972 Ann. Rep. Tokyo
                                                                                      Metrop. Res. Lab. Public
                                                                                      Health 24:409-440)
----------------------------------------------------------------------------------------------------------------

[[Page 38929]]


Chronic dietary (all populations)    NOAEL = 48 mg/kg/day    Chronic RfD = 0.5 mg/   Subchronic (13-week) oral
 diethanolamine salt of alkyl (C8-   UFA = 10x.............   kg/day                  toxicity study in rats
 C24) benzenesulfonic acid           UFH = 10x.............  cPAD = 0.05 mg/kg/day.   (NTP, 1992)
                                     FQPA SF = 10x.........                          Female LOAEL = 124 mg/kg/
                                                                                      day demyelination of the
                                                                                      brain and spinal cord
                                                                                     Male LOAEL = 97 mg/kg/day,
                                                                                      based on decreased testis
                                                                                      and epididymis weight
                                                                                      associated with
                                                                                      degeneration of
                                                                                      seminiferous epithelium,
                                                                                      decreased numbers of
                                                                                      spermatogenic cells,
                                                                                      reduced size of
                                                                                      seminiferous tubules,
                                                                                      decreased sperm, sperm
                                                                                      motility, and sperm count
----------------------------------------------------------------------------------------------------------------
Incidental Oral and Inhalation       NOAEL = 50 mg/kg/day    Residential LOC for     28-day oral (gavage)
 short-term (1 to 30 days) and       UFA = 10x.............   MOE = 100               toxicity study in rats
 intermediate-term (1 to 6 months)   UFH = 10x.............                           with
 dimethylaminopropylamine,           FQPA SF = 1x..........                           dimethylaminopropylamine
 isopropylamine, ethanolamine, and   inhalation toxicity is                          NOAEL = 50 mg/kg
 triethanolamine salts of alkyl (C8-  assumed to be                                  LOAEL = 250 mg/kg based on
 C24) benzenesulfonic acid.           equivalent to oral                              mortality (4/5 females)
                                      toxicity.                                       and clinical signs (males:
                                                                                      irregular respiration and
                                                                                      respiratory sounds;
                                                                                      females: decreased
                                                                                      spontaneous activity,
                                                                                      stilted gait, swollen
                                                                                      abdomen, impaired
                                                                                      respiration) OECD SIDS.
                                                                                      UNEP Publication and BUA
                                                                                      Report, October 1996 plus
                                                                                      weight of evidence of
                                                                                      three studies with
                                                                                      alkylbenzene sulfonates:
                                                                                     1) Rat reproduction study
                                                                                      LOAEL = 250 mg/kg/day
                                                                                      based on decreased Day 21
                                                                                      female pup body weight
                                                                                      (Buehler, E. et al. 1971.
                                                                                      Tox. Appl. Pharmacol.18:83-
                                                                                      91)
                                                                                     2) 9-month drinking water
                                                                                      rat study LOAEL = 145 mg/
                                                                                      kg/day based on decreased
                                                                                      body weight gain, and
                                                                                      serum/ biochemical and
                                                                                      enzymatic changes in the
                                                                                      liver andkidney (Yoneyama
                                                                                      et al. 1976 Ann. Rep.
                                                                                      Tokyo Metrop. Res. Lab.
                                                                                      Public Health 27(2):105-
                                                                                      112)
                                                                                     3) 6-month rat dietary
                                                                                      study LOAEL = 114 mg/kg/
                                                                                      day (0.2%) based on
                                                                                      increased caecum weight
                                                                                      and slight kidney damage
                                                                                      (Yoneyama et al 1972 Ann.
                                                                                      Rep. Tokyo Metrop. Res.
                                                                                      Lab. Public Health 24:409-
                                                                                      440)
----------------------------------------------------------------------------------------------------------------
Incidental Oral and Inhalation       NOAEL = 48 mg/kg/day    Residential LOC for     Subchronic (13-week) oral
 short-term (1 to 30 days) and       UFA = 10x.............   MOE = 1,000             toxicity study in rats
 intermediate-term (1 to 6 months)-- UFH = 10x.............                           (NTP, 1992)
  diethanolamine salt of alkyl (C8-  FQPA SF = 10x.........                          Female LOAEL = 124 mg/kg/
 C24) benzenesulfonic acid.          inhalation toxicity is                           day based on demyelination
                                      assumed to be                                   of the brain and spinal
                                      equivalent to oral                              cord
                                      toxicity.                                      Male LOAEL = 97 mg/kg/day,
                                                                                      based on decreased testis
                                                                                      and epididymis weight
                                                                                      associated with
                                                                                      degeneration of
                                                                                      seminiferous epithelium,
                                                                                      decreased numbers of
                                                                                      spermatogenic cells,
                                                                                      reduced size of
                                                                                      seminiferous tubules,
                                                                                      decreased sperm, sperm
                                                                                      motility, and sperm count
----------------------------------------------------------------------------------------------------------------
Dermal (short- and intermediate-        No systemic toxicity observed in available dermal toxicity study. Low
 term) -- dimethylaminopropylamine,     potential for dermal absorption to ionized amine. No quantitative risk
 isopropylamine, ethanolamine, and                                assessment required
 triethanolamine salts of alkyl (C8-
 C24) benzenesulfonic acid.
----------------------------------------------------------------------------------------------------------------
Dermal (short- and intermediate-     NOAEL = 125 mg/kg/day   Residential LOC for
 term) -- diethanolamine salt of     UFA = 10x.............   MOE = 1,000
 alkyl (C8-C24) benzenesulfonic      UFH = 10x.............
 acid                                FQPA SF = 10x.........
----------------------------------------------------------------------------------------------------------------

