I ,3-Dichloropropene Barcode 0410115 

UNITED STATES ENVIRONMENTAL PROTECTION AGENCY 

WASHINGTON, D.C. 20460 

MEMORANDUM 

Date: September 5, 20 13 

OFFICE OF 

CHEMICAL SAFETY AND 

POLLUTION PREVENTION 

SUBJECT: 1,3-Dicbloropropene. Human Health Assessment Scoping Document in Support 

of Registration Review. 

PC Code: 02900 1 DP Barcode: 0410115 

Decision No.: 476422 Registration No.: NA 

Petition Nos.: NA Regulatory Action: Registration Review 

Risk Assess Type: Scoping Document CaseNo.: NA 

TXRNo.: NA CAS No.: 4643-05-4 and 4643-06-5 

MRIDNo.: NA 40 CFR § 180.636 

FROM: Ideliz Negron-Encarnacion, Ph.D., C~e ~,f. Linda Taylor, Ph.D., Toxicologi ~~0 .-

Matthew Lloyd, MPH, ORE Assessor -~ 

Risk Assessment Branch V N il 

THRU: 

Health Effects Division (7509P) 

Office of Pesticide Programs 

Michael Metzger, Branch Chief 

Risk Assessment Branch V Nil 

Jeffrey Dawson, Senior Scientist 

Immediate Office 

Health Effects Division (7509P) 

Office of Pesticide Programs 

TO: Margaret Hathaway, Risk Manager Reviewer 

Pesticide Re-evaluation Division (7508P) 

Office of Pesticide Programs 

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l ,3-Dichloropropene Barcode 0410115 

EXECUTIVE SUMMARY 

EPA's Health Effects Division (HED) has evaluated the available data and the most recent 

human health risk assessments for the fumigant 1 ,3-dichloropropene (1 ,3-D) to determine the 

scope of work necessary to support the registration review process. HED has considered the 

current use patterns (OPPIN Database and current labels) as well as the available toxicity and 

exposure information for 1 ,3-D. 1 ,3-D is a broad spectrum fumigant registered for pre-plant 

control of nematodes and other soil pests and for post-plant drip irrigation in vineyards to control 

nematodes and Phylloxera. 

Toxicity /Hazard 

The toxicology database for 1 ,3-dichloropropene is complete. No additional toxicology or hazard 

data are required to support registration review. Acute and subchronic neurotoxicity studies in 

rats, which are required in accordance with new data requirements for conventional pesticide 

registration (40 CFR Part 158), have not been submitted for 1,3-D. However, based on a weightof-evidence (WOE) approach considering all the available hazard and exposure information for 

1,3-D, the Hazard and Science Policy Council (HASPOC; TXR # 0056626) concluded that the 

acute and subchronic neurotoxicity studies are not required for 1,3-D at this time. An 

immunotoxicity study was submitted as part of the new EPA guideline requirements and is under 

review. 

There is no evidence that 1 ,3-dichloropropene is a developmental, reproductive, or neurotoxic 

chemical. There is evidence of mutagenicity in the data base, and 1 ,3-D has been classified as 

"likely to be carcinogenic to humans" via both the oral and inhalation routes of exposure. There 

is no concern for increased quantitative or qualitative susceptibility of the young following in 

utero and pre-and post-natal exposure to 1,3-D via inhalation in developmental toxicity studies in 

rats and rabbits or in the reproduction study in rats. Therefore, the risk assessment team 

concluded that the lOX FQPA Safety Factor can be reduced to 1X. 1,3-D has low acute toxicity 

(lethality) by the inhalation route of exposure <1\ld moderate acute toxicity by the oral and dermal 

routes of exposure. It is moderately irritating to.the eye and skin and is a dermal sensitizer. The 

major target organs following repeate~ inhalatiqn and oral exposures to 1,3-D are the 

stomach/forestomach, nasal cavity; and lung in rats and mice. 

Residue Chemistry 

Tolerances are established in the 40 CFR §180.636 for residues of 1,3-D inion grapes. Studies 

were submitted by the registrant to cover several deficiencies noted in the residue chemistry 

chapter in support for the use in vineyards. These studies will be considered by the HED. In 

addition, the tolerance expression needs to be modified according to the new Interim Guidance 

on Tolerance Expressions. 

Dietary Exposure 

Chronic and cancer dietary assessments were conducted for the combined exposure from food 

and drinking water (surface water modeling data and ground water monitoring data). Chronic 

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dietary risk estimates were below HED’s level of concern for the general population and for all 

population subgroups. Cancer risks were not of concern for residues in/on food or ground water 

but were of concern for residues in/on food and surface water. Updated dietary exposure 

assessments for 1,3-D will be necessary (see Section 4.0).

Aggregate Risk Assessment

To date, exposures from the oral (dietary) and inhalation (residential bystander) routes of 

exposure have not been aggregated, as there is not a common toxic effect by these two routes of 

exposure. Similarly, no aggregate cancer assessment was completed because the types of tumors 

observed in the inhalation and oral carcinogenicity studies are different. Based on this, the 

aggregate assessment is based on food and drinking water dietary exposure only, which was 

addressed in the dietary assessment. Any change in endpoint selection for 1,3-D that impacts the 

toxicity determination of the dietary or inhalation routes of exposure may require a revised 

aggregate risk assessment.

Occupational & Residential Exposure

1,3-D is registered for use as a (1) pre-plant agricultural soil fumigant; (2) post-plant drip 

irrigation fumigation; and (3) golf course turf fumigant. 1,3-D is a Restricted Use Pesticide and 

the primary risk concerns are for inhalation exposure for workers involved in soil fumigations 

and for residential bystanders around treated areas. The occupational and residential exposure 

database for 1,3-D is adequate for Registration Review, with the exception of ambient air studies 

for representative airsheds, which the Agency will require and incorporate during Registration 

Review. Additional details on the specific airshed monitoring data are available in Section 14.0.

The following data deficiency was identified for 1,3-D (see Appendix D):

Occupational/Residential Exposure: 

o Ambient Airshed monitoring data

The following regulatory recommendation was identified for 1,3-D:

Modification of the tolerance expression in the 40 CFR § 180.636 according to the new 

HED guidance, see section 3.0.

1.0 1,3-DICHLOROPROPENE FORMULATIONS AND USE PATTERNS 

HED used the Biological and Economics Analysis Division (BEAD) Label Data System to 

identify all agricultural and non-agricultural uses of 1,3-dichloropropene. See 1,3-D the HED 

Master Label Report (02/28/2013) for a complete list. In addition, the BEAD Chemical Profile 

for Registration Review was used to characterize the use pattern of 1,3-D (In Progress; C. Chen 

et al.).
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1,3-Dichloropropene is a soil fumigant containing approximately equal proportions of the cis and 

trans isomers formulated as a pressurized gas, liquid ready to use, emulsifiable concentrate, or a

flowable concentrate. The liquid concentrates are intended for direct metering into drip irrigation 

systems, and other formulations are used in more conventional soil fumigation applications (i.e., 

shank/chisel/plowsole pre-plant soil treatments).The concentrations of the active ingredients in 

the end-use products range from 37.1 to 97.5%. 1,3-Dichloropropene is registered for pre-plant

and for post-plant applications to control nematodes and/or garden symphylans. Registered 

products for pre-plant applications may be applied by drip irrigation, soil injection and row and 

broadcast applications. The only post-plant use registered is for drip irrigation to established 

vineyards. Several 1,3-D products also contain the fumigant chloropicrin to enhance plant 

pathogen and weed control. The human health risk assessment of chloropicrin is addressed

separately.

