Fifth Five Year Review Report for Envirochem Corp. Superfund Site Boone County Indiana


980263

FIFTH FIVE-YEAR REVIEW REPORT FOR
ENVIROCHEM CORP. SUPERFUND SITE
BOONE COUNTY, INDIANA



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Prepared by:
U.S. Environmental Protection Agency
Region 5
Chicago, Illinois

3/2/2023

X Douglas Ballotti

Douglas Ballotti, Director

Superfund & Emergency Management Division

Signed by: DOUGLAS BALLOTTI

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Table of Contents

LIST 01 ABBREVIATIONS & ACRONYMS	ii

I.	INTRODUCTION	1

FIVE-YEAR REVIEW SUMMARY FORM	3

II.	RESPONSE ACTION SUMMARY	3

Basis for Taking Action	3

Response Actions	5

Status of Implementation	8

Institutional Controls	10

Systems Operations/Operation & Maintenance	12

III.	PROGRESS SINCE THE LAST REVIEW	12

IV.	FIVE-YEAR REVIEW PROCESS	15

Community Notification, Involvement & Site Interviews	15

Data Review	15

Site Inspection	18

V.	TECHNICAL ASSESSMENT	18

QUESTION A: Is the remedy functioning as intended by the decision documents?	18

QUESTION B: Are the exposure assumptions, toxicity data, cleanup levels, and remedial action

objectives (RAOs) used at the time of the remedy selection still valid?	19

QUESTION C: Has any other information come to light that could call into question the
protectiveness of the remedy?	20

VI.	ISSUES/RECOMMENDATIONS	21

OTHER FINDINGS	23

VII.	PROTECTIVENESS STATEMENT	25

VIII.NEXT	REVIEW	25

APPENDIX A - REFERENCE LIST

APPENDIX B - LABORATORY DATA

APPENDIX C - SITE INSPECTION FORM

APPENDIX D - PHOTO LOG

APPENDIX E - FIGURES

APPENDIX F - RG TABLES

APPENDIX G- 1,1 -DICHLOROETHANE TOXICOLOGICAL PROFILE

l

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LIST OF ABBREVIATIONS & ACRONYMS

^g/L

microgram per liter

|ig/m3

microgram per cubic meter

ARAR

Applicable or Relevant and Appropriate Requirement

ASC

Acceptable Stream Concentrations

CERCLA

Comprehensive Environmental Response, Compensation, and Liability Act

CFR

Code of Federal Regulations

COC

Contaminant of Concern

CSM

Conceptual Site Model

DCA

Dichloroethane

DCE

Dichloroethene

DNAPL

Dense Non-Aqueous Phase Liquid

ECC

Envirochem Corp.

EPA

United States Environmental Protection Agency

ESD

Explanation of Significant Differences

FYR

Five-Year Review

HDPE

High Density Polyethylene

ICs

Institutional Controls

IDEM

Indiana Department of Environmental Management

MCL

Maximum Contaminant Level

NCP

National Oil and Hazardous Substances Pollution Contingency Plan

NPDES

National Pollutant Discharge Elimination System

NPL

National Priorities List

NSL

Northside Sanitary Landfill Superfund Site

O&M

Operation and Maintenance

OU

Operable Unit

PCE

T etrachl oroethy 1 ene

PRGS

Permeable Reactive Gate System

PRP

Potentially Responsible Party

RAOs

Remedial Action Objectives

RCRA

Resource Conservation and Recovery Act

RGs

Remediation Goals

ROD

Record of Decision

RPM

Remedial Project Manager

Site

Envirochem Corp. Superfund Site

SVE

Soil Vapor Extraction

TBC

To be considered

TBCW

Thin Barrier Curtain Wall

TCA

Trichloroethane

TCE

T ri chl oroethy 1 ene

USACE

United States Army Corps of Engineers

UU/UE

Unlimited Use and Unrestricted Exposure

VOCs

Volatile Organic Compounds

11

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I. INTRODUCTION

The purpose of a Five-Year Review (FYR) is to evaluate the implementation and performance of a
remedy to determine if the remedy is and will continue to be protective of human health and the
environment. The methods, findings, and conclusions of reviews are documented in FYR reports such as
this one. In addition, FYR reports identify issues found during the review, if any, and document
recommendations to address them.

The United States Environmental Protection Agency (EPA) is preparing this FYR pursuant to the
Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA) Section 121, 42
U.S.C. § 9621, consistent with the National Oil and Hazardous Substances Pollution Contingency Plan
(NCP)(40 C.F.R. Section 300.430(f)(4)(ii)), and considering EPA policy.

This is the fifth FYR for the Envirochem Corp. (ECC) Superfund Site (Site). The triggering action for
this statutory review is the completion date of the previous FYR on March 12, 2018. The FYR has been
prepared since hazardous substances, pollutants, or contaminants remain at the site above levels that
allow for unlimited use and unrestricted exposure (UU/UE).

The Site consists of one sitewide operable unit (OU) that will be addressed in this FYR. OU1 includes
all media at the Site, including soil, groundwater, and surface water.

The Envirochem Corp. Superfund Site FYR was led by Matthew Ohl, EPA's Remedial Project
Manager (RPM) for the Site. Participants included Heriberto Leon, EPA's Community Involvement
Coordinator for the Site, Katie Neighbors of the Indiana Department of Environmental Management
(IDEM), and William Clabaugh and Jennifer Grimm of the United States Army Corps of Engineers
(USACE). The Potentially Responsible Party (PRP) group was notified of the initiation of the FYR. The
review began on 3/11/2022.

Site Background

The ECC Site is located east and south of the Boone County Resource Recovery Systems, Inc. facility
on U.S. Highway 421 in a primarily rural area of Boone County, Indiana. It is approximately 5 miles
north of Zionsville and ten miles northwest of Indianapolis. A facility previously located at ECC
processed and reclaimed solvents from 1977 to 1982. The ECC Site, which occupies approximately 6.5
acres of land, was placed on the National Priorities List (NPL) for cleanup in September 1983.

The Northside Sanitary Landfill Superfund Site (NSL) is located immediately to the east of the ECC
Site, and the Third Site (a Non-Time-Critical Removal Action Site) is located immediately to the south
of the ECC Site (Figure 1 in Appendix E). The close proximity of remedial activities at both of these
sites makes them relevant to the ECC Site. The remedy for the NSL includes a cap, containment wall,
and groundwater collection and treatment. A removal action is ongoing at Third Site including the
following actions:

• In-situ chemical oxidation of groundwater and Dense Non-Aqueous Phase Liquids (DNAPL),

• Soil vapor extraction and excavation of soils with off-site disposal,

• Sheet pile wall around the DNAPL area,

• Electrical resistive heating of the DNAPL area and limited adjacent area, and

• Groundwater collection and treatment.

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An unnamed ditch, near the east side of the ECC Site, flows into Finley Creek which flows into Eagle
Creek about a half-mile downstream of the ECC Site. Eagle Creek, in turn, feeds into the Eagle Creek
Reservoir about ten miles further downstream. The Eagle Creek Reservoir has a storage capacity of 7.8
billion gallons and is one of several sources of drinking water for Indianapolis. More information on
water quality is provided in the Water Quality Report by Citizen's Energy Group online at:
http://www.citizensenergvgroup.com/Mv-Home/Utilitv-ServicesAVaterAVater-Qualitv.

The current land use for the surrounding area is residential, commercial, and agricultural. Nearby
residents who are not connected to the municipal water supply use private wells for their water supply.
A well survey conducted in November 2022 using available state data identified one well at the only
occupied residential property that is immediately downgradient of the Site, and no other wells in the
vicinity. The residential well has not shown any contamination.

Recent data indicate the potential migration of dissolved-phase contaminants, including vinyl chloride,
into the sand and gravel aquifer underlying the till unit and away from source areas at the ECC Site
toward Third Site. The Data Review Section of this FYR has additional information on the current
concentrations at the Site and possible plume migration.

As of 2022, the PRPs are currently negotiating a new amendment to the 1991 Amended Consent Decree;
Civil Action No. 83-1419C (Consent Decree, 1991)1 to provide for interim measures to control, capture,
and treat contaminated groundwater while designing additional remedial action alternatives with
construction planned for 2024 after EPA approves the alternative(s) and issues an Explanation of
Significant Differences (ESD) or Record of Decision (ROD) amendment.

1 The 1991 Amended Consent Decree contains the most helpful representation of the Site and therefore is the primary legal
enforcement document referenced in this FYR. It is an amended version of the original 1983 Consent Decree and has been
itself modified through stipulation multiple times since. To avoid unnecessarily regurgitating the long and complex legal
enforcement history of the Site, throughout this FYR, references to the 1991 Amended Consent Decree will be used to refer
to the collective legal enforcement documents governing the Site, which consist of the 1983 CD, the Amended 1991 CD, and
several stipulations to modify the 1991 Amended CD over decades.

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FIVE-YEAR REVIEW SUMMARY FORM

SITE IDENTIFICATION

Site Name: Envirochem Corp.

EPA ID:

IND084259951

Region: 5

NPL Status: Final

State: IN

City/County: Zionsville/Boone

SITE STATUS

Multiple OUs?

No

Has the site achieved construction completion?

Yes

Lead agency: EPA

Author name (Federal or State Project Manager): Matthew Ohl

Author affiliation: EPA

Review period: 3/11/2022 - 10/12/2022

Date of site inspection: 7/29/2022

Type of review: Statutory

Review number: 5

Triggering action date: 3/12/2018

Due date (five years after triggering action date): 3/12/2023

II. RESPONSE ACTION SUMMARY

Basis for Taking Action

Soils at the Site are contaminated with elevated levels of various volatile and semi-volatile organic
compounds and metals, which present potential, unacceptable human health risks through exposures to
soil, surface water, leachate, and groundwater. The potential human health risks are due to levels of
hazardous substances exceeding EPA's risk management criteria for either the average or reasonable
maximum exposure scenarios for residential and site workers, as applicable. Unacceptable risks, as
defined in the National Oil and Hazardous Substances Pollution Contingency Plan (NCP), from
exposure to groundwater are attributed to the presence of various organic and inorganic hazardous
substances that exist at concentrations exceeding their respective State and Federal drinking water
standards. Additionally, there are potential adverse effects to human and ecological receptors from
concentrations in the groundwater/surf ace water that exceed surface water quality standards. Table 1
shows the contaminants of concern for each media at the Site (EPA 1991).

