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1,3-Dichloropropene - Proposed Termination of Special Review 12/99

[Federal Register: January 12, 2000 (Volume 65, Number 8)]
[Notices]
[Page 1869-1887]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr12ja00-73]
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ENVIRONMENTAL PROTECTION AGENCY
[OPP-30000/51A; FRL-6380-6]
1,3-Dichloropropene; Proposed Determination to Terminate Special
Review
AGENCY: Environmental Protection Agency (EPA).
ACTION:  Proposed Determination to Terminate Special Review.
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SUMMARY: This Notice sets forth EPA's proposal to terminate the Special
Review of 1,3-Dichloropropene (1,3-D). This proposal is based on Dow
AgroSciences' changes to their product labels and EPA's determination
that, with these label revisions, the benefits of 1,3-D use outweigh
the risks. In making this determination, EPA considered several
factors, including the risk reduction provided by numerous mitigation
measures that have been added to 1,3-D labels, the benefits of 1,3-D
use and the risks and benefits of alternative soil fumigants, in
particular the phase-out of methyl bromide production and imports by
2005. In December, 1998, EPA issued the Reregistration Eligibility
Decision (RED) document for 1,3-D and has determined that all uses of
1,3-D are eligible for reregistration.
DATES:  Comments, data and information relevant to the Agency's
proposed decision, identified by the docket control number OPP-30000/
51A, must be received on or before March 13, 2000.
ADDRESSES:  Comments may be submitted by mail, electronically or in
person. Please follow the detailed instructions for each method
provided in the "SUPPLEMENTARY INFORMATION" section.
FOR FURTHER INFORMATION CONTACT: Phil Budig, Special Review and
Reregistration Division (7508C), Office of Pesticide Programs,
Environmental Protection Agency, 401 M St., SW., Washington, DC 20460.
Telephone (703) 308-8029. E-mail address: budig.philip@epa.gov.
SUPPLEMENTARY INFORMATION

I. General Information

A. Does this Action Apply to Me?

    You may be affected by this action if you are a pesticide
registrant with registered products which contain 1,3-D as an active
ingredient, or if you are an agricultural producer using products
containing 1,3-D as an active ingredient.

B. How Can I Get Additional Information, Including Copies of Support
Documents?

    1. By mail. You may request copies of this document and supporting
documents by writing to: Public Information and Records Integrity
Branch, Information Resources and Services Division (7502C), Office of
Pesticide Programs, Environmental Protection Agency, 401 M St., SW.,
Washington, DC 20460 or calling 703-305-5805 between 8:30 a.m. and 4
p.m., Monday through Friday, excluding legal holidays. Be sure to
include the docket control number [OPP-30000/51A] in your request.
    2. In person. The Agency has established an official record for
this action under docket control number [OPP-30000/51A]. The official
records consist of the documents specifically referred to in this
action, any public comments received during an applicable comment
period, and other information related to this action, including any
information claimed as confidential business information (CBI). The
official record includes documents that are physically located in the
docket, as well as documents that are referred to in those documents.
The public version of the official record does not include any
information claimed as CBI. The public version of this record,
including printed, paper versions of any electronic comments, is
available for inspection in the Public Information and Records
Integrity Branch (PIRIB), Rm. 119, Crystal Mall #2, 1921 Jefferson
Davis Highway, Arlington, VA, from 8:30 a.m. to 4 p.m., Monday through
Friday, excluding legal holidays. The PIRIB telephone number is 703-
305-5805.
    3. Electronically.  You may obtain electronic copies of this
document and various support documents from the EPA Home page at the
Federal Register - Environmental Documents entry for this document
under "Laws and Regulations" (www.epa.gov/fedrgstr/).

C. How and to Whom do I Submit Comments?

    You may submit comments through the mail, in person, or
electronically:
    1. By mail. Submit comments to Public Information and Records
Integrity Branch, Information Resources and Services Division (7502C),
Office of Pesticide Programs, Environmental Protection Agency, 401 M
St., SW., Washington, DC 20460.
    2. In person. Deliver comments to Public Information and Records
Integrity Branch in Rm. 119, Crystal Mall #2, 1921 Jefferson Davis
Highway, Arlington, VA.
    3.  Electronically. Submit your comments electronically by e-mail
to: opp-docket@epa.gov, or you can submit a computer disk by mail as
described above in Unit I.C.1. Electronic submission on disks will be
accepted in Wordperfect 5.1/6.1 or ASCII file format. Do not submit any
information electronically that you consider to be CBI. Avoid the use
of special characters and any form of encryption. All comments in
electronic form must be identified by the docket control number [OPP-
30000/51A]. Electronic comments may also be filed online at many
federal Depository Libraries.
    The record for the Special Review is kept in paper form.
Accordingly, EPA will transfer all comments received electronically
into printed paper form as they are received and will place the paper
copies in the official record, which will also include all comments
submitted directly in writing. The official record is the paper record
maintained at the address for the Public Information and Records
Integrity Branch listed above.

[[Page 1870]]

D. How Should I Handle Information that I Believe is Confidential?

    Do not submit any information electronically that you consider to
be CBI. You may claim information that you submit in response to this
document as confidential by marking any part or all of that information
as CBI. Information so marked will not be disclosed except in
accordance with procedures set forth in 40 CFR part 2. A copy of the
comment that does not contain CBI must be submitted for inclusion in
the public version of the official record. Information not marked
confidential will be included in the public version of the official
record without prior notice.

E. What Should I Consider as I Prepare my Comments for EPA?

    You may find the following suggestions helpful for preparing your
comments:
    • Explain your views as clearly as possible.
    • Describe any assumptions you used.
    • Provide copies of technical information or data that
support your views.
    • If you estimate potential burden or costs, explain how you
arrived at the estimate you provide.
    • Provide specific examples to illustrate your concerns.
    • Offer alternative ways to improve the Agency's proposed
action.
    • Make sure to submit your comments by the deadline in this
notice.
    • To ensure proper receipt by EPA, be sure to identify the
docket control number assigned to this action in the subject line on
the first page of your response. You may also provide the name, date,
and Federal Register citation.

II. Introduction

    1,3-Dichloropropene (1,3-D) is a soil fumigant used mainly to
control plant-parasitic nematodes. A second formulation containing
chloropicrin also controls soil fungi. The primary registrant of 1,3-D
products is Dow AgroSciences. Dow AgroSciences' main products are
Telone II, which is used to treat soils to be planted to any crop,
including vegetables, orchard trees, and ornamentals, and Telone C-17,
which contains chloropicrin to enhance fungicidal properties. Two other
registrants also reformulate Telone II into eight end-use products. Dow
AgroSciences also holds a Special Local Needs (FIFRA section 24(c))
registration for a pre-plant underground drip product, Telone EC.
    1,3-D is injected as a liquid into the soil by shanks, or knives,
that are inserted 12 to 18 inches beneath the soil surface. The
volatile chemical then diffuses through the air spaces in the soil
inhabited by nematodes and other soil-borne pests. The rate of
diffusion is affected by the size of the soil particles, the amount of
soil moisture present, the amount of organic material, and pH. 1,3-D
can move up and into the atmosphere or down to ground water under
certain conditions. The half-life of 1,3-D in soil depends on several
factors; in field studies the dissipation half-life ranged from 1 to 7
days and in laboratory studies up to 54 days. For more information on
1,3-D use, see Unit VI of this document.
     1,3-D is classified as a B2, or probable human,
carcinogen by both the oral and inhalation routes of exposure. Studies
show that 1,3-D residues do not occur in foods planted to treated soils
when 1,3-D is used as a pre-plant soil fumigant. Oral exposures can
occur through consumption of contaminated ground water. Workers and
residents in the vicinity of treated fields can be exposed to 1,3-D
vapors during application and for approximately a 2-week period as some
of the applied material offgasses following application. 1,3-D is
classified as Toxicity Category II (moderately toxic) for oral toxicity
and primary eye irritation and Toxicity Category III (low toxicity) for
dermal irritation. There are two degradates of toxicological concern,
3-chloroallyl alcohol and 3-chloroacrylic acid.

A. Legal Background

    In order to obtain a registration for a pesticide under the Federal
Insecticide, Fungicide and Rodenticide Act (FIFRA, 7 U.S.C. 136 et
seq., as amended by the Food Quality Protection Act of 1996, Public Law
104-170), an applicant must demonstrate that the pesticide will not
cause "unreasonable adverse affects on the environment" when used
according to label directions [FIFRA section 3(c)(5)]. The term
unreasonable adverse effects on the environment means (1) "any
unreasonable risk to humans or the environment, taking into account the
economic, social and environmental costs and benefits of the use of any
pesticide" [FIFRA section 2(bb)] or (2) "a human dietary risk from
residues that results from use of a pesticide in or on any food
inconsistent with the standard under section 408 of the Federal Food,
Drug and Cosmetic Act" (21 U.S.C. 346a).
    Tolerances, or the establishment of maximum permissible levels of
pesticides in foods, are required when a pesticide or its identifiable
degradates or metabolites are expected to be present in food. The
Federal Food, Drug and Cosmetic Act (FFDCA), 21 U.S.C. 301 et seq., as
amended by the Food Quality Protection Act (FQPA) of 1996, (Public Law
104-170), authorizes EPA to establish such tolerances (21 U.S.C.
346(a)). Without such a tolerance or an exemption from a tolerance, a
food containing a pesticide residue is "adulterated" under section
402 of the FFDCA and may not be legally moved in interstate commerce
(21 U.S.C. 342).
    In determining a pesticide's safety for establishing a tolerance or
an exemption from the requirement of a tolerance, the FFDCA also
requires that EPA examine aggregate exposures from all sources of
pesticide residues, whether infants and children have heightened
susceptibility to pesticide residues, and whether there are cumulative
effects of pesticides and other compounds with a common mechanism of
toxicity (21 U.S.C. 346a).
    Certain pesticides are classified as non-food use when no residues
are expected to occur in crops from pesticide treatment. This class of
pesticides includes several soil fumigants which degrade in the soil to
compounds of non-toxicological concern, and thus are not available for
uptake by plants. Non-food use pesticides do not require a tolerance or
an exemption from a tolerance.
    Under the registration requirements of FIFRA, the burden of proving
that a pesticide satisfies the standard for registration is on the
proponent(s) of registration and continues as long as the registration
remains in effect. Under FIFRA section 6, the Administrator may cancel
the registration of a pesticide or require modification of the terms
and conditions of a registration if the Administrator determines that
the pesticide product causes unreasonable adverse effects to man or the
environment. EPA created the Special Review process to provide a public
procedure to gather and evaluate information about the risks and
benefits of uses that exceed EPA's risk criteria.
    The Act also provides that all pesticides registered prior to
November 1, 1984 must be reregistered. Congress amended FIFRA to
include reregistration for older pesticides because of advances in
scientific knowledge and testing capabilities not available when many
pesticides were first registered.
    The Special Review risk criteria are set out in the regulations at
40 CFR part 154. When EPA believes that a pesticide has met such
criteria, a notice announcing the initiation of the Special Review is
published in the Federal Register. After the Notice of Special Review
is issued, registrants and other interested persons are invited to
review

[[Page 1871]]

the data and risk assessments upon which EPA's determination is based
and to submit data and information to rebut EPA's conclusions. In
addition to submitting rebuttal evidence, commenters may submit
relevant information to support EPA's initial conclusions or to aid in
the determination of whether the economic, social and environmental
benefits of the use of the pesticide outweigh the risks. After
reviewing the comments, EPA makes a preliminary decision of the future
status on the pesticide's registration.
    Typically, a Special Review is concluded in one of three ways. If
information is submitted which successfully rebuts EPA's risk case, the
Agency may propose no changes to the terms and conditions of a
pesticide's registrations. Secondly, EPA may propose changes to the
terms and conditions of registration such that the proposed measures
reduce risk(s) to a point where the benefits of the pesticide's use(s)
outweigh the risk concerns. Such changes might include additional
protective clothing, lower application rates or engineering controls.
    However, EPA may determine that no changes in the terms and
conditions of a registration will adequately assure that use of the
pesticide will not cause any unreasonable adverse effects. If EPA makes
such a determination, it may seek cancellation, suspension, or change
in classification of the pesticide's registration. Any final decision
on a pesticide's registration through the Special Review process is set
forth in a Notice of Final Determination issued in accordance with 40
CFR 154.33.

