water sources (Eckel 2008).  Because the cancer risk from ground water
sources is below the Agency’s level of concern without the benefit of
these processes to aid dissipation, HED believes that the cancer risk
from surface water sources will also be below the Agency’s level of
concern based on its likely dissipation from surface water sources.

Cancer risk for multiple sources (ambient air exposure) of
1,3-dichloropropene was estimated from monitoring data collected from
over 20 sites over multiple years.  These sites were in areas of high
use and urban environments. The cancer risk estimates for all but one
monitoring site, in a high use area, ranged from 2 x 10-6 to 9 x 10-8,
which are below the Agency’s level of concern.  The monitoring data
for this site resulted in a risk estimate of 6 x 10-6, which does exceed
the Agency’s level of concern.  However, the data for this site in the
following year was almost two orders of magnitude lower.  Therefore,
over a lifetime of exposure, the risk estimates would likely be below
the level of concern.  In more populated urban environments air
concentrations were below the analytical limit of detection in 21 of 28
site/year combinations considered.  In the remaining, values were
measured but did not result in cancer risks of concern.  Therefore, the
Agency does not have a concern for the cancer risk from
1,3-dichloropropene.

8.0 	Cumulative Risk Assessment and Characterization  TC \l1 "8.0
Cumulative Risk Assessment and Characterization

Unlike other pesticides for which EPA has followed a cumulative risk
approach based on a common mechanism of toxicity, EPA has not made a
common mechanism of toxicity finding as to 1,3-D and any other
substances and 1,3-D does not appear to produce a toxic metabolite
produced by other substances. For the purposes of this reregistration
action, therefore, EPA has not assumed that 1,3-D has a common mechanism
of toxicity with other substances. For information regarding EPA’s
efforts to determine which chemicals have a common mechanism of toxicity
and to evaluate the cumulative effects of such chemicals, see the policy
statements released by EPA’s Office of Pesticide Programs concerning
common mechanism determinations and procedures for cumulating effects
from substances found to have a common mechanism on EPA’s website at
http://www.epa.gov/pesticides/cumulative/.

9.0	Occupational Exposures  TC \l1 "9.0	Occupational Exposures

This section of the risk assessment focuses on potential exposures and
risk to occupational handlers, to occupational reentry workers who could
be exposed when entering 1,3-D-treated areas to perform crop-production
tasks, and to occupational bystanders who could be exposed when
performing crop-production tasks near (but not inside) 1,3-D-treated
areas.  This assessment describes the occupational exposures for the
proposed new use only.  The occupational assessment for the existing
uses may be found in the most recent risk assessment associated with the
RED (Vogel, 2007).

Since the majority of 1,3-D is used seasonally with typical applications
lasting 2 weeks, 1 to 2 times per year, it is expected that the majority
of worker exposure will be acute and short-term in duration. Due to
model limitations, the PERFUM model was only used to calculate
post-application exposure for the acute durations.  Monitoring data were
used to calculate post-application acute, short-term and cancer risk
(see Appendix E).  However, there is potential for use by commercial
applicators as well as private growers. Since commercial applicators may
apply 1,3-D to many fields over the course of the use season, they are
expected to have a longer durations of  exposure  than private growers.
Therefore, acute, short- and intermediate-term exposures are assessed
for commercial mixer, loaders, and applicators of 1,3-D (see Section 9.0
of the Phase 5 RED).

It should be noted that the RfC methodology used to calculate inhalation
risk incorporates an adjustment for expected duration of exposure. It is
presumed that exposure occurs during the course of an average work week
(8 hours of work per day and 5 days per week).  For this reason, the
worker assessment is considered conservative for both private growers
and commercial applicators.

Since 1,3-D is formulated as a liquid there is some potential for dermal
and eye contact.  The use of mitigation controls such as personal
protective equipment (PPE) and closed transfer systems (as required on
the Cordon™ label) minimizes the potential but does not eliminate it.
Although 1,3-D may be irritating to the skin and eyes, no dermal
endpoints of concern were selected for risk assessment purposes.
However, the high vapor pressure of 1,3-D also makes quantifying any
potential low level exposures very difficult.  Therefore, a quantitative
dermal exposure assessment has not been completed.

9.1	Post-plant Drip Irrigation Fumigations

Mixer/Loader/Applicator Exposure

The registrant has proposed a post-plant drip irrigation use of 1,3-D in
established vineyards.  HED has no new data for worker exposure
resulting specifically from the post-plant drip irrigation application
of 1,3-D.  However, mixing and loading techniques for the proposed use
are expected to be similar to loading techniques assessed for the
existing agricultural uses of 1,3-D.  Specifically, exposure for bulk
and mini-bulk loading methods were assessed in the most recent RED.  No
data are available to assess drip irrigation applicator exposure;
however, since this type application is closed system, exposure is
expected to be negligible.

As noted above, bulk and mini-bulk loading exposure was evaluated in the
Phase 5 RED for 1,3-D.  The data evaluated in the recent RED is the only
data available to assess exposure for loading of 1,3-D.  It should be
noted that the study data used to estimate bulk and mini-bulk loader
exposure are based on a much higher application rate than the proposed
application rate for the post-plant vineyard use. For this reason,
loader exposure for the proposed post-plant use is expected to be
significantly lower than that assessed for bulk and mini-bulk loading
for the existing pre-plant uses of 1,3-D.

Exerted from the Phase 5 RED:

As a result of the March 1992 Data Call-In (DCI), DowElanco submitted
final reports of worker air monitoring studies conducted in 1992 and
1993 at the Moses Lakes, Washington, Buckeye, Arizona, and Hookerton,
North Carolina (MRID 42946201, 42845602).  These studies monitored
loaders, applicators and workers involved in drum and bulk loading and
related applications of various 1,3-D products.  Studies were conducted
in accordance with product label directions and utilizing regional
commercial application techniques associated with application of Telone
II and Telone C-17.  As a result of the Special Review negotiations
between DowElanco and EPA, drum loading of 1,3-D products was phased out
in late 1996.  A delivery method known as mini-bulk was promoted as
replacement for drum loading.  Subsequently, Dow submitted a study
conducted in Ainger, North Carolina, in which mini-bulk cylinder were
used (MRID 43880401).    These three studies were evaluated in the 1998
1,3-D RED to determine exposure and risk for workers involved in 1,3-D
loading and applications.

For the loaders and applicators, two kinds of samples were collected:
four hour samples, and task-specific short duration (4 to 46 minutes)
samples.  The four hour samples provided inherently time- weighted
average air concentrations over a major fraction of a work day, while
the task-specific samples measured the air concentrations associated
only with high-contact activities.  For product loaders, these
activities were the actual loading events.  The 4-hour loader samples
included the loading events, and the time spent on site between loading
events.  In the most recent Ainger, NC worker monitoring study, only
short-term task specific samples were collected.  Sampling occurred only
when workers were actively engaged in loading.  Because the number of
monitored replicates at each site was small, HED pooled the results from
different sites, to obtain the largest possible sample sizes for each
exposure scenario.   Details of the worker monitoring studies are
described in detail in the 1998 RED.

Data evaluated in the 1998 RED was not modified.  The air concentration
values are the same as those used in Table 7 of the 1998 RED document.
However, in the 1998 RED, estimates for commercial handlers and private
growers were presented separately, assuming that private grower will
perform both loading and application and spend most of their work day
engaged in application rather than loading. Exposures estimates for
growers were based on the air concentration for application rather than
loading. Estimates of exposure for commercial loaders and applicators
were presented separately, assuming 5 to10 hours per work day.

The current document provides assessments of commercial loader and
applicator exposure only, for each task monitored (as listed in Table 7
of the 1998 RED document).  Since commercial applicators may apply 1,3-D
to many fields over the course of the use season, they are expected to
have a more exposure than private growers.   To support this assumption,
HED used estimates of daily and yearly work hours as supplied by the
Agency’s Biological and Economic Analysis Division (BEAD).  BEAD
determined that the Total Lifetime Work Hours were 500 hours for private
farmers/growers (5 hrs/day x 10 days/year x 10 years/lifetime) and 3200
hours for commercial handlers (8 hrs/day x 20 days/year x 20
years/lifetime).  HED used BEAD’s assessment of lifetime work hours
for commercial handlers (8 hrs/day x 20 days/year x 20 years/lifetime)
as the basis for the current assessment. Since the estimate lifetime
work hours for commercial handlers are greater than that of the private
growers, the current worker assessment is considered conservative for
both private growers and commercial applicators.

Acute risks (MOEs) are calculated by comparing the maximum air
concentration level of 1,3-D at an individual sample point to the
toxicological human equivalent concentration (HEC) selected for acute
exposures. To calculate the short-and intermediate-term risks to
handlers, the  mean air concentration level of 1,3-D are calculated
across all sites for each different handler task and method of
application.  This mean air concentration levels are compared to the HEC
selected for short- and intermediate-term. Cancer risk is calculated by
multiplying the LADE by the occupational Q1*.  The LADE used for cancer
risk assessment assumes 20 days of exposure per year for 20 years per
lifetime.

Table 14 summarizes the risks for loading activities and applicators
involved in pre-plant broadcast and row applications.  Overall, the data
indicate that risks exceed HED’s level of concern for workers involved
in 1,3-D loading and application when no respiratory protection is used.
 OV respirators, which reduce exposure levels by a factor of 10, are
also considered and reduce exposure do not exceed HED’s level of
concern for most workers involved in 1,3-D application with these
devices.  However, even with the use of OV respirators, which are
required on current 1,3-D labels, the intermediate-term MOEs for bulk
loading exceed HED’s LOC (LOC is for MOEs less than 30).  It is likely
that the risk estimates for bulk loading is conservative because this
assessment assumes that this activity is done over the course of a
normal work week, 8 hours per day, 5 days per week.  The available
monitoring study indicates that actual loading activities comprise a
small part of the entire work day (approximately 15 minutes to 1 hour).
However, since this assessment is for commercial applicators and BEAD
information indicates that commercial applicators can work for 8 hours
/day, HED will use these current inputs until data are available to
support refinements to ensure HED does not underestimated risk.  Data
which indicated the division of work for commercial applicators (i.e.,
time spent loading and time spent applying) could be used to refine the
bulk loading risk estimates.  Note that if bulk loading only occurs for
one hour (or less) per day, the intermediate-term bulk loading risk
would not exceed the LOC.

Table 14:  1,3-D Air Concentrations Monitoring Data for Agricultural
Workers as listed in the 1998 RED

Activity

Sample Duration

Study Site

Total reps

Max	Air Concentration (ppm)	MOE

	Cancer Risk3

	Mean	Median	acute1	Short2	interm2

	Bulk Loadinga	4 hrs	WA, AZ	10	1.29	0.35	0.14	176.35	42.38

	2.43

(24.3)4	1.2E-04

(1.2E-05)4

 Bulk Loadinga	task only	WA, AZ	10	7.05	2.35	1.05	32.20

	6.38

(64)4	0.37

(4) 4	6.6E-04

(6.6E-05)4

Mini-bulk Loadinga	task only	NC	12	0.26	0.10	0.10	886.51

	148.98

	8.54

(85.4)4	2.4E-05

(2.4E-06)4

Bulk, Mini-bulk, and Drum Applicationb	4 hrs & task	WA, AZ, NC	28	1.43
0.29	0.25	158.96

	50.86

	2.92

(29.2)4	1.34E-04

(1.3E-05)4

a With use of dry disconnects

b With use of end-row spill control

1  Acute MOE = HEC (227 ppm)/maximum air concentration value.

2  Short- and Intermediate-term MOE = HEC (15 ppm for short-term and
0.86 ppm for intermediate-term)/mean air concentration value.