Agricultural Uses

1,3-D is registered for pre-plant use on soils being prepared for the production of a variety of 

agricultural crops including vegetables, fruits, nuts, forage crops, tobacco, fiber crops, golf 

course turf and nursery crops. Only the post-plant use in vineyards is considered a food-use, 

since the potential for residues in foods results from that use. End-use products containing this 

active ingredient are listed in the 1,3-D HED Master Label Report (02/28/2013).

Non-Agricultural and Residential Uses

1,3-D has no residential uses but is registered for non-agricultural uses on golf course turf where 

there is potential for non-occupational exposure. Other non-agricultural uses include ornamental 

and/or shade trees, ornamental herbaceous and non-flowering plants, and ornamental woody 

shrubs and vines.

2.0 HAZARD IDENTIFICATION/TOXICOLOGY

The toxicology database for 1,3-dichloropropene is adequate for the purpose of human health 

risk assessment. No additional data are required. The major target organs following repeated oral 

and inhalation exposures to 1,3-D are the stomach/forestomach, nasal cavity, and lung in rats and 

mice. Consistent with the irritant properties of 1,3-D, there was evidence of degenerative 

changes in the nasal olfactory epithelium and histopathological changes of the respiratory 

epithelium in rats and mice after subchronic inhalation exposure. Following chronic inhalation 

exposure, the olfactory region of the nasal cavity appeared to be the target organ in rats while 

lung adenomas were induced in mice. Similarly, following oral exposure, 1,3-D induced 

histopathological lesions in rats and/or mice, including forestomach squamous cell papillomas 

and carcinomas, liver masses/neoplastic nodules, urinary bladder carcinomas, and 

alveolar/brochiolar adenomas. Increases in hematopoietic activity and decreased body weights 

were seen in dogs. 1,3-D showed moderate acute (lethality) toxicity by the oral and dermal 

routes of exposure, low acute (lethality) toxicity by the inhalation route of exposure, was 

moderately irritating to the eye and skin, and was a dermal sensitizer in guinea pigs. 
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For endpoint selection, since an appropriate toxicity endpoint was not identified in the database 

to quantitate risk from a single oral exposure to 1, 3-D, there is no acute reference dose (aRfD). 

The chronic reference dose (cRfD) is based on decreased body weight gain and an increased 

incidence of basal cell hyperplasia of the nonglandular stomach mucosa in the rat chronic 

toxicity/carcinogenicity oral study. The acute inhalation point of departure (POD) in based on 

clinical signs and decreased body weight in the 4-hour acute inhalation study. Dermal endpoints 

were not selected since dermal exposure is not expected given the high vapor pressure of 1,3-D 

and the application methods used. The point of departure (POD) for short-term inhalation 

exposure risk assessment is based on decreased maternal body weight gains in an inhalation 

developmental toxicity study in rabbits. The POD for intermediate-term inhalation exposure risk 

assessment is based on histopathological lesions in the olfactory region of the nasal cavity in a 

13-week inhalation toxicity study in rats. The POD for long-term inhalation exposure risk 

assessment is based on nasal histopathology in the chronic toxicity/carcinogenicity inhalation 

study in mice. 

1,3-D is rapidly absorbed into the bloodstream, extensively metabolized, and rapidly eliminated, 

mainly in the urine and to a lesser extent as CO2 in expired air and in the feces. The primary 

urinary excretion product is the mercapturic acid conjugate of 1,3-dichloropropene and its 

corresponding sulfoxide. 

There was no evidence of reproductive effects in a 2-generation reproduction study in rats via the 

inhalation route. In the developmental toxicity study in rats via inhalation, decreased ossification 

of the vertebral centra was observed at the highest dose tested while decreased maternal body 

weight gain and food consumption were observed at all dose levels. No developmental effects 

were observed in the rabbit developmental toxicity study via inhalation exposure, while maternal 

toxicity was manifested as decreased body weight gains. There is no concern for increased 

quantitative or qualitative susceptibility of the young following in utero (rats and rabbits) and 

pre-and post-natal exposure (rats) to 1, 3-dichloropropene via inhalation in developmental 

toxicity studies in rats and rabbits or in a reproduction study in rats. Additionally, there is no 

evidence of neurotoxicity. Therefore, the risk assessment team concluded that the 10X FQPA 

Safety Factor can be reduced to 1X. 1,3-D has been classified as “likely to be carcinogenic to 

humans” via both the oral and inhalation routes of exposure. Forestomach, liver, mammary, 

thyroid, adrenal, urinary, and lung tumors were observed in the 2-year rat oral carcinogenicity 

study and bronchioloalveolar adenomas were observed in the 2-year mouse inhalation study. 

There is evidence of mutagenicity (gene mutations in bacteria and cultured mammalian cells in 

conjunction with clastogenic activity and sister chromatid exchanges in several mammalian cell 

lines and induction of DNA strand breaks both in vitro and in vivo) in the 1,3-D data base. As a 

result, cancer potency factors (Q1*) have been calculated for oral and inhalation routes of 

exposure.

Attachment A provides a summary of the relevant toxicological endpoints used in the 2008 

human health risk assessment. In a screening literature search, a National Toxicology Program

(NTP) report of potential effects of 1,3-D on the immune system was identified, and this study 

along with the recently submitted immunotoxicity study will be evaluated during registration 

review. During Registration Review, the Agency will reevaluate the 1,3-D endpoints, points of 
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departure (PODs), and uncertainty factors for the various assessments based on current HED 

policy, recently submitted study (immunotoxicity/published data), and any other data.

3.0 RESIDUE CHEMISTRY

1,3-Dichloropropene is a soil fumigant registered for pre-plant use on soils to be planted to all 

crops and for post-plant use in established vineyards using drip irrigation systems only.

Commercial 1,3-D is a mixture of approximately equal proportions of the cis and trans isomers. 

The nomenclature, registration numbers, PC Code and chemical structure of 1,3-D are listed in 

Appendix B. 

The uses of 1,3-D have been classified as food and non-food based on residue chemistry 

considerations. Plant metabolism studies have been conducted with tomatoes, sugar beets, and 

soybeans (C. Olinger, D318734, 5/24/2007). These studies were conducted at greatly 

exaggerated rates considering the proposed use, and prior to planting. Residues of the parent 

were metabolized in the plant to acetic acid and malonic acid and generally incorporated into 

natural plant constituents. Based on this finding, the use of 1,3-D as pre-plant soil fumigant is 

considered a non-food use and tolerances are not needed. Post-plant use in vineyards is 

considered a food use and the residues of concern for tolerance enforcement and risk assessment 

are the cis and trans isomers of the parent, 3-chloroallyl alcohol (CAAL), and 3-chloroacrylic 

acid (CAAC).

A confined rotational crop study conducted with wheat, lettuce, carrots and radishes showed

extensive incorporation of radiolabeled residues into natural plant biochemical constituents. No 

tolerances or plant-back restrictions are required. Livestock metabolism studies are not required 

for 1,3-D due to the absence of residues of concern for pre-plant uses and absence of feed items 

associated with grape vineyards. 

A tolerance for residues of 1,3-D in/on grapes is established in the 40 CFR 180.636. An 

adequate enforcement method was submitted for the determination of parent. An independent 

laboratory validation (ILV) was requested for the method for the determination of CAAL and 

CAAC. The ILV has been submitted to the agency. Multi-residue method data and storage 

stability data in grapes was also required for the parent and it’s CAAL and CAAC metabolites

and already submitted by the registrant as well.