B. Regulatory Background

    1,3-D was placed into Special Review in 1986 (51 FR 36160, October
8, 1986) based on carcinogenicity concerns. At that time, EPA focused
on inhalation exposure to workers who load and apply 1,3-D, as well as
to workers who enter fields shortly after 1,3-D application. EPA also
noted risk concerns for potential dietary exposures through food crops
and ground water contamination with 1,3-D or its contaminant 1,2-
dichloropropane (1,2-D). The focus of the Special Review was to gather
data to better define 1,3-D's toxicity, environmental fate and factors
which most influence exposures and to seek ways to reduce those
exposures.
    In 1986, EPA also issued the Registration Standard for 1,3-D
(Guidance for the Reregistration of Pesticide Products Containing 1,3-
Dichloropropene, USEPA, September 18, 1986). This standard outlined
studies required to fill data gaps and maintain the 1,3-D registration.
Many of the data gaps involved residue chemistry and environmental
fate, which were needed to investigate the Special Review concerns for
worker, dietary and ground water risks. Most studies in the 1986
Registration Standard were scheduled for completion within 2 years.
    In 1990, EPA notified Dow AgroSciences (then DowElanco) of its
concerns regarding the many delays in obtaining the studies required in
the 1986 Registration Standard, namely for the residue chemistry and
several of the retrospective ground water studies. Dow AgroSciences
stated that the delays were due to difficulties in obtaining
radiolabeled 1,3-D and the unexpected collapse of testing systems in
one of the ground water studies. EPA established a new 2-year schedule
for these data. Also in 1990, California suspended 1,3-D use permits
because unexpectedly high levels of the fumigant were found during air
monitoring required under California law. California regulates the use
of certain pesticides by permits, which are issued annually and which
specify use conditions such as the application rates, location and
crops [Ref. 1]. Since 1,3-D use patterns in California were unique to
the state, EPA initiated a review of use and exposure scenarios
throughout the United States. EPA issued a Data Call-In (DCI) in 1991
for information on exposure, usage and product performance by state and
by crop.
    In 1990, Title VI of the Clean Air Act was amended to include
regulation of chemicals which deplete stratospheric ozone. Under the
amendments, EPA's Office of Air and Radiation originally proposed to
phase-out use of methyl bromide by 2001 due to its potential to deplete
stratospheric ozone (56 FR 49548, September 30, 1991). Because the 1,3-
D Special Review considered methyl bromide to be a major alternative to
1,3-D, EPA looked more closely at the risks and benefits of all the
remaining soil fumigants and contact nematicides. Specifically, EPA
looked at the potential increase in benefits and risks associated with
1,3-D use in light of the scheduled phase-out of methyl bromide. The
phase out was extended to 2005 under legislation passed in 1999. For
more information on the methyl bromide phase out, refer to
http://www.epa.gov/docs/ozone/mbr/mbrqa.html.
    EPA contacted Dow AgroSciences in 1992 when the additional residue
chemistry and ground water studies were not submitted according to the
revised schedule. EPA also sought measures to reduce inhalation
exposures, since EPA's assessments based on the incomplete data sets
yielded risk estimates for workers and residents who live near treated
fields that exceeded those EPA generally considers to be acceptable. In
order to maintain 1,3-D registrations, the registrant agreed to set a
strict timetable for completing data submissions, to develop new
exposure data, and to add engineering controls and additional personal
protective gear for workers to all 1,3-D labels [Ref. 2].
    EPA also raised concerns about the results of the retrospective
ground water studies. While results from North Carolina and California
were acceptable, unexpectedly high levels from the Nebraska site, and
the lack of results from Florida required attention. Since Dow
AgroSciences had already approached Florida with plans to expand use as
a methyl bromide alternative, EPA and Florida developed a joint
schedule to oversee the study. EPA believed that the high levels in
Nebraska were linked to cold temperatures, and required a prospective
ground water study in Wisconsin to determine whether 1,3-D can be
safely used in cold climates.
    In 1995, Dow AgroSciences and EPA met a second time to review the
data that had been collected, as well as California's decision to allow
limited re-introduction of 1,3-D use [Ref. 3]. On January 19, 1996, Dow
AgroSciences requested changes to their Telone labels to incorporate
mitigation requirements and also included a time table for submitting
interim and final studies for ground water monitoring taking place in
Florida and Wisconsin [Ref. 4].
    In 1997 and 1998, the results of the ground water studies showed
levels of 1,3-D in ground water which were high enough to warrant
additional mitigation measures. On September 30, 1998, Dow AgroSciences
requested a third modification of their Telone labels to include
measures to mitigate potential exposures through contaminated ground
water (see Table 1 below) (Ref. 5). This label modification was
included as part of the reregistration eligibility determination for
1,3-D. Dow AgroSciences also has agreed to conduct additional studies
on the alcohol and acid degradates of toxicological concern and
additional environmental fate studies. In addition, Dow AgroSciences
agreed to conduct a tap water monitoring study to assess 1,3-D and
degradate levels in water used for drinking. Should residues of 1,3-D
and/or the alcohol or acid degradates be detected at levels exceeding
the Office of Water health advisory of 0.2 parts per billion (ppb), Dow
AgroSciences has

[[Page 1872]]

agreed to implement label use restrictions on further applications in
the vulnerable use areas before the next use season commences. Label
changes may include restrictions based on depth to ground water or soil
type characteristics. Table 1 outlines all of the requirements which
now appear on the new 1,3-D labels (effective August 1, 1999) as well
as measures adopted earlier.

           Table 1.-- Summary of Requirements on 1,3-D Labels
------------------------------------------------------------------------
  Regulatory Action (date when  measures
               took effect)                      Label Requirements
------------------------------------------------------------------------
Registration Standard (1986) (effective     Precautionary statements;
 1987).                                      Cancer hazard warning;
                                             Classification change to
                                             "Restricted Use"
                                             pesticide; Reentry
                                             increased to 72 hours;
                                             Clothing for applicators
                                             and handlers (coveralls,
                                             chemical-resistant gloves
                                             and boots, liquid-proof
                                             hat).
1992 Interim Risk Mitigation (effective     Ground water advisory;
 1992/1993).                                 Lowered maximum rates;
                                             Deletion of selected use
                                             sites; Revised respirator
                                             requirements; Closed
                                             loading requirements;
                                             Technology to minimize 1,3-
                                             D spillage during
                                             application.
Worker Protection Standard (August 1992,    Coveralls over short-sleeved
 see 57 FR 38102).                           shirt and short pants;
                                             Chemical-resistant gloves
                                             and footwear; Chemical-
                                             resistant apron (for direct
                                             handlers).
1995 Risk Mitigation (effective August      A respirator requirement for
 1996).                                      all 1,3-D handlers;
                                             Restricted entry increased
                                             to 5 days; Prohibition of
                                             use within 300 feet of
                                             occupied structures; Soil
                                             moisture and soil sealing
                                             requirements; Modified
                                             application techniques;
                                             Lower maximum use rates.
1998 Risk Mitigation (effective August      100' buffer between drinking
 1999).                                      water wells and treated
                                             fields; prohibition in
                                             areas overlying karst
                                             geology; prohibition of use
                                             in ND, SD, MN, NY, ME, NH,
                                             VT, MA, UT, MT, WI where
                                             ground water is less than
                                             50 feet from the surface
                                             and soils are classified as
                                             hydrologic type "A."
------------------------------------------------------------------------

    Based on the submission of label changes and a completed data base
showing that 1,3-D can be used without unreasonable adverse effects to
humans or the environment, EPA has found all uses of 1,3-D eligible for
reregistration. The Reregistration Eligibility Decision (RED) document
is contained in the 1,3-D docket (the location is listed under
"ADDRESSES" in this Notice), or can also be accessed from the
Internet at http://www.epa.gov/REDs for case 0328. Please refer to the
1,3-D RED for a more detailed discussion of the data summarized in this
Notice.

C. Summary of EPA's Proposed Action

     EPA has determined that the benefits associated with the continued
use of 1,3-D under the recently revised terms and conditions of 1,3-D's
registration outweigh the risks. Thus, EPA is proposing to terminate
the Special Review of 1,3-D.

 III. Summary of Hazard Assessment

A. Short and Intermediate Term Toxicity

     The acute toxicity values and categories for 1,3-D are summarized
in Table 2 below:

            Table 2.-- Acute Toxicity Study Results for 1,3-D
------------------------------------------------------------------------
                                                               Toxicity
             Study Type                      Results           Category
------------------------------------------------------------------------
Acute Oral.........................  LD50 = 300 mg/kg (M),            II
                                      224 mg/kg (F)
Acute Dermal - Rabbit..............  LD50 = 333 mg/kg                 II
Acute Inhalation...................  LC50 = 3.88 mg/L (M),            IV
                                      4.1 mg/L(F)
Primary Eye Irritation.............  Intermediate irritant            II
Primary Skin Irritation............  Slight irritant                 III
Dermal Sensitization...............  Sensitizer              ...........
Acute Neurotoxicity................  None required           ...........
------------------------------------------------------------------------

    EPA has placed 1,3-D in Toxicity Category II (moderately toxic, the
second highest toxicity classification out of four levels). EPA has
reviewed the available toxicological data for 1,3-D and concluded that
the data do not indicate any evidence of significant oral or inhalation
toxicity from a single exposure event that may occur with labeled uses.
    EPA has established an intermediate-term endpoint based on results
from a 2-year combined chronic/carcinogenic inhalation study in rats.
Fischer 344 rats (50/sex/group plus 10/sex/group to 6- and 12-month
exposure groups) were exposed by whole-body inhalation to Telone II
(92.1% active ingredient (a.i.)) at aerosol concentrations of 0, 5, 20
or 60 parts per million (ppm) (equivalent to approximately 0, 0.023,
0.091 or 0.272 mg/L), 6 hours/day, 5 days/week for a total of 509 days
over a 2-year period. There was no effect of exposure to 1,3-D on the
survival of males or females. Slight (approximately 5% in 60 ppm males
and females, as well as 3% in 20 ppm males) decreases in body weight
gains were observed (statistically significant, p<0.05) but generally
only during the first year of the study. The olfactory region of the
nasal cavity appeared to be the target tissue as determined by
histopathological examination. Males and females having been exposed to
60 ppm (no evidence reported at lower concentrations of 20 or 5 ppm)
showed decreased thickness and erosions of the epithelium as well as
minimal submucosal fibrosis. For chronic toxicity, the No-Observed
Adverse Effect Level (NOAEL) was 20 ppm (0.091 mg/L) and the Lowest
Observed Adverse Effect Level (LOAEL) was 60 ppm (0.272 mg/L) based on
histopathological changes in nasal tissue as well as the suggestion of
decrease in body weight gain compared with controls during the first
year of the study.

B. Carcinogenicity

    EPA initiated the Special Review of 1,3-D based on evidence that
1,3-D induced cancer in rats and mice exposed to 1,3-D. The potential
for human carcinogenicity is based on inhalation exposures for workers
handling the fumigant and for area residents who may be exposed to air
borne levels of 1,3-D and oral exposures to levels in contaminated
ground water.
    1. Oral studies. In 1985, the National Toxicology Program (NTP)
tested the chronic toxicity and carcinogenic potential of 1,3-D (Telone
II - 89% 1,3-D, 6% inert ingredients, 1% epichlorohydrin) in F344 rats
and B6C3F1 mice [Ref. 6].
    a. Rat Feeding Study by Gavage. Male and female F344 rats received
oral administration by gavage (feeding tube) of 1,3-D in corn oil at 0,
25, or 50 mg/kg/day, 3 days per week, for 104 weeks. A total of 77 rats
per sex were used for each dose group, including those sacrificed for
examination during the course of testing. Statistically significant
increases in the incidence of the following tumors were observed at the
highest dose tested (HDT) by pairwise comparison with controls:
     i. Forestomach squamous cell papillomas in males and females.
     ii. Combined forestomach squamous cell papillomas and carcinomas
combined in males.
     iii. Liver neoplastic nodules in males and combined neoplastic
nodules and hepatocellular carcinomas in males.
    The increased incidence of forestomach tumors was accompanied

[[Page 1873]]

by a statistically significant positive trend for forestomach basal
cell hyperplasia in male and female rats of both treated groups (25 and
50 mg/kg). There were also positive trends for other tumors in rats
(i.e. in females, mammary gland adenomas or fibromas and thyroid gland
follicular cell adenomas or carcinomas; in males, adrenal gland
pheochromocytomas). The highest dose tested in rats (50 mg/kg) appeared
to be adequate for carcinogenicity testing.
    b. Mouse Feeding Study by Gavage. In the mouse study, groups of 50
mice/sex were fed Telone II in corn oil (with 1% epichlorohydrin as a
stabilizer) through a gavage feeding tube at 0, 50, or 100 mg/kg, 3
days per week for a total of 104 weeks. The results of the study were
confounded by an excessive mortality in control males (those not
receiving 1,3-D) from myocarditis. The survival of female mice was
lower in the high dose group than in the other dose level groups (46/
50, 45/50, 36/50 for control, low dose and high dose respectively).
Significantly elevated incidence of the following tumors were observed
either at the HDT or at both dose levels:
     i. Forestomach squamous cell papillomas or papillomas and
carcinomas combined in males and females, and squamous cell carcinomas
in females.
    ii. Urinary bladder transitional cell carcinomas in males and
females.
     iii. Lung adenomas or adenomas and carcinomas combined in males
and females.
    Several deficiencies were noted in the mouse study, including
excessive mortality in control males and inadequate randomization
procedures at the study initiation. The highest dose tested appears to
have been excessive for testing. While this study was not used for
quantitatively estimating 1,3-D's carcinogenic potential, the Agency
has included the stomach, bladder and lung effects in its weight-of-
the-evidence findings (see Unit III.D of this document.).
    c. Rat study by microencapsulation. In 1992, the registrant
conducted a second feeding study using time-released
(microencapsulated) doses of 1,3-D in food since the stomach tumors
seen in the NTP study occurred in the area where the feeding tube was
inserted. In addition, the NTP study results may have been confounded
by the presence of a stabilizer, epichlorohydrin, which is a known
carcinogen.
    Charles River Fischer 344 ("Fischer 344") rats (60/sex/dose) were
fed doses of 0, 2.5, 12.5, and 25 mg/kg/day for 2 years, with an
examination of one group made after 1 year. Body weight gains were
decreased for males and females at the middle and high doses compared
to controls. There was an increase in liver masses/nodules in males
only at the 12.5 and 25 mg/kg doses. The NOAEL was 2.5 mg/kg. There was
an increased incidence of basal cell hyperplasia of the nonglandular
mucosa of the stomach of both sexes at the 12 and 24 month sacrifice at
the middle and high doses. The incidence of primary hepatocellular
adenomas in male rats exceeded that in the control group at the middle
and high doses tested. The incidence of hepatocellular ademonas in
female rats showed an increase over the control only at the high dose.
The highest dose tested appeared adequate for carcinogenicity testing
[Ref. 7]. EPA used the test results of this study to confirm the
carcinogenicity finding of the earlier study in rats. The results of
this study were also used to develop the chronic non-cancer Reference
Dose.
    d. Mouse study by microencapsulation. Male and female
B6C3F1 mice (50/sex/dose) were fed
microencapsulated 1,3-D at levels of 0, 2.5, 25 or 50 mg/kg/day for 2
years, with an examination of 10 mice/sex/dose made after 1 year. As
seen in the rat study, body weight gains were lower in both sexes at
the middle and high doses compared to controls. In addition,
hepatocytes of the high dose males were decreased in size at the 12 and
24 month sacrifice. While liver effects were seen, there was no
treatment-related incidence of tumors observed in mice ingesting
microencapsulated 1,3-D [Ref. 8]. EPA notes that the negative cancer
findings do not affect the Agency's position on the carcinogenicity of
1,3-D due to the results of the rat study.
    2. Inhalation studies. Because 1,3-D is a volatile compound which
can move up and into the atmosphere after application, EPA also
required studies on the potential carcinogenicity of 1,3-D via the
inhalation route of exposure.
    a. Rat study. In the rat study, 50/sex/group were exposed to 0, 5,
20 or 60 ppm 1,3-D for 6 hours/day, 5 days/week, for approximately 2
years. Ancillary groups of rats (10/sex/group) were similarly exposed
for 6 or 12 months. Clinical signs of toxicity were not observed and no
significant differences in survival were found in any of the test
groups. No significant increase in treatment-related incidence of
tumors in rats was observed [Ref. 9].
    b. Mouse study. The mouse study followed the same study design as
the rat study (50 mice/sex/group dosed at 0, 5, 20, or 60 ppm, 6 hours/
day, 5 days/week for approximately 2 years; 2 groups of mice to be
sacrificed and studied at the 6 month and 1 year mark of the study). In
male mice at the 2-year sacrifice, a statistically significant increase
in the incidence of bronchioloalveolar adenoma (a benign lung tumor)
was found at the highest dose tested (HTD) (60 ppm) by pairwise
comparison with controls (9/50, 6/50, 13/50, and 22/50 for 0, 5, 20,
and 60 ppm respectively). For controls (0 ppm) the historical incidence
for bronchioloalveolar adenoma is in the 7-32% range; this includes a
20% control incidence from another 2-year inhalation study.
Additionally, male mice had a significant difference in lacrimal gland
cystadenomas in the pair-wise comparison of control and the 20 ppm dose
group. No tumors were seen in treated female mice. Although a
hyperplastic response was seen in the urinary bladders of both male and
female mice, no tumorigenic response was found [Ref. 10].
    3. Dermal studies. EPA also has studies that tested the potential
carcinogenicity of 1,3-D through short-term dermal exposure. Van Duuren
et al., (1979) administered subcutaneous injections of 1,3-D weekly to
30 female HA:ICR mice at a dose of 3 mg/mouse. The author noted a
positive finding of fibrosarcomas in 6 of the 30 mice after 538 days.
No tumors developed in untreated or vehicle-treated animals (i.e.
treated with the serum minus the compound being tested).
     The same study also investigated the tumor-initiating potential of
1,3-D when applied to the skin of female HA:ICR mice (30 animals). Mice
received 1,3-D in 0.2 mL acetone as the initiator at a single dermal
dose of 122 mg, followed by promotion with phorbal myristate acetate (5
μg) in acetone 3 times/week for 440-594 days. No significant
differences in tumor incidence were found between the treated and
control animals. Additionally, when 1,3-D was tested for carcinogenic
potential following repeated dermal administration with 122 mg. 1,3-D
in 0.2 mL in 0.2 acetone, 3 times/week for 440-594 days, only 1/30
treated animals had papilloma and carcinoma of the skin; the authors
noted statistical significance was not attained. None of the control
animals developed any skin tumors [Ref. 11]. EPA did not consider this
study in its consideration of 1,3-D's carcinogenicity since the
authors' conclusions and statistical tests used could not be confirmed.
    4. Structure-Activity Relationships. 1,3-D bears a structural
resemblance to several short chain halogenated hydrocarbon compounds
that are known human and/or animal carcinogens, namely vinyl chloride
and epichlorohydrin. There is no