[[Page 38930]]


Cancer (oral, dermal, inhalation)        Classification: Based on SAR analysis, ASABSA is not expected to be
                                       carcinogenic. No evidence of carcinogenicity in the available data or SAR
                                            analysis for alkyl benzenesulfonates, dimethylaminopropylamine,
                                           isopropylamine, ethanolamine, and triethanolamine. No concern for
                                        diethanolamine based on SAR analysis, limited evidence in experimental
                                             animals; not classifiable as to its carcinogenicity to humans
----------------------------------------------------------------------------------------------------------------
 Point of Departure (POD) = A data point or an estimated point that is derived from observed dose-response data
  and used to mark the beginning of extrapolation to determine risk associated with lower environmentally
  relevant human exposures. NOAEL = no observed adverse effect level. LOAEL = lowest observed adverse effect
  level. UF = uncertainty factor. UFA = extrapolation from animal to human (interspecies). UFH = potential
  variation in sensitivity among members of the human population (intraspecies). PAD = population adjusted dose
  (a=acute, c=chronic). FQPA SF = FQPA Safety Factor. RfD = reference dose. MOE = margin of exposure. LOC =
  level of concern. N/A = not applicable.

C. Exposure Assessment

    Very limited information is available for ASABSA with respect to 
plant and animal metabolism or environmental degradation. The Agency 
relied collectively on information provided on the representative 
chemical structures, the generic cluster structures, the modeled 
physicochemical information, as well as the structure-activity 
relationship information. Additionally, information on other 
surfactants and chemicals of similar size and functionality was 
considered to determine the residues of concern for these inert 
ingredients. ASABSA are likely to be fully dissociated in solution. If 
dissociated amine counter ion or alkylbenzenesulfonic acid residues on 
plants and livestock undergo any metabolism or hydrolysis, they will 
likely result as highly polar or conjugated residues, which would not 
be of concern.
    1. Dietary exposure from food and feed uses. In evaluating dietary 
exposure to ASABSA, EPA considered exposure under the petitioned-for 
exemptions from the requirement of a tolerance. EPA assessed dietary 
exposures from ASABSA in food as follows:
    i. Acute exposure. No adverse effects attributable to a single 
exposure of ASABSA were seen in the toxicity databases. Therefore, an 
acute dietary risk assessment for ASABSA is not necessary.
    ii. Chronic exposure. In conducting the chronic dietary exposure 
assessment for ASABSA, EPA used food consumption information from the 
U.S. Department of Agriculture (USDA) 1994-1996 and 1998 Nationwide 
Continuing Surveys of Food Intake by Individuals (CSFII). As to residue 
levels in food, no residue data were submitted for ASABSA. 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 can be found at http://www.regulations.gov in the 
document ``Alkyl Amines Polyalkoxylates (Cluster 4): Acute and Chronic 
Aggregate (Food and Drinking Water) Dietary Exposure and Risk 
Assessments for the Inerts'', 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 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 
concentrations of active ingredient in agricultural products are 
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 relative to that of 
the active ingredient. EPA made a specific adjustment to the dietary 
exposure assessment to account for the use limitations of the amount of 
diethanolamine salts of alkyl (C8-C24) 
benzenesulfonic acid that may be in formulations (no more than 7%, 
which corresponds to a concentration of 2% diethanolamine) and assumed 
that the diethanolamine salts of alkyl (C8-C24) 
benzenesulfonic acid are at the maximum limitations rather than at 
equal quantities with the active ingredient. This remains a very 
conservative assumption because surfactants are generally used at 
levels far below these percentages. For example, EPA examined several 
of the pesticide products associated with the tolerance/commodity 
combination which are the driver of the risk assessment and found that 
these products did not contain surfactants at levels greater than 2.25% 
and that none of the surfactants were diethanolamine salts of alkyl 
(C8-C24) benzenesulfonic acid.
    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.