HED established interim guidance on writing tolerance expressions for enforcement purposes (S. 

Knizner, 27/May/2009). In order to add clarity to the language used to establish the coverage of 

the tolerance expression and measurement of the level of the residue in the Raw Agricultural 

Commodity (RAC) the text in the 40 CFR § 180.636 should read: “(a) General. (1) Tolerances 

are established for residues of 1,3-dichloropropene, including its metabolites and degradates, in 

or on the commodities in the table below. Compliance with the tolerance levels specified below 

is to be determined by measuring cis - and trans -1,3-dichloropropene and its metabolites cis -

and trans -3-chloroacrylic acid, and cis - and trans -3-chloroallyl alcohol, in or on the 

commodity.”
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Conclusions: The submitted residue chemistry studies will be reviewed by HED. In addition,

the tolerance expression in 40 CFR § 180.636 needs to be modified according to the new HED 

guidance.

4.0 DIETARY EXPOSURE

The last dietary assessment for 1,3-D was performed to support the Section 3 requests for use on 

vineyards (C. Olinger, D217283, 06/10/2007). A dietary risk analysis was conducted for the 

combined residues of the parent and metabolites assuming all grapes are treated. The analysis

(food only) showed that all populations are exposed to less than 1% of the population adjusted 

dose (PAD) for chronic risk. This is below the Agency’s level of concern (i.e., when dietary 

exposure exceeds 100% of the PAD). The estimated cancer risk (3x10-7, food only) is also below 

the Agency’s level of concern.

Residues of concern in drinking water are the cis and trans isomers of the parent, the 3-

chloroacrylic acid (CAAC) and 3-chloroallyl alcohol (CAAL) degradates. The Environmental 

Fate and Effects Division (EFED) provided the drinking water assessment using simulation 

models to estimate the potential concentration of 1,3-D and the degradates in surface water while 

tap water monitoring data were used to estimate concentrations in ground water.

A dietary exposure analysis was conducted for the combined exposure from food and water. The 

chronic assessment for 1,3-D and the degradates CAAC and CAAC showed that all populations 

are exposed to less than 1% of the population adjusted dose for food plus water from ground 

water sources and less than 5% of the population adjusted dose for food plus water from surface 

water sources. The cancer risk analysis for the combined residues of parent and CAAC and 

CAAL degradates in food and water from ground water sources did not exceed the level of 

concern. However, the cancer risk analysis for the combined residues of parent and CAAC and 

CAAL degradates in food and water from surface water sources based on modeling data 

exceeded the level of concern. HED considered those estimates to be highly conservative, and 

actual exposures to be likely much lower for a number of reasons such as: volatilization, one of 

the main dissipation routes of 1,3-D, was not accounted for adequately in PRZM-EXAMS; the 

lack of aerobic aquatic and soil metabolism studies; and lack of indirect photolysis studies (C. 

Olinger, D347789, 01/24/2008). Moreover, limited surface water monitoring data (123 samples) 

in areas of high used showed that 1,3-D and its degradates were not detected. In addition, it was 

suggested that additional environmental fate data may be helpful to refine the drinking water 

assessment.

Conclusions: Dietary exposure assessments for 1,3-D may be necessary to consider the most 

recent food consumption data from the 2003-2008 U.S. Department of Agriculture’s National 

Health and Nutrition Examination Survey, What We Eat in America, and to include newly 

estimated drinking water concentrations based on refined drinking water assessments and/or 

from updated drinking water monitoring data. It is noted that new drinking water models may be 

used during registration review which may lead to new EDWCs. In addition, if new points of 

departure are selected a revised dietary assessment may be needed. 
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5.0 TOLERANCE ASSESSMENT AND INTERNATIONAL HARMONIZATION

Where possible, EPA encourages the harmonization of the US Tolerances and Maximum 

Residue Limits (MRLs) in key export markets. A table with the US tolerances, the Canada 

MRLs, Mexico MRLs and Codex MRLs for 1,3-dichloropropene in registered RACs is provided 

in Appendix C- International Residue Limits. There are currently no established Codex, 

Canadian and/or Mexican MRLs for 1,3-dichloropropene in/on grapes; therefore, harmonization 

is not germane to this action. 

6.0 RESIDENTIAL EXPOSURE

The residential exposure databases for 1,3-D are adequate for Registration Review, with the 

exception of ambient monitoring exposure data for representative usage areas in the U.S. 

Additional details on these data are available in Section 14.0. 

There are currently no registered 1,3-D products intended for residential use. However, there are 

registered commercial use patterns where there is potential for residential bystander inhalation 

exposure. Specifically, the Agency assesses non-occupational (bystander) inhalation exposure 

from residential proximity to treated farm fields (i.e., near field sources) and from regional 

ambient air concentrations from many applications within a region (i.e., ambient sources). Field 

volatility studies indicate that peak emissions for 1,3-D from treated field occur up to 72 hours 

after application. Therefore, the Agency assesses acute exposures for near field sources. There is 

also potential for inhalation exposure to 1,3-D via ambient air as a result of regional 1,3-D 

applications. These exposures can be acute as well as longer-term in nature.

There are two recent documents that analyzed acute residential bystander inhalation exposure to 

1,3-D based on numerous flux studies and PERFUM (Probabilistic Exposure and Risk model for 

Fumigants) air modeling for a variety of 1,3-D scenarios (Olinger; D347789; 01/24/2008 and 

Olinger; D337328; 04/12/2007). Data from available field volatility studies have been included 

where possible, for the registered use on established grape vines1, bedded row crops, and others.

For registration review and as per other fumigants, these exposures will need to be further 

characterized as appropriate which may include further computer modeling analyses with

PERFUM, or other applicable modeling system, as needed.

These risk assessments (Olinger; D347789; 01/24/2008 and Olinger; D337328; 04/12/2007) also

addressed ambient air inhalation exposure to 1,3-D based on California ambient air monitoring 

studies. Data in these assessments include targeted monitoring by the California Air Resources 

Board (CARB) (high agricultural use areas in-season) and the Toxic Air Contaminant (TAC) 

program (background levels in urban environments). The assessments included non-cancer and 

cancer risk estimation. The results of these assessments show no non-cancer risk estimates of 

concern for ambient air inhalation exposures to 1,3-D for any of the exposure durations assessed. 

Cancer risk estimates using monitoring data in urban environments were generally. Below 1x10-

 

1 MRID 45296101
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6

and the assumptions in the near field source and ambient source assessments provide a 

conservative assessment of risk.

The cancer risk estimates using monitoring data from high agricultural use areas in-season 

generally ranged from ranged from 2 x 10-6to 9 x 10-8. The cancer assessment is expected to 

represent high-end exposure and risk since it is not likely that a bystander will be exposed to a 

high-use air concentration over a lifetime. Buffer distances for 1,3-dichloropropene were 

established based on the concerns over longer-term exposure (i.e., cancer assessment). 

California Department of Pesticide Regulation (DPR) manages a township cap permitting 

program designed to assist growers in their transition away from methyl bromide as a soil 

fumigant while also protecting public health by minimizing long-term problematic exposure to 

1,3-D in ambient air. The use of 1,3-D has been capped at 90,250 pounds/per year/per township 

under a program of restrictions developed after the pesticide was reintroduced to the California 

market in 1995. The Agency is monitoring California’s Toxic Air Contaminant Identification 

Program to reevaluate ambient 1,3-D exposures. 