[[Page 1874]]

information, however, that establishes a common mode of carcinogenicity
between these chemicals and 1,3-D.

C. Mutagenicity

    A series of mutagenicity studies has been performed which show that
1,3-D has some mutagenic activity. This activity would also provide
support for a carcinogenicity concern. 1,3-D produced gene mutations in
bacterial and mammalian test systems in vitro but did not produce
structural chromosomal aberrations in mammalian test systems. 1,3-D is
also a germ cell mutagen in Drosophila. The Drosophila result suggests
an interaction with germ cells in an eukaryotic organism. There are
studies in the open literature that show the in vivo mouse liver
conversion of 1,3-D to mutagenic cis and trans epoxides, the in vitro
formation of four DNA adducts when 1,3-D epoxides are reacted with 2'-
deoxygenase and the in vivo formation of DNA lesions in the stomach,
colon, liver, kidneys, bladder, lungs, brain and bone marrow.
    For the 1,3-D reregistration and Special Review, Dow AgroSciences
submitted information to support regulation of 1,3-D as a non-linear
carcinogen (i.e., that there is no risk associated with exposure below
a certain dose) because 1.3-D is not mutagenic. EPA has reviewed the
information and determined that the weight-of-the-evidence shows 1,3-D
is mutagenic. [Ref. 12].
    In addition, Dow AgroSciences is performing the Ames assay, mouse
lymphoma and mouse mocronucleus study on the alcohol and acid
degradates to test EPA's assumption that the degradates exhibit the
same mutagenicity as the parent.

D. Human Incidents Data

    The Agency is aware of several reports in the open literature
describing adverse effects related to accidental 1,3-D exposure. In
1973, nine firemen were exposed during a clean-up operation in
California after a 1,3-D transport tank overturned [Ref. 13]. Reports
show two of the nine men exposed were treated for neck pain, nausea and
breathing difficulty following exposure. Follow-up revealed that both
men died from hematological malignancies within 7 years of exposure. In
a separate case in the same report, a farmer was repeatedly sprayed in
the face with 1,3-D through a leaky hose. The man first went to the
doctor in 1975, when he was found to have mucosal lesions in his ear
and pharynx, as well as symptoms of fatigue. He also required
transfusions to correct low red and white blood cell counts. He
returned to field work in 1976, where he was again sprayed with 1,3-D.
The next year, fatigue became more severe and his gums began bleeding.
Red and white cell counts were diminished and the patient was diagnosed
with acute myelomonocytic leukemia. The patient died within 5 weeks of
admission.
    In another report of 1,3-D exposure [Ref. 14], a worker drank a
clear fluid which he thought was water from a container. The first
signs of injury were acute gastrointestinal distress, sweating,
tachycardia, tachypnoea and lividity in the lower legs. His condition
worsened within 9 hours; blood abnormalities did not respond to
numerous treatments. The patient died 38 hours after admission; the
autopsy revealed multiple organ failure and extensive damage to the
respiratory tract and liver. While this case involves an acute
poisoning, rather than a chronic effect, EPA has concluded that this
report supports concern for 1,3-D toxicity to the human hematologic
system as was seen in the other cases cited above. It should be noted
that these accidental exposures to 1,3-D are less likely under the
current labels because of strict requirements for closed loading, check
valves, and protective equipment.
    While these reports alone do not provide an adequate basis for
making a determination of human carcinogenicity (i.e. that 1,3-D is a
Group A, human, carcinogen), they provide evidence to support EPA's
concerns regarding the target organs of 1,3-D's effects in humans
(hematopoietic system, lungs, liver) and its potential to induce
cancer.

E. Weight-of-the-Evidence and Carcinogenicity Summary

    The EPA Cancer Peer Review Committee (CPRC) met in 1989 to consider
all the data relevant to developing a position on 1,3-D's
carcinogenicity. The Committee based its determination on the
following:
     1. The CPRC looked at the original NTP oral carcinogenicity
studies to determine whether the epichlorohydrin stabilizer was the
carcinogenic agent. The CPRC concluded that the tumors could not solely
be attributed to epichlorohydrin because tumors were seen at sites
other than the forestomach (i.e. liver, mammary gland and thyroid) and
the dose of epichlorohydrin was far below that associated with
forestomach tumors in gavage and drinking water carcinogenicity
studies. A comparison between the mutagenic activities of 1,3-D and
epichlorohydrin showed that even if epichlorohydrin did contribute some
activity to the 1,3-D preparation, its relative contribution would be
very small because epichlorohydrin constituted a small percent of the
total test material. Epichlorohydrin by itself did not appear to induce
as large a mutagenic response as 1,3-D on an equimolar basis based on
studies administering epichlorohydrin alone.
     2. 1,3-D, when administered by oral gavage to Fischer 344 rats,
was associated with an increase in (i) forestomach tumors in both
sexes; (ii) liver tumors in males; and (iii) positive trends for other
tumor types in mammary and thyroid glands.
     3. 1,3-D, when administered by oral gavage to
B6C3F1 mice, was associated with an
increase in (i) forestomach tumors; (ii) urinary bladder tumors and
cell changes; and (iii) lung adenomas (benign lung tumors) in both
sexes at both dose levels and lung adenomas and carcinomas combined in
males at both dose levels.
     4. No compound-related increase in tumors was observed in
inhalation studies in Fischer 344 rats. However, the dose levels used
were not considered to be high enough to fully assess the carcinogenic
potential of 1,3-D.
     5. 1,3-D, when administered by inhalation to
B6C3F1 mice, was associated with an
increase in bronchioloalveolar adenomas in males at the highest dose
tested. Cellular changes in the urinary bladder, nasal passages and
non-glandular stomach were noted. Based on toxicity parameters, the
data suggest that higher dosing could have been utilized in this study.
     6. The CPRC concluded that the benign lung tumors observed in mice
after inhalation were biologically significant, because tumor induction
was dose-dependent, tumor incidence was outside the range of historical
controls, and the tumor type was also seen in the mouse oral study.
     7. EPA has concluded that, based on available evidence in
bacterial, Drosophila and mammalian cell mutagenicity studies, 1,3-D
has mutagenic capability.
     8. 1,3-D bears a structural resemblance to several short chain
halogenated hydrocarbons that are known carcinogens.
     9. Confidence in the compound-related induction of tumors was
strengthened by the observation of site concordance for neoplastic and
non-neoplastic effects seen for the two routes (oral and dermal) of
1,3-D administration [Ref. 15].
    Based on the above data (evidence of carcinogenicity in two rodent
species via two different routes of exposure), EPA has classified 1,3-D
as a Group B2, or probable human, carcinogen.

[[Page 1875]]

    For the 1,3-D reregistration and Special Review, Dow AgroSciences
submitted information to support regulation of 1,3-D as a non-linear
carcinogen (i.e., that there is not risk associated with exposure below
a certain dose). The Office of Pesticide Programs has reviewed the
information and determined that the evidence on 1,3-D's mutagenicity
does not support Dow AgroScience's claim that 1,3-D is a candidate for
regulation as a non-linear carcinogen [Ref. 12]. Thus, EPA will
continue to regulate 1,3-D as a B2 carcinogen under a linear
approach.

F. Dose-Response Assessment for 1,3-D

    By using data from carcinogenicity studies, EPA quantifies the
carcinogenic potential of chemicals based on a dose-response
relationship. This measure is known as the carcinogenic potency factor,
or the Q1*. For 1,3-D, EPA has calculated two carcinogenic
potency factors: one for the oral route and the other for inhalation.
The Q1* for the oral route was presented in the 1986 Notice
of Special Review as 1.75  x  10**-1 (mg/kg/day)**-1,
based on the combined tumors (either (i) adrenal and thyroid, (ii)
forestomach or (iii) liver tumors) in the oral gavage rat study using
the Multistage model. In 1994, Office of Pesticide Programs revised the
Q1* for the oral route to 1.22  x  10**-1 based on
a scaling factor of 3/4 instead of 2/3 to extrapolate data from humans
to animals. The Q1* for the inhalation route using the 3/4
scaling factor is 5.33  x  10**-2 (mg/kg/day)**-1,
based on the lung bronchioalveolar tumor rates in male mice [Ref. 16].

G. Toxicity and Carcinogenicity of 1,2-Dichloropropane

     The 1986 Notice initiating the Special Review for 1,3-D mentioned
concerns for the contaminant 1,2-dichloropropane (1,2-D). In the mid
1980's, 1,2-D was registered as an active ingredient and was present in
1,3-D formulations at levels up to 5%. All 1,2-D pesticide
registrations were canceled as of 1987 and 1,2-D levels in the Telone
II formulation (which is also used by reformulators) have been reduced
to less than 0.1% for products sold after August 1, 1999. Nonetheless,
EPA has been tracking 1,2-D levels in ground water studies and reviews
due to 1,2-D's persistence.
    EPA has not conducted a formal evaluation of the toxicology
database for 1,2-D at this time because 1,2-D is no longer registered
as a pesticide. However, 1,2-D has been evaluated by the Office of
Research and Development (ORD) to support development of the Drinking
Water Criteria Document by the Office of Water (USEPA 1987). ORD
evaluated the limited available database for 1,2-D and concluded that
the liver was the principal target organ of toxicity. ORD also found
effects from acute exposures; the effects were seen in the lungs,
liver, kidneys, central nervous system and eyes. A more detailed
description is on EPA's IRIS data base at http://www.epa.gov/ordntrnt/
ORD/dbases/iris/index.html.
    1,2-D has been classified as a Group B2, probable human
carcinogen, with a Q1* of 3.69  x  10**-2(mg/kg/
day)**-1 based on the statistically significant increased
incidence of hepatocellular adenomas and carcinomas in male and female
B6C3F1 mice. In addition, a dose-
related trend in mammary adenocarcinomas was noted in female Fischer
344 rats. This is considered significant because Fischer 344 rats have
a relatively low background incidence of these tumors (56 FR 3540,
January 30, 1991). In addition, 1,2-D was mutagenic in the Salmonella
and in Aspergillus nidulans. 1,2-D also induced sister chromatid
exchange and chromosome aberrations in Chinese hamster ovary cells.
    The Agency has not cumulated 1,3-D risks with the impurity 1,2-D or
other chemicals since no determination has been made that these
chemicals share a common mechanism of toxicity.