[[Page 38931]]

In summary, EPA chose a very conservative method for estimating what 
level of inert residue could be on food, and then used 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.
    iii. Cancer. The Agency used a qualitative structure activity 
relationship (SAR) database, DEREK11, to determine if there were 
structural alerts suggestive of carcinogenicity. No structural alerts 
for carcinogenicity were identified. Additionally, there is not 
evidence of carcinogenicity of the ASABSA amine or alkylbenzenesulfonic 
acid constituents. Therefore, a cancer dietary exposure assessment is 
not necessary to assess cancer risk.
    iv. Anticipated residue and percent crop treated (PCT) information. 
EPA did not use anticipated residue and/or PCT information in the 
dietary assessment for ASABSA. Tolerance level residues and/or 100% 
crop treated were assumed for all food commodities.
    2. Dietary exposure from drinking water. The Agency used screening 
level water exposure models in the dietary exposure analysis and risk 
assessment for ASABSA in drinking water. These simulation models take 
into account data on the physical, chemical, and fate/transport 
characteristics of ASABSA. Further information regarding EPA drinking 
water models used in the pesticide exposure assessment can be found at 
http://www.epa.gov/oppefed1/models/water/index.htm.
    A screening level drinking water analysis, based on the Pesticide 
Root Zone Model/Exposure Analysis Modeling System (PRZM/EXAMS) was 
performed to calculate the estimated drinking water concentrations 
(EDWCs) of ASABSA. Modeling runs on four surrogate inert ingredients 
using a range of physical chemical properties that would bracket those 
of ASABSA were conducted. Modeled acute drinking water values ranged 
from 0.001 parts per billion (ppb) to 41 ppb. Modeled chronic drinking 
water values ranged from 0.0002 ppb to 19 ppb. Further details of this 
drinking water analysis can be found at http://www.regulations.gov in 
the documents ``Dimethylaminopropylamine, Isopropylamine, Ethanolamine 
and Triethanolamine Salts of Alkyl (C8-C24) 
Benzenesulfonic Acid (JITF CST 8 Inert Ingredients). Human Health Risk 
Assessment to Support Proposed Exemption from the Requirement of a 
Tolerance When Used as Inert Ingredients in Pesticide Formulations and 
Diethanolamine Salt of Alkyl (C8-C24) 
Benzenesulfonic Acid (DEA - JITF CST 8 Inert Ingredient). Human Health 
Risk Assessment to Support Proposed Exemption from the Requirement of a 
Tolerance When Used as Inert Ingredients in Pesticide Formulations,'' 
in docket ID number EPA-HQ-OPP-2008-0889.
    For the purpose of the screening level dietary risk assessment to 
support this request for an exemption from the requirement of a 
tolerance for ASABSA, a conservative drinking water concentration value 
of 100 ppb based on screening level modeling was used to assess the 
contribution to drinking water for chronic dietary risk assessments for 
the parent compounds and for the metabolites of concern. These values 
were directly entered into the dietary exposure model.
    3. 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). ASABSA may be used as 
inert ingredients in pesticide products that are registered for 
specific uses that may result in outdoor residential exposures. A 
screening level residential exposure and risk assessment was completed 
for pesticide products containing ASABSA as inert ingredients. In this 
assessment, representative scenarios, based on end-use product 
application methods and labeled application rates, were selected. For 
each of the use scenarios, the Agency assessed residential handler 
(applicator) inhalation and dermal exposure for use scenarios with high 
exposure potential (i.e., exposure scenarios with high-end unit 
exposure values) to serve as a screening assessment for all potential 
residential pesticides containing ASABSA. Similarly, residential 
postapplication dermal and oral exposure assessments were also 
performed utilizing high-end exposure scenarios. Further details of 
this residential exposure and risk analysis can be found at http://
www.regulations.gov in the document ``JITF Inert Ingredients. 
Residential and Occupational Exposure Assessment Algorithms and 
Assumptions Appendix for the Human Health Risk Assessments to Support 
Proposed Exemption from the Requirement of a Tolerance When Used as 
Inert Ingredients in Pesticide Formulations,'' in docket ID number EPA-
HQ-OPP-2008-0710.
    4. 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 ASABSA to share a common mechanism of toxicity 
with any other substances, and ASABSA do not appear to produce a toxic 
metabolite produced by other substances. For the purposes of this 
tolerance action, therefore, EPA has assumed that ASABSA do 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.