Conclusions: As per prior fumigant risk assessments, bystander risk to 1,3-D from soil 

fumigations may need to be evaluated and updated during registration review should additional 

information about soil emissions become available , the label prescribed use conditions change, 

and/or the relevant durations of the applicable HECs change. Additional or updated PERFUM 

modeling and ambient air analyses may also be required if the points of departure (PODs) or

uncertainty factors (UFs) for the residential exposure assessment change. Additionally, HED 

plans to reevaluate bystander cancer risk estimates based on required ambient air monitoring 

data. 

During Registration Review, HED also plans to update the fumigant factors document (Dawson, 

Smith, and Shelat; D385314; 1/11/2011) which affects all of the soil fumigants, including 1,3-D.

The fumigant factors document lays out recommendations for good agricultural practices as they 

are associated with buffer reduction credits, and builds on previous analyses of factors impacting 

fumigant emissions from soil fumigant applications.

7.0 AGGREGATE EXPOSURE AND RISK ASSESSMENT

For the acute, short-, intermediate-, and long-term assessments the toxicity endpoints selected for 

inhalation and dietary exposures are not expected to be aggregated as there is not a common 

toxicity observed. 1,3-D has been classified as likely to be carcinogenic to humans via the oral 

and inhalation routes. However, the types of tumors observed in the inhalation and oral studies 

were different, see section 2.0. Therefore, oral and inhalation cancer risks will not be aggregated.

For the acute dietary exposure scenario, the aggregate exposure and risk estimates for 1,3-D 

include only food and drinking water, and risk estimates are currently below HED’s level of 

concern.

Conclusions: Dietary exposure estimates for 1,3-D and its metabolites may be revised during 

registration review. Any change in endpoint selection for 1,3-D that impacts the toxicity 
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determination of the dietary or inhalation routes of exposure may require a revised aggregate risk 

assessment.

8.0 OCCUPATIONAL EXPOSURE 

The HED occupational exposure databases for 1,3-D are adequate for Registration Review.

There are several main categories of registered occupational uses of 1,3-D, including the 

following: (1) use as a pre-plant agricultural soil fumigant; (2) use as a post-plant drip irrigation 

fumigation; and (3) golf course turf fumigations.

Occupational Handlers

There is potential for occupational handler inhalation exposure to 1,3-D based on the registered 

use pattern. Dermal exposure is not expected given the high vapor pressure of 1,3-D and based 

on the application methods used. Therefore, HED has not estimated occupational risk estimates 

associated with dermal exposures. Because 1,3-D formulations are Restricted Use Pesticides, it 

may only be applied under the direct supervision of a trained, certified applicator. 

There are two recent documents that analyzed occupational handler inhalation exposure to 1,3-D 

(Olinger; D347789; 01/24/2008 and Olinger; D337328; 04/12/2007).

HED assessed inhalation exposure for representative occupational uses of 1,3-D for the acute, 

short- and intermediate-term exposure durations, as well as a cancer exposure assessment. That 

said, the majority of worker exposure will be for the acute and short-term exposure durations 

given the 1,3-D use pattern. Chemical-specific worker exposure data are available, and were 

used to the extent possible to address occupational handler exposure. The available data used in 

the occupational handler assessments, along with the corresponding activities considered in the 

research, to date include: 

MRID 42946201 and 42845602: drum and bulk loaders and applicators, irrigation 

maintenance worker, rock removers, bed shapers;

MRID 43880401: mini-bulk loaders and applicators;

MRID 45120702/45400202: pre-bed row applications (Yetter rig), shovel men, operators, 

drivers.

The occupational risk assessment did identify risk estimates of concern without respirator 

protection, but the 1,3-D labels include OV respirators (i.e. PF10 respiratory protection) during 

the loading and application of 1,3-D. Assuming use of appropriate respiratory protection, the 

occupational risk estimates do not exceed HED’s level of concern (i.e., MOEs > 30) for all noncancer assessments. Cancer risk estimates for the occupational use of 1,3-D are refined in that 

they rely on both available chemical-specific air monitoring and chemical-specific lifetime use 

information provided by BEAD. Cancer risk estimates based on the 2007/2008 risk assessments 

are in 10-5to 10-6range, taking into account personal protective equipment and engineering 

controls for handling and application of 1,3-D.
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Occupational Post Application

HED also performed occupational bystander assessments based on available field volatility data 

for 1,3-D scenarios involving pre- and post-plant drip irrigation, and row applications.

As part of the 1998 RED, the Agency placed various restrictions on reentry of workers into 

fumigated fields (i.e., 5 day restricted entry interval (REI)). Additionally, the organic vapor (OV)

respirator requirement on 1,3-D labels apply to all occupational workers before and during a 5 

day REI. With these risk mitigations in place, risks to reentry workers did not exceed the HED’s 

level of concern for either non-cancer risk estimates. Buffer distances for 1,3-D were established 

based on longer-term exposure (i.e., cancer risk estimates).

Conclusions: The occupational exposure database is adequate to support the Registration 

Review process for the HED uses of 1,3-D. Additional or updated PERFUM modeling and 

ambient air analyses may be required during Registration Review if the points of departure 

(PODs) or uncertainty factors (UFs) for the occupational bystander exposure assessment change. 

Additionally, cancer risk estimation may be revisited based on HED evaluating the 

chronic/carcinogencity study, worker risk estimate policy revisions, and updated chemicalspecific lifetime use information.

9.0 PUBLIC HEALTH AND PESTICIDE EPIDEMIOLOGY DATA

Adapted from: E. Evans and S. Recore, D411762, 05/15/2013

OPP’s Incident Data System (IDS) includes reports of alleged human health incidents from 

various sources, including mandatory Federal Insecticide, Fungicide and Rodenticide Act 

(FIFRA) Section 6(a)(2) reports from registrants, other federal and state health and 

environmental agencies, and individual consumers. IDS records incidents resulting in higher 

severity outcomes in more detail, in a module called the Main IDS module. Main IDS incidents 

involving only one pesticide are considered to provide more certain information about the 

potential effects of exposure from the pesticide. The less severe human incidents (minor, 

unknown, or no effects outcomes) are reported by registrants as counts called aggregate 

summaries and are recorded in a separate module called Aggregate IDS. 

For the Main IDS, from January 1, 2008 to February 19, 2013, there were 5 incidents reported 

for single chemical only in the database. One incident, an allergic reaction that was classified as 

major severity because it involved a severe allergic reaction, was determined to be a reaction to a 

prescription and not the pesticide. This incident does not appear to be related to the implicated 

product. Three of the other incidents were classified as moderate severity and one was classified 

as minor severity. In Aggregate IDS, from January 1, 2008 to February 19, 2013, there were 20 

reported incidents involving telone. These incidents were classified as minor severity.

The SENSOR-Pesticides database covers 11 states from 1998-2009, although reporting varies 

from state to state. A query of SENSOR-Pesticides 1998-2009 finds a total of 18 cases, 

stemming from ten events, involving Telone. Of these 18 cases, 15 were low in severity, one 
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was moderate in severity and two were high in severity. The high severity cases occurred in 

Washington in 2008 (railroad switchman transporting the product) and North Carolina in 2008 

(worker unclogging disconnected lines) and involved telone products co-formulated with 

chloropicrin. Six cases were reported following one drift/volatilization event that occurred in 

Florida in 2006 in which a pesticide application made to a golf course drifted onto a residential 

area. All 6 cases were low in severity. 