IV. Summary of Exposure

A. Dietary Exposure

    1. Food sources. The 1986 Registration Standard concluded that the
characteristics of 1,3-D were not well enough understood to ascertain
whether residues might be expected in raw agricultural commodities, and
therefore metabolism data were required for reregistration.
    In 1992, Dow AgroSciences submitted metabolism studies
demonstrating that 1,3-D is extensively metabolized and incorporated
into natural components such as sugars, amino acids and fatty acids.
EPA determined that residues of 1,3-D and its degradates of
toxicological concern are not expected in foods from pre-plant fumigant
uses of 1,3-D. Thus, EPA has determined that the pre-plant fumigation
uses of 1,3-D are non-food uses and no tolerances or exemptions from
the requirement for a tolerance are required. [Ref. 17].
    2. Drinking water sources. Although EPA believes there are no
residues of 1,3-D in foods grown on 1,3-D treated soils, studies show
that 1,3-D can contaminate ground water, including that which is used
for drinking water. While 1,3-D was not specifically placed into
Special Review because of ground water concerns, EPA noted that 1,3-D
could reach ground water since monitoring had yielded detections of
1,3-D and 1,2-D. EPA's Office of Water (OW) has not established a
Maximum Contaminant Level (MCL) set for 1,3-D. For carcinogens, OW
typically sets a Maximum Contaminant Level Goal (MCLG) at zero. In
1987, OW set the Health Advisory level of 0.2 ppb, which is the daily
level of consumption over a lifetime associated with a 1  x
10**-6 cancer risk. Health Advisories are not enforceable
standards, but rather are advisory in nature.
    The MCL for 1,2-D is 0.005 mg/L (5 μg/L or 5 ppb). For 1,2-
D, EPA's Office of Water has a children's 10-day Health Advisory of
0.09 mg/L (90 μg/L or 90 ppb).
    1,3-D is considered highly mobile and is more persistent when 1,3-D
enters ground water in colder climates. 1,3-D has been detected and its
presence confirmed in ground water in New York, Florida, Nebraska,
Washington state and the Netherlands under normal field use. In 1991,
the General Accounting Office (GAO) issued a report which listed
detections of 1,3-D in seven states. This list also included detections
of the impurity 1,2-D [Ref. 18].
    The 1986 Registration Standard required that retrospective ground
water monitoring studies be conducted at five sites. From the study
results, no 1,3-D was found at the California, North Carolina or
Washington state sites. Retrospective ground water monitoring studies
require sampling in known use areas for a pesticide, but do not require
extensive information on past use, well integrity or other historical
information to help characterize any detections. A sinkhole collapsed
and interfered with obtaining results at the Florida site. 1,3-D
residues were found at the Nebraska site, leading EPA to suspect that
the increased persistence of 1,3-D under colder conditions had
contributed to 1,3-D's presence in ground water there.
    In 1995 and 1996, Dow AgroSciences initiated prospective ground
water studies in Wisconsin and Florida. Prospective studies are
conducted under predetermined conditions in areas of no known prior
use, thereby reducing the chance that prior use or changes in use
practices could interfere with study results. The Wisconsin site was
chosen to better define 1,3-D's fate in a cold climate. Dow
AgroSciences initiated the Florida study to determine if 1,3-D products
could be used without adverse effects to ground water.
    At the Wisconsin study site, 1,3-D, its degradates and 1,2-D were
found in both on-site wells and in one off-site monitoring well at
concentrations well

[[Page 1876]]

above levels considered acceptable. These levels were detected for more
than a year after the 1,3-D application occurred (see Unit V.B.1.c. for
more information on concentrations associated with unacceptable risks).
Cancer risks associated with prolonged exposures to the detected levels
were unacceptably high for all age groups, as were chronic non-cancer
risks for infants and children. In the Wisconsin study, on-site wells
yielded concentrations of 1,3-D as high as 579 ppb. Concentrations of
1,3-D in off-site wells were as high as 84 ppb [Ref. 19].
    In the Florida study, 1,3-D, its degradates and 1,2-D were also
found, though at lower levels than those seen in the Wisconsin study.
In Florida, residents tap both surficial aquifers and deeper ground
water for drinking water and thus the study was designed to look at
levels 10 feet and 70 feet below the surface. There were also a limited
number of off-site wells to look at downgradient concentrations from a
single application. Time-weighted average (TWA) concentrations of 1,3-D
plus its degradates in the on-site wells were 1.15 ppb in 10 feet wells
and 0.17 ppb in the 70 feet wells (note that time-weighted averages are
used to describe the exposures to pesticides which pose chronic risks,
while peak levels are used to describe exposures to pesticides which
pose acute risks). TWA concentrations of 1,3-D plus degradates measured
in wells located 100 feet down-gradient from the treated field were
0.074 ppb. Levels of 1,3-D plus its degradates did not persist beyond a
year after application [Ref. 20].
    EPA also reviewed the U.S. Geological Survey's (USGS) National
Water Quality Assessment (NAWQA) reports. The assessment, which is on-
going, monitors both surface and ground water for pesticides, nitrates
and other contaminants in the United States. Some USGS-monitored sites
were located in counties that have reported the highest use rates of
1,3-D, although there was no information in the reports to directly
link 1,3-D treatments with sampled wells. Moreover, the assessment did
not test for 1,3-D's alcohol and acid degradates. None of the NAWQA
reports released to date have shown detections of 1,3-D in ground or
surface water. 1,2-D detections were widespread and thought to be
related to past use of 1,2-D as a soil fumigant. Although no
information in the reports directly links 1,3-D use to the monitored
wells, the absence of detections suggests that 1,3-D use probably does
not result in widespread aquifer contamination. For more details on the
NAWQA program and 1,3-D and 1,2-D sampling, please refer to
http://water.usgs.gov/lookup/get?nawqa/.
    EPA used the results of the prospective ground water studies to
assess exposure to 1,3-D and its degradates in drinking water because
of the Agency's confidence in the high quality of the data. EPA has
estimated dietary exposure to 1,3-D via drinking water using these
study results and a daily water consumption value of 2 L/day for adult
males and females with bodyweights of 70 kg and 60 kg, respectively,
and 1 L/day consumption for infants and children with a 10 kg
bodyweight. The following equation used to estimate exposure to 1,3-D
through drinking water for adult males is provided as an example of how
EPA calculated exposure to 1,3-D and its degradates in drinking water:
    Exposure (mg/kg/day)(Adult male) = (conc'n, μg/L)(2 L/
day)(0.001 mg/μg) / 70 kg adult body weight

    The following table 3 presents the exposure estimates for 1,3-D,
its degradates and 1,2-D.

                           Table 3.-- Chronic Exposure Estimates for 1,3-D, 1,3-D+ Degradates, and 1,2-D
       (Based on Time-Weighted Average (TWA) concentrations from the Florida and Wisconsin Prospective Ground Water
Studies)
------------------------------------------------------------------------------------------------------------------------
                                               Florida Prospective Study (365 days)                 Wisconsin
Prospective
                                  -------------------------------------------------------------- Study (after 337 days,
on-
                                       10-ft wells           70-ft wells       10-ft wells, 100 ft off-site     site
wells)
                                  -------------------------------------------------           site  --------------------
                                                                               -----------------  shallow aquifer (15-22
   Populations         Compound                                                                              ft)
                                     TWA    Exposure      TWA      Exposure      TWA                ---------------
                                     mg/L   mg/kg/day)    mg/L     mg/kg/day)    mg/L   Exposure\1\    TWA
                                                                                        mg/kg/day)     mg/L     Exposure
                                                                                                              
mg/kg/day)
--------------------------------------------------------------------------------------------------------------------
Adult males..........  1,3-D         0.30   8.6x10**-6    0.04     1.1x10**-6    0.026     134    3.8x10**-3
Adult females........                       1x10**-5               1.3x10**-6                       4.5x10**-3
Infants & Children...                       3x10**-5               4x10**-6                         1.3x10**-2
--------------------------------------------------------------------------------------------------------------------
Adult males..........  1,3-D +       1.15   3.3x10**-5    0.17     4.9x10**-6    0.074     357    1x10**-2
                        Degradates
Adult females........                       3.8x10**-5             5.6x10**-6                       1.2x10**-2
Infants & children...                       1.2x10**-4             1.7x10**-5                       3.6x10**-2
--------------------------------------------------------------------------------------------------------------------
Adult males..........  1,2-D         0.22   6.3x10**-6    0.06     1.7x10**-6     NA        1.69    4.9x10**-5
 Adult females.......                       7.3x10**-6             2x10**-6                         5.6x10**-5
Infants & children...                       2.2x10**-5             6x10**-6                         1.7x10**-4
--------------------------------------------------------------------------------------------------------------------
\1\ Note these wells were not used for risk assessment purposes, therefore, TWA concentration values are only presented
to compare to levels found in
  other wells.

    In summary, the prospective studies show that 1,3-D can move to
ground water under use conditions allowed on 1,3-D labels. EPA believes
that the conditions most likely to result in 1,3-D treatment-related
ground water contamination are shallow water tables, cold temperatures
and high soil permeability. 1,3-D labels have a ground

[[Page 1877]]

water advisory and, as of August 1, 1999, will require a 100 feet
setback from drinking water wells. The labels will also prohibit use in
ND, SD, MN, NY, ME, NH, VT, MA, UT, MT, WI where ground water is less
than 50 feet from the surface and soils are classified as hydrologic
type "A," and in areas overlying karst geology.

B. Non-Dietary Exposure and Mitigation

    Dow AgroSciences conducted several studies to assess both worker
and residential exposures to air borne concentrations of 1,3-D. The
Agency and Dow AgroSciences designed special studies not only to
measure air levels following fumigation, but also to determine which
measures are best suited to mitigate exposures. This section describes
those studies, their limitations, and how EPA reached regulatory
decisions based on the study results [Ref. 21].
    1. Worker and area resident exposure studies-- a. Exposure studies
in the Notice of Special Review. In the 1986 Notice of Special Review,
the non-dietary worker exposure assessment was based on nine studies
conducted in California and Florida. The excess lifetime cancer risk
estimates based on these exposure studies ranged from 10**-5
(one excess cancer death in 10,000 exposed workers over a lifetime) to
10**-2 (one excess cancer death in 100 exposed workers over a
lifetime). In the 1986 Registration Standard, EPA noted the variability
in the data and risk estimates, but ascribed this to 1,3-D's high
volatility and variations in crop practices. During the reregistration
process, the registrant submitted environmental fate studies which
showed that in controlled laboratory studies, 1,3-D behaves differently
according to soil type, temperature, the amount of organic matter in
the soil and other variables [Ref. 22]. There were, however, only
limited data describing how 1,3-D moves in the field under actual use
conditions. EPA determined that, in order to make regulatory
determinations for the Special Review, study designs would have to take
into account some of the environmental conditions that appeared to
influence air borne concentrations under actual field conditions.
    b. Exposure studies for the PD2. When EPA and Dow AgroSciences met
in 1992 to assess the potential effectiveness of risk reduction
measures, the discussions focused on the environmental factors and work
practices which would likely lead to the highest exposures and how best
to control exposures. The registrant agreed to take certain steps,
including reducing maximum application rates, reducing high exposures
to loaders during fumigant transfers, using closed systems and
discontinuing the practice of continuously pumping 1,3-D when the
application rig was lifted out of the ground at row turns. These
exposure reduction measures were placed on 1,3-D labels in 1992 and
1993.
    In addition to label changes, the meetings defined exposure study
designs which would take into account the different use conditions in
the United States and the effectiveness of mitigation measures (e.g.,
enclosed cabs, respirators, loading from 1,000 gallon bulk containers
instead of 55 gallon drums). The 1,000 gallon bulk containers, also
called mini-bulk or traveler systems, reduce exposures because the
frequency of loading events is reduced. AgroSciences conducted air
monitoring studies in three locations to measure exposures to fumigant
loaders, applicators, re-entry workers and area residents.
    For the three study sites, two types of sampling for worker tasks
took place: 4 hour sampling to estimate full-day exposure and short
term sampling. The three representative sites chosen each had different
soil types, moisture conditions, organic soil content and cropping
patterns.
    For residential exposure estimates, data were pooled to account for
random shifts in prevailing wind direction. For residents, EPA also
assumed 16 hours/day spent in and around the house. EPA also assumed
1,3-D air concentrations to be the same indoors and outdoors since 1,3-
D is a small, highly volatile chemical and since there are no data
demonstrating any indoor/outdoor difference. Exposure estimates for
residents are presented in Table 5 in Unit IV of this document, at
fixed distances from a treated field.
    Moses Lake, Washington. This study was conducted in October and
November of 1992. 1,3-D was applied at 25 gallons per acre in loamy
sand soil. The delivery system used was bulk loading with dry
disconnects. Application was by the broadcast method. This type of
application is crucial to root crops because the economically important
part of the plant is entirely underground and is susceptible to direct
nematode damage. For residential air monitoring, there were 20
monitoring locations surrounding the 20-acre treatment test site.
    Buckeye, Arizona. This study was conducted in March of 1993. 1,3-D
(Telone II) was applied by the row method at a rate of 12 gallons per
acre. In the row method less material is used, since the fumigant is
being applied to discrete rows of soil, generally for vegetable crops,
cotton and tobacco. The soil was sandy loam, and bulk loading was used
both with and without dry disconnects. A second study performed in
Buckeye, AZ was similar to the first, except that drum loading was
used. For residential air monitoring, there were 28 locations
surrounding the 20-acre plot.
    Hookerton, North Carolina. This study was conducted in December of
1992. Telone C-17 was used at a rate of 20 gallons per acre to a field
that was sandy loam. Drum loading was used and applied by the broadcast
method. For residential air monitoring, there were 20 monitoring
locations surrounding the 12-acre test plot.
    Ainger, North Carolina. In April of 1995, after the 1992
negotiations and data call-in, Dow AgroSciences conducted an additional
worker exposure monitoring study using a new mini-bulk packaging and
delivery system for 1,3-D (the "traveler" study). 1,3-D was applied
using the row method at a rate of 10 gallons/acre to a tobacco field.
The soil type was not specified.
    Lifetime exposures were estimated by using information Dow
AgroSciences collected on use and usage of 1,3-D. In 1991, Dow
AgroSciences surveyed the 17 states where 1,3-D was used (the survey
did not include California) to obtain information on use patterns
around the country. Information included the crops planted on 1,3-D
treated soil, the amount of 1,3-D (and its alternatives) handled, and
the amount of time spent handling 1,3-D.
    Exposure estimates for workers are presented in Table 4, while
estimates for exposure to residents around treated fields are presented
in Table 5.

[[Page 1878]]

                   Table 4.--1,3-D Air Concentration Monitoring Data for Agricultural Workers
-------------------------------------------------------------------------------------------------------
                                                                                   Air Concentration
                                                                        Total       (μg/m**3)
             Activity         Sample Duration         Study sites       reps. -------------------------
                                                                                    Range        Mean
-------------------------------------------------------------------------------------------------------
Loading \a\................  4 hr                  WA, AZ                    10        177-5932     1,631
Loading \a\................  task only             WA, AZ                    10       526-32490    10,833
Loading \a\................  task only             NC                        12         52-1180       464
Application \b\............  4 hr & task           WA, AZ, NC                28         43-6581     1,359
-------------------------------------------------------------------------------------------------------
\a\ With use of dry disconnects
\b\ With use of end-row spill control

Table 5.-- Offsite Air Monitoring data using average concentrations from
                     three study sites (AZ, NC, WA)
------------------------------------------------------------------------
                                              Mean Conc. 7   Mean conc.
                                              day (μ     15 day
       Distance from treated field (m)           mg/m**3)    (μg/
                                                                 m**3)
------------------------------------------------------------------------
1600 (AZ)...................................            3             2
1,200 (AZ)..................................            6             4
800.........................................           11             7
500.........................................           19            10
125 Edge of buffer zone\1\..................           92            56
25..........................................          196            63
5...........................................          185            67
onsite......................................          181           171
------------------------------------------------------------------------
\1\ Edge of buffer zone - EPA uses this distance to approximate risks at
  300 feet buffer.