3

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Table 1: Site Contaminants of Concern by Media Type

Contaminant

Groundwater

Surface Water

Soil

Acetone

~



~

Chlorobenzene

~



~

Chloroform

~

~

~

1,1-Dichloroethane (DCA)

~



~

1,1-Dichloroethene (DCE)

~

~

~

Ethylbenzene

~

~

~

Methylene Chloride

~

~

~

Methyl Ethyl Ketone

~



~

Methyl Isobutyl Ketone

~



~

Tetrachloroethylene (PCE)

~

~

~

Toluene

~

~

~

1,1,1-Trichloroethane (1,1,1-TCA)

~

~

~

1,1,2-TCA

~

~

~

Trichloroethylene (TCE)

~

~

~

Xylene

~



~

Bis(2-ethylhexyl) phthalate

~

~



Bi-n-Butyl Phthalate

~

~



Diethyl Phthalate

~

~



Isophorone

~





Naphthalene

~

~



Phenol

~

~

~

Antimony

~





Arsenic

~

~



Barium

~





Beryllium

~





Cadmium

~





Chromium VI

~

~



Lead

~

~



Manganese

~





Nickel

~

~



Silver

~





Tin

~





Vanadium

~





Zinc

~

~



Cyanide

~

~



PCBs

~

~



1,2-DCE*

~

~

~

Vinyl Chloride*

~

~

~

Bis (2-ethylhexyl) phthalate*

~

~



Di-n-butyl phthalate*

~

~



1,2-Dichlorobenzene *

~

~

~

Diethyl phthalate*

~

~



Isophorone*







Napthalene*

~

~



Phenol*

~

~

~

* Identified during Remedial Design

4

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Response Actions

EPA issued a Record of Decision (ROD) on September 25, 1987, selecting a combined remedy for the
Site and the adjacent NSL Site (EPA 1987). The 1987 ROD provided for a low-permeability cover
system over the contaminated areas and a groundwater extraction and treatment system. The combined
remedial action objectives (RAOs) for the Site and the NSL from the 1987 ROD are as follows (EPA
1987):

•	Soils and Landfill Contents: Minimize risk to public health and environment from direct contact,
inhalation or ingestion of NSL landfill contents, contaminated surface or subsurface soils on
ECC and NSL, leachate soils and sediment in the old creek beds of Findley Creek.

•	Groundwater and Leachate: Minimize current and possible future risk to public health from
direct consumption of contaminated groundwater by nearby users. Manage migration of
contaminated groundwater and leachate to the unnamed ditch and Finley Creek so public health
and the environment are adequately protected from surface water and sediment contamination
and ingestion of contaminated aquatic life.

•	Surface Water and Sediment: Minimize and mitigate the threat to the environment and public
health from direct contact, inhalation, and ingestion of contaminants in the surface water and
sediment resulting from future release of hazardous substances from landfill leachate and
groundwater discharge.

Based on a treatability study performed by the PRPs, EPA, and IDEM, it was later determined that
actively treating the contaminant source at the Site would be feasible and preferable to only containing
these materials as provided for in the 1987 ROD. Therefore, EPA issued an Amended ROD in June
1991, establishing separate, complementary remedial approaches for the ECC (EPA 1991) and NSL
Sites.

The updated RAOs from the 1991 Amended ROD are as follows:

•	preventing direct contact, inhalation, and ingestion of contaminated soils, landfill contents,
groundwater, leachate, and sediment;

•	limit infiltration;

•	controlling migration of contaminants to groundwater, surface water and sediments; and

•	removing and destroying volatile organic compounds (VOCs) and selected base neutral/acid
organics from the soils through soil vapor extraction (SVE).

As amended, the 1987 and 1991 RODs for the Site required the following remedies:

•	Access Restrictions: Placement of deed restrictions on the landfill property and the ECC site to
prevent future development of the land and to prohibit use of groundwater or the installation of
wells onsite; thereby protecting against direct contact with contaminated soil and groundwater or
further migration that could result from site excavation and development. Access to the site to be
controlled by completing the fencing around the site perimeter and posting signs.

•	SVE: Construction of a system utilizing injection and extraction trenches to vaporize and extract
VOCs and phenols from contaminated soils. These contaminants would be captured and

5

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removed utilizing granular activated carbon. The goal of the SVE system was to clean the soil
contamination source areas to levels that would assure long-term protection of groundwater and
surface water.

• Resource Conservation and Recovery Act (RCRA) Compliant Cap and Surface Controls:
Construction of a multi-layered cap over the entire Site. The cap would comply with RCRA
Subtitle C performance-based standards. (The presence of the cap would also improve the
efficiency of the SVE system by reducing the amount of air and vapor that could escape from
that system.) The 1987 ROD also included the removal of contaminated sediments, which is then
presumed to be put under this cap. Surface controls included rerouting of the unnamed ditch west
of the Site to keep surface waters further away from contaminated soil areas, and demolition and
disposal of on-site buildings.

• Contingent Groundwater Treatment: Groundwater collection and treatment would be required if
SVE did not achieve soil cleanup standards within a five-year operation period, or if at that time
surface water or groundwater samples still showed unacceptable levels of contamination.
Collected groundwater would be treated to meet effluent standards before discharge into Finley
Creek. Groundwater collection and treatment would continue until cleanup standards were met.

• Monitoring of leachate, groundwater, surface water, and sediments.

The objectives of the cap are to prevent direct contact with contaminated soils, reduce infiltration, and
enhance the SVE system. The objective of the SVE activity is to remove and destroy VOCs and selected
base neutral/acid organics from the soils.

The groundwater Remediation Goals (RGs) in the 1991 ROD Amendment were listed as site-specific
Acceptable Stream Concentrations (ASCs) that were derived from Maximum Contaminant Levels
(MCLs), MCL proposed goals, or lifetime drinking water health advisories, Acceptable Subsurface
Water Concentrations, and Acceptable Soil Concentrations (EPA, 1991). The RGs have been revised
through coordination with EPA, IDEM, and the PRPs throughout the project history. The RGs were last
revised in 2010. The current groundwater ASCs are shown in Table 6 within the Data Review Section.

EPA issued an Explanation of Significant Differences (ESD) in July 1997 to excavate and remove soils
in the southern portion of the Site that were not being addressed through the SVE system (EPA, 1997).
The 1997 ESD also revised several Site cleanup criteria, the remediation boundary and cap
requirements.

Due to the limited success of the SVE system to treat groundwater and meet cleanup standards, EPA
issued another ESD in September 2006, which revised the remedy to include a groundwater collection
trench with a permeable reactive gate system (PRGS) to passively collect and treat groundwater before it
left the Site. The new SVE trenches were connected to the existing SVE system and operated using all
of the basic operations of the existing SVE system. The purpose of these measures is to capture and treat
through the SVE system the more mobile contaminants in the vicinity of the SVE trenches and moisture
in sand seams that enter the SVE trenches (EPA, 2006).

A summary and comparison of the Remedial Components for ECC taken from the 2006 ESD is included
as Table 2. It describes the changes to the ROD and the remedy components that have been documented
with a decision document. Additional revisions to the remedy have been implemented but have not been

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documented within a decision document. Please refer to the Status of Implementation for additional
changes to the remedy.

Table 2: ECC Site Remec

ial Components Comparison (EPA, 2006)

1987 ROD

1991 ROD Amendment

1997 ESD

2006 ESD

Northside Sanitary Landfill
and ECC Sites' combined
remedy

Separate but compatible
remedies for ECC and LSF

Leachate collection and
onsite treatment (expect to
continue in excess of 30
years)

N/A

Combined cover over both
Sites

N/A

Access restrictions

ECC SITE REMEDY

Soil Vapor Extraction
(SVE) using SVE trenches
with potential to remediate
the site in five years or less.

SVE remedy is modified to
allow use of SVE wells in
addition to SVE trenches
and to provide that materials
from southern part of Site
would be excavated and
moved to the central and
northern parts of the Site for
SVE treatment. The
excavation in the southern
portion of Site is to be filled
with clean fill. Area of Site
also expanded slightly on
the western side.

SVE trenches will be used
to augment the Additional
Work described below.

Onsite SVE compliance
criteria established for
subsurface water, surface
water, and soils. If onsite
cleanup levels are achieved,
supplemental offsite and
surface water sampling
provided for.

Additional chemicals added
to onsite SVE compliance
criteria and several site
cleanup criteria recalculated
using site-specific organic
carbon fraction rather than
literature values.

N/A

RCRA compliant cap over
the Site

Composition of the RCRA
cap on the northern and
central parts of the Site
modified, final cap to be
extended over the southern
area to the extent that area
does not meet RCRA clean
closure requirements.

RCRA cover determined not
to be needed on the southern
portion of the Site.

ECC Additional Work

Installation of a subsurface
water collection trench on
the eastern, southern, and
part of western sides of the
Site including high density
polyethylene (HDPE) liner
to contain contaminated
groundwater.

No Change

Additional SVE trenches
will be installed along the
approximate alignment of
the former subsurface water
collection trench. After
operation of the SVE system
component of the modified
Additional Work is
completed (expected to be

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approximately 1-2 years
including an active
monitoring phase) any
residual water in the
trenches will be contained
by a barrier wall (replacing
the HDPE liner). Any water
that is not contained will be
discharged through an
installed reactive gate where
it will be treated.

Collection of subsurface
water in the trench system
(expected to continue in
excess of 30 years) and on
or offsite treatment of
collected water.

No Change

Collection of subsurface
water in the SVE system
during operation of the
system and on or offsite
treatment of collected water.
After operation of the SVE
system, onsite treatment
through the reactive gate (to
be evaluated as part of five-
year review)

Monitoring of offsite wells
and surface water

No Change

Monitoring of discharge
from the reactive gate
added.

Site may be evaluated for
potential commercial or
industrial (not residential)
reuse after 2 to 3 years
provided reuse is protective
of the groundwater remedy
and the environment.

Appendix F includes the full list of the RGs for all media from the 1991 ROD Amendment, as well as
the current RGs.

The 1997 ESD and 2006 ESD did not revise the RAOs from the 1991 ROD Amendment. The Remedial
Actions and RGs for the Site have been revised multiple times following the 2006 ESD, and the RAOs
may no longer accurately reflect the objectives of the current remedy. A revised decision document
should be completed.