D. Safety Factor for Infants and Children

    1. In general. Section 408(b)(2)(C) of FFDCA provides that EPA 
shall apply an additional tenfold (10X) margin of safety for infants 
and children in the case of threshold effects to account for prenatal 
and postnatal toxicity and the completeness of the database on toxicity 
and exposure unless EPA determines based on reliable data that a 
different margin of safety will be safe for infants and children. This 
additional margin of safety is commonly referred to as the FQPA safety 
factor (SF). In applying this provision, EPA either retains the default 
value of 10X, or uses a different additional safety factor when 
reliable data available to EPA support the choice of a different 
factor.
    2. Prenatal and postnatal sensitivity.--i. Dimethylaminopro-
pylamine, isopropylamine, ethanolamine, and triethanolamine salts of 
alkyl (C8-C24) benzenesulfonic acid. The 
available mammalian toxicology database for dimethylaminopropylamine, 
isopropylamine, ethanolamine, and triethanolamine salts of alkyl 
(C8-C24) benzenesulfonic is complete with respect 
to assessing the increased susceptibility to infants and

[[Page 38932]]

children as required by FQPA for the dimethylaminopropylamine, 
isopropylamine, ethanolamine and triethan-olamine salts of alkyl 
(C8-C24) benzenesulfonic acid. There was no 
increased susceptibility to the offspring of rats following prenatal 
and postnatal exposure in the OPPTS Harmonized Test Guidelines 870.3550 
and 870.3650 reproductive/developmental screening studies, and 
developmental effects studies.
    There was no increased susceptibility to the offspring of rats 
following prenatal and postnatal exposure in the OPPTS Harmonized Test 
Guideline 870.3650 study with isopropylamine dodecylbenzene sulfonate. 
Developmental toxicity was not observed, whereas parental toxicity was 
manifested as excessive salivation in both sexes, soft feces in males, 
and lesions of the forestomach in both sexes. No increased 
susceptibility was observed in offspring of rats following exposure in 
the OPPTS Harmonized Test Guideline 870.3550 study with 
dimethylaminopropylamine. Developmental toxicity was not observed, 
whereas parental toxicity was manifested as decreased body-weight gain 
and clinical signs. Susceptibility was not demonstrated in the 
offspring in a rat developmental toxicity study with isopropylamine 
following inhalation exposure. Developmental toxicity was not observed, 
whereas parental toxicity was manifested as decreased body weight and 
body-weight gain. In developmental toxicity studies with ethanolamine 
following dermal (rat and rabbit) exposure, developmental and maternal 
toxicity were not observed. In a developmental toxicity study, 
increased susceptibility to the offspring was not observed following 
oral exposure to ethanolamine. Developmental toxicity was observed 
(decreased body weight in female fetuses on PND 1-4) at the same dose 
level where maternal toxicity was observed (decreased body weight 
during the latter part of gestation and throughout lactation). Since a 
clear NOAEL of 120 mg/kg/day was identified for offspring effects, and 
the selected point of departure of 50 mg/kg/day (mortality and clinical 
signs) for the dietary and inhalation risk assessments is protective of 
the offspring effects, there are no residual concerns.
    There is no evidence in the available toxicity studies or 
scientific literature to indicate neurotoxic effects of these amines in 
laboratory animals. The clinical signs observed in females in the 28-
day study with dimethylaminopropylamine (stilted gait and decreased 
spontaneous activity are considered agonal in nature.
    The prenatal developmental and reproduction studies with 
alkylbenzene sulfonates showed no qualitative or quantitative evidence 
of increased susceptibility. Several reproduction and many 
developmental studies have been performed with alkylbenzene sulfonates 
in a number of animal species. In the developmental studies, whenever 
toxicity was observed in adults, it was generally for mild effects 
(slight body weight changes, intestinal disturbances) except for severe 
dermal irritation effects in dermal developmental studies. Any 
developmental toxicity observed in these same studies included minor 