3  Cancer Risk = Q1*(1.8 x 10-2 ppm) x ( 8 hours/24 hours -) x LADE
(median air concentration value x 20 days/365 days per year x 20
years/70 year lifetime).

4 () = addition of OV respirator.

Occupational Bystander Exposure

One field volatility study is available to address post-application
exposure from this use (MRID 45296101).  Using this field volatility
study, modeling is done for the post-plant drip irrigation using the
PERFUMS model. The resulting buffer distances were estimated to be zero
(see section 6.1 for details).  However, the Agency has some concerns
with the quality of this study.  First, the application rate used in the
study was 5.4 lbs ai/acre, while the maximum application rate allowable
is 17.74 lbs ai/acre.  In general, the Agency believes that scaling down
from the maximum application rate is acceptable, assuming a linear
relationship between application rate and flux rate.  However, the
Agency has concerns with the practice of scaling up flux rates to the
maximum application rate, as it is unclear if soil saturation may occur
that causes more off-gassing (flux) than expected.  Additionally, while
flux rates were calculated from this study data, the regression analysis
for most periods yielded poor r-squared values and reordering of the
data was required.  This is a standard practice, but a better designed
study probably would have yielded better results.  A smaller field and
samplers placed closer to the edges of the field (e.g., the samplers in
this study were roughly 300 ft away whereas most studies have samplers
approximately 30 ft away) would have produced a higher quality of data.
As a result, the Agency has low confidence in the flux rates obtained
from this study.

ble post-plant study only monitored air concentrations of 1,3-D at 300
feet from the treated field, HED recommends that the Cordon™ label
require a buffer distance of 300 feet until the requested confirmatory
field volatility data for this use are received and reviewed.

The Agency has limited data (i.e, one field volatility study) to assess
the post-plant drip irrigations use.  However, the Agency has additional
field volatility data for the existing pre-plant drip irrigation use of
1,3-D, which is very similar to the proposed post-plant drip irrigation
use.  To further characterize the potential risks resulting from the
proposed use, the HED has provided a summary of risk results for the
pre-plant irrigation uses.  This assessment indicates low concern for
occupational bystander exposure resulting from the existing drip
irrigation uses.  Additionally, it should be noted that the proposed
post-plant drip irrigation uses  are applied at significantly lower
application rates than the existing pre-plant drip irrigation uses.  For
this reason, exposure and risk related to the proposed use is expected
to be significantly lower than that of the pre-plant drip irrigation
uses (presented below).

Exerted from the Phase 5 RED:  Pre-plant Drip Irrigation Applications:
TC \l3 "Pre-plant Drip Irrigation Applications:  HED has no data for
worker exposure resulting from the drip irrigation application of 1,3-D.
 However, there are field volatility data available to address off-site
exposure from this use.  The ISCST3 Model is used to estimate
occupational bystander exposures following/during a single pre-plant
drip irrigation application of 1,3-D to outdoor agricultural fields.
The model allows HED to examine the effect of several variables,
including field size, emission ratios, wind speed, and atmospheric
stability.  Air concentration levels estimated by the ISCST3 Model are
based on the assumption that occupational bystanders would be exposed
during an eight-hour work day.  [Details of the ISCST3 analysis are
available in Appendix C. ]. Table 17 shows the acute risks (MOEs)
estimated by comparing the toxicological human equivalent concentration
of concern to the estimated air concentration levels.  Generally, risks
do not exceed HED’s level of concern ((LOC is for MOEs less than 30).
Although the ISCST3 model assessment is considered be a high-end
estimate of actual exposure, HED does not have data to refine the
current assessment.

As noted above, the modeling analysis done for the existing pre-plant
drip irrigation use indicates that there is low concern for acute
occupational bystander exposure resulting from 1,3-D application.
However, field volatility studies for 1,3-D indicate that peak emissions
from treated fields occur up to 72 hours after application.  At this
time, the models cannot readily be used to evaluate exposures of longer
duration.  When appropriate distributional models are available,
short-term, intermediate-term and cancer risk may be reassessed with
models that can better estimate longer term, average exposures (e.g., a
SOFEA© analysis based on existing uses).

Table 17. ISCST3 MOEs At Selected Distances Downwind For Occupational
Exposure to Pre-Plant Agricultural Field Fumigations, Telone EC

App. Meth.	ER

(%)	Fld

Size

(A)	DW Dist.

(M)	Differing  Meteorological Conditions

1 m/s

2.3 mph	1.4 m/s

3.1 mph	1.8 m/s

4 mph	2.2 m/s

5 mph	2.7 m/s

6 mph	3.1 m/s

7 mph	3.6 m/s

8 mph	4.0 m/s

9 mph	4.5 m/s

10 mph	4.5 m/s

10 mph

Stab D	Stab C	Stab C	Stab C	Stab C	Stab C	Stab C	Stab C	Stab C	Stab B

Drip Irrigation, Raised Bed, Untarped	7.8	1	25	105	228	293	359	441	505
588	650	732	1040

	100	238	565	727	889	1083	1253	1444	1600	1825	3059

	500	1316	4727	6118	7429	8667	10400	11556	13000	14857	34667

5	25	67	148	190	233	286	328	381	423	477	675

	100	130	296	381	466	571	658	765	846	954	1405

	500	406	1253	1600	1962	2419	2737	3250	3586	4000	8667

10	25	57	126	162	198	243	279	324	360	405	575

	100	102	235	302	370	454	520	605	671	754	1106

	500	279	782	1010	1238	1507	1733	2000	2261	2537	5200

20	25	49	109	140	171	210	241	280	310	350	498

	100	82	190	245	299	366	421	488	545	612	889

	500	203	536	689	839	1030	1182	1368	1529	1733	3250

40	25	42	95	122	149	183	211	244	272	305	439

	100	67	157	202	246	302	348	403	448	505	743

	500	153	395	507	619	759	874	1020	1130	1268	2261

Drip Irrigation, Raised Bed, Tarped	2.2	1	25	375	813	1051	1284	1576	1793
2080	2311	2600	3714

	100	852	2000	2600	3152	3852	4522	5200	5778	6500	10400

	500	4727	17333	20800	26000	34667	34667	52000	52000	52000	104000

5	25	241	531	680	832	1020	1169	1368	1507	1705	2419

	100	462	1061	1368	1651	2039	2364	2737	3059	3355	4952

	500	1444	4522	5778	6933	8667	9455	11556	13000	14857	34667

10	25	203	450	578	707	867	1000	1156	1284	1444	2039

	100	365	839	1083	1316	1625	1857	2167	2419	2667	4000

	500	1000	2811	3586	4333	5474	6118	7429	8000	8667	17333

20	25	174	388	500	612	748	860	1000	1106	1253	1793

	100	294	680	874	1072	1316	1507	1733	1926	2167	3152

	500	727	1926	2476	2971	3714	4160	4952	5474	6118	11556

40	25	151	340	437	533	654	754	874	972	1095	1576

	100	240	562	722	881	1083	1238	1444	1600	1793	2667

	500	545	1405	1825	2213	2737	3152	3586	4000	4522	8000

10.0	Data Needs and Label Requirements  TC \l1 "10.0	Data Needs and
Label Requirements

10.1	Toxicology  TC \l2 "10.1	Toxicology

No additional studies are required at this time.

10.2	Residue Chemistry  TC \l2 "10.2	Residue Chemistry

The following confirmatory studies are needed to support an
unconditional registration.

860.1340 Residue Analytical Methods

An independent laboratory validation is required for the tolerance
enforcement method that determines the 3-chloroacrylic acid and
3-chloroallyl alcohol metabolites.

OPPTS Guideline 860.1360 Multiresidue Methods

Multiresidue method data are required for 1,3-dichloropropene and its
3-chloroacrylic acid and 3-chloroallyl alcohol  metabolites.

OPPTS Guideline 860.1380 Storage Stability

A storage stability study demonstrating stability of 1,3-dichloropropene
and its 3-chloroacrylic acid and 3-chloroallyl alcohol  metabolites in
grapes for at least 154 days is required.

10.3	Occupational and Residential Exposure  TC \l2 "10.3	Occupational
and Residential Exposure

No additional studies are required at this time.

References

Abel, S., 6/26/00; D260209 and D260210 (Environmental Fate Assessment).

Eckel, W., 1/18/08, Characterization of the Drinking Water Assessment
for Telone.

Olinger, C.; 5/24/2007; DP D318734; Amended Registration for Grapes:
Summary of Analytical Chemistry and Residue Data.

Olinger, C.; 6/13/07; DP D340060; Amended Registration for Grapes:
Summary of Analytical Chemistry and Residue Data.

Olinger, C.; 12/14/07; DP Barcode: D346778; Follow-up on Proposed New
Use for Drip Irrigation in Vineyards: Drinking Water and Residential
Assessments.

Vogel, D. et al; 4/12/2007; DP D337328; 1,3-Dichloropropene: HED Human
Health Risk Assessment for Phase 5.

Appendix A: Executive Summaries for Critical Studies and Toxicological
Profile  TC \l1 "Appendix A

Executive Summaries for Critical Studies and

 Toxicological Profile

Acute Inhalation Exposure

Critical Studies: Acute Inhalation Studies - Rats

EXECUTIVE SUMMARY:   In one acute inhalation study (MRID No.4022093),
Wistar rats were exposed to Telone II at 454, 647, 699, 762, 832 or 958
ppm for 4 hours (whole body exposure).  The mortality rates were as
follows: 0, 20, 30, 50, 100 and 100% at 454, 647, 699, 762, 832 and 958
ppm dose levels, respectively. In a second study (MRID 41672201),
Fischer 344 rats were exposed to cis- 1, 3 dichloropropene at 0, 583,
771, or 1020 ppm for 4 hours (whole body exposure).  No animals died at
583 ppm; however, body weight loss (13% decrease in body weight) during
days 2 through 7 was seen in rats exposed to this concentration. Rats
regained their weight on day 8. At 1020 ppm, all exposed animals died
immediately following the exposure and 771 ppm exposed animals died
during the 14 day observation period.  Accordingly, 454 ppm or an HEC of
75.67 ppm (non-occupational risk assessment) or 227.0 ppm (occupational
risk assessment) was selected as the NOAEL  based on decreased body
weights at the LOAEL of 583 ppm.

	Short-term Inhalation Exposure

Critical Study: Developmental Toxicity Study - Rabbits

EXECUTIVE SUMMARY :  In a developmental toxicity study (MRID 001444715
and 00152848), New Zealand rabbits (17-24 females/group) were exposed to
aerosol concentrations of 1,3-D (90.1%) at 0, 20, 60 or 120 ppm
(equivalent to approximately 0, 0.091, 0.272 or 0.545 mg/L) 6 hours/day
during gestation days 6 through 18.  The maternal NOAEL was 20 ppm
(0.091 mg/L).  The maternal LOAEL was 60 ppm (0.272 mg/L) based on
decreased body weight gains compared with controls.  The developmental
NOAEL was 120 ppm (0.545 mg/L).  The developmental LOAEL was >120 ppm (>
0.545 mg/L, HDT).  No Telone II related malformations were reported.