Status of Implementation

EPA and IDEM have jointly overseen cleanup activities at the Site under authority of CERCLA. EPA
and IDEM entered into a Consent Decree with certain PRPs who agreed to perform the final remedy for
the Site. The Consent Decree was approved by the U.S. District Court for the Southern District of
Indiana on September 10, 1991. The Consent Decree requires those PRPs to implement the remedy
selected by EPA (with IDEM's concurrence) in the June 7, 1991 ROD Amendment.

The PRPs have, under EPA and IDEM supervision:

(1) obtained the necessary access agreements in July 1993, with the Site owners, to permit
cleanup of contaminated areas and support activities on adjacent property;

(2) completed Site preparation work, including an upgrade of Site fencing, removal of Site
structures and debris, decontamination and disposal of tanks, construction of pads for future
decontamination and storage activities, Site grading and construction of drainage channels;

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(3) secured, inventoried, analyzed and removed drums of contaminated material that had

accumulated on-site during previous investigations and response activities; and

(4) designed and implemented the Site remedy.

During the course of the remedial design investigations, the PRPs identified nine organic compounds in
Site groundwater that had not been identified at levels of concern in the Remedial Investigation (and
thus did not have cleanup standards in the ROD). The parties discussed and agreed to a mechanism for
establishing appropriate cleanup standards for certain portion of these additional compounds and made
minor adjustments to other cleanup standards based on additional site-specific information. As stated
earlier, the ASCs were last revised in 2010.

The PRPs also proposed to excavate soils at the southern end of the Site when they determined that the
high-water table in that area would likely hamper the effectiveness of SVE in that area. EPA and IDEM
agreed with that proposal as part of the remedy, as reflected in the 1997 ESD. The concrete pad
overlying this area was crushed and excavated with the underlying soil. The excavated soils and crushed
concrete were moved to the northern area of the Site and covered along with the other material to be
treated using SVE. The remedy was also modified in the 1997 ESD so that only an interim cap would be
constructed prior to operating the SVE system, with a full RCRA cap to be constructed only after SVE
was complete. The final cap has now been constructed but does not extend over the excavated area at the
southern end of the Site. This cover consisted of a minimum of 3 feet of compacted native soil, a
geomembrane with low permeability, and 1 foot of topsoil to support vegetation. The 2006 ESD
determined that the southern portion of the Site did not need a cap; however, as further data was
collected, the effects of precipitation became better understood and EPA determined that the cap needed
to be extended over the southern portion of the Site after all. An effort to extend the cap over the
excavated area is currently planned to be completed in 2024 and should be reflected in a forthcoming
Memo to the Site File, ESD or ROD Amendment.

The PRPs ceased the SVE operations in 2001, when it was determined that the system would not
achieve the ASCs for groundwater. This failure to meet the ASCs triggered the 1991 Amended ROD
and the 1991 Consent Decree requirement for implementation of the contingent groundwater collection
and treatment remedy. The 2006 ESD reflected a negotiated refinement to that Additional Work. SVE
trenches were installed along the same general alignment along two sides of the capped area. The SVE
trenches were used to try to capture additional mobile contaminants in the trench area. The trench
system also included a Thin Barrier Curtain Wall (TBCW) and a PRGS to further contain and control
any contaminated groundwater and surface water.

In 2012, the PRPs discontinued operation of the active SVE system (EPA 2013), but the trench system
continues to passively capture some shallow water, which is treated as necessary and discharged. Due to
periodically high-water volumes and questions concerning the efficiency of long-term containment, the
existing remedial components are under further review, as described in more detail below. This review
may lead to further refinements of the remedial action.

In 2013-2014, contractors of the PRPs, Ramboll Environ and Geosyntec, installed piezometers and
conducted test trenching to identify water collection and transmission zones. In 2015, the effectiveness
of the collection system was evaluated. In 2016 a Supplemental Water Contribution Assessment Report
Revision 2 was prepared, a comprehensive data review was completed, and the Conceptual Site Model
(CSM) was reviewed and updated.

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From 2017 through 2022, additional remedial actions have been identified and evaluated, including the
installation of new extraction wells south of the TBCW downgradient of the Site and the resumption of
active pumping from multiple groundwater collection trenches. These additional remedial action
alternatives will be implemented as appropriate after EPA evaluates and selects remedial alternatives in
a decision document. The design is intended to control and manage surface water and groundwater at the
Site and when implemented to ensure updated RAOs are met.

Institutional Controls

Institutional Controls (ICs) are non-engineered instruments, such as administrative and/or legal controls
that help minimize the potential for exposure to contamination and protect the integrity of the remedy.
Compliance with ICs is required to assure long-term protectiveness for those areas that do not allow for
UU/UE.

The remedy embodied in the 1991 Amended ROD and 1991 Amended Consent Decree, requires
placement of deed restrictions on the Site property to prevent future development of the land and to
prohibit the use of groundwater or the installation of wells. While those obligations exist, the Site cannot
be disturbed or developed. The PRPs are obliged to maintain the cap and the remedy elements under the
1991 Amended Consent Decree.

As required by the Consent Decree, the PRPs entered an access agreement with the Bankert family, who
own the Site property through a trust and live adjacent to and southwest of the Site. In addition to
providing unrestricted access for Site work, the Bankert family also agreed "that they will not construct
or place any improvements within the Remedial Action Boundary or Support Zone Area Boundary ...
unless and until the Court enters an order in USA v. Enviro-Chem determining that [the PRPs] have no
further obligations.... " These areas include all the relevant portions of the Site and are identified on the
ICs map included in Appendix E. The objective of the access agreement is to ensure access by the PRPs,
project personnel, EPA, and IDEM and prevent any use of the Site property and any disturbance of the
cap or the remedy elements. The agreement was recorded with the Boone County Recorder's office on
July 16, 1993, and states that these covenants run with the land (See Table 3 below).

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Table 3: Summary of Planned and/or Implemented ICs.

Media, engineered
controls, and areas
llial do not support
11/1T. based on
current conditions

ICs
Needed

ICs ( ailed
lor in the
Decision
Documents

Impacted
Parcel(s)

Objective

Title of l(
Instrument
Implemented
and Dale (or
pl nil nod)

Soil and sediment
containment area on
Envirochem Property -
Cap and Other Remedy
Components

Yes

See

Appendix
E

Prohibit
interference
with remedy
components;
Prohibit use of
property; Prohibit
construction or
placement of any
improvements

Restrictive
covenant in
access agreement
that states it runs
with the land
recorded at Boone
County

Recorder's Office
on July 16, 1993.

Groundwater impacted
by contamination at or
from the Envirochem
property which exceeds
cleanup standards

Yes

See

Appendix
E

Prohibit
installation
of wells; Prohibit
use of

groundwater

Restrictive
covenant in
access agreement
that states it runs
with the land
recorded at Boone
County

Recorder's Office
on July 16, 1993.

A map showing the area to which the ICs apply is shown on Figure 3 in Appendix E.

Status of Access Restrictions and ICs: ICs in the form of a restrictive covenant within an access
agreement are in place. Fencing and warning signs are present and are included in the Site inspection
photographs in Appendix D.

Current Compliance: Based on the 7/29/2022 Site inspection and discussions with the PRPs'
consultants, EPA is not aware of Site or media uses which are inconsistent with the stated objectives to
be achieved by the ICs. No Site uses which are inconsistent with the implemented ICs or IC objectives
have been noted during the Site inspection.

IC Follow-up Actions Needed: Following the implementation of the planned extraction wells, EPA
will reevaluate groundwater contaminant migration data to determine the need to expand ICs. EPA will
ensure any additional ICs needed are implemented. In addition, the O&M Plan will be updated to
include procedures for long-term stewardship of ICs.

Long-Term Stewardship: The PRPs are providing for long-term stewardship of remedy components,
including ICs. Long-term stewardship involves ensuring effective procedures are in place to properly
maintain and monitor the Site. Long-term stewardship is necessary to ensure that the ICs are maintained,
monitored, and enforced. Compliance with ICs is necessary to ensure that the remedy continues to
function as intended and that it remains protective. Thus, long-term stewardship is necessary to ensure
the continued protectiveness of the remedy. Revisions to the remedy are ongoing and a revised O&M
Plan will be drafted once the ongoing revisions to the remedial actions are completed. The revised O&M

-------
Plan will include procedures to ensure long-term stewardship of ICs, including regular inspections of the
engineering controls and access controls at the Site, reviews of the ICs, and annual ICs reports with
results of the inspection and review, and certification to EPA that ICs remain in-place and are effective.

Systems Operations/Operation & Maintenance

Since the 2018 FYR, the PRPs have primarily operated the combined SVE/groundwater collection
system as a passive collection system. The SVE component is not active, and only groundwater and
precipitation that naturally flows into the collection trenches are then collected and treated. In Spring
2022, an active pumping system was installed for Trench 6, which depresses the groundwater level
around Trench 6 to assist with hydraulic capture and enhances the removal of VOCs within the
groundwater. One or more additional active pumping systems are proposed and are expected to be
installed in early 2023. Revisions to the remedy are ongoing and a revised O&M Plan will need to be
drafted after the remedy revisions are complete.

Since the last FYR, the PRPs have maintained the cover at the Site with periodic mowing and
inspections for erosion and settlement. They have repaired the perimeter fencing and cleared excess
vegetation from the inside of the fence to allow for better inspection and maintenance. They have also
operated and maintained the groundwater treatment system used to treat the passively collected
groundwater. Please see the Site Inspection section of this FYR for further details on the O&M of
remedy components.

III. PROGRESS SINCE THE LAST REVIEW

This section includes the protectiveness determinations and statements from the last FYR as well as the
recommendations from the last FYR and the current status of those recommendations.

Table 4: Protectiveness Determinations/Statements from the 2018 FYR

ou#

Protectiveness
Determination

Protectiveness Statement

01 and
Sitewide

Protectiveness
Deferred

A protectiveness determination of the remedy at the
Envirochem Corp. Superfund site cannot be made at this
time until further information is obtained. Further
information will be obtained by taking the following actions:

• Conduct vapor intrusion investigation;

• Expand monitoring network and conduct groundwater
monitoring to determine extent of groundwater plume and its
quality;

• Evaluate the need for ICs to cover the extent of the
contaminated groundwater plume offsite and implement if
needed;

• Update groundwater monitoring plan to include 1,4-
dioxane and implement; and

• Add residential wells monitoring to groundwater
monitoring plan and sample residential wells.