increases in visceral/skeletal anomalies and some fetal losses; but 
only at maternally toxic doses. In one reproduction study, there were 
slight changes in hematology and histopathology (both within historical 
control ranges) and slight decreases in body weight in the offspring at 
the highest dose of 250 mg/kg/day (at which there were no effects on 
the parental generation). There were no effects in either the parents 
or offspring in the other two alkyl benzensulfonate reproductive 
toxicity studies at the high dose tested of 70 and 170 mg/kg/day, 
respectively.
    ii. Diethanolamine salt of alkyl (C8-C24) 
benzenesulfonic acid (DEA). There is no OPPTS Harmonized Test Guideline 
870.3650 combined repeated dose toxicity study with the reproduction/
developmental toxicity screening test available on DEA. The toxicology 
database on DEA consists of open literature studies that include oral 
and dermal exposure developmental toxicity studies in rats and a dermal 
exposure developmental toxicity study in rabbits. There are no 
reproductive toxicity or neurotoxicity studies available on DEA.
    No evidence of increased susceptibility to the offspring of rats or 
rabbits following prenatal dermal exposure was located. There was 
qualitative prenatal susceptibility in the rat oral developmental 
toxicity study. The developmental findings with a NOAEL of 50 mg/kg/day 
were well-characterized and included increased developmental 
sensitivity in the form of increased postnatal day (PND) 0 through 4 
mortality and post implantation loss, and reduced pup body weight at 
125 mg/kg/day (developmental LOAEL). The maternal toxicity NOAEL/LOAEL 
of 50/125 mg/kg/day was based on increased absolute liver weight. 
Developmental toxicity was demonstrated in the rat following dermal 
exposure to the maternal animal during gestation days (GD) 6 through 
15, as evidenced by increased incidence of skeletal variations at 1500 
mg/kg/day (HDT). The NOAEL for developmental toxicity was 500 mg/kg/
day; the LOAEL for maternal toxicity was 150 mg/kg (LDT) based on 
microcytic anemia with abnormal red blooc cell morphology. The degree 
of concern for the increased qualitative susceptibility seen in the 
oral developmental toxicity study in rats (prenatal exposure) is low 
since a clear NOAEL/LOAEL was established for oral developmental 
toxicity and since a more sensitive endpoint of concern (48 mg/kg/day, 
the NOAEL from the rat subchronic toxicity study) has been utilized in 
assessing the risks from incidential and chronic oral exposure to the 
diethanolamine salt of alkyl (C8-C24) benzenesulfonic acid.
    Demyelination has been observed in the brain (medulla) and spinal 
cord of rats following oral and dermal exposure, and decreased testis 
and epididymis weights associated with degeneration of seminiferous 
epithelium, decreased numbers of spermatogenic cells, reduced size of 
seminiferous tubules, decreased sperm; decreased sperm motility and 
sperm count have been observed in male rats following oral exposure.
    DEA is structurally related to the essential nutrient choline, and 
choline deficiency during pregnancy has been shown to reduce 
neurogenesis and increase apoptosis in rat and mouse fetal hippocampus. 
In the open literature, DEA has been shown to alter neurogenesis and 
induce apoptosis in fetal mouse hippocampus following dermal exposure 
of the maternal animal to DEA during pregnancy.
    The existing toxicology database is not adequate for assessing the 
sensitivity of infants and children to DEA exposure because a 
reproduction study is not available and in light of the findings in 
adult animals (demyelination in the brain and spinal cord and 
degeneration of the seminiferous tubules of the testis) that suggest 
the potential for developmental, reproductive, and/or 
neurodevelopmental toxicity in the young animal. The particular 
findings in the parental animals lead to uncertainties for the 
offspring. There is a concern for neurodevelopment since this is not 
addressed in the currently available database.
    3. Conclusion.--i. Dimethylaminopropylamine, isopropylamine, 
ethanolamine, and triethanolamine salts of alkyl (C8-
C24) benzenesulfonic acid. EPA has determined that reliable 
data show that the safety of infants and children would be adequately 
protected if the