	Intermediate-term Inhalation Exposure

Critical Study: 13-Week Inhalation Toxicity Study - Rats

EXECUTIVE SUMMARY: In a subchronic (13-week) toxicity study (MRID
00146461)  Fischer 344 rats (10 sex/group) were exposed to
concentrations of Telone II at 0, 10, 30, 90 or 150 ppm, 6 hours/day, 5
days/week for 13 weeks. Both sexes of rats at 90 and 150 ppm exhibited a
significant decreases in body weights while rats at 30, 60 and 150 ppm
exhibited treatment-related histopathological lesions in the nasal
turbinates.  The NOAEL was 10 ppm (0.045 mg/L) and the LOAEL was 30 ppm
(0.136 mg/L), based on histopathological lesions in the nasal
turbinates.

Long-term Inhalation Exposure

Critical Study: Chronic toxicity/carcinogenicity study - Mice

EXECUTIVE SUMMARY:  In a chronic toxicity/carcinogenicity study (MRID
40312301), B6C3F1 mice (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%) at aerosol concentrations of 0, 5, 20 or 60 ppm
(equivalent to approximately 0, 0.023, 0.091 or 0.272 mg/L) 6 hours/day,
5 days/week for a total of 510 days over a two-year period.  There was
no effect on survival (at least 80% in each group).  There was a
statistically significant decrease in body weight gain in 60 ppm males
(3-9%) and females (2-11%).  Urinary bladder effects were noted
primarily in females at 20 and 60 ppm (slight, moderate or marked
roughened, irregular and opaque surfaces were reported in 20/50 at 20
ppm and 30/49 at 60 ppm compared with 3/50 slight in the control group).
 Hypertrophy and hyperplasia of the nasal respiratory mucosa (very
slight/slight) were observed in most 60 ppm mice of both sexes and in 20
ppm females.  Degeneration of olfactory epithelium (very slight/slight)
was noted in most 60 ppm mice of both sexes.  Hyperplasia of the
epithelial lining of the nonglandular portion of the stomach was
observed in 60 ppm males (0, 5, 20 and 60 ppm: males = 0, 3, 1 and 8;
females = 0, 0, 0 and 2).  For chronic toxicity, the NOEL was 5 ppm
(0.023 mg/L) and the LOEL was 20 ppm (0.091 mg/L) based on urinary
bladder hyperplasia and hypertrophy/hyperplasia of the nasal respiratory
mucosa.  Hyperplasia of the epithelial lining of the nonglandular
portion of the stomach was observed in a higher incidence compared with
controls in 60 ppm males and, to a lesser extent, 60 ppm females.  There
was evidence of carcinogenicity.  Bronchioloalveolar adenomas appeared
in a higher incidence in 60 ppm males only compared with controls (0, 5,
20 and 60 ppm = 9/50, 6/50, 13/50 and 22/50).  Although the lung tumors
noted in the mouse inhalation study were benign, 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 bioassay.

Discussion of Tumor Data: Telone II was associated with a significant
positive dose related trend in lung bronchioloalveolar adenomas (benign
tumors) in male mice.  A pair-wise comparison at the top dose, 60 ppm,
showed a significant increase of bronchioloalveolar adenomas from
control (22/60 of animals at risk (37%) versus control of 9/57 of
animals at risk (16%)).  Historical control data from seven studies
indicated a control range of 7-32% for lung bronchioloalveolar adenoma;
this included a 20% control incidence from another 2 year inhalation
study.  The incidence of lung tumors in male mice in this study was
outside the historical range.  While there were some increases in the
incidences of other tumor types (benign lacrimal gland tumors in males
and mesenteric lymph node lymphosarcomas in females), these were not
considered convincing by the Peer Review Committee to be of great
concern (Memo from Kerry Dearfield to Herman Toma, Second Peer Review of
Telone II, dated December 8, 1989).  The only agreed upon tumor of
concern was the increase in lung tumors in male mice after inhalation
exposure.  It was noted that female mice in the NTP study also had a
dose related increase in lung tumors after an oral exposure.

Chronic Oral Exposure

Critical Study:  Combined Chronic Toxicity/Carcinogenicity Study in Rats

EXECUTIVE SUMMARY:  In a chronic toxicity/carcinogenicity study (MRID
43763501), Telone II (96% a.i.) was administered as microcapsules by
dietary admix to Fischer 344 rats (60/sex/group with 10/sex/group
sacrificed at 12 months) at levels of 0, 2.5, 12.5 or 25 mg/kg/day for
two years. Body weight gains were decreased for males (8 and 21%) and
females (15 and 25%) at 12.5 and 25 mg/kg/day compared to controls. Food
consumption was decreased in females at 25 mg/kg/day. There was an
increase in liver masses/nodules in males only at 12.5 and 25 mg/kg/day.
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
sacrifices at 12.5 and 25 mg/kg/day. For chronic toxicity, the NOEL was
2.5 mg/kg/day and the LOEL was 12.5 mg/kg/day based on a decrease in
body weight gain compared with controls and an increase in the incidence
of basal cell hyperplasia of the nonglandular mucosa of the stomach.
There was evidence of carcinogenicity. The incidences of rats with
primary hepatocellular adenomas were as follows respectively (0, 2.5,
12.5 or 25 mg/kg/day): males = 2/50, 1/50, 6/50 and 9/50; females =
0/50, 0/50, 0/50 and 4/50. These data indicate that exposure to Telone
II increases the incidence of these tumors in males at the two highest
doses and in females at the highest dose. The highest dose tested in
this study (25 mg/kg/day) was considered adequate to assess the
carcinogenic potential of 1,3-D in rats.

Discussion of Tumor Data:  The incidences of rats with primary
hepatocellular adenomas were as follows respectively (0, 2.5, 12.5 or 25
mg/kg/day): males = 2/50, 1/50, 6/50 and 9/50; females = 0/50, 0/50,
0/50 and 4/50. These data indicate that exposure to Telone II increases
the incidence of these tumors in males at the two highest doses and in
females at the highest dose.

EXECUTIVE SUMMARY: In a study reported by the National Toxicology
Program (NTP) in 1985 (MRID 0014669), 1,3-D (89.0% a.i.) was
administered in corn oil (with 1.0% epichlorohydrin as a stabilizer)  by
gavage to Fischer 344 rats (52/sex/group) at doses of 0, 25 or 50
mg/kg/day three times per week for 104 weeks.  A total of 77 rats per
sex was used for each dose group, including those sacrificed for
examination during the course of testing.  Basal cell or epithelial
hyperplasia of the forestomach was reported.  The NTP concluded that
there was “clear evidence of carcinogenicity” for males and “some
evidence of  carcinogenicity” for females.

Discussion of Tumor Data:  Statistically significant increases in the
incidence of the following tumors were observed in the highest dose
tested (HDT) by pairwise comparison with controls:

1) forestomach squamous cell papillomas in males and females;

2) combined forestomach squamous cell papillomas and carcinomas combined
in males; and

3) liver neoplastic nodules in males and combined neoplastic nodules and
hepatocellular carcinomas in males.

The increased incidence of forestomach tumors was accompanied by a
statistically significant positive trend for forestomach basal cell
hyperplasia in male and female rats of both treatment 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.

	 In 1992, the registrant conducted a second feeding study using
timed-released (microencapsulated) doses of 1,3-D in food since the
stomach tumors seen in the NTP study coincided with 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.

	In a chronic toxicity/carcinogenicity study (MRID No. 43763501), Telone
II (96% a.i.) was administered as microcapsules by dietary admix to
Fischer 344 rats (60/sex/group with 10/sex/group sacrificed at 12
months) at levels of 0, 2.5, 12.5 or 25 mg/kg/day for two years.

	Body weight gains were decreased for males (8 and 21%) and females (15
and 25%) ar 12.5 and 25 mg/kg/day compared to controls.  Food
consumption was decreased in females at 25 mg/kg/day.  There was an
increase in liver masses /nodules in males only at 12.5 and 25
mg/kg/day.  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 sacrifices at 12.5 and 25 mg/kg/day.  For chronic toxicity, the
NOAEL was 2.5 mg/kg/day and the LOAEL was 12.5 mg/kg/day based on a
decrease in body weight gain compared with controls and an increase in
the incidence of basal cell hyperplasia of the nonglandular mucosa of
the stomach.  There was evidence of carcinogenicity.

Discussion of Tumor Data:  The incidences of rats with primary
hepatocellular adenomas were as follows respectively (0, 2.5, 12.5 or 25
mg/kg/day): males = 2/50, 1/50, 6/50 and 9/50; females = 0/50, 0/50,
0/50 and 4/50.  These data indicate that exposure to 1,3-D increases the
incidence of these tumors in males at the two highest doses and in
females at the highest dose.  The highest dose tested in this study (25
mg/kg/day) was considered adequate to assess the carcinogenic potential
of 1,3-D in rats.

Critical Study: Combined Chronic Toxicity/Carcinogenicity Study in Mice

EXECUTIVE SUMMARY: In a study with B6C3F1 mice (50/sex/group) reported
by the NTP in 1985 (MAID 00146469), Telone II (89.0 % a.i.) was
administered in corn oil (with 1.0% epichlorohydrin)  by gavage at doses
of 0, 25 or 50 mg/kg/day three times per week for 104 weeks.  The study
in males was not considered to be adequate because of the mortality of
controls at weeks 48-51(25/50, myocarditis) and the 104-week survival
for males (8/50, 28/50 and 31/50).  Squamous cell papillomas of the
forestomach (0/50, 1/50 and 2/50 for females), squamous cell carcinomas
of the forestomach (0/50, 0/50 and 2/50 for females), transitional cell
carcinomas of the urinary bladder 0/50, 8/50 and 21/48 for females) and
alveolar/bronchiolar adenomas (0/50, 3/50 and 8/50 for females) were
seen.  In males, the study was considered to be inadequate for
carcinogenicity (due to mortality of controls).  For females, there was
clear evidence of carcinogenicity”.

Discussion of Tumor Data:   A statistically elevated incidence of the
following tumors was observed at either HDT or a both dose levels:

1) forestomach squamous cell papillomas or papillomas and carcinomas
combined in males and females, and squamous cell carcinomas in females;

2) urinary bladder transitional cell carcinomas in males and females;

3) 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.  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.