It is expected that these actions will take approximately 4.5
years to complete, at which time a protectiveness
determination should be made.

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Table 5: Status of Recommendations from the 2018 FYR

Issue

Recommendations

Current
Status

Current Implementation Status
Description

Completion

Date (if
applicable)

Remedy failure.

Complete design,
selection, and
construction of
additional remedial
measures

Addressed
in Next
FYR

Additional remedial measures are in
the process of being evaluated and
implemented, including a cap
extension, additional extraction wells
to the south of the Site, and additional
active pumping systems within the
groundwater collection trenches.



Additional ICs
may be needed.

Evaluate the need for
ICs to cover the extent
of the contaminated
groundwater plume
offsite and implement if
needed.

Addressed
in Next
FYR

The extent of groundwater
contamination to the southwest will
be reassessed after installation and
operation of extraction wells EW-1
and EW-2. After this action, the need
for additional ICs for the
contaminated groundwater plume will
be evaluated.



Potential vapor

intrusion

pathway.

Conduct vapor
intrusion investigation

Addressed
in Next
FYR

Soil gas sampling for the nearby
residence has been completed during
summer months. No detections have
been noted at wells adjacent to
residence, but additional seasonal data
is needed to fully evaluate pathway.



Contaminated
groundwater
plume is not
under control
and is
migrating
offsite.

Expand monitoring
network and conduct
groundwater
monitoring to
determine extent of
groundwater plume and
its quality

Completed

Supplemental sampling of area
downgradient of site completed in
2020, and additional wells installed
(Geosyntec, 2020). Data show that
contaminated groundwater has
migrated offsite, but has not reached
residential receptors. See the Data
Review section for more information.

12/09/2020

New

contaminant of
concern found,
1,4-dioxane.

Update groundwater
monitoring plan to
include 1,4-dioxane and
implement

Addressed
in Next
FYR

Monitoring wells S-5, S-6, and MW-
14 were sampled and analyzed for
1,4-dioxane in June 2020.
Concentrations in a single well (MW-
14) were above IDEM guidelines.
Groundwater monitoring plan has not
been updated to include continued
sampling of 1,4-dioxane. Further
evaluation of 1,4-dioxane is required.
See Data Review Section for more
information.



Residential wells
in the vicinity of
the Site may be
impacted by the
migration of the
contaminated
groundwater
plume.

Add residential wells
monitoring to
groundwater
monitoring plan and
sample residential wells

Completed

One residential well was found to be
within the possible impact area of the
ECC groundwater plume.
Groundwater monitoring plan updated
and the residential well and
residential sump were sampled
multiple times during semiannual
sampling events, with no detections

2/18/2021

13

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of COCs. No other residential wells
were identified within the vicinity of
the Site.

Lack of long-
term

stewardship of
ICs.

Update O&M Plan to
include long-term
stewardship procedures
for ICs

Ongoing

O&M Plan will be updated and
revised once remedial action revisions
are completed.

OTHER FINDINGS from the 2018 FYR

In addition, the 2018 FYR identified the following recommendations that may improve management of
O&M, but do not affect current nor future protectiveness. A status update is provided for each below.

• A comprehensive evaluation of monitoring objectives and the means to satisfy them should be
completed, followed by a document that establishes the program and provides a means for modifying the
program as conditions change over time. The plan should provide clear justification for what
locations/depths require sampling and water level monitoring and how that data will meet the program's
objectives. EPA's data quality objectives ("DQOs") system (reference EPA/240/B-06/001) provides the
appropriate framework for implementing this recommendation. The plan should consider the installation
of additional monitoring wells in both the till and sand units. Current coverage is inadequate,
particularly in the till unit, the central area of the Site, and along the west boundary.

Status update: Additional monitoring wells along the western and southwestern boundary have been
installed based on individual investigation results, but no comprehensive evaluation of the Site has been
completed. After the current remedy activities are completed, a comprehensive evaluation should be
conducted to ensure additional measures are not required.

• The onsite O&M Manual for the wastewater remediation system is dated 1999, and the O&M Manual
for the air stripper is dated 2011. Current O&M manuals, process flow diagrams, and process and
instrumentation diagrams have not been developed. The treatment system has undergone several
modifications, additions, and reconfigurations since its initial construction. Maintaining up-to-date
documentation and plans for treatment systems is a best practice and should be performed. Treatment
system logs should also be maintained on site.

Status update: The current treatment system at ECC is scheduled to be replaced in 2023. The design of
the new system will be approved by EPA and IDEM, and the O&M Manual will be updated for the new
system based on updated best practices.

• Components of the onsite groundwater treatment system are not properly labeled. Labeling is
warranted to identify the components and the tap locations for systems operations. Also, the National
Pollutant Discharge Elimination System (NPDES) discharge permit is not properly labeled, meaning it is
not physically displayed clearly onsite.

Status update: Treatment influent and effluent lines are now labeled with flow direction, but labels are
still not present on all groundwater treatment system components. Unused and unmaintained
components of past treatment systems are also co-mingled with the active treatment system and are not
immediately distinguishable as such. The Third Site treatment system has been removed from the ECC
treatment facility. As the new ECC treatment system is installed, it is recommended that unused
equipment be removed and relocated, the NPDES permit be posted clearly, and the system be labeled to
show the treatment process flow.

-------
• A cap inspection and performance monitoring program should be established to ensure the cap
maintains its function over time. An accompanying monitoring plan should be developed to describe the
procedures used to maintain and inspect the cap and remedy for any deficiencies that develop.

Status update: Cap inspection is included in O&M, but a performance monitoring program will need to
be developed after the cap is extended.

• Only one perimeter warning sign was observed at the subject property entrance. No other warning
signs were present. Additional warning signs should be posted along the length of the perimeter fence.
Warning signs should prohibit entry to the property, the installation of wells, and the use of
groundwater.

Status update: Additional signs have been installed on the perimeter fence identifying the site (Photo
30 in Appendix D). Signs do not prohibit entry or notify trespassers of the prohibitions on well
installation or groundwater use, and updated signs should be installed.

• Vegetative growth is present along the exterior of the perimeter fence. The integrity of this access
control may be impacted by the vegetative growth. In addition, vegetative growth is present in the
perimeter drainage ditch and associated culverts. The vegetative growth might impact storm water
control and/or allow surface water infiltration points. Additional vegetative control should be conducted.
Status update: Vegetative growth within the geo-membrane-lined drainage channel (Photos 6 and 7 in
Appendix D) is controlled through O&M and was not present during the Site inspection. No
uncontrolled vegetative growth within the fenced area was observed during the Site Inspection. Heavy
vegetation remains along the exterior of the eastern perimeter fence, along the Unnamed Ditch (Photos
19 and 20 in Appendix D). This vegetation does not impact the effectiveness of the surface water
drainage system or the ability to collect surface water samples but could limit future accessibility if not
properly maintained. The addition of routine vegetative clearance within the fenced area of the
Unnamed Ditch should be investigated and implemented, if practical.

IV. FIVE-YEAR REVIEW PROCESS

Community Notification, Involvement & Site Interviews

A public notice was made available by a newspaper posting in the Lebanon Reporter, titled, "USEPA
Begins Review of EnviroChem Corp. Superfund Site"), on 3/29/2022, stating that there was a FYR and
inviting the public to submit any comments to EPA. A similar announcement was published on the Site
web page along with the Site team's contact information. No comments were received as of the
preparation of this FYR. EPA determined that it would not conduct formal interviews as part of this
FYR given its other efforts described herein. The results of the review and the report will be made
available at the Site information repository located at Hussey-Mayfield Memorial Public Library, 250 N.
Fifth Street, Zionsville, IN 46077-0840.

Data Review

Table 6 shows the current Chemicals of Concern for ECC and the ASCs for groundwater that may
discharge to surface water. The current values replace the values included in the 1991 ROD.

Table 6: Current Groundwater to Surface Water ASCs for Chemicals of Concern

Chemical

ASC micrograms per liter (jig/L)

1,2-Dichloroethene (1,2-DCE)

320

Ethylbenzene

3,280

-------
Methylene Chloride

15.7

Tetrachloroethylene (PCE)

8.85

Toluene

3,400

1,1,1-Trichloroethane (TCA)

5,280

1,1,2-TCA

41.8

Trichloroethylene (TCE)

80.7

Vinyl Chloride

525

These are the Chemicals of Concern that are included in the current monitoring program. Other COCs
had been identified in the 1991 ROD but are no longer included in analyses. Additionally, there were 3
new COCs added during remedial design. See Table 1 for a full list of COCs. The list of current COCs
and associated ASCs should be included in an updated decision document. The current ASCs, which are
located in Table 6 above, were modified in a 2010 letter (EPA 2010).

Groundwater:

During the semi-annual sampling events, samples have been collected from within each of the seven
SVE collection trenches (Trench 1 through Trench 7) as well as the collection manhole, from within
paired piezometers straddling the TBCW (PT-1 and PT-2, PT-3, and PT-4), and from five sand/gravel
monitoring wells (S-l, S-4B, S-5, S-6, and MW-14). Additionally, groundwater samples were collected
from the basement sump and residential supply well of the nearby property (currently the only nearby
residential well). The results of the most recent sampling event in June 2022 are summarized in this
section. Sampling locations are shown in Figure 5 of Appendix E. Additional sampling data can be
found in Appendix B.

•	1,2-DCE concentrations above the ASCs were identified at Trench 1, Trench 2, Trench 3,
Trench 6, and within the manhole that collects groundwater from the trenches before being
pumped to the treatment system (9,100 micrograms per liter (|ig/L), 4,400 |ig/L, 730 |ig/L,
and 970 |ig/L respectively). TCE concentrations were exceeded at Trench 6 and the
collection manhole (120 |ig/L and 260 |ig/L). Vinyl chloride concentrations were exceeded at
Trench 1 and Trench 2 (3,200 |ig/L and 1,700 |ig/L).

•	1,2-DCE and vinyl chloride were found within PT-1 (2.7 |ig/L and 1.5 |ig/L) and PT-3 (3.0
|ig/L and 1.6 |ig/L). These concentrations were below the ASCs and were not exceeded
during the previous five years. Both piezometers with concentrations above the LOD were
located outside of the TBCW.

