[Federal Register Volume 65, Number 8 (Wednesday, January 12, 2000)]
[Notices]
[Pages 1869-1887]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 00-188]


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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: [email protected].
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: [email protected], 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 
g) 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 g/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 g/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, g/L)(2 L/
day)(0.001 mg/g)  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 wells)
                                              ------------------------------------------------------           site           --------------------------
                                                                                                    --------------------------   shallow aquifer (15-22
          Populations              Compound                                                                                               ft)
                                               TWA g/L        kg/day)       m>g/L        kg/day)       m>g/L     Exposure\1\  TWA g/L     Exposure (mg/
                                                                                                                                               kg/day)
--------------------------------------------------------------------------------------------------------------------------------------------------------
Adult males....................  1,3-D             0.30     8.6  x  10-6      0.04     1.1  x  10-6      0.026                       134    3.8  x  10-3
Adult females..................                             1  x  10 -5                1.3  x  10-6                                         4.5  x  10-3
Infants & Children.............                             3  x  10-5                 4  x  10-6                                           1.3  x  10-2
--------------------------------------------------------------------------------------------------------------------------------------------------------
Adult males....................  1,3-D +           1.15     3.3  x  10-5      0.17     4.9  x  10-6      0.074                       357    1  x  10-2
                                  Degradates
Adult females..................                             3.8  x  10-5               5.6  x  10-6                                         1.2  x  10-2
Infants & children.............                             1.2  x  10-4               1.7  x  10-5                                         3.6  x  10-2
--------------------------------------------------------------------------------------------------------------------------------------------------------
Adult males....................  1,2-D             0.22     6.3  x  10-6      0.06     1.7  x  10-6     NA                          1.69    4.9  x  10-5
 Adult females.................                             7.3  x  10-6               2  x  10-6                                           5.6  x  10-5
Infants & children.............                             2.2  x  10-5               6  x  10-6                                           1.7  x  10-4
--------------------------------------------------------------------------------------------------------------------------------------------------------
\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       (g/m3)
             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 (g/m3)    (g/
                                                                 m3)
------------------------------------------------------------------------
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, g/
m3)(mg/1,000 g)(ventilation rate, m3/
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 m3/h (light    0.81 m3/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                                                                      g/                                                         Int.-
  Method              Example Crop                          Task                 m3 from     hr/d      day/yr           LADD         Cancer Risk    Term
                                                                                 Table 4                                                            MOEa
--------------------------------------------------------------------------------------------------------------------------------------------------------
 
      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    g/  hr/d  g/                     LADD         Cancer Risk    Term
                                  m3              m3 from     hr/d   d/yr                                   MOEa
                                                  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