Toxicity Profile

Guideline No./ Study Type	MRID No./ Classification /Doses	Results

Subchronic Toxicity Studies*

870.3100

90-Day oral toxicity rodents

[Fischer 344 rats]	42954802

Acceptable/guideline

0, 5, 15, 50 or 100mg/kg/day in diet

	NOAEL = 5 mg/kg/day

LOAEL = 15 mg/kg/day based on hyperkeratosis and/ or basal cell
hyperplasia in the non-glandular portion of the stomach (both sexes)

870.3100

90-Day oral toxicity rodents

[B6C3F1 mice] 	42954801

Acceptable/guideline 0,15, 50, 100 or 175 mg/kg/day in diet

	NOAEL = 15 mg/kg/day

LOAEL = 50 mg/kg/day based on decreased body weights and body weight
gain (both sexes)

870.3100

90-Day oral toxicity nonrodent

	See 870.4100b, below

	870.3465

30-Day inhalation toxicity rodent [Fischer 344 rats]	00039685

Acceptable/guideline

0, 3, 10 or 30 ppm (0, 0.0136, 0.045 or 0.136 mg/L) 6 hours/day, 5
days/week 	NOAEL = 30 ppm (0.136 mg/L), highest dose tested

LOAEL = >30 ppm

870.3465

30-Day inhalation toxicity rodent [CD-1 mice] 	00039685

Acceptable/guideline

0, 3, 10 or 30 ppm (0, 0.0136, 0.045 or 0.136 mg/L) 6 hours/day, 5
days/week 	NOAEL = 30 ppm (0.045 mg/L), highest dose tested

LOAEL = >30 ppm (0.136 mg/L)

870.3465

90-Day inhalation toxicity rodent [Fischer 344 rats] 	00146461

Acceptable/guideline

0, 10, 30, 90 or 150  ppm (0, 0.045,  0.136, 0.408,or 0.680 mg/L) 6
hours/day, 5 days/week 	NOAEL = 10 ppm (0.045 mg/L)

LOAEL =  30 ppm (0.136 mg/L) based on histopathological lesions in the
nasal turbinates

870.3465

30-Day inhalation toxicity rodent [B6C3F1 mice]	00146461

Acceptable/guideline

0, 10, 30, 90 or 150  ppm (0, 0.045,  0.136, 0.408,or 0.680 mg/L) 6
hours/day, 5 days/week	NOAEL = 10 ppm (0.045 mg/L)

LOAEL =  30 ppm (0.136 mg/L) based on histopathological lesions in the
nasal turbinates

Developmental and Reproductive Toxicity Studies*

870.3700a

Prenatal developmental in rodents

[Fischer 344  rats]	00144715, 00152848

Acceptable/guideline

0, 20, 60 or 120  ppm (0, 0.091,  0.272 or 0.545 mg/L) by inhalation 6
hours/day during gestation days 6 through 15	Maternal NOAEL = <20 ppm
(0.091 mg/L) LOAEL = 20 ppm (0.091 mg/L) based on decreased body weight
gain and food consumption

Developmental NOAEL <120 ppm (0545 mg/L), highest concentration tested

LOAEL =120 ppm (0545 mg/L) based on increased delay in ossification of
the vertebral centra

870.3700b

Prenatal developmental in nonrodents

[New Zealand White Rabbit]	00144715, 00152848

Acceptable/guideline

0, 20, 60 or 120  ppm (0, 0.091,  0.272 or 0.545 mg/L) by inhalation 6
hours/day during gestation days 6 through 18	Maternal NOAEL = 20 ppm
(0.091 mg/L) LOAEL = 60 ppm (0.272 mg/L) based on decreased body weight
gain

Developmental NOAEL 120 ppm (0545 mg/L), highest concentration tested

LOAEL >120 ppm (0545 mg/L)

870.3800

Reproduction and fertility effects

[Fischer 344 rats]	40312401, 40835301

Acceptable/guideline

 0, 10, 30 or 90  ppm (0, 0.045, 0.136, or 0.408 mg/L) by inhalation 6
hours/day, 5 days/week

  ♂♀ parents after weaning and continued for 12 weeks, 5 days/week
Parental/Systemic NOAEL = 30 ppm (0.136 mg/L)

 LOAEL = 90 ppm (0.408 mg/L) based on decreased body weight gain,
microscopic non-glandular stomach lesions and hyperplasia of the nasal
respiratory epithelium with focal degeneration of the olfactory tissue

Reproductive NOAEL = 90 ppm (0.408 mg/L), highest concentration tested

LOAEL >90 ppm (0.408 mg/L)

Offspring NOAEL = 90 ppm (0.408 mg/L), highest concentration tested

LOAEL >90 ppm

Chronic Toxicity Studies*

870.4100b

Chronic toxicity nonrodent

[Beagle dog]	42441001

Acceptable/guideline

0, 0.5, 2.5 or 15 mg/kg/day microcapsules by dietary admix 	NOAEL = 2.5
mg/kg/day

LOAEL = 15 mg/kg/day  based on decreased body weight gain, microcytic
anemia, an increase in hematopoietic activity in both sexes and possible
increased liver weights in males

870.4300

Combined Chronic Oral  Toxicity/Carcino-genicity for 2 year rat study

[Fischer 344 rats]	43763501

Acceptable/guideline

0, 2.5, 12.5 or 25 mg/kg/day microcapsules by dietary admix	Chronic
Toxicity NOAEL = 2.5 mg/kg/day

LOAEL = 12.5 mg/kg/day based on decreased body weight gain and an
increase in the incidence of basal cell hyperplasia of the non-glandular
mucosa of the stomach

Carcinogenicity:  Increased incidence of rats with primary
hepatocellular adenomas: 0, 2.5, 12.5 and 25 mg/kg/day = ♂ 2/50, 1/50,
6/50 and 9/50;  ♀ 0/50, 0/50, 0/50 and 4/50

870.4300

Combined Chronic Toxicity/Carcinogenicity (104 week)

[Fischer 344 rats]	00146469, NTP study

Acceptable/guideline

0, 25 or 50 mg/kg/day by oral gavage 3 times/week for 104 weeks 	Chronic
Toxicity NOAEL = not established

LOAEL = 25 mg/kg/day based on increased tumor incidence

lomas of the forestomach: 0, 25 and 50 mg/kg/day = ♂ 1/52, 1/52  and
9/52;  ♀ 0/52, 2/52, 3/52.  Squamous cell carcinomas: ♂ 0/52, 0/52
and 4/52.  Neoplastic nodules of the liver: ♂ 1/52, 6/52  and 7/52:
♀ 6/52, 6/52, 10/52.

NTP concluded that there was “clear evidence of carcinogenicity” in
males and “some evidence” of carcinogenicity in females

870.4300

Combined Chronic Toxicity/Carcino-genicity (104 week)[B6C3F1 mice]
43757901

Acceptable/guideline

0, 2.5, 25 or 50 mg/kg/day microcapsules by dietary admix	Chronic
toxicity NOAEL = 2.5 mg/kg/day

 LOAEL = 25 mg/kg/day based on lower body weights and decreased body
weight gain (both sexes)

Carcinogenicity: No evidence of carcinogenicity but study not adequate
for assessment due to several deficiencies in conduct.

870.4300

Combined Chronic Toxicity/Carcino-genicity (104 week)[B6C3F1 mice]
00146469, NTP study

Acceptable/guideline

0,  25 or 50 mg/kg/day by oral gavage 3 times/week for 104 weeks
Chronic Toxicity NOAEL = not established

LOAEL = 25 mg/kg/day based on increased mortality in males

nd 50 mg/kg/day = ♀ 0/50, 1/50, 2/50.  Squamous cell carcinomas of
thee forestomach:  ♀ 0/50, 0/50, 2/50. Transitional cell carcinomas of
the urinary bladder: ♀ 0/50, 8/50, 21/50.

Alveolar/bronchiolar adenomas: ♀ 0/50, 3/50, 8/50.

In ♂, study was inadequate for carcinogenicity.

NTP concluded that there was “clear evidence of carcinogenicity” in
females

870.4300

Combined Chronic Toxicity/Carcino-genicity (2 years) [Fischer 344 rats]
40312201  Acceptable/guideline

0, 5, 20  or 60  ppm (0, 0.023, 0.091 or 0.272 mg/L) by inhalation 6
hours/day, 5 days /week for 509 days  	Chronic Toxicity NOAEL = 20 ppm
(0.091 mg/L)

LOAEL = 60 ppm (0.272 mg/L) based on histopathological changes in nasal
tissue (males and females) and a suggestion of decreased body weight
gain (first year of the study only)

There was no evidence of carcinogenicity

870.4300

Combined Chronic Toxicity/Carcino-genicity (2 years) [B6C3F1 mice]
40312301  Acceptable/guideline

0, 5, 20  or 60  ppm (0, 0.023, 0.091 or 0.272 mg/L) by inhalation 6
hours/day, 5 days /week for 510 days  	Chronic Toxicity NOAEL = 5 ppm
(0.023 mg/L)

LOAEL = 20 ppm (0.091 mg/L) based urinary bladder hyperplasia, and
hypertrophy/hyperplasia of the nasal respiratory mucosa

Carcinogenicity: Increased incidence of bronchioloalveolar adenomas: 0,
5, 20 or 60 ppm  = ♂ 9/50, 6/50, 13/50 or 22/50. Although the lung
tumors were benign, tumor induction was concentration dependent, the
tumor incidence was dose dependent, the tumor incidence was outside of
the historical controls, and the tumor type was seen in the mouse oral
bioassay.

Genotoxicity Studies

Gene Mutation

870.5300

In vitro mammalian cell in culture gene mutation assay

Chinese hamster ovary (CHO) cells	47020332

Acceptable/guideline

50-250 µM -S9

 to cytotoxicity (≥200 µM -S9) or the highest dose tested +S9

Gene Mutation

870.5300

Drosophila melanogaster sex-linked recessive lethal mutations 	00146469
(1985)

Acceptable/guideline

0, 5750 ppm/feeding	Positive: Induction of sex-linked recessive lethal
mutations but negative for the induction of reciprocal translocations at
 5750 ppm National Toxicology Program (NTP); Valencia et al., Environ
Mutagenesis 7:325-348.

Gene Mutation

870.5300

Host Mediated assay 	00039688

Acceptable/guideline

0, 30, 60 mg/kg (oral gavage administration at 1, 2 & 3 hrs) 	Negative
up to the highest dose tested

Cytogenetics

870.5375

In vitro mammalian cytogenetics assay

CHO cells	NTP (1989)

Acceptable/Guideline

4.91-49.1 µg/mL -S9 (Trial 1)

 50-100 µg/mL -S9 (Trial 2)

10-50 µg/mL +S9 (Trial 1 only)	Negative up to concentrations causing
50% reduction in cell confluency (≥50 µg/mL ± S9)NTP: Loveday  et
al., Environ Mutagenesis 13:6–94.

Cytogenetics

870.5395

In vivo mouse

micronucleus assay 	259101 (1985)

Acceptable/guideline

0, 38, 115, 380 mg/kg  	Negative up to a lethal dose (380 mg/kg)

Cytogenetics

870.5450

Dominant Lethal Mutation in Sprague Dawley Rats 	44302801 (1997)

Acceptable/guideline

0-150 ppm, 7 da/wk, 10 wks (whole body inhation)	Negative up to the
LOAEL of 150 ppm, based on adverse effects on body weight.

Other Effects

870.5500

Bacterial DNA repair

Bacillus subtilis H15 & M45	00039688 (1978)

Acceptable/guideline

50-1,250 µg/well	Positive: Preferential inhibition of the DNA repair
deficient strain at 1250 µg/well

Other Effects

870.5550

Unscheduled DNA Synthesis Primary rat hepatocytes	00146467(1985)

Acceptable/guideline

3x10-3 to 1x 10-6M	Negative up to a cytotoxic level (3 x 10-4 M)

Other Effects

870.5900

In vitro sister chromatid exchange(SCE)

↑in SCE induction at 30-50  µg/mL -S9 & 10 -30 µg/mL +S9. These
levels were not cytotoxic.