•	1,2-DCE and vinyl chloride were found within S-6 (27 |ig/L and 2.8 |ig/L) and MW-14 (24
|ig/L and 21 |ig/L). These concentrations were below the ASCs and were not exceeded
during the previous five years.

•	There have been no VOC detections in the residential supply groundwater well or within the
basement sump.

Monitoring wells S-5, S-6, and MW-14 were sampled for 1,4-dioxane in June 2020. Concentrations of
1,4-dioxane within the wells were 0.11 |ig/L, 0.67 |ig/L, and 19 |ig/L respectively. The nearby property
sump and supply well were sampled for 1,4-dioxane in 2021, and no detections were identified. There is
no site-specific ASC for 1,4-dioxane. The EPA Tap Water RSL for 1,4-dioxane is 0.46 |ig/L and the
IDEM drinking water guideline for 1,4-dioxane is 7.7 |ig/L.

16

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A Mann-Kendall trend analysis was conducted for the COCs that were exceeded within the SVE
trenches and are included with the laboratory data in Appendix B. Only trenches that exhibited the
exceedances were included in the analysis. Results of the Mann-Kendall trend analysis show that PCE
and TCE concentrations within the system are decreasing, but there is no overall trend for 1,2-DCE or
vinyl chloride. The continued concentrations give evidence that precipitation is infiltrating around the
engineered cap to the leachate and supporting contaminant migration into the passive collection
trenches.

In December 2020, a supplemental sampling report was completed to investigate offsite migration of
contaminants within the upper till and upper sand and gravel unit in the area to the south of the Site
downgradient of Trench 6. Figure 5 of Appendix E shows the location of the investigation. Data showed
that the distribution of VOCs in the upper till unit is confined to the area south of the TBCW
downgradient of PS-5 (at S-6 and S-8), and the VOC concentrations are below the ASCs. Within the
upper sand and gravel unit, a plume of chlorinated solvents is migrating downgradient of the southern
end of the ECC Site in a south/southeast direction (Geosyntec, 2020).

Based on a survey of nearby residential groundwater wells conducted in November 2022, only one
residential well is within the potential impacted area of the ECC groundwater plume as determined in
the 2020 Supplemental Sampling Report (Geosyntec 2020). Three rounds of groundwater sampling of
the basement sump at the that residence were conducted in 2020 and 2021. All VOC concentrations
were below detection levels. The basement sump sampling was temporarily discontinued in 2022 due to
a request from the property owners but will resume in 2023. Groundwater sampling of the sump of the
residential well used at the residence is now included in routine sampling events. Concentrations of
VOCs have been below detection limits within the well, and monitoring will continue to ensure
protectiveness.

Surface Water:

Surface water samples are collected at three locations within the Unnamed Ditch during the semiannual
sampling events and analyzed for the COCs listed in Table 6. All COC concentrations were below
detection limits during this FYR period.

Vapor Intrusion Investigation:

Due to the proximity of the groundwater plume to the occupied-nearby property (the location of the
single residential well), a Vapor Intrusion investigation was recommended in the previous FYR and was
initiated in 2020. Soil gas samples were collected in June 2020, August 2020, and September 2021 in the
vicinity of the nearby property and compared to the EPA and IDEM Residential Soil Gas Screening
Criteria (Ramble 2021), shown in Table 7. Because of saturated conditions during the June 2020 and
August 2020 sampling events, only one location was able to be sampled per event; SG-07S and SG-04S
respectively. See Figure 5 in Appendix E for sampling locations. While the soil gas near the ECC Land
Use Control (LUC) area showed exceedances in the concentrations of TCE (up to 35 micrograms per
cubic meter (|ig/m3), and vinyl chloride (up to 6.5 |ig/m3), samples collected from the area closest to the
residence were less than screening criteria for all analytes at both the sub-slab and basement depths. This
data supports that the vapor intrusion pathway is incomplete for the nearby residence. Although this data
was collected during the spring and summer seasons, this data is anticipated to be the same or greater
than the winter months. This assumption is based on the following rationale: 1) colder groundwater
temperatures are expected during winter and fall, 2) the distance of the residence to the well, and 3) the
higher volatilization of VOCs during the warmer seasons. The screening criteria are conservative and

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likely overestimate the attenuation factor at the Site based on the tight soil formation and the frequently
saturated soil conditions. To verify, a winter sampling event was conducted in December 2022, but no
soil gas data is available for the fall and winter season as of the writing of this report. The analysis of all
soil gas data will be performed and incorporated into the next FYR.

Table 7. Soil gas screening criteria in micrograms per cubic meter (|ig/m3)

Criteria

PCE

TCE

1,1,1-
TCA

1,1,2-
TCA

Methylene
Chloride

Toluene

Ethylbenzene

EPA Soil Gas
Screening
Level(1)

360

15.9

5.6

173,000

5.8

20,800

173,000

37.3

IDEM Soil
Gas Screening
Level(2)

420

52,000

2.1

6,300

52,000

110

Table 7 Notes:

(1)USEPA soil gas screening levels from the Regional Screening Levels Users Guide (2020) based on 10-6 target risk, hazard quotient = 1 and attenuation factor of 0.03
(USEPA 2015)

(2) IDEM soil gas screening level based on a default shallow soil gas attenuation factor of 0.1 (IDEM 2022)

Based on the data review of the last five years, the current remedy is not achieving the RAOs (from the
1991 ROD Amendment) at ECC. These RAOs do not coincide with the current remedy and need to be
updated. There is not a downward trend of all contaminants to support reaching groundwater RGs, and
contaminants continue to migrate from the leachate into the groundwater and migrate offsite.

Site Inspection

The inspection of the Site was conducted on 7/29/2022. In attendance were Matthew Ohl, EPA's RPM
for the Site; Katie Neighbors, IDEM; and William Clabaugh, USACE; Andrew Gremos of Ramboll
Environ, contractor for the Trustees that represent the PRPs; and Greg Scarpone of the subcontractor
IWM Consulting Group, LLC. The purpose of the inspection was to review the cap, cover, fencing,
buildings, monitoring wells, and all components of the remedy as required in the O&M Plan.

Attendees inspected the perimeter fence and associated signage, drainage, and vegetative cover of the
engineered cap, the treatment system and associated buildings, and piezometers and monitoring wells.
No issues were identified during the Site Inspection through visual inspection. The ICs appeared to be in
place and effective as there was no indication of trespassers, non-authorized excavation, or groundwater
use. See Appendix C for the Site Inspection Checklist and Appendix D for the photolog of the visit.

V. TECHNICAL ASSESSMENT

QUESTION A: Is the remedy functioning as intended by the decision documents?

No. The remedy is not functioning as intended by the decision documents. Data collected during this and
previous FYRs show that the soil cover and the groundwater collection system are not functioning as
intended and require additional remedial measures to meet cleanup levels and RAOs. As described in the
Status of Implementation section, the selection, design, and approval process for these additional
remedial measures are ongoing and an updated decision document is required. The following list
summarizes the status of the remedy:

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• The collection of the groundwater beneath the engineered cap through passive drainage using the
existing SVE trenches has shown to be insufficient to treat the entire contaminant mass. Active
pumping at Trench 6 has been implemented in Spring 2022, and additional measures are
ongoing.

• There is evidence of contaminant mass located outside of the TBCW on the south side of the Site
(Geosyntec, 2020). This contamination is outside of the current treatment area. Additional
measures to contain and capture this contaminant mass are planned to be implemented. Two
extraction wells will be installed to hydraulically capture and treat the contamination. Additional
monitoring will be needed once the extraction wells are in operation to ensure that the plume is
fully captured and not migrating. An issue and recommendation have been included in this FYR
to address this issue. Residential groundwater sampling for the nearby residential well is ongoing
and results have not shown contamination.

• Data collected during this FYR period indicates that the current engineered cap is not preventing
precipitation from infiltrating into the groundwater within the Land Use Control area. A cap
extension with drainage improvements is being designed and implemented that will prevent
contaminant leaching into groundwater and will divert storm runoff and limit clean precipitation
from entering the SVE trenches. By accomplishing these objectives, the cap extension will
improve the efficiency of the system and meet RAOs.

The ICs in place are functioning as intended to prevent exposures in the areas the ICs currently address.
If the data collected after the installation of the two extraction wells shows incomplete capture of the
plume, additional ICs may need to be implemented over an expanded plume area. In addition, the O&M
Plan will be updated to include procedures for long-term stewardship of ICs.

QUESTION B: Are the exposure assumptions, toxicity data, cleanup levels, and remedial action
objectives (RAOs) used at the time of the remedy selection still valid?

Question B Summary:

No. The exposure assumptions, toxicity data, and cleanup levels are still valid; however, the RAOs have
not changed since the 1991 ROD Amendment and no longer reflect the current remedy. The RGs have
been modified as more details and information is collected. The recommendation to update and revise
the RAOs is included in this FYR. The changes to the RAOs, exposure assumptions, toxicity data, and
cleanup levels are discussed below.

Changes in Cleanup Levels and RAOs: As discussed in the 2018 FYR, the 1991 ROD Amendment,
which the PRPs have agreed to implement under the 1991 Amended Consent Decree, confirms that "As
remedial action progresses, these benchmark levels must be reviewed because the underlying standards
and criteria change over time as scientific knowledge increases." The ASCs used as acceptable levels for
groundwater that may discharge to surface water are found in the remedial design and are shown in
Table 6. These ASCs were revised in 2010 from the original values listed in the 1991 ROD amendment.
No revisions since 2010 have occurred and recommendations to address updating and documenting the
RAOs and RGs are included in this FYR. Although the ASCs have not been revised since 2010, there is
no current groundwater use, and all perimeter wells show non-detect. Therefore, any changes in the RGs
do not affect the remedy.

-------
Federal and state standards for surface water quality and protection of aquatic life have not changed
since the time of the ROD, as amended. The RGs are site-specific values and have not been revised
since 2010. Therefore, there have been no changes that would affect the remedy.

The 2018 FYR also recommended an evaluation on the emerging contaminant 1,4-dioxane. 1,4-Dioxane
was identified at MW-14 outside of the TBCW at concentrations that exceed IDEM guidelines. It is
unknown at this time if 1,4-dioxane is a potential COC, and further investigation is needed.