Conclusions: Based on the low frequency and severity of incident cases reported for Telone in 

both IDS and SENSOR-Pesticides, there does not appear to be a concern at this time that would 

warrant further investigation. The Agency will continue to monitor the incident information and 

if a concern is triggered, additional analysis will be included in the risk assessment.

10.0 ENVIRONMENTAL JUSTICE

Potential areas of environmental justice concerns, to the extent possible, were considered in this 

human health risk assessment, in accordance with U.S. Executive Order 12898, "Federal Actions 

to Address Environmental Justice in Minority Populations and Low-Income Populations," 

(http://www.eh.doe.gov/oepa/guidance/justice/eo12898.pdf. As a part of every pesticide risk 

assessment, OPP considers a large variety of consumer subgroups according to well-established 

procedures. In line with OPP policy, HED estimates risks to population subgroups from 

pesticide exposures that are based on patterns of that subgroup’s food and water consumption, 

and activities in and around the home that involve pesticide use in a residential setting. 

Extensive data on food consumption patterns are compiled by the USDA under the Continuing 

Survey of Food Intake by Individuals (CSFII) and are used in pesticide risk assessments for all 

registered food uses of a pesticide. These data are analyzed and categorized by subgroups based 

on age, season of the year, ethnic group, and region of the country. Additionally, OPP is able to 

assess dietary exposure to smaller, specialized subgroups and exposure assessments are 

performed when conditions or circumstances warrant. Whenever appropriate, non-dietary 

exposures based on home use of pesticide products and associated risks for adult applicators and 

for toddlers, youths, and adults entering or playing on treated areas post-application are 

evaluated. Further considerations are currently in development as OPP has committed resources 

and expertise to the development of specialized software and models that consider exposure to 

bystanders and farm workers as well as lifestyle and traditional dietary patterns among specific 

subgroups.

11.0 CUMULATIVE RISK ASSESSMENT

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 tolerance 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 
1,3-Dichloropropene Barcode D410115

Page 13 of 30

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/.

12.0 ENDOCRINE DISRUPTOR SCREENING PROGRAM

As required by FIFRA and FFDCA, EPA reviews numerous studies to assess potential adverse 

outcomes from exposure to chemicals. Collectively, these studies include acute, subchronic and 

chronic toxicity, including assessments of carcinogenicity, neurotoxicity, developmental, 

reproductive, and general or systemic toxicity. These studies include endpoints which may be 

susceptible to endocrine influence, including effects on endocrine target organ histopathology, 

organ weights, estrus cyclicity, sexual maturation, fertility, pregnancy rates, reproductive loss, 

and sex ratios in offspring. For ecological hazard assessments, EPA evaluates acute tests and 

chronic studies that assess growth, developmental and reproductive effects in different 

taxonomic groups. As part of its most recent registration decision for 1,3-D, EPA reviewed these 

data and selected the most sensitive endpoints for relevant risk assessment scenarios from the 

existing hazard database. However, as required by FFDCA section 408(p), 1,3-D are subject to 

the endocrine screening part of the Endocrine Disruptor Screening Program (EDSP). 

EPA has developed the EDSP to determine whether certain substances (including pesticide 

active and other ingredients) may have an effect in humans or wildlife similar to an effect 

produced by a “naturally occurring estrogen, or other such endocrine effects as the Administrator 

may designate.” The EDSP employs a two-tiered approach to making the statutorily required 

determinations. Tier 1 consists of a battery of 11 screening assays to identify the potential of a 

chemical substance to interact with the estrogen, androgen, or thyroid (E, A, or T) hormonal 

systems. Chemicals that go through Tier 1 screening and are found to have the potential to 

interact with E, A, or T hormonal systems will proceed to the next stage of the EDSP where EPA 

will determine which, if any, of the Tier 2 tests are necessary based on the available data. Tier 2 

testing is designed to identify any adverse endocrine-related effects caused by the substance, and 

establish a dose-response relationship between the dose and the E, A, or T effect. 

Under FFDCA section 408(p), the Agency must screen all pesticide chemicals. Between 

October 2009 and February 2010, EPA issued test orders/data call-ins for the first group of 67 

chemicals, which contains 58 pesticide active ingredients and 9 inert ingredients. A second list of 

chemicals identified for EDSP screening was published on June 14, 20132and includes some 

pesticides scheduled for Registration Review and chemicals found in water. For further 

information on the status of the EDSP, the policies and procedures, the lists of chemicals, future 

lists, the test guidelines and the Tier 1 screening battery, please visit our website.3

 

2

See http://www.regulations.gov/#!documentDetail;D=EPA-HQ-OPPT-2009-0477-0074 for the final second list of 

chemicals.

3

http://www.epa.gov/endo/
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In the interim, EPA is making no human health or environmental safety findings associated with 

the EDSP screening of 1,3-D. Before completing this Registration Review, the Agency will 

make an EDSP FFDCA section 408(p) determination.

13.0 HUMAN STUDIES

The chemical specific studies used to develop the previous occupational handler assessment 

have not been reviewed for compliance with required ethical standards for conducting human 

studies. Prior to final decisions under Registration Review for 1,3-D the Agency will ensure 

that the studies are subjected to the appropriate review.

The study MRIDs are as follows:

An Evaluation of 1,3-Dichloropropene Worker Exposures Associated With TELONE 

“Soil Fumigant Loading Application and Re-entry Final Report

o MRIDs: 42946201/42845602

An Evaluation of Worker Exposure to Airborne Concentrations of 1,3-dichloropropene 

during loading and application of TELONE Soil Fumigants Packaged in Traveler 

Cylinders

o MRIDs: 43880401

Water and Air Concentrations of 1,3-Dichloropropene Following a Golf Course Turf 

Application in the Southeast United States

o MRIDs: 45120702/45400202

14.0 DATA REQUIREMENTS

This data is required in order to complete the 1,3-D registration review risk assessment. 

Occupational/Residential Exposure: 

o Airshed monitoring data4for:

 Southeast climate zone (e.g., Florida, Georgia, or Virginia)

 Mid-Atlantic to Upper mid-west climate zone (e.g. Michigan, Wisconsin)

 Pacific North-West climate zone (e.g. ,Idaho, Washington)

 The Southwest climate zone (e.g. California, Arizona)

Additional information about the required ambient monitoring data can be found in HED’s 2008 

memo “Health Effects Division Recommendations for Fumigant Data to Refine Exposure 

Assessments” (D353724). This “special study” data requirement is necessary because the 

available ambient data used in the assessment is dated and did not take place in high use areas. 

Additional justification for the study requirement is identified in Appendix D.

 

4

“Special Study” data requirement. See Appendix D for more information
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15.0 REFERENCES

 

EPA 2002. 2002 Edition of the Drinking Water Standards and Health Advisories. EPA

822/R/02/038. Washington, DC: Office of Water, EPA.

Van Alstine, J., (April 23, 2013), TXR #0056626, 1,3-Dichloropropene (1,3-D): Summary of 

Hazard and Science Policy Council (HASPOC) Meetings of March 28, 2013: Recommendations 

on the Requirement of the Neurotoxicity Battery (Acute and Subchronic Neurotoxicity Studies).

J. Dawson and C. Smith, 07/01/2008, D353724, Health Effects Division Recommendations for 

Fumigant Data to Refine Exposure Assessments.

1,3-D RED Document; December, 1998.

1,3-Dichloropropene: HED Human Health Risk Assessment For Phase 5; DP Barcode: D337328, 

PC Code: 029001; April 12, 2007.