METABOLITES OF 1,3-DICHLOROPROPENE

Gene Mutation

870.5100

In vitro bacterial reverse gene mutation assay Salmonella  typhimurium
TA98, TA100, TA1535, TA1537

Escherichia coli WP2 (uvrA)	44940327 (1999) 3-Chloroacrylic acid

Acceptable/guideline

500 - 5000 µg/plate ±S9	Negative in independently performed
preincubation assays up to the limit concentration

Gene Mutation

870.5100

In vitro bacterial reverse gene mutation assay Salmonella  typhimurium
TA98, TA100, TA1535, TA1537

Escherichia coli WP2 (uvrA)	44940326 (1999) 3-Chloroallyl alcohol

Acceptable/guideline

33.3 - 5000 µg/plate ±S9	Negative in independently performed
preincubation assays up to the limit concentration

Gene Mutation

870.5300

In vitro mammalian cell in culture gene mutation assay

mouse lymphoma L5178Y	44940311 (1999) 3-Chloroallyl alcohol

Acceptable/guideline

Trial 1:12.5- 925 µg/mL -S9; 1.5-100 µg/mL +S9

↑ MF at 400 and 500  µg/mL -S9 & 75 and 100 µg/mL +S9: no difference
in the induction of small or large mutant colonies

Cytogenetics

870.5395

In vivo mouse (CD-1) micronucleus assay	44940312 (1999) 3-Chloroacrylic
acid

Acceptable/guideline

62.5-250 mg/kg (♂)

62.5-200 mg/kg (♀)	Negative up to overtly toxic (death and/or
decreased activity) highest doses

MECHANISM STUDIES

Gene Mutation

In vitro bacterial reverse gene mutation assay Salmonella  typhimurium
TA100  plus mouse lung homogenate	44460501

Unacceptable               /non-guideline

100-450 µg/plate - metabolic activation;

̊C under N2) or +S9 because of low level microsomal/oxidative proteins
in the lung preparation

Gene Mutation

In vivo with transgenic Big Blue B6C3F1 mice gene mutation assay target
gene (lacI) 	44470501 Unacceptable /non-guideline

0, 10, 60, 150 ppm (via whole body inhalation) 6 hrs/da, 5 da/wk, 2 wks
Negative in lung and liver tissue but test system uncertainties weaken
the understanding of the negative response.

Other Mutagenic Effects

In vitro DNA binding assays	44446301 Unacceptable /non-guideline

11 mM reacted w calf thymus DNA ± S9 (Aroclor 1254-induced rat liver)
± GSH	Inconclusive -S9; negative +S9 ± GSH but uncertainties regarding
use of optimum conditions

Mechanism of Tumorigenicity

♂B6C3F1 mice & ♂ Fischer 344 rats	44446302 Unacceptable

/non-guideline

0, 5,12.5, 25, 100 mg/kg (oral gavage-rats) 3, 12 26 days

0, 10, 30, 60, 150 ppm (whole body inhalation- mice)  6 hrs/da, 5 da/wk,
2 wks	RATS:. No mortality or clinical signs  S ↓GSH at 25 & 100 mg/kg
(adaptive process) but liver tumors were seen in the 2-yr bioassay at
12.5 mg/kg.  No conclusion possible for apoptosis or cell proliferation
because of variability in data.  No conclusion possible for DNA adduct
formation because of variability in data & small sample size.

MICE:   No mortality or clinical signs.  Data show conjugation of 1,3-D
w GSH in lung tissue, no clear effect  on cell proliferation or
apoptosis in bronchiole epithelium or bladder transitional cells or DNA
adduct formation in lungs  but extreme variability and small sample size
compromised the findings.

Concerns regarding whether a biological effective dose was achieved.

GSH Activity in Several Mammalian Cell Lines: ♂B6C3F1 mice & ♂
Fischer 344 rats primary rat hepatocytes, CHO cells, Chinese hamster
lung cells, Salmonella typhimurium 	44460503 Unacceptable

/non-guideline

GSH measurements in cell lines reacted with various substrates:
13C-1,3-D; 4-chloro-1,3-dinitrobenzene; para-nitro-phenylethylbromide;
trans-4-phenyl-3-buten-2-one	No conclusions relative to the correlation
between physiological levels of GSH and mitigation of  mutagenicity

Low level GSH activity with S. typhimuruim but conflicting results with
various mammalian cell lines (i.e.,  high & low level GSH activity with
cell lines producing negative mutagenicity data and high GSH activity
with 2 cell lines that were positive in standard mutagenicity assays)

Bioavailabity of Microencapsulated Telone II in Female Rats	44460502
Unacceptable

/non-guideline

Phase I: 25 mg/kg 13C-1,3D coadministered w 25 mg/kg microencap-sulated
1,3-D sampled at 1,3,5,10,15, 20, 30,40,50,or 60 min.

Phase II:  25 or 50 mg/kg 13C-1,3D + microencap-sulated 1,3-D; 25 or 50
mg/kg 13C-1,3D + 7.5 or 15 mg/kg  microencap-sulated 1,3-D	No
conclusions because of unclear study design, technical deficiencies and
biased treatment of the data.

Initiation-Promotion: Mechanism of Mouse Lung Tumors

♂A/J mice	45897502B&D  Unacceptable

/non-guideline

16 mg/kg vinyl carbamate(VC)  (initiator) ± 0, 60 ppm 1,3-D (whole body
inhalation 6 hrs/da, 5 da/wk, 25 wks) 	Lung adenomas in 1,3-D alone 26%
vs 10% in air control suggest initiating event. Lack of ↑total tumors
for VC-treated alone vs. VC + 1.3-D does not support a promoter role for
1,3-D

Initiation-Promotion: Mechanism of Rat Liver Tumors  ♂ Fischer 344
rats	45897502C&D Unacceptable

/non-guideline

100 mg/kg diethylnitrosamine (DEN, initiator) + 0, 25 mg/kg/da 1,3-D; 80
mg/kg phenobarbital (PB, promoter); or 5-10 mg/kg 2-acetylaminofluorene
(2-AAF, complete carcinogen)  	Data do not  support a promotional role
for 1,3-D.

  SEQ CHAPTER \h \r 1 Appendix B: Methodologies for Inhalation Risk
Calculations

1,3-Dichloropropene (Telone II) Array

  SEQ CHAPTER \h \r 1 METHODOLOGIES FOR INHALATION RISK CALCULATIONS

In evaluating the risks that a compound may pose to human health after
exposure via the inhalation route, different methodologies have been
historically used by the USEPA and the California Department of
Pesticide Regulation (CDPR).  The Agency’s approach to calculating
risks due to inhalation exposure is based on the

guidance methodology developed by the Office of Research and Development
(ORD) for the derivation of inhalation reference concentrations (RfCs)
and human equivalent concentrations (HECs) for use in margin of exposure
(MOE) calculations (RfC methodology).   The two approaches differ in
their use of species-specific parameters to derive HECs.  Therefore, the
differences noted in the risk assessments of each organization are due,
in part, to their use of different methodologies and use of different
uncertainty factors (UFs).  The Agency’s approach to calculating risks
due to inhalation exposure is based on the guidance methodology
developed by the Office of Research and Development (ORD) for the
derivation of inhalation reference concentrations (RfCs) and human
equivalent concentrations (HECs) for use in margin of exposure (MOE)
calculations (RfC methodology).  An example of CDPR’s methodology, and
the species-specific parameters used in this approach can be found in
the CDPR website and their 1,3-D risk assessment, Appendix G at the
following web address:    HYPERLINK http://www.cdpr.ca.gov
www.cdpr.ca.gov/docs/dprdocs/methbrom/append_g.pdf .  As OPP understands
the importance to harmonize, to the extent possible, with other
regulatory agencies, this risk assessment will present HECs derived
using both methodologies.

The RfC methodology applies a dosimetric adjustment that takes into
consideration not only the differences in ventilation rate (MV) but also
the physicochemical properties of the inhaled compound, the type of
toxicity observed (e.g. systemic vs. port of entry) and the
pharmacokinetic (PK) but not pharmacodynamic (PD) differences between
animals and humans.

Based on the RfC guidance (1994), the methodology for RfCs derivation is
an estimate of the quantitative dose-response assessment of chronic
non-cancer toxicity for individual inhaled chemicals and includes
dosimetric adjustment to account for the species-specific relationships
of exposure concentration to deposited/delivered dose. This adjustment
is influenced by the physicochemical properties of the inhaled compound
as well as the type of toxicity observed (e.g. systemic vs. port of
entry), and takes into consideration the PK differences between animals
and humans.  Though the RfC methodology was developed to estimate
toxicity of inhaled chemicals over a lifetime, it can be used for other
inhalation exposures (e.g. acute and short-term exposures) since the
dosimetric adjustment incorporates mechanistic determinants of
disposition that can be applied to shorter duration of exposures
provided the assumptions underlying the methodology are still valid.
These assumptions, in turn, vary depending on the type of toxicity
observed and will be discussed later on in this document.  Thus the
derivation of a HEC for inhaled gases is described by the following
equation:

   ADVANCE \u 13

Where:

PODstudy: Point of departure identified in the critical toxicology study

Danimal exposure: Duration of animal exposure (hrs/day; days/wk)

Danticipated exposure: Anticipated human duration of exposure (hrs/day;
days/wk)

RGDR: Regional Gas Dose Ratio

For gases eliciting both port of entry and systemic effects,
calculations to estimate  the inhalation risk to humans are dependent on
the regional gas dose ratio (RGDR).  In the case of systemic effects,
the RGDR is defined as the ratio of the blood:gas partition coefficient
of the chemical for the test species to humans (Hb/g animal/Hb/g human).
 When this ratio is unknown or when the Hb/g animal > Hb/g human a
default value of  1.0 is used as the RGDR.  This default is based on the
observation that for chemicals where partition coefficient data are
available in both rats and humans the RGDR value has usually been
comparable or slightly higher than 1.  Thus, the use of an RGDR of 1
results in a protective calculation of the inhalation risk.   Some of
the key assumptions fundamental to the use of the RfC methodology to
derive a HEC based on systemic effects include:

1) all the concentrations of inhaled gas within the animal’s body are
periodic with respect to time (i.e. periodic steady state - the
concentration vs time profile is the same for every week).  Periodicity
must be attained for at least 90% of the exposure.

2) in the respiratory tract, the air, tissue, capillary blood
concentration are in equilibrium with respect to each other.

3)systemically, the blood and tissue concentrations are in equilibrium
with respect to each other.

In the case of 1,3-Dichloropropene, the physicochemical properties and
metabolism data for the compound indicate that these conditions (i.e.
periodicity and equilibrium between different compartments) will be
achieved in a very short period of time.  Under these conditions,
therefore, the use of the RfC methodology to estimate acute inhalation
risk is appropriate.

When the critical toxic effect in a study occurs in the respiratory
tract (i.e port of entry effects), the RGDR is not related to the
blood:gas partition coefficient of the compound but rather the ratio of
the minute volume (MV) to the surface area (SA) of the affected region.
In these instances, attaining periodicity or equilibrium between the
compartments is not critical (since the effect is a function of the
direct interaction between the inhaled compound and the affected region
in the respiratory tract) and the RGDR may be calculated using the
following equation:

   ADVANCE \u 19

Where:

MV animal: Minute volume for the test species (varies depending on body
weight)

SA animal: Surface area of the affected region in animals

MV human: Minute volume for humans (default value is 13.8 l/min)

SA human: Surface area of the affected region in humans

The MV animal is calculated using the allometric scaling provided in
USEPA (1988a).  The equation for calculation of the MV animal is:

lnMV animal = b0 + b1ln(BW)

Where:

ln MV animal : natural logarithm of the minute volume

b0 : species specific intercept used in the algorithm to calculate
minute volumes based on body weight

b1: species specific coefficient used in the algorithm to calculate
minute volumes based on body weight

ln BW: natural logarithm of the body weight (expressed in kg)

The values for the species-specific parameters used to calculate the MV
animal based on body weight and the values for the surface areas of
various regions of the respiratory tract (extrathoracic, thoracic, and
pulmonary) are provided in the EPA document “Methods for Derivation of
Inhalation Reference Concentrations and Application of Inhalation
Dosimetry” (1994).