Changes in Toxicity and Other Contaminant Characteristics: The RGs are site-specific values and have
not changed since the 2018 FYR. Toxicity and other factors for some COCs have not changed
significantly since the 1987 ROD except for 1,1-DCA. EPA and IDEM agreed to add a minor change in
the cleanup standard for 1,1-DCA. The change in the 1,1-DCA cleanup standard was based on
information about the cancer potency of 1,1-DC A developed since the time of the 1991 ROD
Amendment. Since that time, a general scientific consensus has developed that concludes 1,1-DCA does
not pose the level of cancer risk previously believed. For more information see the Agency for Toxic
Substances and Disease Registry's toxicological profile for 1,1-DCA in Appendix G.

As a result, the risk calculation and cleanup standard for DCA were re-calculated to reflect this
information and have become less stringent. Toxicity factors for other COCs at the Site have not changed
in a way that could affect the protectiveness of the remedy. Other contaminant characteristics have not
changed in a way that could affect the remedy.

Changes in Risk Assessment Methods: Changes in risk assessment methodologies since the time of the
ROD do not significantly impact the protectiveness of the remedy.

Changes in Exposure Pathways: Land use or reasonably anticipated future land use on or near the Site
has not changed. Physical Site conditions or the understanding of these conditions have not changed in a
way that could affect the protectiveness of the remedy. The vapor intrusion pathway was not investigated
at the time of the ROD, and a vapor intrusion evaluation was recommended in the 2018 FYR. A vapor
intrusion investigation was initiated in 2020 and data collected during the spring/summer sampling event
support that there is no complete VI pathway. Seasonal soil gas data is required to fully evaluate the VI
pathway.

There are no changes in the physical conditions that would affect the protectiveness of the remedy.

Expected Progress Towards Meeting RAOs

• Concentrations within the collection trenches do not show a decreasing trend for all

contaminants, and obtainment of the RAOs is not expected to occur until an effective remedial
action has been implemented.

This FYR includes a recommendation to complete a new decision document to update the remedy,
RAOs, and RGs, and during that process the site-specific RGs should be reevaluated.

QUESTION C : Has any other information come to light that could call into question the protectiveness
of the remedy?

-------
No. There has been no additional information that has come to light that has called into question the
protectiveness of the remedy. There have been no impacts on the Site due to natural disasters or climate
change, and none are projected.

VI. ISSUES/RECOMMENDATIONS

Issues/Recommendations

Ol (s) without Issues/Recommendations Identified in the l-ive-Year Review:

None

Issues and Recommendations Identified in the l-ive-Year Review:

OU(s):

OUl/Sitewide

Issue Category: Remedy Performance

Issue: The contaminated groundwater plume has migrated outside
of the groundwater capture area south of the ECC site.

Recommendation: Extraction wells should be installed as planned
to capture the contaminant plume and additional monitoring should
be conducted to ensure that contamination is hydraulically
captured, and the contamination is not mobile.

Affect Current
Protectiveness

Affect Future
Protectiveness

Party
Responsible

Oversight
Party

Milestone Date

Yes

PRP

EPA

12/31/2023

OU(s):

OUl/Sitewide

Issue Category: Institutional Controls

Issue: Additional ICs may be required to address contaminant plume
downgradient of the Site past the TBWC.

Recommendation: After installation and operation of the planned
extraction wells and additional monitoring, an assessment should be
conducted on the need for additional ICs based on the revised plume
properties.

Affect Current
Protectiveness

Affect Future
Protectiveness

Party
Responsible

Oversight
Party

Milestone Date

Yes

PRP

EPA

12/31/2024

-------
OU(s):

OUl/Sitewide

Issue Category: Remedy Performance

Issue: ASCs and other components of the remedy have been revised
through memorandum or letter and further remedial measures will be
proposed to address groundwater contamination.

Recommendation: Implement a decision document reflecting updated
RAOs, remediation goals/cleanup levels, and changes to the remedy.

Affect Current
Protectiveness

Affect Future
Protectiveness

Party
Responsible

Oversight
Party

Milestone Date

No

Yes

EPA

EPA

12/31/2024



OU(s):

OUl/Sitewide

Issue Category: Operations and Maintenance

Issue: O&M Plan needs to be updated.

Recommendation: Complete an updated O&M Plan to include all
changes to the remedy.

Affect Current
Protectiveness

Affect Future
Protectiveness

Party
Responsible

Oversight
Party

Milestone Date

No

Yes

PRP

EPA

12/31/2024



OU(s):

OUl/Sitewide

Issue Category: Remedy Performance

Issue: Current remedies including the soil cap and groundwater
collection system are not functioning as intended to meet RAOs and
cleanup levels.

Recommendation: Complete selection, design, and construction of
additional remedial measures that will meet updated RAOs and
cleanup levels.

Affect Current
Protectiveness

Affect Future
Protectiveness

Party
Responsible

Oversight
Party

Milestone Date

No

Yes

PRP

EPA

12/31/2024



OU(s):

OUl/Sitewide

Issue Category: Monitoring

Issue: Potential Vapor Intrusion Pathway

22

-------


Recommendation: Continue Vapor Intrusion investigation by
collecting soil gas data during the winter months to obtain complete
seasonal data.

Affect Current
Protectiveness

Affect Future
Protectiveness

Party
Responsible

Oversight
Party

Milestone Date

No

Yes

PRP

EPA

7/31/2024

OU(s):

OUl/Sitewide

Issue Category: Monitoring

Issue: New Potential Contaminant of Concern found, 1,4-dioxane

Recommendation: Complete full evaluation of 1,4-dioxane as a
potential COC because concentrations were identified above screening
criteria. Nature and extent of 1,4-dioxane contamination needs to be
evaluated.

Affect Current
Protectiveness

Affect Future
Protectiveness

Party
Responsible

Oversight
Party

Milestone Date

No

Yes

PRP

EPA

7/31/2024

OU(s):

OUl/Sitewide

Issue Category: Operations and Maintenance

Issue: Lack of long-term stewardship of ICs.

Recommendation: Update O&M Plan to include long-term
stewardship procedures for ICs.

Affect Current
Protectiveness

Affect Future
Protectiveness

Party
Responsible

Oversight
Party

Milestone Date

No

Yes

PRP

EPA

12/31/2024

OTHER FINDINGS

In addition, the following are recommendations that were identified during the FYR and may improve
performance of the remedy, reduce costs, and improve management of O&M but do not affect current
nor future protectiveness of the remedy:

• It is recommended that the pump-and-treat system at ECC be updated, as the equipment onsite
has exceeded the recommended service life. Installation of a new system is tentatively scheduled
for 2024, and the schedule should be reviewed to see if installation can be completed earlier
during planned remedial measures.

23

-------
• A comprehensive evaluation of monitoring objectives and the means to satisfy them should be
completed, followed by a document that establishes a monitoring program/plan and provides a
means for modifying the program as conditions change over time. The plan should provide clear
justification for what locations/depths require sampling and water level monitoring and how that
data will meet the program's objectives. EPA's data quality objectives ("DQOs") system
(reference EPA/240/B-06/001) provides the appropriate framework for implementing this
recommendation. The plan should consider the installation of additional monitoring wells in both
the till and sand units. Current coverage is inadequate, particularly in the till unit, the central area
of the Site, and along the west boundary.

• The onsite O&M Manual for the wastewater remediation system is outdated, and the O&M
Manual for the air stripper is dated 2011. Current O&M manuals, process flow diagrams, and
process and instrumentation diagrams have not been developed. The treatment system has
undergone several modifications, additions, and reconfigurations since its initial construction.
Maintaining up-to-date documentation and plans for treatment systems is a best practice and
should be performed. Treatment system logs should also be maintained onsite.

• Some components of the onsite groundwater treatment system are not properly labeled. Labeling
is warranted to identify the components and the tap locations for systems operations for existing
lines and any future modifications to the system. Also, the NPDES discharge permit should be
properly posted. The Third Site treatment system has been removed from the ECC treatment
facility. As the new ECC treatment system is installed, it is recommended that unused equipment
be removed and relocated, and the system be labeled to show the treatment process flow.

• A cap performance monitoring program should be established to provide additional insurance
that the cap maintains its function over time. The performance monitoring program should be
added to the existing cap inspection plan.

• Heavy vegetation remains along the exterior of the eastern perimeter fence, along the Unnamed
Ditch and should be removed.

-------
VII. PROTECTIVENESS STATEMENT

OU1 and Sitewide Protectiveness Statement

Protectiveness Determination:

Short-term Protective

Protectiveness Statement:

The remedy at ECC currently protects human health and the environment. The cover prevents
exposure to contaminated soil within the ECC area, and ICs are in place and effective for areas
currently known to present unacceptable risks and prevent exposure to groundwater and
contaminated soil. Exposure pathways that could result in unacceptable risks are being
controlled. There is no current use of groundwater or surface water at ECC. The monitoring
program will identify any exceedances of RGs or other potential issues that could affect the
remedy before impacts fully occur. However, for the remedy to be protective in the long-term,
the following actions need to be taken to ensure future protectiveness:

- Additional remedy actions are required to meet RAOs and cleanup levels.

- Extraction wells need to be installed to capture the contaminant plume migrating offsite.

- The Vapor Intrusion investigation needs to be completed by collecting soil gas data during the
winter months.

-1,4-dioxane needs to be fully evaluated as a potential COC and included in the monitoring
program to determine the nature and extent of contamination.

-Changes to the current ASCs, RAOs, RGs, COCs, and the remedy need to be documented in a
decision document.

-The O&M Plan needs to be updated based on changes to the remedy and to include long-term

stewardship procedures for ICs.

-An evaluation of new ICs needs to be conducted.

VIII. NEXT REVIEW

The next FYR report for the Envirochem Corp. Superfund Site is required five years from the
completion date of this review.

-------
APPENDIX A - REFERENCE LIST

Geosyntec Consultants. 2020. "Enviro-Chem Superfund Site Supplemental Sampling Report".
December.

Geosyntec Consultants. 2016. "ECC Site CSM" Presentation. July.

IDEM. 2022. "Risk-based Closure Guide". July.

Ramboll Environ US Corporation. 2022. "June 2022 Surface and Subsurface Water Sampling Enviro-
Chem Superfund Site, Zionsville, Indiana EPA ID: IN084259951". September.