1,3-Dichloropropene: Proposed New Use for Drip Irrigation in Vineyards: HED Human Health 

Risk Assessment; DP Barcode: D340059, PC Code: 029001; June 6, 2007.

Review of Special Local Need Registration 24(c) for Telone II (EPA Reg. 62719-32) to Control 

Potato Cyst Nematodes (PCN) in Soils Involved with the USDA/ISDA PCN Eradication 

Program - SLN: ID-070015 (PC Code 029001, DP Barcode 345158); November 16, 2007.

1,3-Dichloropropene: Follow-up on Proposed New Use for Drip Irrigation in Vineyards: 

Drinking Water and Residential Assessments; DP Barcode: D346778, PC Code: 029001; 

December 14, 2007.

1,3-Dichloropropene: Proposed New Use for Drip Irrigation in Vineyards: Revised HED Human 

Health Risk Assessment; DP Barcode: D347789, PC Code: 029001; January 24, 2008

Health Effects Division Recommendations for Fumigant Data to Refine Exposure Assessments. 

D353724; July 1, 2008.

1,3-Dichloropropene, PC Code 029001, DP Barcode 369764; Responses To Technical Issues 

Associated With Telone Use In Florida On Golf Courses and Labeling Issues In California;

October 27, 2009.
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Appendix A: Toxicology Profile and Executive Summaries

A.1 Toxicology Data Requirements

The requirements (40 CFR 158.340) for food uses for 1,3-Dichloropropene are in Table 1. Use of the new guideline 

numbers does not imply that the new (1998) guideline protocols were used.

Study

Technical

Required Satisfied

870.1100 Acute Oral Toxicity.......................................................

870.1200 Acute Dermal Toxicity ..................................................

870.1300 Acute Inhalation Toxicity..............................................

870.2400 Primary Eye Irritation....................................................

870.2500 Primary Dermal Irritation ..............................................

870.2600 Dermal Sensitization......................................................

yes

yes

yes

yes

yes

yes

yes

yes

yes

yes

yes

yes

870.3100 Oral Subchronic (rodent)...............................................

870.3150 Oral Subchronic (nonrodent) .........................................

870.3200 21-Day Dermal ..............................................................

870.3250 90-Day Dermal ..............................................................

870.3465 90-Day Inhalation..........................................................

yes

yes

yes

CR

yes

yes

yes

noA

-

yes

870.3700a Developmental Toxicity (rodent)...................................

870.3700b Developmental Toxicity (nonrodent).............................

870.3800 Reproduction .................................................................

yes

yes

yes

yes

yes

yes

870.4100a Chronic Toxicity (rodent) ..............................................

870.4100b Chronic Toxicity (nonrodent)........................................

870.4200a Oncogenicity (rat)..........................................................

870.4200b Oncogenicity (mouse)....................................................

yes

yes

yes

yes

yes

yes

yes

yes

870.5100 Mutagenicity—Gene Mutation - bacterial.....................

870.5300 Mutagenicity—Gene Mutation - mammalian................

870.5xxx Mutagenicity—Structural Chromosomal Aberrations...

yes

yes

yes

yes

yes

yes

870.6100a Acute Delayed Neurotoxicity (hen)...............................

870.6100b 90-Day Neurotoxicity (hen)...........................................

870.6200a Acute Neurotoxicity Screening Battery (rat) .................

870.6200b 90-Day Neurotoxicity Screening Battery (rat)...............

870.6300 Develop. Neurotoxicity .................................................

no

no

yes

yes

CR

no

no

waived*

waived*

-

870.7485 General Metabolism ......................................................

870.7600 Dermal Penetration ........................................................

870.7800 Immunotoxicity .............................................................

yes

CR

yes

yes

-

yes

*HASPOC TXR#0056626; A highly volatile chemical; very low dermal exposure anticipated relative to inhalation; 

realistic quantification of dermal risk is not possible (study not required).

CR = Conditionally Required.
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A.2. Acute Toxicology

Acute Profile of 1,3-Dichloropropene

Guideline No. Study Type MRIDs # Results Toxicity

Category

870.1100 Acute Oral (rat) 40220901 LD50 = 224 mg/kg II

870.1200 Acute Dermal (rabbit) 40220902 LD50 = 333 mg/kg II

870.1300 Acute Inhalation (rat) 40220903 LC50 = 3.88 mg/L IV

870.2400 Primary Eye Irritation (rabbit) 40220904 Severe irritant II

870.2500 Primary Skin Irritation (rabbit) 40220905 Slight irritant III

870.2600 Dermal Sensitization (guinea pig) 40220906 Sensitizer --

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 (1993)

Acceptable/guideline

0, 5, 15, 50 or 100 

mg/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 (1993)

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 (1978)

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 (1978)

Acceptable/guideline 

0, 3, 10 or 30 ppm (0, 

0.0136, 0.045 or 0.136 

NOAEL = 30 ppm (0.045 mg/L), highest dose tested 

LOAEL = >30 ppm (0.136 mg/L)
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Guideline No./ Study 

Type

MRID No./ Classification 

/Doses

Results

mg/L) 6 hours/day, 5 

days/week 

870.3465

90-Day inhalation 

toxicity rodent [Fischer 

344 rats] 

00146461 (1984)

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 (1984)

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 

(1983)

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 

(1983)

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(1987)

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 

(premating) 6 hours/day, 7 

days/week (F0 breeding at 

weeks 11-13, during 

gestation and lactation; F1a

and F1b, dams from 

gestation day 20 until 

postpartum day 5; F1 ♂♀ 

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
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Guideline No./ Study 

Type

MRID No./ Classification 

/Doses

Results

870.4100b

Chronic toxicity 

nonrodent

[Beagle dog]

42441001 (1992)

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/Carcinogenicity for 2 year rat 

study 

[Fischer 344 rats]

43763501 (1995)

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/Carcinogenici

ty (104 week)

[Fischer 344 rats]

00146469 (1985)

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 

Carcinogenicity: Increased incidence of squamous cell 

papillomas 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/Carcinogenicity (104 

week)[B6C3F1 mice]

43757901 (1995)

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/Carcinogenicity (104 

week)[B6C3F1 mice]

00146469 (1985)

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 

Carcinogenicity: Increased incidence of squamous cell 

papillomas of the forestomach: 0, 25 and 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/Carcinogenicity (2 years) 

[Fischer 344 rats]

40312201 (1987) 

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 

40312301 (1987) 

Acceptable/guideline

Chronic Toxicity NOAEL = 5 ppm (0.023 mg/L)

LOAEL = 20 ppm (0.091 mg/L) based urinary bladder 
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Guideline No./ Study 

Type

MRID No./ Classification 

/Doses

Results

Toxicity/Carcinogenicity (2 years) 

[B6C3F1 mice]

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 

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

50-200 μM +S9

Negative up to cytotoxicity (≥200 μM -S9) or the highest dose 

tested +S9 

Gene Mutation

870.5300

Drosophila 

melanogaster sexlinked 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 (1978)

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

00039688 (1978)

Acceptable/guideline

Positive: Preferential inhibition of the DNA repair deficient 

strain at 1250 μg/well
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Guideline No./ Study 

Type

MRID No./ Classification 

/Doses

Results

Bacterial DNA repair 

Bacillus subtilis H15 & 

M45

50-1,250 μg/well

Other Effects 

870.5550 

Unscheduled DNA 

Synthesis Primary rat 

hepatocytes

00146467(1985)

Acceptable/guideline

3x10-3to 1x 10-6M

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

Other Effects 

870.5900

In vitro sister 

chromatid 

exchange(SCE)