The magnitude of the UFs applied is dependent on the methodology used to
calculate risk.  When using the methodology developed by CDPR, a 100X UF
is applied (10X for interspecies extrapolation and 10X for intraspecies
variation).  In contrast, the RfC methodology takes into consideration
the PK differences but not the PD differences.  Consequently, the UF for
interspecies extrapolation may be reduced to 3X (to account for the PD
differences) while the UF for intraspecies variation is retained at 10X.
 Thus, the UF when using the RfC methodology is customarily 30X.

The HED Arrays for 1,3-D may be found on the following pages.

¶ Bolded studies used for endpoint selection

‡ 3X UF for LOAEL to NOAEL extrapolation is being recommended due to
the mild nature of effects (decreased body weight) noted at the LOAEL

* Input parameters for the derivation of RGDRs were obtained from
“Methods for Derivation of Inhalation Reference Concentrations and
Application of Inhalation Dosimetry” (USEPA, 1994) Tables 4-4, 4-5,
and 4-6.

Key for Array Table

LOAEL: Lowest observed adverse effect level

NOAEL: No observed adverse effect level

Da: Daily animal exposure (hrs/day)

Dh: Anticipated daily human exposure (hrs/day)

Wa: Weekly animal exposure (days/week)

Wh: Anticipated weekly human exposure (days/week)

RGDR: Regional Gas Dose Ratio

HEC: Human Equivalent Concentration

inter: interspecies extrapolation uncertainty factor

intra: intraspecies variation uncertainty factor

UF: Other uncertainty factor(s)

¶ Bolded studies used for endpoint selection

‡ 3X UF for LOAEL to NOAEL extrapolation is being recommended due to
the mild nature of effects (decreased body weight) noted at the LOAEL

§ Offspring were not directly exposed to the compound

* Input parameters for the derivation of RGDRs were obtained from
“Methods for Derivation of Inhalation Reference Concentrations and
Application of Inhalation Dosimetry” (USEPA, 1994) Tables 4-4, 4-5,
and 4-6.

Key for Array Table

LOAEL: Lowest observed adverse effect level

NOAEL: No observed adverse effect level

Da: Daily animal exposure (hrs/day)

Dh: Anticipated daily human exposure (hrs/day)

Wa: Weekly animal exposure (days/week)

Wh: Anticipated weekly human exposure (days/week)

RGDR: Regional Gas Dose Ratio

HEC: Human Equivalent Concentration

inter: interspecies extrapolation uncertainty factor

intra: intraspecies variation uncertainty factor

UF: Other uncertainty factor(s)

Appendix C:  Summary Of Cordon® PERFUM Buffer Distributions Based On
Ventura California Weather And Data for Post-plant Drip Irrigation Use
in Vineyards Data

\Appendix D:  Summary Of 1,3-D Bystander Exposure from Known Area
Sources Estimated Using the Monitoring Method

Summary of Bystander Exposure from Known Area Sources Estimated Using
the Monitoring Method

When assessing bystander exposure to 1,3-D, HED evaluated pre-plant
agricultural field fumigations; post-plant drip irrigation fumigations
and turf fumigations.

The use of the field volatility data in this assessment is based on the
previous bystander exposure review of 1,3-D.  Details of study quality
and data analysis can be found in the following memo; REVISED
Post-application Non-occupational Bystander Risk Estimates for Proposed
Label Change from 300 to 100 foot Buffer Zone for Telone II, Telone
C-17, and Telone C-35, S.Weiss, D284547, 11/1/02).

In summary, twenty studies, with field volatility data collected near
1,3-D treated fields, have been submitted to the Agency since 1989.
Some of the studies (MRID#s 426973-01, 427742-01, 428456-01) reflect
application methods that are no longer used, and therefore are not
included in this assessment.  Eleven of the studies are used to estimate
risk for bystander exposure from the broadcast and row uses of 1,3-D.
Several studies (MRID#s 447956-02, 451129-02, 452961-01) are used to
estimate use drip application methods.  Bystander inhalation exposure
estimates for the turf uses of 1,3-D are based on air concentration
measurements reported in field volatility studies, MRID 451207-01 and
451207-02. One field volatility study is available to address off-site
exposure resulting from the post-plant use.  Bystander inhalation
exposure estimates are based on air concentration measurements reported
in this study, (MRID 452961-01).  Study descriptions are available in
Appendix A of Memo, S.Weiss, D284548, 11/1/02.

Generally, HED calculates non-cancer risks (i.e. acute, short-,
intermediate-term, and chronic exposure) using maximum label application
rates and cancer risks using “typical” rates.  The registrant
suggests that the field volatility study were conducted at typical
rates(from 96 to 224 lb ai/A).   BEAD states these rates would be
typical for all crops except for tree/vine crops and pineapples. Since
these two crops only accounted for about 9 percent of the total pounds
of 1,3-D applied , the rates in the field volatility studies cover the
majority of current uses.   However, HED risk estimates must reflect the
entire range of potential exposures, including those at the high end of
the exposure distribution.   Therefore, when appropriate, risk
calculations are adjusted to account for the maximum label application
rate (linear extrapolation) and risks are calculated for both the
typical and maximum rates.  Cancer risk is calculated based on typical
rates only.

Acute MOEs are calculated by comparing the maximum 24 hour time-weighed
average (TWA) from each field volatility study to the toxicological
human equivalent concentration (HEC) selected for acute risk assessment.

Consistent with the most recent review of bystander exposure (Memo,
S.Weiss, D284548, 11/1/02), the consecutive seven day average air
concentration were also estimated from each field volatility study.  The
highest average seven day average each direction is compared to the
selected HEC to estimate short-term risk for bystanders.

This is consistent with the pattern of toxicity observed in short-term
guideline toxicity studies.  In the study used for the short-term risk
assessment - the developmental toxicity study in rabbits - the endpoint
of concern is a decrease in body weight gain.  This effect was not
observed until several days after exposure began suggesting that a
multiple-day rolling average is appropriate to assess risks.

In the field volatility studies, 1,3-D peak offgassing occurs 1 to 3
days after application. Additionally since 1, 3-D products are used only
1 to 2 times per field each year, the majority of bystander exposure
resulting directly from treatment of agricultural fields is expected to
be  acute or short-term.  Intermediate-term exposure (consecutive
exposures lasting 30 days to several months) is expected to be less
likely.  Chronic exposure is not expected since it unlikely that
bystanders will be continually exposed to significant concentrations of
1,3-D for 6 consecutive months or longer.

Cancer risks are calculated using  the average air concentration for all
locations (extrapolated from each field volatility study). It is assumed
that the number of days of exposure per year is equal to the number of
days that samples were taken in each study (i.e. 7 to 21 days).  Since
inter-year and seasonal variability in wind direction will prevent any
single location from being predominately down wind, using the average
air concentration of all directions is appropriate to assess cancer risk
resulting from a lifetime of exposure.

None of the acute or short-term risks exceed HED’s LOC.  Using the
average air concentrations, several of the estimated cancer risks exceed
HED’s LOC for cancer for the existing pre plant uses (generally 1 x
10-6).   Since a particular field is not likely to be treated more than
once or twice each year, and a bystander is not likely to be present
downwind of the field during this entire period, every year for 50
years, after every application, this assessment is expected to provide
an upper-end estimate of cancer risk.  Bystander exposure resulting from
the agricultural and golf course uses of 1,3-D are summarized in Tables
E1 through E3.

Table E1.  Acute Non-Cancer Risk for Bystander Exposures Based on Field
Volatility Data	Maximum 24 hr TWA Air Concentration

Acute MOE1

Study Location/

MRID#

Formulation	Application  Rate

study

(g/A)

label max

(g/A)

#

Distance

(m)	study

(ppm)	label max

(ppm)

study	label max

Broadcast Applications

2	Imperial Valley, CA; 1989	422657-01	Telone II	12.1	35	30	0.008	0.022
9800	3400

3	Salinas Valley, CA; 1992	425451-01	Telone II	12.3	35	30	0.009	0.027
8100	2800

16	Collier County, FL; 1999	451207-02	Telone II	5.12	35	30	0.018	0.125
4100	610

17	Highlands County, FL; 1998	451207-01	Telone II	5.19	35	30	0.070	0.469
1100	160

18	Waushara County, WI; 2001	454002-03	Telone II	26.8	35	61	0.015	0.020
4900	3800

16	Collier County, FL; 1999	451207-02	Telone II	5.12	35	61	0.010	0.070
7400	1100

17	Highlands County, FL; 1998	451207-01	Telone II	5.19	35	61	0.018	0.124
4100	610

Row Applications

7	San Joaquin Valley, CA; 1995	 442585-01	Telone II	12.6	35	30	0.016
0.097	4800	780

19	Immokalee, FL; 2001	454002-02	Telone II	28.40	35	30	0.041	0.050	1900
1500

19	Naples, FL; 2001	454002-02	Telone II	25.30	35	30	0.138	0.191	550	400

6	Moses Lake, WA; 1992	 NR424663-01	Telone II	*	*	91	0.191	--	400	--

Drip Irrigation Application

8	Rio Grande Valley, TX 1998	447956-02	Telone EC	8.65	18	30	0.054	0.112
1400	670

15	Douglas, GA; 2000	451129-02	In-Line	24.6	20.5	30	0.047	0.039	1600
1900

8	Rio Grande Valley, TX 1998	447956-02	Telone EC	8.65	18	91	0.021	0.044
3600	1700

15	Douglas, GA; 2000	451129-02	In-Line	24.6	20.5	91	0.019	0.016	3900
4700

20	Gilroy, CA, 1998 (post-plant)	 452961-01	Telone II	5.4	17.74	91	0.001
--	54000	--

1  Acute MOE = HEC (75.67 ppm)/maximum 24 hour TWA

Table E2.  Short-Term 1,3-D Risk for Bystander Exposures Based on Field
Volatility Data

	Application Rate	Highest 7-day Air

concentration	Short-term MOE1

#	Study Location/	MRID#	Formulation

	Distance

(m)	study

(g/A)	Label max

(g/A)	study

(ppm)	label max

(ppm)

study	label max

Broadcast Applications

2	Imperial Valley, CA; 1989	422657-01	Telone II	30	12.1	35	0.006	0.017
870	300

3	Salinas Valley, CA; 1992	425451-01	Telone II	30	12.3	35	0.004	0.011
1300	470

16	Collier County, FL; 1999	451207-02	Telone II	30	5.12	35	0.003	0.018
1900	270

17	Highlands County, FL; 1998	451207-01	Telone II	30	5.19	35	0.013	0.085
400	60

18	Waushara County, WI; 2001	454002-03	Telone II	61	26.8	35	0.008	0.010
640	490

16	Collier County, FL; 1999	451207-02	Telone II	91	5.12	35	0.0003	0.002
14000	2100

17	Highlands County, FL; 1998	451207-01	Telone II	91	5.19	35	0.006	0.039
870	130

Row Applications

7	San Joaquin Valley, CA; 1995	 442585-01	Telone II	30	12.6	35	0.006
0.034	900	150

19	Immokalee, FL; 2001	454002-02	Telone II	30	28.40	35	0.024	0.029	210
170

19	Naples, FL; 2001	454002-02	Telone II	30	25.30	35	0.058	0.080	90	60

6	Moses Lake, WA; 1992	NR424663-01	Telone II	91	*	*	0.078	–	60

Drip Irrigation Applications

	Rio Grande Valley, TX 1998	447956-02	Telone EC	30	8.65	18	0.012	0.025
420	200

15	Douglas, GA; 2000	451129-02	In-Line	30	24.6	20.5	0.015	0.012	330	400

8	Rio Grande Valley, TX 1998	447956-02	Telone EC	91	8.65	18	0.005	0.011
980	470

15	Douglas, GA; 2000	451129-02	In-Line	91	24.6	20.5	0.006	0.005	900	1100

20	Gilroy, CA, 1998 (post-plant)	 452961-01	Telone II	91	5.4	17.74
0.0003

16000

	1 Short-term MOE = HEC(5.0 for short-term)/highest 7 day air
concentration.

Appendix E:  Model Information and History

Industrial Source Complex 3 (ISC3)