Ramboll Environ US Corporation. 2021. "Monthly Progress Report - September 2021 Environ-Chem
Superfund Site, Zionsville, Indiana". October.

Ramboll Environ US Corporation. 2016. "Supplemental Water Contribution Assessment Report,
Revision 2". January.

USEPA. 1991. "Superfund Record of Decision: Enviro-Chem (Northside Sanitary Landfill)
(Amendment), IN". June.

USEPA. 1987. "Superfund Record of Decision: Northside Sanitary Landfill / Environmental
Conservation and Chemical, IN". September

USEPA. 1997. "Explanation of Significant Difference: Enviro-Chem Superfund Site: Zionsville,
Indiana". July

USEPA. 2006. "Explanation of Significant Difference: EnviroChem Site: Zionsville, Indiana".
September

USEPA. 2010. "RE. Envirochem Site, Zionsville, Indiana. Consent Decree, Civil Action No. IP 83-
1419-C-M/S. Trench Water Levels and Proposed Acceptable Stream Criteria". 26 April

USEPA. 2013. "Fourth Five-Year Review Report for EnviroChem Corp Site. Zionsville. Boone County,
Indiana". April

USEPA. 2015. "OSWER Technical Guide for Assessing and Mitigating the Vapor Intrusion Pathway
From Subsurface Vapor Sources To Indoor Air Vapor Sources To Indoor Air". June

USEPA. 2018. "Fourth Five-Year Review Report for EnviroChem Corp. Superfund Site. Boone County,
Indiana". March

USEPA. 2022. "Regional Screening Level (RSL) Resident Tap Water Table (TR=lE-06, HQ=1)".
November

Consent Decree, United States of America vs. Environmental Conservation and Chemical Corporation,
Et Al. (Civil Action NO. 83-1419 C, Indianapolis, 1991).

26

-------
APPENDIX B

LABORATORY DATA

-------
Subsurface Water Monitoring Well Data ( micrograms per liter [|j.g/L])

Well

coc

ASC

Jun-18

Dec-18

Jun-19

Dec-19

Jun-20

Dec-20

Jun-21

Dec-21

Jun-22



1,2-DCE

320

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<1.0

<0.50



Ethylbenzene

3280

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



Methylene Chloride

15.7

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



PCE

8.85

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

ECC-SSW-S1

Toluene

3400

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



1,1,1-TCA

5280

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



1,1,2-TCA

41.8

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



TCE

80.7

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



Vinyl Chloride

525

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



1,2-DCE

320

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<1.0

<0.50



Ethylbenzene

3280

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



Methylene Chloride

15.7

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

ECC-SSW-
S4B

PCE

Toluene

8.85
3400

<0.50
<0.50

<0.50
<0.50

<0.50
<0.50

<0.50
<0.50

<0.50
<0.50

<0.50
<0.50

<0.50
<0.50

<0.50
<0.50

<0.50
<0.50

1,1,1-TCA

5280

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



1,1,2-TCA

41.8

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



TCE

80.7

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



Vinyl Chloride

525

0.5

0.56

<0.50

0.61

<0.50

0.76

0.59

<0.50

0.45



1,2-DCE

320

1.2

0.81

0.56

<0.50

<0.50

<0.50

0.49

<0.50

<0.50



Ethylbenzene

3280

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



Methylene Chloride

15.7

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



PCE

8.85

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

ECC-SSW-S5

Toluene

3400

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



1,1,1-TCA

5280

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



1,1,2-TCA

41.8

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



TCE

80.7

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



Vinyl Chloride

525

2.2

1.7

1.9

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

Notes:

Dichloroethene (DCE)
Tetrachloroethene (PCE)

Trichloroethane (TCA)
Trichloroethene (TCE)

-------
Subsurface Water Monitoring Well Data (ng/L)

Well

coc

ASC

Jun-18

Dec-18

Jun-19

Dec-19

Jun-20

Dec-20

Jun-21

Dec-21

Jun-22



1,2-DCE

320

4.9

8.9

11.0

19.0

21.0

29.0

20.0

31.0

27.0



Ethylbenzene

3280

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



Methylene Chloride

15.7

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



PCE

8.85

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

ECC-SSW-S6

Toluene

3400

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



1,1,1-TCA

5280

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



1,1,2-TCA

41.8

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



TCE

80.7

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



Vinyl Chloride

525

0.75

1.1

1.3

1.8

2.2

2.9

2.5

3.1

2.8



1,2-DCE

320

41.0

60.0

37.0

49.0

34.0

45.0

32.0

58.0

24.0



Ethylbenzene

3280

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



Methylene Chloride

15.7

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



PCE

8.85

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

ECC-SSW-























Toluene

3400

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

MW-14





















1,1,1-TCA

5280

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



1,1,2-TCA

41.8

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



TCE

80.7

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50

<0.50



Vinyl Chloride

525

16.0

19.0

19.0

20.0

22.0

23.0

25.0

33.0

21.0

-------
Subsurface Trench Data (ng/L)

Trench

coc

ASC

Jun-18

Dec-18

Jun-19

Dec-19

Jun-20

Dec-20

Jun-21

Dec-21

Jun-22



1,2-DCE

320

3100

3900

7100

760

7400

2100

25000

7900

9100



Ethylbenzene

3280

<2.5

<2.5

<2.5

<0.5

<2.5

<5.0

0.5

<0.5

<50.0



Methylene Chloride

15.7

<2.5

<2.5

<2.5

<0.5

<2.5

<5.0

2.5

0.82

66



PCE

8.85

19.0

16.0

21.0

8.4

6.9

7.2

19.0

8.0

<50.0*

ECC-SSW-T1

Toluene

3400

4.6

11.0

12.0

<0.5

7.9

5.4

90.0

22.0

<50.0



1,1,1-TCA

5280

140

150

260

56

110

55

490

130

88



1,1,2-TCA

41.8

<2.5

<2.5

<2.5

<0.5

<2.5

<5.0

2.8

1

<50.0*



TCE

80.7

16.0

16.0

25.0

3.3

13.0

10.0

12.0

10.0

<50.0



Vinyl Chloride

525

990

670

1300

190

2400

880

6000

3000

3200



1,2-DCE

320

5000

1000

6100

880

4300

1000

1800

820

4400



Ethylbenzene

3280

79

4.7

66

10

36

29

45

13

91



Methylene Chloride

15.7

<5.0

<2.5

<0.5

2.7

<2.5

<2.5

<0.5

8.5

<25.0*



PCE

8.85

7.2

4.9

2.4

4.6

5.3

3.7

5.0

5.3

<25.0*

ECC-SSW-T2

Toluene

3400

280

18.0

510

54.0

260

120

140

170

350



1,1,1-TCA

5280

630

160

730

190

620

210

360

210

740



1,1,2-TCA

41.8

<5.0

<2.5

3.4

0.62

3.0

<2.5

2.8

0.6

<25



TCE

80.7

26.0

7.8

3.3

12.0

6.9

6.8

4.3

8.3

<25



Vinyl Chloride

525

850

150

510

150

960

140

770

100

1700



1,2-DCE

320

560

360

660

310

460

450

410

770

730



Ethylbenzene

3280

0.74

<2.5

<0.5

<0.5

<2.5

<0.5

<0.5

<0.5

<5.0



Methylene Chloride

15.7

1.3

<2.5

<0.5

0.76

<2.5

<0.5

0.4

2.6

<5.0



PCE

8.85

3.2

2.0

3.8

2.6

2.6

2.4

2.4

3.1

4.5

ECC-SSW-T3

Toluene

3400

0.53

<2.5

<0.5

<0.5

2.6

<0.5

1.2

0.94

<5.0



1,1,1-TCA

5280

89

53

120

88

88

100

150

190

150



1,1,2-TCA

41.8

6.2

<2.5

0.53

0.45

6.9

0.42

1.6

0.63

<5.0



TCE

80.7

8.3

3.2

6.3

6.8

3.9

5.3

5.0

6.3

6.6



Vinyl Chloride

525

85

2.6

69

6.1

170

18

130

77

270

Notes:

Red text indicates exceedance of ASCs
* Exceeds ASC due to Detection Limits

-------
Subsurface Trench Data (ng/L)

Trench

coc

ASC

Jun-18

Dec-18

Jun-19

Dec-19

Jun-20

Dec-20

Jun-21

Dec-21

Jun-22



1,2-DCE

320

220

230

470

170

200

95

170

370

170



Ethylbenzene

3280

<0.5

<2.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



Methylene Chloride

15.7

<0.5

<2.5

<0.5

<0.5

<0.5

<0.5

<0.5

0.85

<0.5



PCE

8.85

2.2

<2.5

3.5

2.3

2.3

1.2

2.5

2.2

5.7

ECC-SSW-T4

Toluene

3400

<0.5

<2.5

<0.5

0.91

<0.5

<0.5

<0.5

<0.5

<0.5



1,1,1-TCA

5280

42

38

110

55

87

56

93

120

90



1,1,2-TCA

41.8

1.6

<2.5

1.50

0.64

1.5

0.62

1.3

0.84

1.2



TCE

80.7

8.8

4.7

9.2

5.4

6.0

3.0

7.1

4.8

10



Vinyl Chloride

525

0.6

<2.5

1.7

3.8

<0.5

<0.5

0.79

2.9

0.51



1,2-DCE

320

130

220

420

190

160

81

140

360

94



Ethylbenzene

3280

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



Methylene Chloride

15.7

0.41

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

0.78

<0.5



PCE

8.85

2.3

2.2

4.3

2.3

2.7

2.5

2.5

2.8

7.8

ECC-SSW-T5

Toluene

3400

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



1,1,1-TCA

5280

37

37

120

46

88

58

89

120

89



1,1,2-TCA

41.8

1.6

0.87

1.60

0.65

1.4

0.57

1.3

0.86

1.1



TCE

80.7

8.8

4.7

11.0

5.1

6.6

5.0

7.8

5.0

11



Vinyl Chloride

525

<0.5

<0.5

<0.5

0.46

<0.5

<0.5

0.56

1.7

<0.5

-------
Subsurface Trench Data (ng/L)