CHO cells

NTP (1989)

Acceptable/Guideline

0.995-29.900 μg/mL -S9 

(Trial 1)

30-50 μg/mL -S9 (Trial 2)

2.990-29.900 μg/mL +S9 

(Trial 1 only)

Positive: Significant and concentration-related ↑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

Trial 2:12.5- 500 μg/mL -

S9; 3-100 μg/mL +S9

Positive: Dose-related and reproducible ↑ 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 
1,3-Dichloropropene Barcode D410115

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Guideline No./ Study 

Type

MRID No./ Classification 

/Doses

Results

Immunotoxicity

870.7800

(sheep red blood cell 

assay)

49074801 (2010)

28-day dietary 

male F344/DuCrl Rats

Under review

MECHANISM STUDIES

Gene Mutation

In vitro bacterial 

reverse gene mutation 

assay Salmonella 

typhimurium TA100 

plus mouse lung 

homogenate

44460501 (1998)

Unacceptable /nonguideline

100-450 μg/plate -

metabolic activation;

150-1000 μg/plate + 

untreated mouse lung 

homogenate -glutathione 

(GSH)or 75-1000 μg/plate 

+GSH; 75-1000 μg/plate ± 

GSH + mouse lung S9 

(pretreated with 63 ppm 

1,3-D, 5da/wk, 2.5 wks) 

Negative at any concentration ± GSH and ± untreated or 1,3-D 

lung S9 but under conditions that would not favor a mutagenic 

response -S9 (no epoxidized soybean stabilizer, purification 

through silicic column and storage at 5C 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 (1998)

Unacceptable /nonguideline

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 (1997)

Unacceptable /nonguideline

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 (1997)

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 inhalationmice) 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 

44460503 (1998)

Unacceptable

/non-guideline

GSH measurements in cell 

No conclusions relative to the correlation between physiological 

levels of GSH and mitigation of mutagenicity
1,3-Dichloropropene Barcode D410115

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Guideline No./ Study 

Type

MRID No./ Classification 

/Doses

Results

mice & ♂ Fischer 344 

rats primary rat 

hepatocytes, CHO 

cells, Chinese hamster 

lung cells, Salmonella 

typhimurium 

lines reacted with various 

substrates: 13C-1,3-D; 4-

chloro-1,3-dinitrobenzene; 

para-nitrophenylethylbromide; trans4-phenyl-3-buten-2-one

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 + microencapsulated 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

45897502 (1998) C&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.
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Summary of Toxicological Doses and Endpoints for 1,3-Dichloropropene for Use in Human 

Risk Assessments

Table x.x. Summary of Toxicological Dose and Endpoints for Use in 1,3-Dichloropropene Dietary Risk Assessments

Exposure/

Scenario Point of Departure

Uncertainty/

FQPA Safety 

Factors

Level of Concern 

for Risk 

Assessment

RfD, PAD

Study and Toxicological Effects

1,3-D Combined with Degradates: 3-Chloroallyl Alcohol and 3- Chloroacrylic Acid 

Acute Dietary 

Exposure (any 

Subpopulation)

No endpoint attributable to a single exposure was identified.

Chronic Dietary 

Exposure

NOAEL = 2.5 

mg/kg/day

UFA= 10x

UFH=10x

FQPA SF= 1x

Chronic PAD = 

0.025 mg/kg/day

2- year combined chronic toxicity/ 

carcinogenicity study (rat) 

LOAEL = 12.5 mg/kg/day

Decreased body weight gain, increased 

incidence of basal cell hyperplasia of 

nonglandular stomach mucosa 

Cancer (oral) Classified as “likely to be carcinogenic in humans. 

Q1 * = 1.22 x 10-1 (mg/kg/day)-1

2- Year Combined 

Chronic/Carcinogenicity study -Rats

Combined forestomach, liver, mammary 

thyroid, adrenal, urinary, lung tumors, 

multistage model, 3/4 scaling factor. 

UF = uncertainty factor. NOAEL = no observed adverse effect level. LOAEL = lowest observed adverse effect level. RfD = 

reference dose. PAD = Population Adjusted Dose; UFA = extrapolation from animal to human (interspecies). UFH = 

potential variation in sensitivity among members of the human population (intraspecies). NA = Not Applicable

Table 3.3. Summary of Toxicological Dose and Endpoints for Use in 1,3-Dichloropropene Human Health Inhalation Risk 

Assessment (Non-Occupational)

Exposure

Scenario Point of Departure

Uncertainty/

FQPA Safety Factors

HED HECs

Study and Toxicological Effects

Acute Inhalation NOAEL = 454 ppm

75.67 ppm

UFH = 10X

UFA = 3X

FQPA = 1X

acute (4-hour) inhalation studies (rat) 

LOAEL = 583 ppm, based on clinical signs 

(tremors, convulsions, salivation, lacrimation, 

diarrhea, lethargy) and decreased body weight 

(mortality observed at >647 ppm)

Short-Term 

Inhalation (1 to 30 

days) 

NOAEL = 20 ppm

(maternal)

5.0 ppm

UFH = 10

UFA = 3

FQPA = 1X

developmental inhalation toxicity study (rabbit )

LOAEL = 30 ppm, based on maternal decreased 

body weight gains

Intermediate -term 

Inhalation (1-6 

months)

NOAEL = 10 ppm

0.205 ppm

UFH = 10X

UFA = 3X

FQPA = 1X

13-week inhalation study (rat)

LOAEL = 30 ppm, based on nasal histopathology

Long-Term 

Inhalation (>6 

months)

NOAEL = 5 ppm

0.182 ppm

UFH = 10X

UFA = 3X

FQPA = 1X

Chronic toxicity/carcinogenicity study (mouse)

LOAEL = 20 ppm, based on nasal histopathology

Cancer (inhalation) Classification: Likely to be carcinogenic to humans 

Q1 * = 4 x 10-6 (μg/m3)

-1

2-year inhalation bioassay – mouse 

bronchioloalveolar adenomas

UF = uncertainty factor; HEC = Human Equivalent Concentration; HED = Human Equivalent Dose; NOAEL = no observed 
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Table 3.3. Summary of Toxicological Dose and Endpoints for Use in 1,3-Dichloropropene Human Health Inhalation Risk 

Assessment (Non-Occupational)

Exposure

Scenario Point of Departure

Uncertainty/

FQPA Safety Factors

HED HECs

Study and Toxicological Effects

adverse effect level; LOAEL = lowest observed adverse effect level; UFA = extrapolation from animal to human (interspecies). 