 V. Worker and Area Resident Risk Assessment

    Cancer risk is the product of exposure and cancer potency. EPA used
the results of the air monitoring studies to assess inhalation
exposure. EPA used the air levels at the 125 meter distance, which is
used to represent the 300 foot buffer, to approximate an upper-bound
worst case scenario for inhalation risk. EPA used the levels detected
in the 10-foot wells from the Florida prospective ground water
monitoring study as an upper-bound worst case scenario for drinking
water risk. Because the new 1,3-D labels will prohibit 1,3-D use in
areas similar to the Wisconsin site, those levels were not used to
develop risk estimates for the general population.

A. The Cancer Potency Estimate

    EPA calculates lifetime cancer risks as the product of exposure and
the cancer potency estimate (Q1*). EPA has classified 1,3-D
as a Group B2 (probable human) carcinogen based on tumor
induction in rats and mice by the oral and inhalation routes of
exposure. The inhalation Q1* is 5.33  x  10**-2
(mg/kg/day)**-1. For oral (water) exposures, the
Q1* is 1.22  x  10**-1 (mg/kg/day)**-1.

B. The Risk Assessment

    1. Dietary risk assessment. The dietary risk assessment for 1,3-D
is based solely on drinking water exposures through contaminated ground
water. Studies show that 1,3-D and its degradates of toxicological
concern do not appear in foods grown on treated soils as long as 1,3-D
is applied as a pre-plant soil fumigant. The assessment does not
include any exposure through surface water. While models used to
estimate movement of pesticides to surface water show the potential for
1,3-D movement to surface water, these models are not designed to track
volatile, soil applied pesticides. EPA will review the results of a
run-off study Dow AgroSciences is conducting in order to assess whether
run-off to surface water is a significant source of dietary exposure.
    The dietary (drinking water) risk assessment consists of exposures
to 1,3-D and its two degradates of toxicological concern, 3-chloroallyl
alcohol and 3-chloroacrylic acid. EPA does not have toxicity data on
the degradates, and thus assumed that the degradates are of equal
toxicity and carcinogenicity to 1,3-D. A separate assessment is
presented based on 1,2-D levels found in the prospective studies.
    a. Acute- and intermediate-term drinking water risks. No acute or
intermediate endpoints were identified for 1,3-D exposure, and thus no
acute or intermediate risk assessment was conducted.
    b. Chronic drinking water risk. For chronic non-cancer risks, EPA
determined that an oral Reference Dose (RfD) should be 0.025 mg/kg/day
based on a NOAEL of 2.5 mg/kg/day from a 2-year chronic/carcinogenicity
study in rats and an uncertainty factor of 100. The RfD is a level at
or below which daily aggregate exposure over a lifetime is not expected
to pose appreciable non-cancer chronic risk to human health; EPA
generally considers exposures which occupy less than 100% of the RfD to
be acceptable.
    The chronic drinking water risk is calculated as a percent of the
RfD taken up by drinking water. For 1,3-D, groundwater is considered to
be the only source for chronic drinking water exposure to 1,3-D, and
exposure includes the acid and alcohol degradates.
    The following calculation was used:
    % RfD = (Drinking Water Exposure, mg/kg/day) / RfD of
0.025 mg/kg/day  x  100%

    Drinking water exposures for the U.S. population were developed
using concentrations from the Florida prospective ground water
monitoring study. For all population sub-groups (adult males, adult
females, infants/children), the % RfD was less than 1, and therefore is
considered acceptable [Ref. 23].
    c. Cancer risk estimates - drinking water. For 1,3-D, EPA looked at
aggregate risks from multiple routes of exposures (i.e., food, water,
air, dermal). In order to aggregate exposures from multiple routes of
exposure, EPA developed Drinking Water Levels of Comparison (DWLOC's).
A DWLOC, which is not an enforceable standard, is the concentration of
a pesticide in drinking water that would be acceptable as an upper
limit in light of total aggregate exposure to that pesticide from all
other exposure routes. The DWLOC for 1,3-D is based on ground water
levels as EPA did not have information to determine whether surface
water should also be a component of the DWLOC.
    For 1,3-D, EPA has calculated two DWLOC's. For residents who live
near treated fields, as defined at the 300 feet buffer, the DWLOC for
cancer is zero because the inhalation risk estimates were calculated to
be greater than 1  x  10**-6 for this population. While the
cancer risk estimates at distances between 300 feet up to 800 meters
are presented as greater than 1  x  10**-6, EPA believes these
risks are overstated because the value of all mitigation measures has
not been factored into the assessment. Thus, EPA believes the DWLOC of
zero is overly conservative.
    For the general population, defined as residents who live at
distances greater than 300 feet from 1,3-D treated fields,

[[Page 1879]]

the DWLOC for cancer has been calculated to be 0.3 ppb, which is the
level of daily consumption of a pesticide over a lifetime associated
with a 10**-6 risk. The DWLOC for cancer differs from OW's
Health Advisory (HA) of 0.2 ppb, in part because of differing
assumptions on exposure, but also because the DWLOC is based on more
reliable cancer data developed after the 1987 HA had been established.
    EPA compared the ground water levels of 1,3-D found in the
Wisconsin and Florida study sites to the DWLOC for cancer of 0.3 ppb.
In the Wisconsin study, time-weighted average levels were 357 ppb, far
greater than the 0.3 ppb level considered to be acceptable. In the
Florida study, time-weighted average levels from on-site wells were
1.15 ppb, which is associated with lifetime cancer risks of 4  x
10**-6 [Ref. 24]. As of August 1, 1999, 1,3-D labels will
require applicators to leave a 100 foot set-back from any drinking
water well. Therefore the levels from on-site wells in the studies
would overestimate risks at an application site. EPA did not have
accurate information to develop risk estimates with the 100 foot buffer
because the registrant requested the setback from drinking water wells
after ground water studies were well underway. Although the information
from the off-site wells is limited, EPA views these levels (27 ppb in
WI, 0.074 ppb in FL) as indicative of an expected decline in residues
with the well setback from a one-time application.
    Although EPA is not performing a cumulative risk assessment for
1,3-D and 1,2-D, EPA developed a DWLOC for 1,2-D to compare with the
levels found in the ground water studies. The oral Q1* for
1,2-D was used to calculate a DWLOC for cancer effects, which is 1 ppb.
This 1,2-D DWLOC of 1 ppb compares to 0.22 ppb found in 10' Florida
wells, 0.06 ppb found in 70' Florida wells and 1.7 ppb found in the WI
study. It should be noted that the new labels prohibit use of 1,3-D
products in areas with conditions similar to Wisconsin. The inhalation
exposure studies did not monitor for levels of 1,2-D in air. Therefore,
the DWLOC only estimates oral exposures.
    2. Inhalation risk assessment-- a. Factors that influence
exposures. Occupational and residential/bystander inhalation exposure
occurs as a result of 1,3-D volatilization. 1,3-D is a volatile
chemical which is applied at least 12 inches below the soil surface.
The liquid 1,3-D then diffuses through the soil spaces and as much as
25% can volatilize into the atmosphere.
    Volatilization can also occur during product loading; several
measures have been added to 1,3-D labels to minimize leaks. 1,3-D
products do not require mixing and are loaded into tanks which are
attached to tractors or application rigs directly from a bulk or mini-
bulk container through closed loading systems. Bulk loading from tanker
trucks is the predominant practice where custom applicators are the
primary 1,3-D users (e.g., the Pacific Northwest). Mini-bulk systems
are portable 1,000-gallon "traveler" cylinders with dry disconnects
to prevent 1,3-D leaks.
    Variations in use patterns and application methods can affect
exposures. The rate and amount of 1,3-D volatilization is affected by
application method, soil sealing method, soil composition (e.g., amount
of clay and organic matter), soil moisture, and a variety of other
local environmental factors. Meteorological conditions, such as
temperature, precipitation, wind, and atmospheric stability vary
greatly from day to day and also have an effect on exposure. Studies
showed that average exposures are inversely related to distance from
the treated field; 1,3-D air concentrations measured 125 meters from
treated fields were 45 to 72 percent lower than air concentrations
measured 5 meters from treated fields [Ref. 25].
    b. Exposure estimates used for risk assessment. EPA based its risk
assessment on 1,3-D air concentrations measured from the monitoring
sites in Washington, Arizona and the two sites in North Carolina (one
using drum loading for residential exposure and another using mini-bulk
for worker exposure). Only inhalation exposure was estimated; dermal
exposure is expected to be negligible because of 1,3-D's volatility and
the protective measures required on 1,3-D product labels.
    Because the number of monitored replicates at each site was small
(5 to 13), EPA pooled the results from different sites to obtain the
largest possible sample sizes for each exposure scenario.
    For intermediate-term worker exposure, 4-hour samples were used
over the first 7-day period to calculate the mean air concentrations
over all pooled replicates. All worker air concentration estimates were
adjusted using a protection factor of 0.10 for respirators. For
intermediate term risks, EPA calculates a Margin of Exposure, or MOE.
The MOE is a quotient of the NOAEL divided by estimated human
exposures. EPA generally regards MOE's of less than 100 to be
unacceptable. For 1,3-D, the Agency chose an intermediate term NOAEL of
0.091 mg/L, derived from the 2-year combined chronic/carcinogenicity
inhalation study in rats.
    For intermediate-term residential/bystander exposure, a time-
weighted average (TWA) air concentration was calculated for the first 8
days of exposure only (day of application and the first 7 days of a 14-
day study). These are the mean 7-day air concentrations in Table 5 in
Unit IV of this document, which were used to calculate intermediate
term MOE's, also using the NOAEL of 0.091 mg/L.
    For lifetime worker and residential/bystander exposure, the TWA air
concentration was calculated for the entire sampling period for each
monitoring station. This time-weighted average was the arithmetic mean
of the mean daily air concentrations. For all but the on-site samples,
this calculation included the air concentrations measured during the
application process. This value was normalized over a 24 hour period,
and incorporated into an overall 15 day TWA (the day of application
plus the 14 days following). The exposure period of 15 days is used
based on study results showing almost complete volatilization during
the 2-week period following application.
    For each distance from a treated field, the mean TWA over all four
directions (N, S, E, W) was calculated for the entire monitoring
period. Data for all three sites were then pooled, and an overall
average for each distance was calculated for the entire data set. These
values appear in Table 5 under the heading of "Mean conc. 15 day" air
concentrations.
    Exposures to agricultural handlers entering treated fields after
the 5 day Re-entry Interval (REI) were calculated using the on-site air
monitoring data from the residential/bystander studies. For each of the
three monitored sites, the TWA 1,3-D air concentration was calculated
for the period consisting of days 6-14 post-application and was
adjusted by 0.10 for a respirator.
    Chronic, lifetime exposures to workers and area residents were
expressed as lifetime average daily dose (LADD). The LADD of 1,3-D was
calculated according to the following formula:
    LADD (mg/kg/day) = [(air concentration, μg/
m**3)(mg/1,000 μg)(ventilation rate, m**3/
hr)(hr/day) (days/yr)(1 yr/365 days)(yrs exposed/70 yrs)] /
70 kg body wt

using the following values for workers and residents/bystanders:

[[Page 1880]]

Table 6.--Assumptions Used in Assessing Worker and Residential/Bystander
                                  Risk
------------------------------------------------------------------------
                                                          Residents/
                                        Workers           Bystanders
------------------------------------------------------------------------
Ventilation rate................  1.74 m**3/h (light    0.81 m**3/h
                                   work)
Lifetime Exposure...............  30 years, grower,   30 years
                                   20 years,
                                   commercial
Average Lifetime................  70 years            70 years
Exposure Duration...............  crop specific       16 h/day
Exposure Frequency..............  crop specific       15 days/event, 1
                                                       event/yr
------------------------------------------------------------------------

    LADDs for commercial "for-hire" handlers were calculated by first
estimating average daily doses (ADDs) in mg/kg/day, from the air
concentrations. Information on days per year and hours per day were
obtained for each crop, state by state, from Dow AgroSciences' Use, and
Usage Summary Report (1991). However, for loaders, the report lists
only the total hours per day spent actively engaged in loading (0.5 to
1.25 hour/day), not total hours spent on site. To estimate ADDs, the
Agency therefore assumed loaders to be on site for the same number of
hours per day as the applicators (5 to 10 hours/day, depending on state
and crop).
    LADDs for growers assumed that the majority of the work day is
spent applying 1,3-D, and only as much time as is required to load the
tank is spent engaged in loading. Therefore, the 4-hour samples were
used in the calculation of the portion of the exposure resulting from
application, and the task-specific samples were used to calculate the
exposure incurred while loading (because four-hour samples were not
collected for the mini-bulk study, the Agency made the assumption that,
for the use of mini-bulk cylinders, the task-specific loader air
concentrations are experienced for the duration of a work cycle). The
loading and application exposures were then added to estimate the total
exposure for these individuals. For growers, the Agency assumed that
the same person conducts both loading and application of 1,3-D. Tables
7 through 9 present worker and residential/bystander risk.

                                   Table 7.-- 1,3-D Custom Handler Intermediate-Term Non-Cancer Risks and Cancer Risks
----------------------------------------------------------------------------------------------------------------------
                                                Conc.
 Delivery                                    μg/                                                         Int.-
  Method      Example Crop           Task      m**3 from     hr/d      day/yr           LADD         Cancer Risk    Term
                                               Table 4                                                            MOE\a\
----------------------------------------------------------------------------------------------------------

      Bulk  Cotton, AZ         Loader              1,631      10         36    1.1  x  10**-3    6.1  x  10**-5    560

                               Applicator          1,359      10         20    5.3  x  10**-4      2.8 x 10-5    670

      Bulk  Potatoes, WA       Loader              1,631       8         24    6.1  x  10**-4    3.2  x  10**-5    560

                               Applicator          1,359       8         24    5.1  x  10**-4    2.7  x  10**-5    670

 Mini-bulk  Tobacco, NC        Loader                464       5         10    4.5  x  10**-5    2.4  x  10**-6   1960

                               Applicator          1,359       5         10    1.3  x  10**-4    7.0  x  10**-6    670
------------------------------------------------------------------------------------------------------------------
\a\ Adjusted for wearing of respirator or use of enclosed tractor cab (PF = 0.1). MOEs greater than 100 are generally
considered to be acceptable.