ISC3 (http://www.epa.gov/scram001/dispersion_alt.htm) was developed by
the U.S. Environmental Protection Agency (EPA) as a replacement for
ISC2.  ISC3 is a steady-state Gaussian plume model which can be used to
assess pollutant concentrations from a wide variety of sources including
point and area sources.  ISC3 operates in both long-term and short-term
modes.  OPP has operated the model in short-term mode in its fumigant
assessments and used the designation ISCST3.  ISCST3 allows for three
different types of outputs: (1) summaries of high values (highest,
second highest, etc.) by receptor for each averaging period and source
group combination, (2) summaries of overall maximum values (e.g., the
maximum 50) for each averaging period and source group combination, and
(3) tables of concurrent values summarized by receptor for each
averaging period and source group combination for each day of data
processed. The third output option was used when OPP ran the ISCST3
model.  These outputs can be produced all the way down to an hourly
basis.

Up until the end of 2005, ISC3 was the Agency's recommended air
dispersion model for steady state sources.  It should be noted that ISC3
can still be used as an alternative to the recommended models in
Appendix W in regulatory applications with case-by-case justification
(see Appendix W to 40 CFR Part 51, Section 3.2).

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e of the main weaknesses of ISCST3 is in its treatment of calm periods.
A calm period in ISCST3 is when the wind speed is less than 1.0 m/s.
When this occurs, ISCST3 assumes that there is no wind blowing and
assigns a wind speed of 0.0 m/s and this can result in a
misrepresentation of the fumigant plume.  For the Agency's fumigant
assessments, ISCST3 was run using the "regulatory option" for addressing
calm periods.

American Meteorological Society/Environmental Protection Agency
Regulatory Model (AERMOD)

AERMOD (http://www.epa.gov/scram001/dispersion_prefrec.htm#aermod) was
developed by American Meteorological Society (AMS) and the U.S.
Environmental Protection Agency (EPA).  ISC was replaced by AERMOD as
the preferred air dispersion model for near-field, steady state sources
in the Agency's Guidelines on Air Quality Models as of December 9, 2005.
 AERMOD is a Gaussian plume model which can be used to assess pollutant
concentrations from a wide variety of sources including point and area
sources.  AERMOD incorporates air dispersion based on planetary boundary
layer turbulence structure and scaling concepts, including treatment of
both surface and elevated sources, and both simple and complex terrain.
The AERMOD modeling system consists of two pre-processors and the
dispersion model.  The meteorological preprocessor AERMET, uses
meteorological data and surface characteristics to calculate boundary
layer parameters (e.g. mixing height, friction velocity, etc.) needed to
run AERMOD.  The terrain pre-processor AERMAP both characterizes the
terrain and generates receptor grids for AERMOD.  AERMOD allows for
three different types of outputs: (1) summaries of high values (highest,
second highest, etc.) by receptor for each averaging period and source
group combination, (2) summaries of overall maximum values (e.g., the
maximum 50) for each averaging period and source group combination, and
(3) tables of concurrent values summarized by receptor for each
averaging period and source group combination for each day of data
processed.  These outputs can be produced all the way down to an hourly
basis.

As the replacement to ISC3, AERMOD currently contains new or improved
algorithms for: 1) dispersion in both the convective and stable boundary
layers; 2) plume rise and buoyancy; 3) plume penetration into elevated
inversions; 4) computation of vertical profiles of wind, turbulence, and
temperature; 5) the urban nighttime boundary layer; 6) the treatment of
receptors on all types of terrain from the surface up to and above the
plume height; 7) the treatment of building wake effects; 8) an improved
approach for characterizing the fundamental boundary layer parameters;
and 9) the treatment of plume meander.  Many of these improvements have
little to no effect on OPP's approach to modeling fumigant applications
as area sources.

AERMOD allows for the conservative assessment of concentrations of
fumigants coming off of treated fields under specific meteorological and
application conditions.  However, AERMOD has a similar weakness to ISC3
in its treatment of calm periods.  A calm period in AERMOD is when the
wind speed is less than 1.0 m/s.  When this occurs, AERMOD assumes that
there is no wind blowing and assigns a wind speed of 0.0 m/s and this
can result in a misrepresentation of the fumigant plume.  Also, AERMOD
does not allow for the probabilistic treatment of variables such as the
meteorological conditions.

CALPUFF

CALPUFF (http://www.epa.gov/scram001/dispersion_prefrec.htm#calpuff) is
a non-steady-state meteorological and air quality modeling system
developed by the Atmospheric Studies Group at TRC Solutions.  It is
maintained by the model developers and distributed by TRC
(http://www.src.com/html/calpuff/calpuff1.htm).  CALPUFF v.5 has been
adopted by the Agency in its Guideline on Air Quality Models as the
preferred model for assessing long range transport of pollutants and on
a case-by-case basis for certain near-field applications involving
complex meteorological conditions (i.e., non-steady state).  The
modeling system consists of three main components and a set of
preprocessing and postprocessing programs.   The main components of the
modeling system are CALMET (a diagnostic 3-dimensional meteorological
model), CALPUFF (an air quality dispersion model), and CALPOST (a
postprocessing package).

The output files that CALPUFF creates for each run include unformatted
data files containing grids of time-averaged concentrations,
time-averaged dry deposition fluxes, and time-averaged wet deposition
fluxes.  These outputs in CALPUFF v.5 can be produced all the way down
to an hourly basis.  The post-processing program CALPOST is designed to
produce ranked tabulations of averages of selected concentration data
from these data files. CALPOST writes a text file containing the input
data summary and output tables.

Although CALPUFF v.5 is on the Agency's guideline for air models, there
is also currently a CALPUFF v.6 that has not yet been reviewed by the
Agency.  CALPUFF v.6 includes a number of technical enhancements over
v.5 but the major one that could have effects on OPP's modeling of
fumigant emissions is the option to use subhourly (i.e., 1 minute, 5
minute, etc.) meteorological data.

Probabilistic Exposure and Risk model for FUMigants (PERFUM)

PERFUM (http://www.exponent.com/practices/health/PERFUM.html) was
developed to address the issue of bystander exposures following
agricultural applications of fumigants.  The core of the PERFUM modeling
system is the US EPA dispersion model ISCST3 which at the time PERFUM
was developed was the Agency's recommended air dispersion model for
steady state sources.  ISCST3 as described above calculates
concentrations but is not designed to determine a buffer zone.  PERFUM
was designed to specifically take the ISCST3 outputs and use them to
produce buffer zone outputs in a distributional format.

PERFUM allows users to develop an understanding of the distributions of
potential bystander exposures and thus more fully characterize the range
of risks resulting to bystanders around treated fields.  ISCST3 is an
integral part of the PERFUM model and the basic physics and code of
ISCST3 remain unchanged.  PERFUM essentially provides ISCST3 with daily
meteorological data over 5 years as well as flux estimates within the
uncertainty of those data.  PERFUM then uses this information to create
distributional outputs for pre-defined receptor locations.

Fumigant Emissions Modeling System (FEMS)

FEMS (http://www.sullivan-environmental.com) was developed to address
the issue of bystander exposures following agricultural applications of
fumigants.  FEMS allows the user to define a number of options prior to
running the model including: the fumigant to be applied, the frequency
of fumigation, the sealing method employed, field size and shape,
consecutive day/contiguous field applications, application season, the
averaging time for the concentrations, and the dispersion model used
(ISCST3, CALPUFF v.5, or CALPUFF v.6).  FEMS also allows the user to
include Monte Carlo treatments of all the key model inputs like
meteorological conditions, emissions data, day the application starts,
etc.

Once the core dispersion model is selected, FEMS simulates the
application of a fumigant and it's off-gassing over a 4 day simulation
using 4 hour time steps.  The model estimates fumigant concentrations at
various receptors beyond the perimeter of the applied field that are
matched to the averaging time of interest for the user.  Aside from
estimating the fumigant concentrations, FEMS keeps track of the number
of times that concentrations exceed the concentration of concern at each
receptor.

Once FEMS completes the modeling simulation, the distribution of
concentrations is computed for each receptor.  FEMS produces two main
outputs.  The first is a frequency distribution that looks at the number
of times that concentrations exceed the concentration of concern at each
receptor.  The second involves establishing the distributions of
concentrations for each receptor and then taking the maximum number of
periods per averaging time of interest above the concentration of
concern and computing them as a function of distance from the field.
Buffer zones are then established based on the most conservative
concentrations that were modeled as a function of distance.

Soil Fumigant Exposure Assessment System (SOFEA)

SOFEA (http://www.epa.gov/oscpmont/sap/meetings/2004/index.htm) was
developed to evaluate and manage human inhalation exposure potential
associated with agricultural applications of fumigants.  SOFEA
calculates fumigant concentrations in air arising from volatility losses
from treated fields for entire agricultural regions using multiple
sources (treated fields), GIS information, agronomic specific variables,
user specified buffer zones and field intervals.  SOFEA uses a modified
version of ISCST3 as its dispersion model.   SOFEA also uses Monte Carlo
techniques to vary the following parameters: weather information, field
size, application date, application rate, application method, pesticide
degradation rates in air, sealing method, field re-treatment, and buffer
setbacks.

Multi-year, multiple field simulations can be conducted with SOFEA using
random field placement in all agricultural areas or by selectively
placing fields in historical or prospective use areas.  Regional land
use information can be used to refine the placement of treated fields,
dispersion calculations, and exposure assessments.  SOFEA has been
previously used for regulatory decision making in California.

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Page   PAGE  32  of   NUMPAGES  84

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[Federal Register: April 3, 2006 (Volume 71, Number 63)]
[Proposed Rules]
[Page 16534-16535]
[DOCID:fr03ap06-23]

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

ENVIRONMENTAL PROTECTION AGENCY

40 CFR Parts 50 and 51

[EPA-HQ-OAR-2005-0159; FRL-8052-8]
RIN 2060-AN40

Notice of Public Hearing for the Proposed Rule--The Treatment of
Data Influenced by Exceptional Events

AGENCY: Environmental Protection Agency (EPA).

ACTION: Announcement of public hearing.

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

SUMMARY: The EPA is announcing two public hearings for the proposed
rule on ``The Treatment of Data Influenced by Exceptional Events''
which was published in the Federal Register on March 10, 2006.

DATES: The public hearings will be held on April 18, 2006, and April
25, 2006. Please refer to SUPPLEMENTARY INFORMATION for additional
information on the hearings.