[[Page 38933]]

FQPA SF were reduced to 1X. That decision is based on the following 
findings:
    a. The toxicity database for dimethylaminopropylamine, 
isopropylamine, ethanolamine, and triethanolamine salts of alkyl 
(C8-C24) benzenesulfonic acid is considered 
adequate for assessing the risks to infants and children to 
dimethylaminopropylamine, isopropylamine, ethanolamine and 
triethanolamine salts of alkyl (C8-C24) 
benzenesulfonic acid exposures (the available studies are described in 
Unit IV.D.2.).
    b. No susceptibility was demonstrated in the offspring in the OPPTS 
Harmonized Guideline 870.3650 combined repeated dose toxicity study 
with the reproduction/developmental toxicity screening test in rats 
with isopropylamine dodecylbenzene sulfonate following prenatal and 
postnatal exposure.
    c. No susceptibility was demonstrated in the offspring in the OPPTS 
Harmonized Guideline 870.3550 reproduction/developmental toxicity 
screening test with dimethylaminopropylamine following prenatal and 
postnatal exposure.
    d. No susceptibility was demonstrated in the offspring in an 
inhalation developmental toxicity study with isopropylamine.
    e. The prenatal developmental and reproduction studies with 
alkylbenzene sulfonates showed no qualitative or quantitative evidence 
of increased susceptibility. Slight changes in hematology and 
histopathology (both within historical control ranges) and slight 
decreases in body weight in the offspring at the highest dose of 250 
mg/kg/day (at which there were no effects on the parental generation) 
were seen with alkylbenzenesulfonate in one reproduction study, however 
there were no effects in either the parents or offspring in the other 
two alkyl benzensulfonate reproductive toxicity studies at the high 
dose tested of 70 mg/kg/day and 170 mg/kg/day, respectively. Since the 
selected point of departure of 50 mg/kg/day (mortality and clinical 
signs) for the dietary and inhalation risk assessments is protective of 
the offspring effects, there are no residual concerns.
    f. No susceptibility was demonstrated in the offspring in dermal 
(rat and rabbit) and oral (rat) developmental toxicity studies with 
ethanolamine. Developmental toxicity was observed following oral 
exposure with ethanolamine at the same dose level where maternal 
toxicity was observed. Since a clear NOAEL of 120 mg/kg/day was 
identified for offspring effects, and the selected point of departure 
of 50 mg/kg/day (mortality and clinical signs) for the dietary and 
inhalation risk assessments is protective of the offspring effects, 
there are no residual concerns.
    g. No evidence of neurotoxicity was demonstrated in the database 
for alkylbenzene sulfonates, dimethylaminopropylamine, isopropylamine, 
ethanolamine, and triethanolamine and isopropylamine salt of 
dodecylbenzenesulfonic acid and thus there is no need for a 
developmental neurotoxicity study or additional UFs to account for 
neurotoxicity.
    h. There are no residual uncertainties identified in the exposure 
databases. The food and drinking water assessment is not likely to 
underestimate exposure to any subpopulation, including those comprised 
of infants and children. The food exposure assessments are considered 
to be highly conservative as they are based on the use of the highest 
tolerance level from the surrogate pesticides for every food and 100 
PCT is assumed for all crops. EPA also made conservative (protective) 
assumptions in the ground and surface water modeling used to assess 
exposure to ASABSA in drinking water. EPA used similarly conservative 
assumptions to assess post application exposure of children as well as 
incidental oral exposure of toddlers. These assessments will not 
underestimate the exposure and risks posed by ASABSA.
    ii. Diethanolamine salts of alkyl (C8-C24) 
benzenesulfonic acid. EPA has determined that the FQPA SF should be 
retained. That decision is based on the following findings:
    a. Although no increased susceptibility was demonstrated in the 
offspring in the available dermal studies in rats and rabbits following 
prenatal exposure to DEA, and the degree of concern is low for the 
increased qualitative susceptibility seen in the oral developmental 
toxicity study in rats, considering the limited data in the literature 
on DEA, which indicate a potential for developmental and/or 
reproductive and/or developmental neurotoxicity effects, the toxicology 
database for DEA is not considered adequate for assessing the 
sensitivity of infants and children to DEA when used as an inert 
ingredient (the available studies are described in Unit IV.D.2.).
    b. There are no neurotoxicity studies available on DEA.
    c. There are no reproductive toxicity studies available on DEA.
    d. There are no developmental toxicity studies available on DEA 
that assess neurodevelopment.

E. Aggregate Risks and Determination of Safety

    EPA determines whether acute and chronic pesticide exposures are 
safe by comparing aggregate exposure estimates to the aPAD and cPAD. 
The aPAD and cPAD represent the highest safe exposures, taking into 
account all appropriate SFs. EPA calculates the aPAD and cPAD by 
dividing the POD by all applicable UFs. For linear cancer risks, EPA 
calculates the probability of additional cancer cases given the 
estimated aggregate exposure. Short-, intermediate-, and chronic-term 
risks are evaluated by comparing the estimated aggregate food, water, 
and residential exposure to the POD to ensure that the MOE called for 
by the product of all applicable UFs is not exceeded.
    1. Acute risk.There was no hazard attributable to a single exposure 
seen in the toxicity database for ASABSA. Therefore, ASABSA are not 
expected to pose an acute risk.
    2. Chronic 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 this unit 
for chronic exposure, including the limitation of use of diethanolamine 
salts of alkyl (C8-C24) benzenesulfonic acid to 
not more than 7% of the pesticide product, the chronic dietary exposure 
from food and water to dimethylaminopropylamine, isopropylamine, 
ethanolamine and triethanolamine salts of alkyl (C8-
C24) benzenesulfonic acid, is 23% of the cPAD for the U.S. 
population and 75% of the cPAD for children 1 to 2 years old, the most 
highly exposed population subgroup. The chronic dietary exposure from 
food and water to diethanolamine salts of alkyl (C8-
C24) benzenesulfonic acid is 19% of the cPAD for the U.S. 
population and 56% of the cPAD for children 1 to 2 years old, the most 
highly exposed population subgroup.
    3. Short-term 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).
    ASABSA are used as inert ingredients in pesticide products that are 
currently registered for uses that could result in short-term 
residential exposure and the Agency has determined that it is 
appropriate to aggregate chronic exposure through food and water with 
short-term residential exposures to ASABSA. Using the exposure 
assumptions described in this unit, EPA has concluded that the combined 
short-