                   Table 8.-- 1,3-D Grower Intermediate-Term Non-Cancer risks and Cancer Risks
----------------------------------------------------------------------------------------------------------------
                                                       Application:
                               Loading         ---------------------------
 Delivery                       Conc.              Conc.                                                   Int.-
  Method     Example Crop    μg/  hr/d  μg/                     LADD         Cancer Risk    Term
                                  m**3              m**3 from     hr/d   d/yr                                   MOE\a\
                                                  Table 4
----------------------------------------------------------------------------------------------------------------

     Bulk  Cucurbits, TX          10833   0.25      1,359        6     15    6.3  x  10**-4    3.4  x  10**-5    670

     Bulk  Pineapples, HI        1,0833   1.25      1,359        6     11    9.3  x  10**-4    5.0  x  10**-5    670

Mini-bulk  Tobacco, NC              464   0.5       1,359        5    3.5    9.6  x  10**-5    5.1  x  10**-6    670

Mini-bulk  Peanuts, GA              464   1         1,359        3      5    8.8  x  10**-5    4.7  x  10**-6    670
----------------------------------------------------------------------------------------------------------------
\a\ Adjusted for wearing of respirator or use of enclosed tractor cab (PF = 0.1)

                                    Table 9.--Residential/Bystander Exposure
-------------------------------------------------------------------------------------------------------
 Distance                                              Doses (mg/kg/day)
   from                                        --------------------------------                  Int.-
 treated                   Study Site(s)                                          Cancer Risk     Term
 field(m)                                             ADD            LADD                         MOE
-------------------------------------------------------------------------------------------------------
    1,600  AZ                                     7.6  x  10**-7    3.3  x  10**-7    1.7  x  10**-8    2,800
    1,200  AZ                                     2.9  x  10**-5    1.2  x  10**-5    6.6  x  10**-7    1,600
      800  overall                                5.7  x  10**-5    2.4  x  10**-5    1.3  x  10**-6    8,500
      500  overall                                7.7  x  10**-5    3.3  x  10**-5    1.8  x  10**-6    6,100
     1125  overall                                2.6  x  10**-4    1.1  x  10**-4    5.9  x  10**-6    1,700
       25  overall                                4.8  x  10**-4    2.1  x  10**-4    1.1  x  10**-5      920
        5  overall                                5.1  x  10**-4    2.2  x  10**-4    1.2  x  10**-5      870
   Onsite  overall                                8.3  x  10**-4    3.6  x  10**-4    1.9  x  10**-5      500
-------------------------------------------------------------------------------------------------------
\1\Labels require buffer zone of 300 ft (approximately 125 meters) from an occupied structure.

[[Page 1881]]

C. Aggregate and Cumulative Risk

    Aggregate risk, which considers the various routes of exposure for
a pesticide, and cumulative risk, which looks at the risks posed from
all pesticides with a common mechanism of action are factors that EPA
must consider when it evaluates risks from a pesticide chemical residue
under the Federal Food, Drug and Cosmetic Act, as amended by the Food
Quality Protection Act. These requirements apply specifically to
tolerance actions. As mentioned in the Introduction, EPA classifies
1,3-D as a non-food use chemical. Thus, tolerances are not required.
Therefore, EPA regulates 1,3-D under FIFRA's risk/benefit standard.
However, these risk assessment factors reflect advances in risk
assessment methodology which EPA believes are appropriate when
assessing 1,3-D's risk, even though no tolerance action is involved.
    EPA has aggregated inhalation and oral exposures to 1,3-D. The
aggregate risk estimate is calculated as follows:
    cancer risk inhalation + cancer risk water
= aggregate lifetime cancer risk

    In calculating aggregate risk, EPA has determined that a reasonable
worst-case exposure scenario would be comprised of the inhalation risk
at the 300 foot buffer, derived from the average of three air
monitoring studies, and water exposure risk from the on-site
concentrations from the Florida study. EPA did not use the Wisconsin
study values because, as of August 1, 1999, use in areas similar to
this site is prohibited. Thus, the aggregate risk is estimated as
follows:
    6  x  10**-6 inhalation + 4  x
10**-6 water = 1  x  10**-5

    This aggregate cancer risk estimate, however, is based on
assessments which contain numerous uncertainties from both the
inhalation and water routes of exposure. Those uncertainties are
detailed in Unit V.D. below.
    For cumulative risk, EPA has made a determination not to cumulate
the risks posed by exposures to 1,3-D and any other chemical. This
determination could change in the future based on policy changes or new
mechanistic data on 1,3-D or other chemicals.

D. Strengths, Weaknesses and Uncertainties of the Risk Assessment

    The evidence for the inhalation carcinogenicity endpoint is strong.
Carcinogenicity was confirmed at multiple sites in two species of test
animals. Further, the lung tumors used for quantitative risk assessment
were seen in both the mouse oral and inhalation studies. Positive
results in bacterial, Drosophila and mammalian mutagenicity studies
also contribute to the weight-of-the-evidence for carcinogenicity. EPA
acknowledges that there are uncertainties in extrapolating from rodent
studies to possible human effects. While there are human incidents
suggesting a link between 1,3-D exposure and hematological
malignancies, they are too few to support a change to the cancer
classification.
    The main difficulty in assessing exposure is trying to measure air
concentrations of a volatile chemical under highly variable conditions.
Although there is an extensive exposure monitoring data base for 1,3-D,
many factors influence exposure. Many of these factors are specific to
the application method and local environmental conditions. Soil
conditions (moisture, organic content, temperature), soil sealing
methods, injection depth and meteorological conditions all affect 1,3-D
air concentrations to various degrees. Since these factors are
uncontrollable under field conditions, additional studies are not
likely to yield information which would substantially improve the
accuracy of the current risk assessment.
    In addition, based on available data, EPA extrapolated to estimate
levels of use on crops and in states for which there was no actual
data. The assessment also assumes that treatment patterns are the same
every year; however, the 1992 Use, Usage and Product Performance DCI
noted that treatment typically varies from year to year, depending on
anticipated pest pressures, crop rotations, weather conditions, and
economic factors.
    There is also no information available to assess whether there are
current 1,3-D handlers whose exposure would increase due to the methyl
bromide phase out. A cursory review of usage over the past five years
shows that there has been an overall increase in 1,3-D use. EPA
believes this increase is due, in part, to growers making the
transition away from methyl bromide. EPA believes that the phase out
will increase the numbers of people exposed, but not any one 1,3-D
user's exposure, because growers typically use either 1,3-D or methyl
bromide.
    EPA believes residential risks may be overstated because most
individuals are not likely to spend 16 hours a day at a fixed distance
from a treatment site for the 2-week period following fumigation over
30 years.
    Drinking water risks were based on levels found in on-site wells.
Because the new labels will require a 100 foot setback, these levels
are likely overestimates, and thus add to the uncertainty in the risk
estimates presented in this document.
    Most importantly, the protective value of only some of the
mitigation measures required on 1,3-D labels can be quantified. Given
that many of the measures have not been factored into the assessment,
risks are likely to be lower than those presented.

E. Comments on Risk from the Notice of Special Review and EPA's
Response

    Several comments on the health concerns were submitted in response
to EPA's 1986 decision to initiate a Special Review. Many of these
comments are no longer applicable as changes have been made to the
formulation of 1,3-D products, use patterns and 1,3-D labels. For
completeness of the record, EPA will present and respond to these
comments.
    Comment. The Natural Resources Defense Council (NRDC) submitted
extensive comments on 1,3-D. First, NRDC criticized the exposure
assessment for not taking into account dermal exposure. Secondly, they
mentioned that bioaccumulation in aquatic animals should be addressed.
In addition, NRDC asserted that tolerances or an exemption from a
tolerance should be established to cover residues of 1,3-D in
commodities grown in treated soil.
    EPA's Response. At the time of the Notice of Special Review, EPA's
position was that, due to 1,3-D's volatility, the dermal contribution
to risk was minimal compared to the inhalation risk. Because of closed
loading and other personal protective equipment requirements, dermal
exposure to workers should be minor, if any. Dermal exposure to
bystanders and those living 300 feet from treated fields is not
expected.
    As to bioaccumulation in aquatic animals, the Registration Standard
noted that laboratory studies show the parent compound, 1,3-D, is low
to moderately toxic to waterfowl and upland game birds, moderately
toxic to fish and highly toxic to freshwater invertebrates. In water,
1,3-D rapidly

[[Page 1882]]

dissolves by photolysis and hydrolysis, reducing the potential for
exposure to non-target organisms and thus the potential for
bioaccumulation [Ref. 26].
    Regarding tolerances, EPA has determined that residues of concern
are not likely to appear in foods from pre-plant fumigant uses of 1,3-D
and has classified such 1,3-D uses as non-food uses which do not
require tolerances.
    Comment. NRDC asserted that ground water should have been included
as a trigger for the Special Review, and that 1,2-D and 3-chloroallyl-
alcohol should have been examined in greater detail.
    EPA's Response. At the time EPA issued the Notice of Special
Review, a main force driving the ground water concern was the higher
percentage of 1,2-dichloropropane in Telone products. Since that time,
the amount of 1,2-D has been reduced, although EPA is still tracking
how 1,2-D moves in the environment.
    EPA agrees with NRDC's comment that the acid and alcohol degradates
should be included in the 1,3-D risk assessment. In the dietary
assessments, EPA required that Dow AgroSciences track the residue
chemistry of the alcohol and acid degradates. There were no residues of
either 1,3-D or its degradates in crops planted to 1,3-D treated soils.
For water monitoring and subsequent risk assessments, EPA included the
degradate levels and assigned the same toxicity and carcinogenicity as
the parent. Dow AgroSciences is conducting several toxicity and
environmental fate studies to test this assumption. EPA did not include
ecological risk as a trigger for the Special Review; the 1998
reregistration review of ecological data supports that 1,3-D use does
not pose unacceptable ecological risks.
    Comment. The state of Massachusetts commented that residues of 1,3-
D had never been detected in ground water there, but that an on-going
monitoring system was in place.
    EPA's Response. EPA is aware that 1,3-D has not been detected to
date in Massachusetts. However EPA's review of 1,3-D monitoring is on-
going and the Agency would like to receive any available information
about 1,2-D and 1,3-D monitoring (including degradates) from the
states.
    Comment. The U.S. Department of the Interior commented that the
Notice of Special Review did not take into account the effects of 1,3-D
on wildlife.
    Response. In the Registration Standard, EPA noted that there were
no known effects on wildlife or endangered species. Studies submitted
for reregistration show that 1,3-D is moderately toxic to waterfowl and
upland game birds. In ecotoxicity tests, 1,3-D is moderately toxic to
coldwater fish, moderately toxic to warm water fish and highly toxic to
freshwater invertebrates. EPA believes that, since 1,3-D is injected
into the soil and dissipates relatively soon thereafter, there should
be low exposure to wildlife through plants or insects. While ecological
effects were not included in the Notice of Special Review, EPA has
reviewed data applicable to wildlife effects for reregistration and
found that 1,3-D is not likely to pose unreasonable risks to wildlife.
Because use of 1,3-D is expected to expand to coastal areas, Dow
AgroSciences is conducting estuarine ecotoxicity and environmental fate
data on 1,3-D and the alcohol and acid degradates. EPA will take
appropriate regulatory action if the study results show that the
increased 1,3-D use poses unreasonable risks.

VI. Benefits Assessment

    1,3-D is a pre-plant soil fumigant labeled for the control of all
plant-parasitic nematodes and some plant diseases, insects and weeds.
Nematodes are the principle target pests for most use sites. 1,3-D,
methyl bromide, metam-sodium and chloropicrin are broad-spectrum soil
fumigants registered for use on all food and non-food sites. Dazomet is
a nematicide registered for selected sites. Non-fumigant alternatives
are aldicarb, ethoprop, fenamiphos, oxamyl and terbufos. Non-chemical
alternatives (e.g., fallowing, non-host crop rotations, resistant
varieties, soil solarization, deep plowing of crop residue) are often
classified as supplemental control measures because they are used in
conjunction with the pesticide alternatives. The amount of 1,3-D used
is variable from year to year. EPA estimates that 20 to 40 million
pounds of the active ingredient 1,3-D are applied yearly to
approximately 400,000 to 500,000 acres.

A. Scope and Methodology

    Individual site analyses were completed for 1,3-D use on 15 sites.
Most of the usage data in the benefits analyses were obtained from the
1991 Use, Usage and Product Performance DCI; other information was
gathered from USDA published statistics, state extension officials and
crop specialists, literature searches and comments on the Notice of
Special Review. The 15 sites comprised about 95% of the 1,3-D usage
between 1988 and 1990.
    EPA has conducted three reviews of benefits information: (1) the
1986 Initiation of Special Review; (2) a 1994 analysis based mainly on
information from the 1991 DCI [Ref. 27]; and (3) a 1997 update of the
1994 analysis [Ref. 28]. The 1994 review estimated economic impacts if
1,3-D were restricted or canceled. The 1997 review was not as
comprehensive as the DCI and 1994 analysis, and thus the more recent
analysis may not have captured the full extent of use between 1994 and
1997.
    The basic economic approach used was a partial budgeting method and
simple supply-demand analysis using possible cost changes and yield
effects. If 1,3-D use were canceled for a given site, EPA made
projections on the alternatives that growers would use to control the
target pests on acreage currently treated with 1,3-D. The assessment
does not project economic impacts if both 1,3-D and methyl bromide are
unavailable.
    California 1,3-D usage was not included in the benefits assessment
because of California's suspension of use permits between 1990 and 1994
and the limited re-introduction of 1,3-D since then.