ADDRESSES: Public Hearing: The public hearings will be held at the
following locations:
    1. Research Triangle Park, N.C.: Date of hearing: April 18, 2006.
The Sheraton Imperial Hotel, 4700 Emperor Blvd., Durham, N.C. 27703,
Phone:<PHONE_NUMBER>.
    2. Denver, CO: Date of hearing: April 25, 2006. The Adams Mark
Hotel, 1550 Court Place, Denver, CO 80202, Phone:<PHONE_NUMBER>.

FOR FURTHER INFORMATION CONTACT: If you would like to speak at the
public hearing or have questions concerning the public hearing, please
contact Ms. Pamela Long at the address provided below under
SUPPLEMENTARY INFORMATION.
    Questions concerning the proposed rule entitled ``The Treatment of
Data Influenced by Exceptional Events'' should be addressed to Mr.
Larry Wallace, Ph.D., U.S. EPA, Office of Air Quality Planning and
Standards, Air Quality Policy Division, (C539-01), Research Triangle
Park, N.C. 27711, telephone number<PHONE_NUMBER>, e-mail at
<EMAIL_ADDRESS>or Mr. Neil Frank, U.S. EPA, Office of Air

Quality Planning and Standards, Air Quality Assessment Division, (C304-
01), Research Triangle Park, N.C. 27711, telephone number (919) 541-
5560, and e-mail address<EMAIL_ADDRESS>
SUPPLEMENTARY INFORMATION: The EPA has proposed a rule to govern the
review and handling of air quality monitoring data influenced by
exceptional events. Exceptional events are events for which the normal
planning and regulatory process established by the Clean Air Act is not
appropriate. In this rulemaking action, EPA is proposing to: Implement
section 319(b)(3)(B) and section 107(d)(3) authority to exclude air
quality monitoring data from regulatory determinations related to
exceedances or violations of the National Ambient Air Quality Standards
(NAAQS) and avoid designating an area as nonattainment, redesignating
an area as nonattainment, or reclassifying an existing nonattainment
area to a higher classification if a State adequately demonstrates that
an exceptional event has caused an exceedance or violation of a NAAQS.
    Public hearings: The proposal for which EPA is holding the public
hearings was published in the Federal Register on March 10, 2006 (71 FR
21592) and is available on the following Web site: http://www.epa.gov/ttn/oarpg/t1pfpr.html.
 The public hearings will provide interested

parties the opportunity to present data, views, or arguments concerning
the proposed rule. The EPA may ask clarifying questions during the oral
presentations, but will not respond to the presentations at that time.
Written statements and supporting information submitted during the
comment period will be considered with the same weight as any oral
comments and supporting information presented at the public hearings.
Written comments must be postmarked by May 10, 2006, which is the
closing date for the comment period, as specified in the proposal for
the rule.
    The two public hearings will be held in Research Triangle Park,
N.C. on April 18, 2006 and Denver, CO on April 25, 2006. Both public
hearings will begin at 9 a.m. (local time) and continue until 5 p.m. on
each day, if necessary, depending on the number of speakers. The EPA
may end the hearing early (no

earlier than 2 p.m.) if all registered speakers have had an opportunity
to speak.
    Commenters desiring to speak at the hearing should notify Ms.
Pamela Long, (C539-01), U.S. EPA, Research Triangle Park, N.C. 27711,
<EMAIL_ADDRESS>(919) 541-0641 by 12 p.m. Eastern time on April 13,

2006. We request that commenters contact Ms. Long at U.S. EPA, Research
Triangle Park, N.C. 27711, by e-mail at<EMAIL_ADDRESS>or by
telephone at<PHONE_NUMBER>, and provide the requests to speak at the
hearing. Ms. Long will arrange a time slot for participants to speak at
the hearing.
    Commenters should notify Ms. Long if they will need specific
equipment, or if there are other special needs related to providing
comments at the hearing. Persons desiring to present oral testimony
that have not made arrangements in advance can register by 2 p.m. on
the day of the hearing. The EPA will provide equipment for commenters
to show overhead slides or make computerized slide presentations if we
receive special requests in advance. Oral testimony will be limited to
5 minutes for each commenter. The EPA encourages commenters to provide
EPA with a copy of their oral testimony electronically (via e-mail,
computer disk, or CD) or in hard copy form.
    The hearing schedule, including lists of speakers, will be posted
on EPA's Web site http://www.epa.gov/ttn/oarpg/t1pfpr.html. Verbatim

transcripts of the hearings and written statements will be included in
the docket for the rulemaking.

How Can I Get Copies of This Document and Other Related Information?

    The EPA has established the official public docket for the proposed
rule entitled ``The Treatment of Data Influenced by Exceptional
Events'' under Docket ID No. EPA-HQ-OAR-2005-0159. As stated
previously, the proposed rule was published in the Federal Register on
March 10, 2006 (71 FR 12592) and is available at http://www.epa.gov/ttn/oarpg/t1pfpr.html
.

    Dated: March 27, 2006.
Gregory Green,
Acting Director, Office of Air Quality Planning and Standards.
[FR Doc. 06-3154 Filed 3-31-06; 8:45 am]

BILLING CODE 6560-50-P


May 27, 2014

Administrator Gina McCarthy
U.S. Environmental Protection Agency
1200 Pennsylvania Ave., N.W.
Washington, D.C. 20460

Re: Inappropriate Foreign RIN generation on renewable fuel that never arrives in the United States (not intended for use in the 48 contiguous states or Hawaii).

Dear Administrator McCarthy:

Today, we bring to your attention an important matter that, if not addressed, will continue to hamper the efforts of EPA in eliminating fraud from the Renewable Fuel Standard (RFS).

We have reason to believe that RINs are being generated by bonded foreign producers for renewable fuel that is subsequently sold to destinations or companies outside the United States that are not obligated parties or other regulated entities under the RFS. In other words, RINs are being generated on fuel that never reaches the United States. Additionally, we understand that these RINs are not being retired, which is a violation under the regulation.

The National Biodiesel Board (NBB) is the national trade association representing the biodiesel industry as the coordinating body for research and development in the United States. NBB's membership includes biodiesel producers, feedstock organizations and suppliers, fuel marketers and distributors, and technology providers.

We have worked very closely with EPA through the development of the Quality Assurance Plan (QAP), which was created to help eliminate fraud under the RFS, and we continue to work with your teams on enforcement-related issues.

The regulation states, as a requirement for RIN generation, that renewable fuel must be "produced or imported for use as transportation fuel, heating oil, or jet fuel in the 48 contiguous states or Hawaii." If a RIN is generated by a foreign bonded renewable fuel producer on a batch of renewable fuel that is not produced or imported for use in the 48 contiguous states or Hawaii, those RINs should be retired based on §80.1431(a)(ix) [was otherwise improperly generated]. Additionally, per §80.1431(b)(1), "(t)he party must retire the invalid RINs in the applicable RIN transaction reports under §80.1451(c)(2) for the quarter in which the RINs were determined to be invalid".

This situation presents problems on many levels for the industry and the program, one of which is that on the EPA's EMTS it can appear to market participants that there are more RINs available for compliance than actually exist.  In fact, these RINs should have never been generated - or perhaps are waiting to be retired.

EPA has the ability to eliminate this and decrease the risk for potential fraudulent RINs in the system.

NBB supports additional assurances that foreign producers of renewable fuel are in compliance with the RFS2, and we support additional provisions to assist EPA's enforcement efforts. Specifically we encourage EPA to require each gallon of imported biofuel be subject to a Quality Assurance Plan and a bond of at least 10% of the value of the imported gallons.

In our comments on Pathways II, the QAP proposal, and the 2014 RVO, we discuss at length how a "quality assurance plan" should be applied to foreign biofuel producers. Specifically, we believe it is critical that the EPA strengthen its oversight of foreign-generated fuel seeking to participate in the RFS.

In our comments, we asked the question: How does EPA best protect obligated parties and the RFS from fraud or invalid RINs that are illegally or invalidly generated from foreign producers? We noted that without a QAP in place it is nearly impossible to track where the feedstocks come from  -  once biodiesel is in its final form and shipped to the United States it is nearly impossible to tell whether it was made from recycled cooking oil, palm oil or some other oil that may or may not qualify for the program. It is also impossible to distinguish a D4 gallon of biodiesel from a D6 gallon.

Issues with foreign RIN generation continue to surface in the program. The feedstock restrictions require a rigorous tracking program. Unfortunately, with little inspection, review or other enforcement mechanism on imported fuels, we have no reason to believe that once a company is registered with the EPA that their feedstocks are consistent with those feedstocks registered. Again, we think this is an important issue for the EPA to get right, as there are currently hundreds of millions and potentially billions of RINs that will likely be generated under the program.

Import issues are difficult and should be decided in a coordinated fashion as it relates to all pending proposals under the RFS, including QAP, the pathways II and the RVO discussion. We strongly encourage the EPA to update the regulatory system, based on the EPA's limited enforcement ability, and create a system in which all foreign-produced renewable fuel (where RINs are generated by the foreign producer or a domestic importer) would be required to subscribe to a QAP.  A functioning QAP program of this type is the only way to ensure that RINs are generated only on gallons of qualifying renewable fuels that actually arrive in the 48 contiguous states or Hawaii. It would also ensure that invalidly generated RINs be retired in a timely manner. NBB has suggested retirement in 30 days. Furthermore, we would encourage the EPA to require bonding for this same group of foreign producers, because it would add another level of security for valid RIN generation.

Additionally, and we did not include this nuance in our formal comments, we would encourage a regulatory change that would require that RIN generation by a bonded foreign renewable fuel producer, or other importer, occur only at the point of sale of a batch of fuel to a US registered company. Based on the current regulations, RIN generating "bonded" producers have the ability to generate RINs upon "production or sale."  This change  -  requiring RIN generation at the point of sale for foreign produced product, rather than the point of production  -  would eliminate excess RIN generation for renewable fuel that never comes to the US and eliminate confusion over the potential use of invalid RINs for compliance.

Finally, on a related issue to foreign RIN generation.  We are aware that there are instances where foreign producers that have been approved for multiple pathways under the RFS use the multiple pathways or "D" codes to manipulate appropriate RIN generation. For example, a bonded foreign company could be approved to generate RINs under at least three different D codes (4, 5 and 6).   That same company could produce an 80/20 mix of renewable fuel with corresponding RINs attached at generation (80% D6 RINs and 20% D4 RINs). When shipped this 80/20 mix is then split into five tankers - one to the United States and four to other destinations. Under this scenario, the producer is required to retire RINs for the fuel that did not arrive in the US. The producer should retire 80% as D6 RINs and 20% as D4 RINs from each shipment that did not make it to the United States; however, we have reason to believe that some companies retire only the 80% of the least valuable RINs (in this case 80% of D6 RINs)  -  and never retire any of the 20% of the D4 RINs. This type of "selective" RIN retirement action is clearly inappropriate and we do not believe that EPA has approved it for any renewable fuel producer.

Again, the options to address this potentially troubling issues would be to require a QAP on each gallon arriving in the United States and to allow RIN generation specifically on those gallons that arrive in the United States (rather than those gallons "intended to arrive" in the United States).

As always, we look forward to discussing these issues with your team.

Sincerely,

Anne Steckel
Vice-President, Federal Affairs
National Biodiesel Board

cc:  	Janet McCabe, Acting Assistant Administrator for the Office of Air and Radiation
      Cynthia Giles, Assistant Administrator, Office of Enforcement and Compliance Assurance (OECA)