[[Page 38934]]

term aggregated food, water, and residential exposures result in 
aggregate MOEs of 220 and 260 for adult males and females, 
respectively. Adult residential exposure combines high end outdoor 
dermal and inhalation handler exposure with a high end post application 
dermal exposure from contact with treated lawns. EPA has concluded the 
combined short-term aggregated food, water, and residential exposures 
result in an aggregate MOE of 110 for children. Children's residential 
exposure includes total exposures associated with contact with treated 
lawns (dermal and hand-to-mouth exposures). As the level of concern is 
for MOEs that are lower than 100, these MOEs are not of concern.
    4. Intermediate-term 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).
    ASABSA are used as inert ingredients in pesticide products that are 
currently registered for uses that could result in intermediate-term 
residential exposure and the Agency has determined that it is 
appropriate to aggregate chronic exposure through food and water with 
intermediate-term residential exposures to ASABSA. Using the exposure 
assumptions described in this unit, EPA has concluded that the combined 
intermediate-term aggregated food, water, and residential exposures 
result in aggregate MOEs of 540 and 570 for adult males and females, 
respectively. Adult residential exposure includes high end post 
application dermal exposure from contact with treated lawns. EPA has 
concluded that the combined intermediate-term aggregated food, water, 
and residential exposures result in an aggregate MOE of 110 for 
children. Children's residential exposure includes total exposures 
associated with contact with treated lawns (dermal and hand-to-mouth 
exposures). As the level of concern is for MOEs that are lower than 
100, these MOEs are not of concern.
    5. Aggregate cancer risk for U.S. population. The Agency has not 
identified any concerns for carcinogenicity relating to ASABSA.
    6. Determination of safety. Based on these risk assessments, EPA 
concludes that there is a reasonable certainty that no harm will result 
to the general population or to infants and children from aggregate 
exposure to residues of ASABSA.

V. Other Considerations

A. Analytical Enforcement Methodology

    An analytical method is not required for enforcement purposes since 
the Agency is establishing an exemption from the requirement of a 
tolerance without any numerical limitation.

B. International Residue Limits

    The Agency is not aware of any country requiring a tolerance for 
ASABSA nor have any CODEX Maximum Residue Levels been established for 
any food crops at this time.

VI. Conclusion

    Therefore, an exemption from the requirement of a tolerance is 
established for residues of dimethylaminopropylamine, isopropylamine, 
ethanolamine, and triethanolamine salts of alkyl (C8-
C24) benzenesulfonic acid when used as an inert ingredient 
in pesticide formulations applied to growing crops under 40 CFR 180.920 
and to animals under 40 CFR 180.930 and to diethanolamine salts of 
alkyl (C8-C24) benzenesulfonic acid when used as 
an inert ingredient at levels not to exceed 7% by weight in pesticide 
formulations applied to growing crops under 40 CFR 180.920 and to 
animals under 40 CFR 180.930.

VII. Statutory and Executive Order Reviews

    This final rule establishes an exemption from the requirement of 
tolerances under section 408(d) of FFDCA in response to a petition 
submitted to the Agency. The Office of Management and Budget (OMB) has 
exempted these types of actions from review under Executive Order 
12866, entitled Regulatory Planning and Review (58 FR 51735, October 4, 
1993). Because this final rule has been exempted from review under 
Executive Order 12866, this final rule is not subject to Executive 
Order 13211, entitled Actions Concerning Regulations That Significantly 
Affect Energy Supply, Distribution, or Use (66 FR 28355, May 22, 2001) 
or Executive Order 13045, entitled Protection of Children from 
Environmental Health Risks and Safety Risks (62 FR 19885, April 23, 
1997). This final rule does not contain any information collections 
subject to OMB approval under the Paperwork Reduction Act (PRA), 44 
U.S.C. 3501 et seq., nor does it require any special considerations 
under Executive Order 12898, entitled Federal Actions to Address 
Environmental Justice in Minority Populations and Low-Income 
Populations (59 FR 7629, February 16, 1994).
    Since tolerances and exemptions that are established on the basis 
of a petition under section 408(d) of FFDCA, such as the exemptions in 
this final rule, do not require the issuance of a proposed rule, the 
requirements of the Regulatory Flexibility Act (RFA) (5 U.S.C. 601 et 
seq.) do not apply.
    This final rule directly regulates growers, food processors, food 
handlers, and food retailers, not States or tribes, nor does this 
action alter the relationships or distribution of power and 
responsibilities established by Congress in the preemption provisions 
of section 408(n)(4) of FFDCA. As such, the Agency has determined that 
this action will not have a substantial direct effect on States or 
tribal governments, on the relationship between the national government 
and the States or tribal governments, or on the distribution of power 
and responsibilities among the various levels of government or between 
the Federal Government and Indian tribes. Thus, the Agency has 
determined that Executive Order 13132, entitled Federalism (64 FR 
43255, August 10, 1999) and Executive Order 13175, entitled 
Consultation and Coordination with Indian Tribal Governments (65 FR 
67249, November 9, 2000) do not apply to this final rule. In addition, 
this final rule does not impose any enforceable duty or contain any 
unfunded mandate as described under Title II of the Unfunded Mandates 
Reform Act of 1995 (UMRA) (Public Law 104-4).
    This action does not involve any technical standards that would 
require Agency consideration of voluntary consensus standards pursuant 
to section 12(d) of the National Technology Transfer and Advancement 
Act of 1995 (NTTAA), Public Law 104-113, section 12(d) (15 U.S.C. 272 
note).