UFH = potential variation in sensitivity among members of the human population (intraspecies). NA = Not Applicable

Table 3.4. Summary of Toxicological Dose and Endpoints for Use in 1,3-Dichloropropene Human Health 

Inhalation Risk Assessment (Occupational)

Exposure

Scenario Point of Departure Uncertainty FactorsHED HECs Study and Toxicological Effects

Acute NOAEL = 454 ppm 227.0 ppm

UF = 30

acute inhalation studies –rat

LOAEL = 583 ppm, based on clinical 

signs (tremors, convulsions, salivation, 

lacrimation, diarrhea, lethargy), 

decreased body weight (mortality 

observed at >647 ppm)

Short-Term 

Inhalation (1 to 30 

days) 

NOAEL = 20 ppm

(maternal) 15.0 ppm

UF = 30

developmental inhalation toxicity study -

rabbit 

LOAEL = 30 ppm, based on maternal 

decreased body weight gains

Intermediate-Term 

Inhalation (1 to 6 

months)

NOAEL = 10 ppm

0.86 ppm

UF = 30

13-week inhalation toxicity -rat 

LOAEL = 30 ppm, based on 

histopathological lesions in olfactory 

region of nasal cavity

Long-Term Inhalation 

(>6 months)

NOAEL = 5 ppm

0.77 ppm

UF = 30

Chronic toxicity/carcinogenicity study -

mice

LOAEL = 20 ppm, based on nasal 

histopathology

UF = uncertainty factor; HEC = Human Equivalent Concentration; HED = Human Equivalent Dose; NOAEL = no 

observed adverse effect level; LOAEL = lowest observed adverse effect level; NA = Not Applicable,
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Appendix B: Chemistry

1.0 PHYSICAL/CHEMICAL PROPERTIES CHARACTERIZATION

1.1 Identification of Active Ingredient

Table 2.1. Test Compound Nomenclature

Compound Structure

Common name cis-1,3-Dichloropropene trans-1,3-Dichloropropene

Company experimental name 1,3-D

IUPAC name (EZ)-1,3-Dichloropropene

CAS name 1,3-Dichloro-1-propene

CAS registry number 542-75-6

End-use product (EP) CordonTM, TeloneTM

Compound Structure

Common name cis-CAAL trans-CAAL

IUPAC name (EZ)-3-chloroprop-2-en-1-ol

CAS registry number 4643-05-4 4643-06-5

Compound Structure

Common name cis-CAAC trans-CAAC

IUPAC name (EZ)-3-chloroacrylic acid

CAS name 1609-93-4 2345-61-1

1.2 Physical and Chemical Properties

Cl

Cl

Cl Cl

Cl OH

Cl

OH

O

Cl OH

Cl O

OH

Table 2.2. Physicochemical Properties of the Technical Grade Test Compound 1,3-Dichloropropene.

Parameter Value Reference

Molecular Weight 110.97 g/mol

Boiling point 104 C for cis isomer;

112.6 C for trans isomer

1,3-Dichloropropene Reregistration 

Eligibility Decision Document 

(12/1998)

pH

The molecule does not contain 

ionizable groups. It is not an acid or 

base.

Density 1.209 g/mL at 25 C 1,3-Dichloropropene Reregistration 

Eligibility Decision Document 

Water solubility (12/1998)

2,180 mg/L for cis isomer;

2,320 mg/L for trans isomer
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Cis and trans 1,3-dichloropropene (MW = 110.97 g/mol) are liquids with boiling point of 104 

and 112.6 C, respectively. These have high water solubility (2 g/L) and high vapor pressure 

(34.3 mm Hg for cis isomer and 23.0 mmHg for trans isomer at 25 C). 

Solvent solubility Not available

Vapor pressure 34.3 mm Hg for cis isomer at 25 C;

23.0 mm Hg for trans isomer at 25 C

1,3-Dichloropropene Reregistration 

Eligibility Decision Document 

(12/1998)

Dissociation constant, pKa The molecule does not dissociate.

Octanol/water partition coefficient, Log(KOW)

1,3-dichloropropene 2.04

trans isomer 2.22 @ 25oC

cis isomer 1.82 @ 20oC 

The Pesticide Manual, 11th Ed., 

1997.

UV/visible absorption spectrum Not available
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Appendix C: International Residue Limits 

1,3-Dichloropropene (PC Code 029001)

Summary of US and International Tolerances and Maximum Residue Limits 

Residue Definition:

US Canada Mexico1 Codex

40 CFR 180.636:

Tolerances are established for the combined residues 

of the fungicide cis - and trans -1,3-dichloropropene 

and its metabolites cis - and trans -3-chloroacrylic 

acid, and cis - and trans -3-chloroallyl alcohol 

None None

Commodity Tolerance (ppm) /Maximum Residue Limit (mg/kg)

US Canada Mexico1 Codex

Grapes 0.018

Completed: M. Negussie; 04/23/2013

1 Mexico adopts US tolerances and/or Codex MRLs for its export purposes.
1,3-Dichloropropene Barcode D410115

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Appendix D: Data Requirements

Guideline Number: Special Study

Study Title: Ambient Air Monitoring

Rationale for Requiring the Data

The Agency evaluated risks from single sources using monitoring data and modeling techniques that 

relied on data which represent currently required agricultural practices as well as innovations designed to 

further reduce emissions. Risks from exposures to ambient 1,3-D, however, were estimated from 

monitoring data collected solely in California to represent conditions at a regional and state-wide level. 

The California monitoring data are dated (i.e., did not capture emissions that result from currently 

mandated good agricultural practices). The California Air Resources Board (CARB) generated most of 

the data considered in the Agency's risk assessment for 1,3-D’s registered uses. Fumigants like 1,3-D are 

also widely used in other states such as Florida.

The Agency’s risk assessment for 1,3-D identified the uncertainties associated with relying on the CARB 

data and concluded that it was difficult to determine how the use of the data would either over- or underpredict actual exposures for those living in high use areas under currently mandated agricultural 

practices. The following describes the major factors that lead to this uncertainty:

o The CARB monitoring data was based on cultural practices used in the 2000 to 2001 period which 

does not reflect today’s required practices.

o The CARB monitoring data does not reflect usage in high use regions other than California, such as 

Florida.

o The CARB monitoring data were intended to be used to evaluate sub-chronic/seasonal exposures and 

not for evaluating chronic exposure.

The Agency intends to call-in ambient 1,3-D studies for representative highest use areas of the US5. 

Representative areas include:

Southeast (e.g. Florida/Georgia/Virginia)

Mid-Atlantic to Upper Mid-west (e.g., Michigan/Wisconsin)

Pacific Northwest (e.g., Idaho/Washington)

Southwest (e.g. California/Arizona)

The goal is to determine whether exposures in high use areas from ambient levels of 1,3-D are of concern 

given the current use patterns and good agricultural practices required on the 2010 amended labels. 

Criteria that must be considered in selecting the sites include:

Areas of highest 1,3-D use

Duration of the season of use for a candidate study area

Geographically unique features that could effect ambient concentration levels (e.g. valleys, flat 

terrain)

Weather considerations which may adversely impact ambient exposures

Proximity of use to populations

Proximity of use to sensitive sites (e.g. schools) 

Proximity of use to minority populations to address environmental justice concerns 

Logistical access

The sampling design must focus on community level exposures in a longitudinal fashion. Monitoring 

samples should be collected at least twice per week during the use season and once per week during the 

 

5

See HED’s memo, “Recommendations for Fumigant Data to Refine Exposure Assessments” D353724 for 

additional information. Specific airsheds to be determined based on consultation with the Agency. At least two 

airsheds shall be monitored in appropriate use seasons over the course of a 2 year interval. All sites will be defined 

based on criteria similar to CARB (High areas of use in high seasons of use).
1,3-Dichloropropene Barcode D410115

Page 30 of 30

non-use season for a period of two consecutive years. 

Practical Utility of the Data

How will the data be used? 

The ambient concentrations from high use areas will be used to confirm that exposure to ambient 1,3-D

is below the Agency's level of concern in light of the changes in use patterns required by the 2010 

amended labels.

How could the data impact the Agency’s future decision-making?

If the data indicates that risks from ambient exposure to 1,3-D are a risk of concern, the Agency will 

consider requiring additional risk mitigation measures (e.g., recapture systems, lowering application 

rates, establishing use caps in high use areas, and other emission reduction controls). If data indicates 

that risks are not a concern, no changes to risk mitigation measures currently required by EPA would be 

needed.