 B. Impacts if 1,3-D were not Available

    Based on the 1994 review, short-term grower economic impacts for
all sites are estimated to range from $37 million to $89 million
annually. EPA considers these impacts to be substantial. These impacts
are the result of increased costs for alternative treatments and
reduced yields with the use of alternatives and are presented in Table
11. EPA estimates project that growers would shift an average of 50% of
their use to the fumigant alternatives and 44% of the use to non-
fumigant alternatives. The remaining 6% represents a shift to non-
chemical and unknown alternatives. Metam-sodium is the fumigant
alternative with the largest quantity of additional acres treated,
followed by methyl bromide and chloropicrin. Aldicarb is the non-
fumigant alternative with the largest shift in additional acres
treated, followed by ethoprop and fenamiphos.
    Crops with the greatest total value of impacts if 1,3-D were
canceled would be Irish potatoes, tobacco, sugar beets, cucurbits
(e.g., cucumbers, pumpkins, squashes), onions, strawberries and
peppers. Geographically, the regions most affected would be the Pacific
Northwest (Washington, Oregon and Idaho) and the southeastern states
(Georgia, Alabama, Florida, Virginia and North and South Carolina).
Impacts on users growing fruit and nut trees and grapevines, crucifers,
pineapples and strawberries would occur when methyl bromide is no
longer available as an alternative. The following table 10 presents
estimated usage of 1,3-D and reflects a recent update.

[[Page 1883]]

                              Table 10.-- Major 1,3-D Usage Sites - 1997 Review\1\
------------------------------------------------------------------------------------------------------
                                       Acres      % Crop    lbs a.i.
                                      Treated    Treated    applied
                                       (000)   -----------   (000)
                     Crop           -----------           -----------  States where most usage occurs
                                      weighted   weighted   weighted
                                      average    average    average
------------------------------------------------------------------------------------------------------
Crucifers..........................         10          4       2000  AZ,TX,GA, SC, NC,CA
Peppers............................          5          4        400  NM,NC,CA
Cucurbits..........................         13          2        600  TX,AZ,SC, NC,GA,CA
Sugar Beets........................         45          3       4000  NE,WY,CO, ID
Cotton.............................         85          1       2000  AZ,NC,GA, FL,CA
Tobacco............................         80         11       7200  NC,SC,GA
Irish Potato.......................         80          6     13,500  WA,ID,OR, CO,ND,MI
Sweet Potato.......................     N/A\2\     N/A\2\     N/A\2\  NC, GA, SC
Peanut.............................         12          1        700  AL,GA,TX
Fruit/Nut Trees and Grape Vines....         27          6       2400  CA,SC,NC, AZ,GA,NJ
Onions.............................          5          5       1000  OR,WA,ID
Tomato.............................          2          0        200  GA,FL,AL
Carrots............................          2          2        150  CA,WA,TX
Pineapple..........................          5         14       1300  HI
Strawberries.......................          1          1         80  CA,FL,NJ
------------------------------------==================================================================
Total..............................        382                 35530
------------------------------------------------------------------------------------------------------
\1\ Usage data covers 1990-1995 for most sites and as early as 1987 for other sites, primarily using data from
  the 1991 Use, Usage and Product Performance DCI. California data is only available for 1994 and 1995, due to
  the 1991-1993 use permit suspension and limited re-entry program. "Weighted average" weights the more recent
  years' estimates because they tend to be more reliable estimates than for possibly outdated earlier estimates.

\2\N/A - not available for sweet potatoes during the 1997 review.

    The following table 11 presents the 1994 summary of short term
(annual) economic assessment.

            Table 11.-- Summary of Short-term, Annual Impacts if 1,3-D Were Canceled (1991 Estimates)
------------------------------------------------------------------------------------------------------------
                                  Average                        Total Short term Annual Impact from Use of
                                  Pounds    Average   Average        Next-Best Alternative(s)(in $000)
                Crop               a.i.      acres    Percent ----------------------------------------------
                                  applied   treated    crop-    Increase in Treatment
                                   (000)     (000)    treated           Costs            Yield Losses Cost
------------------------------------------------------------------------------------------------------------
Carrots........................       450         4         1  500-1,000               400
Cotton.........................      1550        31         8  insignificant           300-3,300
Crucifers......................       950        26         4  unknown\1\              unknown\1\
Cucurbits......................      1500        19         5  6,000-6,500             unknown
Fruit/Nut Trees & Grapevines...     2,500         9         2  0-500                   none in short run\2\
Onions.........................     1,750        10         2  1,500-8,000             unknown
Peanuts........................       750        12         3  insignificant           insignificant
Peppers........................     3,650        18         4  5,600-6,700             none in short run\2\
Pineapples.....................     1,950         6         2  400-500                 (2,100-2,700)
Potatoes (Irish)...............    16,500        95        24  4,000                   9,000-22,000
Strawberries...................        75        <1        <1  100                     none in short run\2\
Sugar Beets....................     4,500        51        13  insignificant           1,000-13,000
Sweet Potatoes.................     1,900        29         7  insignificant           unknown
Tobacco........................     8,150        91        23  2,000-3,000             8,000-13,000
Tomatoes.......................       300         2         1  insignificant           none in short run\2\
============================================================================================================
Total..........................    46,475       403            20,000-40,000           317,000-49,000
------------------------------------------------------------------------------------------------------------
\1\ The information from the 1991 DCI did not provide enough comparative information for alternatives and thus
  no estimates could be derived.
\2\ Methyl bromide is the main alternative; absent development of a suitable alternative, losses would occur
  without 1,3-D after the 2005 phase-out.
\3\ With next best alternative (methyl bromide), yield increases would be expected.

C. Strengths and Limitations in the Benefits Assessment

    The data used to conduct the benefits assessment for 1,3-D are
relatively comprehensive. The results of the Use, Usage and Product
Performance DCI allowed EPA to identify specific use states, amount of
1,3-D used, acreage treated and use of alternatives for many use sites.
EPA was able to quantify potential economic impacts where yield

[[Page 1884]]

data for 1,3-D and its alternatives was available.
    However, there are weaknesses associated with this assessment, as
the information is now as much as 10 years old. Changes in the
regulatory status of alternatives, agricultural markets and the laws
governing agriculture are likely to have influenced some 1,3-D users'
practices. Although the 1997 review shows a decrease in use from the
1994 analysis, a cursory review of 1,3-D trends indicates that 1,3-D
use has been increasing, and likely will continue to do so. This is
mainly due to increased usage in California as the state's permitting
program has increased the amount of 1,3-D used there. In addition, 1,3-
D use has increased (mainly in Florida and California) as growers seek
alternatives to methyl bromide. Overall, the figures presented in
Tables 10 and 11 likely understate to some degree the benefits
associated with current 1,3-D use. EPA is interested in obtaining
comments (preferably data) from areas or for crops which have
experienced substantial fluctuations in 1,3-D use over the past 5 to 7
years.
    There are also limitations in how the assessment was conducted.
Some of the data EPA collected on product performance came from crop
specialists' opinions where studies were not available. Also, usage
data for a few vegetable crops were aggregated under different
groupings for some states. For example, one state listed tomatoes as an
individual crop, while another listed tomatoes under the grouping
"vegetables."
    For crops where methyl bromide is the fumigant of choice, EPA
attempted to predict whether 1,3-D would be used when methyl bromide is
no longer available, and the resulting increase in 1,3-D usage. Crop
specialists and growers are not sure what major pest(s) are currently
being controlled by methyl bromide since it is a broad spectrum
biocide. Accordingly, it is not clear to what extent 1,3-D would serve
as a suitable alternative for all of the methyl bromide uses. In
addition, the pending phase-out of methyl bromide has spurred a great
deal of research on alternative nematode controls; development of less
costly or more effective alternatives could also have an effect on
future use of 1,3-D. Because of the uncertainties related to the methyl
bromide phase-out, EPA decided to present its benefits assessment on a
short-term, annual basis. Despite the uncertainties associated with the
pending phase-out, EPA believes the information accurately depicts the
high benefits associated with 1,3-D use.
    The 1,3-D benefits assessment provides valuable information
defining use and usage patterns. The benefits analyses present
biological and economic information on the use and usage of 1,3-D.
Biological assessments provided information on pests controlled and
their damage, use rates, methods of application and the comparative
performance of alternatives. Economic analyses estimated the total
usage, the cost of market shifts to alternatives and the relative
impacts on users and the industry.

 VII. Risks Associated with 1,3-D Alternatives

    In developing a regulatory proposal, EPA considered whether
canceling 1,3-D use could actually increase risk based on shifts to the
next best alternative. The main limitation in developing a comparative
risk assessment is that the main alternatives pose acute rather than
chronic risks, making these different endpoints difficult to compare.
As such, this Unit provides only a summary of the risks of alternative
nematicides.
    For the two fumigant alternatives, methyl bromide and metam sodium,
short-term animal studies were used to determine at what level of
exposure adverse effects are observed. The NOAEL is the lowest tested
level where no observable adverse effects are seen. A quotient of the
NOAEL over human exposures is used to calculate an MOE. EPA generally
regards MOEs of less than 100 to be unacceptable.

A. Methyl Bromide

    Like 1,3-D, methyl bromide is a liquid soil fumigant that is
injected into the soil. Since methyl bromide is more volatile than 1,3-
D, tarping generally follows application in order to improve methyl
bromide retention in the treated volume of soil.
    Inhalation of 1,600 ppm for 10-20 hours, or 7,900 ppm for 1.5 hours
is lethal to humans [Ref. 29]. The lowest inhalation level found to
cause toxicity in humans is 35 ppm in air. At lower levels, there can
be neurological effects and low-level chronic exposures are associated
with dizziness, vision and hearing disturbances, and personality
changes. Most human exposures are through inhalation. OSHA has
established a Permissible Exposure Level of 20 ppm time-weighted
average over an 8-hour period [Ref. 30].
    For methyl bromide, EPA did not have a complete data base on usage.
Therefore, the risk assessment was conducted on the crop where the
total amount of methyl bromide used is highest - strawberries. The
study used was conducted by the Alliance of the Methyl Bromide Industry
in June 1993 to measure worker exposure only; there was no monitoring
to assess residential exposure [Ref. 31]. No mitigation is factored
into the assessment, even though a self-contained breathing apparatus
(SCBA) is required when methyl bromide levels exceed the Threshold
Limit Value of 5 ppm. The NOAEL is 20 ppm based on a rabbit study. MOEs
for workers range from 5 to 7,600. The workers most at risk are those
who remove the tarps several days after application. MOEs for this
group of handlers range from 5 to 19.
    Ground water testing for methyl bromide has been conducted in
California, Florida and Hawaii. Of 20,429 wells tested, 2 wells in
California contained methyl bromide residues at 2.5 and 6.4 ppb. There
is no Maximum Contaminant Level (MCL) established for methyl bromide.
    As mentioned in Unit II.B. of this document, methyl bromide
production and importation is scheduled for phase-out in 2005 because
of its potential to deplete stratospheric ozone.

B. Metam Sodium

    Metam sodium is also a liquid soil fumigant typically applied by
injection or chemigation methods. Chemigation application is preferred
because water is required for transporting the chemical through the
soil. The type of irrigation system used depends on the crop grown and
farm size. Metam sodium rapidly breaks down to methyl isothiocyanate
(MITC) and carbon disulfide (CS2), which are both
developmental toxicants based on animal studies. California now
requires buffer zones for fields near residential areas based on the
odor nuisance associated with CS2.
    The MOEs, based on MITC and CS2, for mixer/loaders and
applicators for several types of application systems range from 23
(shank injection similar to 1,3-D applications) to 261 (center pivot
irrigation). MOEs for residents are estimated to be 135 at the 500
meter buffer. The Agency does not have information on ground water
monitoring for metam sodium or MITC [Ref. 32].

C. Aldicarb

    Aldicarb is a granular carbamate pesticide. Aldicarb controls
insects, mites and nematodes and is used on certain crops where 1,3-D
is also used: cotton, citrus, peanuts, sugar beets, sweet potatoes and
tobacco. Use on Irish potatoes is restricted to the Pacific Northwest,
Florida and certain counties in Utah and Nevada. EPA has classified
aldicarb in "Toxicity Class I," meaning it is highly toxic by the
oral, dermal and

[[Page 1885]]

inhalation routes of exposure. In 1993, EPA identified aldicarb as one
of the five most acutely toxic pesticides to handlers and field
workers. Since then, both EPA and Rhone-Poulenc, the main producer of
aldicarb, have pursued risk mitigation proposals to reduce the risk to
handlers and applicators of aldicarb.
    Residues of aldicarb have been detected in foods, and in some
cases, the higher levels exceeded levels of concern for acute toxicity.
EPA has taken steps to reduce the possibility of high residues in
foods, especially potatoes.
    Aldicarb has been detected in ground and drinking water supplies.
EPA is in the process of establishing an MCL for aldicarb and for the
sulfoxide and sulfone degradates.
    Since the detection of aldicarb residues in wells on Long Island,
New York in 1979, an extensive amount of ground water monitoring has
been conducted by the registrants and state and local authorities.
Aldicarb residues have been detected in ground water in 26 states. EPA
has identified a positive correlation between aldicarb detections in
ground water and vulnerable soils (i.e., soil conditions that are more
likely to lead to ground water contamination), usage, and climatic
data. Geologic and hydrologic factors, such as the lateral movement of
water along an impermeable layer, are viewed as significant in
controlling the movement of aldicarb to ground water. Other controls,
such as well set-backs, have not been completely effective in
preventing ground water contamination. Because of this, EPA has been
looking at a variety of controls to augment set-backs such as
regulating based on local soil and water conditions, and lower rates to
control the potential for ground water contamination [Ref. 33].

D. Fenamiphos

    Fenamiphos is an organophosphate, contact nematicide which is sold
as either a granular or an emulsifiable concentrate. Fenamiphos is used
primarily on tobacco, orchard crops, cotton, peanuts, citrus,
grapevines, and pineapples as an alternative to 1,3-D or as a
supplemental nematicide once crop growth is underway. Fenamiphos has a
low soil/water partition coefficient, resistance to hydrolysis, and low
Health Advisory level (2 ppb). The risk concerns with fenamiphos and
its degradates are high acute toxicity (Classified in EPA's Toxicity
Category I), residues in food, ground water contamination and surface
water contamination. The parent compound, fenamiphos, has been detected
in ground water in Florida at over 10 times the adult health advisory
of 2 ppb. High levels of the two major degradates of toxicological
concern have also been found in ground water in Florida. Unlike 1,3-D
and methyl bromide, fenamiphos does not volatilize rapidly. Bird and
fish kills have been associated with fenamiphos use, and label
restrictions (setbacks from waterways) have been placed on fenamiphos
labels. EPA is also looking into ecological concerns for terrestrial,
fresh water and marine/estuarine animals.
    In conjunction with the overall review of organophosphates, EPA is
posting risk and use information for fenamiphos on the internet. The
most current risk assessment for fenamiphos is available on
www.epa.gov/oppsrrd1/op/status.htm.