VIII. Congressional Review Act

    The Congressional Review Act, 5 U.S.C. 801 et seq., generally 
provides that before a rule may take effect, the agency promulgating 
the rule must submit a rule report to each House of the Congress and to 
the Comptroller General of the United States. EPA will submit a report 
containing this rule and other required information to the U.S. Senate, 
the U.S. House of Representatives, and the Comptroller General of the 
United States prior to publication of this final rule in the Federal 
Register. This final rule is not a ``major rule'' as defined by 5 
U.S.C. 804(2).

[[Page 38935]]

List of Subjects in 40 CFR Part 180

    Environmental protection, Administrative practice and procedure, 
Agricultural commodities, Pesticides and pests, Reporting and 
recordkeeping requirements.

    Dated: July 30, 2009.
Lois Rossi,
Director, Registration Division, Office of Pesticide Programs.

0
Therefore, 40 CFR chapter I is amended as follows:

PART 180--[AMENDED]

0
1. The authority citation for part 180 continues to read asfollows:

    Authority: 21 U.S.C. 321(q), 346a and 371.


0
2. In Sec.  180.920, the table is amended by adding alphabetically the 
following inert ingredients:


Sec.  180.920  Inert ingredients used pre-harvest; exemptions from the 
requirement of a tolerance.

* * * * *

------------------------------------------------------------------------
        Inert Ingredients               Limits               Uses
------------------------------------------------------------------------
                              * * * * * * *
Diethanolamine salts of alkyl     Not to exceed 7%    Surfactants,
 (C8-C24) benzenesulfonic acid     of pesticide        related adjuvants
 (CAS Reg. Nos. 26545-53-9 and     formulation.        of surfactants
 68953-97-9).
                              * * * * * * *
Dimethylaminopropylamine,                             Surfactants,
 isopropylamine, ethanolamine,                         related adjuvants
 and triethanolamine salts of                          of surfactants
 alkyl (C8-C24) benzenesulfonic
 acid (CAS Reg. Nos. 26264-05-1,
 27323-41-7, 55470-69-4, 68411-
 31-4, 68584-24-7, 68584-25-8,
 68648-81-7, 68648-96-4, 68649-
 00-3, 68910-32-7, 68953-93-5,
 90194-42-6, 90194-53-9, 90218-
 35-2, 157966-96-6, 319926-68-6,
 877677-48-0, 1093628-27-3).
                              * * * * * * *
------------------------------------------------------------------------


0
3. In Sec. 180.930, the table is amended by adding alphabetically the 
following inert ingredients:


Sec.  180.930  Inert ingredients applied to animals; exemptions from 
the requirement of a tolerance.

* * * * *

------------------------------------------------------------------------
        Inert Ingredients               Limits               Uses
------------------------------------------------------------------------
                              * * * * * * *
Diethanolamine salts of alkyl     Not to exceed 7%    Surfactants,
 (C8-C24) benzenesulfonic acid     of pesticide        related adjuvants
 (CAS Reg. Nos. 26545-53-9 and     formulation.        of surfactants
 68953-97-9).
                              * * * * * * *
Dimethylaminopropylamine,                             Surfactants,
 isopropylamine, ethanolamine,                         related adjuvants
 and triethanolamine salts of                          of surfactants
 alkyl (C8-C24) benzenesulfonic
 acid (CAS Reg. Nos. 26264-05-1,
 27323-41-7, 55470-69-4, 68411-
 31-4, 68584-24-7, 68584-25-8,
 68648-81-7, 68648-96-4, 68649-
 00-3, 68910-32-7, 68953-93-5,
 90194-42-6, 90194-53-9, 90218-
 35-2, 157966-96-6, 319926-68-6,
 877677-48-0, 1093628-27-3).
                              * * * * * * *
------------------------------------------------------------------------

[FR Doc. E9-18698 Filed 8-4-09; 8:45 am]

BILLING CODE 6560-50-S