E. Summary of the Risks Associated with Alternatives to 1,3-D

    EPA reviewed the risks associated with the alternatives to 1,3-D to
determine whether cancellation of 1,3-D registrations would actually
reduce risks or shift risks due to exposure to alternatives. The Agency
found that considerable risks are associated with the most likely
alternative nematicides. Like 1,3-D, the four major alternatives pose
risks to workers. Aldicarb and fenamiphos residues also present dietary
concerns. There are ground water contamination concerns associated with
the use of fenamiphos and aldicarb. Fenamiphos also is a surface water
contaminant and has caused fish kills. While there is no way to compare
chronic and acute risks directly, EPA believes the potential acute
risks of 1,3-D's alternatives raise concerns about the desirability of
shifting use from 1,3-D to the next-best alternatives.

VIII. Risk/Benefit Analysis

A. Introduction to the 1,3-D Risk/Benefit Analysis

    FIFRA directs EPA to consider both the risks and benefits of a
pesticide's use when developing and choosing among regulatory options.
In looking at the benefits, EPA considers the availability and
effectiveness of alternative treatments and the risks posed by the
alternatives. In addition, EPA takes into account uncertainties in both
the risk and benefits assessments.
    In 1996, FQPA amended the requirements for what EPA must consider
in taking any action on pesticide tolerances, including aggregate and
cumulative risks, and whether infants and children have heightened
susceptibility to a pesticide's effects. Although there are no
tolerance actions related to this proposal, EPA believes the FQPA
considerations are appropriate to include in the 1,3-D risk assessment.
Although there are no residues in crops grown in treated soils, there
is dietary risk since 1,3-D can migrate to ground water that is used
for drinking water.
    Both the 1,3-D risk and benefits assessments are weakened by
numerous uncertainties, despite efforts by both EPA and Dow
AgroSciences to develop specialized and comprehensive data on
exposures, carcinogenicity and use and usage information. EPA also
considered whether additional data could be developed to assign a
mitigation value to the measures that have been incorporated into 1,3-D
registrations or to overcome other weaknesses in the data base. Given
that many of the factors that have a substantial influence over 1,3-D
exposures are uncontrollable in normal field settings, the potential
for improving the current risk assessment with additional data is
minimal. Instead, EPA evaluated both the nature of the uncertainties
and the current data base to weigh the risks and benefits of 1,3-D use.

B. Summary of Mitigation Measures on 1,3-D Labels and Risk

    In 1992 and in 1995, Dow AgroSciences requested label changes to
reduce levels of 1,3-D which volatilize into the atmosphere during
fumigant transfers, application and the post-fumigation time period.
Measures added to 1,3-D labels were shut-off valves to prevent 1,3-D
from spilling at row turns, closed loading systems, soil sealing, a
300-foot no-treatment buffer from occupied structures, improved product
stewardship, a phase-out of drum delivery, and reduced application
rates. These measures reduced exposures not only for workers, but for
anyone in the vicinity of treated fields.
    On September 30, 1998, Dow AgroSciences requested additional
modifications to the terms and conditions of 1,3-D registrations to
include a use prohibition in certain northern tier states (ND, SD, MN,
NY, ME, NH, VT, MA, UT, MT, WI) where ground water is less than 50 feet
from the surface and soils are Hydrogeologic Type A, a 100-foot no-
treatment buffer around drinking water wells, prohibition of use in
areas overlying karst geologies and additional monitoring to confirm
that use of 1,3-D does not pose unreasonable risks.
    EPA has determined that 1,3-D is a probable human carcinogen. The
quantified portion of the risk assessment for 1,3-D shows that
inhalation cancer risk estimates for workers are estimated

[[Page 1886]]

to be in the 10**-5 to 10**-6 range. Residents who
live near treated fields are also exposed to 1,3-D as it volatilizes
from treated fields. Not taking into account any of the mitigation
provided for on 1,3-D labels, studies show that risks for area
residents who live within 300 feet of treated fields can be as high as
6  x  10**-5. EPA views this as an overestimate of exposures
under typical use patterns and believes that the label measures such as
soil sealing, lowered rates, soil moisture, and deeper injection,
reduce exposures to an acceptable level. EPA has determined that 1,3-D
and its degradates can migrate to ground water under normal use
conditions. Using the results of the on-site wells in the Florida
prospective ground water study, lifetime cancer risk estimates are 4
x  10**-6 from drinking water. Because the new labels will
require a 100 foot setback from drinking water wells, EPA believes this
drinking water risk is an overestimate. From these estimates, EPA
calculated the aggregate risk (oral plus inhalation) to be 1  x
10**-5.
    EPA also recognizes aspects of the assessments that may understate
risk. An increase in 1,3-D use since the 1991 assessment could result
in higher risk if a worker's exposure duration is increased based on
handling more product. Although the 1,3-D studies were designed to
mimic higher-end exposure scenarios, they never measured exposure from
application at more than one site at a time. Thus, EPA was not able to
assess the impact on air and water levels in areas experiencing
multiple 1,3-D treatments. Dow AgroSciences is conducting air
monitoring in California where multiple fields undergo simultaneous
treatment. EPA has arranged to obtain this information to assess the
impact on air levels.
    Although the final risk estimates were derived from an assessment
that does not consider the reduction offered by several mitigation
measures, EPA believes that cumulatively all of the measures on the
1,3-D labels adequately reduce exposures.

C. Summary of Benefits

    1,3-D is registered for use on all vegetable, field, fruit and nut
and nursery crops. As a fumigant, it is considered more effective than
other fumigant and non-fumigant alternatives, except for methyl
bromide, and certain uses of aldicarb and metam sodium. As a pre-plant
fumigant, 1,3-D treatments are only applied once per crop planting;
whereas the non-fumigant alternatives may require multiple
applications, including to growing crops.
    Nematode infestations typically lead to lowered yields and, in the
case of root crops, may also lead to smaller and disfigured roots.
Other types of pests also controlled by 1,3-D, such as certain
soilborne diseases, generally cause similar types of yield impacts.
Because residues in crops and rotational crops are not an issue,
growers have an option in selecting which crops to plant after soils
have been treated with 1,3-D.
    Although methyl bromide is considered an effective alternative, its
production and importation are scheduled to be completely phased out by
the year 2005. It is anticipated that 1,3-D will be used to replace an
unknown amount of the current methyl bromide soil fumigation usage when
the phase-out occurs. Additionally, all the fumigant and non-fumigant
alternatives pose acute risks, including potentially unacceptable
dietary risks.
    EPA has estimated that if 1,3-D were not available, annual losses
to growers resulting from yield losses and/or increased treatment costs
would range from $37-89 million (or higher depending on the
availability of alternatives). Significant impacts would be incurred by
growers of Irish potatoes, tobacco, sugar beets, curcubits, onions,
strawberries and peppers. The regions most affected would be the
Pacific Northwest and south-eastern states.
    The main weaknesses in the benefits case are that the information
used is several years old and there are uncertainties associated with
the anticipated phase-out of methyl bromide use and the regulatory
status of the remaining nematicides. Restrictions on the alternatives
are likely to substantially increase the benefits related to 1,3-D use.

D. Summary of Risk/Benefit Determination

    In assessing the risk/benefit balance for 1,3-D, EPA evaluated the
mitigation provided by all of the mitigation measures included on 1,3-D
labels. The Agency has sought a wide variety of measures, including
those which can be both qualitatively and quantitatively assessed, to
reduce risks to the greatest extent possible. EPA has determined that
the exposure reduction derived from quantitative and qualitative risk
mitigation measures, taken together, provide acceptable exposure
reduction for those who handle 1,3-D products, as well as for those who
live near treated fields. EPA used this determination in 1998 to
support the Agency's decision that all uses of 1,3-D are eligible for
reregistration.
    Accordingly, EPA has determined that the benefits of 1,3-D use
outweigh the risks, taking into account mitigation measures on the
labels, lack of safe, effective alternatives and benefits associated
with 1,3-D's use. Therefore, EPA is proposing to terminate the 1,3-D
Special Review.
    Nothing in today's proposal affects EPA's ability to seek
additional data or changes to the terms and conditions of 1,3-D
registrations should the need arise. On-going reviews of studies being
conducted for reregistration, such as the tap water monitoring program,
present opportunities to review the status of 1,3-D registrations in
the future. Should those data, or any other information, show that 1,3-
D use poses unreasonable risks to the environment, EPA could seek
additional mitigation, and if appropriate, initiate regulatory action
involving 1,3-D.

 IX. References

    1. California Environmental Protection Agency, Press Release,
April 16, 1990.
    2. Smith, Leonard L. Jr., Letter to Anne Lindsey, October 7,
1992.
    3. California Environmental Protection Agency, Memo to County
Agricultural Commissioners, "Stewardship Program and Suggested
Permit Conditions for the Statewide Use of Telone II (1,3-
Dichloropropene), February 15, 1996.
    4. Gibson, James E., Ph.D., Letter to Steve Johnson, January 19,
1996.
    5. Roby, D.M., Letter to Jim Jones Requesting Modifications to

Dow AgroSciences' Telone Labels, September 30, 1998.
    6. National Toxicology Program, Toxicology and Carcinogenesis
Studies of Telone II in F344/N Rats and
B6C3F1 Mice, U.S. Health and Human
Services NTP TR 269, NIH Publ. No.85-2525. 1985. start
    7. Levy, Alan, Telone II (1,3-Dichloropropene) - A Review of a
Chemical Carcinogenicity Rat Study Submitted Under Section 6(a)(2)
of FIFRA, January 17, 1996.
    8. Levy, Alan, Telone II (1,3-Dichloropropene) - A Review of a
Chemical Carcinogenicity Mouse Study Submitted Under Section 6(a)(2)
of FIFRA, November 6, 1996.
    9. Lomax L.W. et. al., The Chronic Toxicity and Oncogenicity of
Inhaled Technical Grade 1,3-dichloropropene in Rats and Mice,
Fundamental and Applied Toxicology. 12:418-431, 1989.
    10. Levy, Alan, Review of Telone II Soil Fumigant: 2-Year
Inhalation Chronic Toxicity-Oncogenicity Study in Mice, February 5,
1988.
    11. Van Duuren et alia, Carcinogenicity of Halogenated Olefinic
and Aliphatic Hydrocarbons in Mice, Journal of the National Cancer
Institute. 63: 1433-1439, 1979.
    12. McCarroll, Nancy, Review of Mutagenicity, Mechanism and
Metabolism Studies with Telone II (1,3-Dichloropropene), July 15,
1999.
    13. Markovitz, A. and Crosby, W., "Chemical Carcinogenesis: A
Soil Fumigant 1,3-Dichloropropene as Possible Cause of

[[Page 1887]]

Hematologic Malignancies," Archives of Internal Medicine. Vol 144,
pp. 1409-1411, July 1984.
     14. Hernandez, A. F. et. al., "Clinical and Pathological

Findings in Fatal 1,3-Dichloropropene Intoxication," Human and
Experimental Toxicology (MacMillan Press Ltd, 1994) pp. 303-306.
    15. Dearfield, K., Second Peer Review of Telone II, December 8,
1989.
    16. Fisher, B., 1994, Telone II - Revised Q1*, (3/4
Interspecies Scaling Factor), Mouse
(B6C3F1) Inhalation Study, December
19, 1994.
    17. Abbotts, John, EPA Memo to Christina Scheltema, April 29,
1997.
    18. USEPA, Pesticides in GW Database - A Compilation of
Monitoring Studies: 1971-1991, EPA 731-12-92-001, OPPTS, September
1992.
    19. Carleton, J., Review of Sixth and Seventh Progress Reports
for Small Scale Prospective Ground Water Monitoring Study in
Wisconsin, April, 14, 1999.
    20. Waldman, E., Air, Surface Water and Ground Water Field Study
of 1,3-D in a South Florida Vegetable Production System - first year
report, March 1997.
    21.Scheltema, C., Revised Occupational and Residential
Assessments for Telone, June 14, 1996.
    22. Poff, K., Review of Column Leaching of Aged Residues and Two
Field Volatility Studies, September 20, 1993.
    23. Scheltema, C., Revised Drinking Water Risk Estimates, 1998.
    24. USEPA, Reregistration Eligibility Decision (RED) for 1,3-
Dichloropropene, December 1998.
    25. Carleton J., Revised Worker and Residential Exposure and
Risk Assessments based on Data Submitted in Response to the Worker
and Biomonitoring DCI (March 1993) for the Special Review Chemical
1,3-Dichloropropene, May 31, 1995.
    26. EFED Chapter for the 1,3-D Reregistration Eligibility
Decision (RED) Document, July 15, 1997.
    27. Zavolta S. and Michell, R., Preliminary Benefits Analysis of
1,3-Dichloropropene Use, April 1994.
    28. Zavolta, S., Memo Updating 1994 PBA, May 8, 1997.
    29. USEPA, Chemical Fact Sheet for Methyl Bromide, Fact Sheet
No. 98, August 22, 1986.
    30. National Institute for Occupational Safety and Health, 1978,
Occupational Health Guidelines for Methyl Bromide.
    31. Mehta, A., Worker Exposure Assessment During Methyl Bromide
Soil Fumigation, EPA Memo to Flora Chow, March 15, 1994.
    32. Mehta, Worker and Residential/Bystander Risk Assessment of
Metam Sodium During Soil Applications, EPA memo to Jay Ellenberger
and Jack Housenger, June 22, 1994.
    33. EPA Questions and Answers, Reinstating the Use of Aldicarb
on Potatoes, September 22, 1995.

List of Subjects

    Environmental protection, pesticides and pest.

    Dated: December 17, 1999.

Susan H. Wayland,

Deputy Assistant Administrator for Prevention, Pesticides and Toxic
Substances.
[FR Doc. 00-188 Filed 1-11-00; 8:45 am]
BILLING CODE 6560-50-F