Trench

coc

ASC

Jun-18

Dec-18

Jun-19

Dec-19

Jun-20

Dec-20

Jun-21

Dec-21

Jun-22



1,2-DCE

320

3800

3200

3300

2900

5100

3100

2900

2500

490



Ethylbenzene

3280

<2.5

<0.5

<2.5

<2.5

<25

<2.5

<2.5

<0.5

<2.5



Methylene Chloride

15.7

2.1

1.1

<2.5

<2.5

<25*

<2.5

<2.5

0.6

<2.5



PCE

8.85

9.9

8.6

6.1

7.6

<25*

8.6

6.2

6.5

2.1

ECC-SSW-T6

Toluene

3400

<2.5

<0.5

<2.5

<2.5

<25

<2.5

<2.5

<0.5

<2.5



1,1,1-TCA

5280

4200

1900

2400

1900

4900

2300

1800

1200

360



1,1,2-TCA

41.8

6.9

4.8

4.20

2.90

<25

3.50

3.6

3.40

<2.5



TCE

80.7

1500.0

600.0

310.0

420.0

1200.0

360.0

86.0

160.0

120



Vinyl Chloride

525

68

69

38

66

100

38

76

150

32



1,2-DCE

320

<0.5

<0.5

0.87

0.55

0.91

<0.5

2.2

<0.5

1



Ethylbenzene

3280

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



Methylene Chloride

15.7

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



PCE

8.85

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

ECC-SSW-T7

Toluene

3400

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



1,1,1-TCA

5280

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



1,1,2-TCA

41.8

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



TCE

80.7

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



Vinyl Chloride

525

<0.5

<0.5

1.7

0.67

1.5

<0.5

3.0

<0.5

3.0

-------
Thin Barrier Curtain Wall Perimeter Data (iig/L)

Well

coc

ASC

Aug-18

Dec-18

Jun-19

Dec-19

Jun-20

Dec-20

Jun-21

Dec-21

Jun-22



1,2-DCE

320

5.2

4.7

4

3.7

2.7

3.6

3.4

5.5

2.7



Ethylbenzene

3280

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



Methylene Chloride

15.7

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

ECC-SSW-PT-1
Outside TBCW

PCE

Toluene

8.85
3400

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

1,1,1-TCA

5280

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



1,1,2-TCA

41.8

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



TCE

80.7

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



Vinyl Chloride

525

2.8

0.73

1.8

0.71

1.6

0.97

2.1

1.1

1.5



1,2-DCE

320

<0.5

<0.5

0.67

<0.5

<0.5

<0.5

<0.5

0.4

<0.5



Ethylbenzene

3280

<0.5

<0.5

0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



Methylene Chloride

15.7

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

ECC-SSW-PT-2
Inside TBCW

PCE

Toluene

8.85
3400

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

1,1,1-TCA

5280

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



1,1,2-TCA

41.8

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



TCE

80.7

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



Vinyl Chloride

525

0.54

0.56

0.72

0.44

0.43

0.69

0.56

0.5

0.55

-------
Thin Barrier Curtain Wall Perimeter Data (iig/L)

Well

coc

ASC

Aug-18

Dec-18

Jun-19

Dec-19

Jun-20

Dec-20

Jun-21

Dec-21

Jun-22



1,2-DCE

320

6.3

5.1

3.9

5.5

4

4.2

4.5

4.2

3



Ethylbenzene

3280

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



Methylene Chloride

15.7

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

ECC-SSW-PT-3
Outside TBCW

PCE

Toluene

8.85
3400

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

1,1,1-TCA

5280

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



1,1,2-TCA

41.8

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



TCE

80.7

<0.5

<0.5

0.41

0.51

0.43

0.58

0.42

0.45

<0.5



Vinyl Chloride

525

2.7

0.69

1.1

1.8

0.97

0.88

2.6

2.7

1.6



1,2-DCE

320

0.55

1.1

0.73

0.67

0.67

0.69

0.5

0.67

0.48



Ethylbenzene

3280

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



Methylene Chloride

15.7

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

ECC-SSW-PT-4
Inside TBCW

PCE

Toluene

8.85
3400

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

1,1,1-TCA

5280

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



1,1,2-TCA

41.8

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



TCE

80.7

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



Vinyl Chloride

525

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

-------
Surface Water Data (ng/L)

Location

coc

ASC

Jun-18

Dec-18

Jun-19

Dec-19

Jun-20

Dec-20

Jun-21

Dec-21

Jun-22



1,2-DCE

320

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



Ethylbenzene

3280

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



Methylene Chloride

15.7

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

ECC-SSW-
SW1

PCE

Toluene

8.85
3400

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

1,1,1-TCA

5280

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



1,1,2-TCA

41.8

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



TCE

80.7

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



Vinyl Chloride

525

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



1,2-DCE

320

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



Ethylbenzene

3280

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



Methylene Chloride

15.7

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

ECC-SSW-
SW1

PCE

Toluene

8.85
3400

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

1,1,1-TCA

5280

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



1,1,2-TCA

41.8

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



TCE

80.7

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



Vinyl Chloride

525

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



1,2-DCE

320

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



Ethylbenzene

3280

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



Methylene Chloride

15.7

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

ECC-SSW-
NSL

PCE

Toluene

8.85
3400

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

<0.5
<0.5

1,1,1-TCA

5280

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



1,1,2-TCA

41.8

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



TCE

80.7

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5



Vinyl Chloride

525

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

<0.5

-------
Soil Gas Data (micrograms per cubic meter [ng/m3])



Sample

PCE

TCE

cis-1,2-

trans-

Vinyl

1,1,1-

1,1,2-

Methylene

Toluene

Ethyl-

Sample ID

Date

DCE

1,2-DCE

Chloride

DCE

DCE

Chloride

benzene

UESEPA Soil Gas
Serening Levels



360

15.9

N/A

N/A

5.6

173,000

5.8

20,800

173,000

37.3

IDEM Soil Gas
Screening Levels



420

21

N/A

N/A

17

52,000

2.1

6,300

52,000

110

SG-04S

Jun-20

8.8

<4.2

<3.1

<3.1

<2.0

<4.3

<4.3

<27

<3.0

<3.4

SG-07S

Aug-20

42

<4.5

<3.3

<3.3

<2.1

<4.6

<4.6

<29

<3.2

<3.6

SG-04

Sep-21

18

30

<2.8

<2.8

<1.8

34

<3.9

<25

<2.7

<3.1

SG-05

Sep-21

43

11

<2.9

<2.9

<1.8

<4.0

<4.0

<25

3.3

<3.1

SG-06

Sep-21

86

35

9

<3.1

6.5

<4.2

<4.2

<27

12

4.2

SG-07S

Sep-21

<5.0

<4.0

<2.9

<2.9

<1.9

<4.0

<4.0

<26

3.2

<3.2

SG-07D

Sep-21

<5.0

<4.0

<2.9

<2.9

<1.9

<4.0

<4.0

<26

<2.8

<3.2

Notes:

Red text indicates exceedance of screening criteria

-------
2020 Supplemental Sampling for Groundwater (ng/L)

Analyte

ASC

MW-14

PZT-1

PZT-2

PZT-3

PZT-4

S-5

S-6

S-7

S-8

1,1,1-TCA

5,280

0.50 U

0.50 U

0.50 U

0.50 U

16

0.50 U

0.50 U

0.50 U

0.50 U

1,1,2-TCA

41.8

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

1,2-DCE (Total)

320

34

200

200

140

49

0.50 U

21

150

1800

Ethylbenzene

3280

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

Methylene chloride

15.7

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

PCE

8.85

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

Toluene

3,400

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

TCE

80.7

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

Vinyl chloride

525

22

32

24

46

22

0.50 U

2.2

25

190

Analyte

ASC

S-9

S-10

S-ll

S-12

S-13

S-14

T-ll

T-12

T-13

1,1,1-TCA

5,280

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

1,1,2-TCA

41.8

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

1,2-DCE (Total)

320

1300

1400

580

8.4

1200

1.9

0.47 J

2

1.4

Ethylbenzene

3280

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

Methylene chloride

15.7

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

PCE

8.85

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

Toluene

3,400

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

TCE

80.7

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

0.50 U

1.5

0.50 U

Vinyl chloride

525

110

180

360

8.3

190

13

2.9

0.50 U

0.50 U

Notes:

Red text indicates exceedance of ASCs

-------
GSI MANN-KENDALL TOOLKIT

for Constituent Trend Analysis

Evaluation Date:
Facility Name:
Conducted By:

22-Sep-22

ECC

William Clabaugh

Job ID:
Constituent:
Concentration Units:

Five Year Review

PCE

ug/L

Sampling Point ID:I Trench 6

EE sum? I

B! SSHI^EiSI

PCE CONCENTRATION (ug/L)

1

Jun-18

9.9













2

Dec-18

8.6













3

Jun-19

6.1













4

Dec-19

7.6













5

Jun-20















6

Dec-20

8.6













7

Jun-21

6.2













8

Dec-21

6.5













9

Jun-22

2.1













10

















11

















12

















13

















14

















15

















16

















17

















18

















19

















20

















Coefficient of Variation:
Mann-Kendall Statistic (S):
Confidence Factor:
Concentration Trend:

O)
3

£
O

c

0)

o
c
o
o

09/17

04/18

10/18

05/19

12/19

06/20

01/21

07/21

02/22

08/22

Sampling Date

Notes:

1.	At least four independent sampling events per well are required for calculating the trend. Methodology is valid for 4 to 40 samples.

2.	Confidence in Trend = Confidence (in percent) that constituent concentration is increasing (S>0) or decreasing (S<0): >95% = Increasing or Decreasing;
> 90% = Probably Increasing or Probably Decreasing; < 90% and S>0 = No Trend; < 90%, S<0, and COV > 1 = No Trend; < 90% and COV < 1 = Stable.
Methodology based on "MAROS: A Decision Support System for Optimizing Monitoring Plans", J.J. Aziz, M. Ling, H.S. Rifai, C.J. Newell, and J.R. Gonzales,
Groundwater, 41 (3):355-367, 2003.

DISCLAIMER: The GSI Mann-Kendall Toolkit is available "as is". Considerable care has been exercised in preparing this software product; however, no party, including without
limitation GSI Environmental Inc., makes any representation or warranty regarding the accuracy, correctness, or completeness of the information contained herein, and no such
party shall be liable for any direct, indirect, consequential, incidental or other damages resulting from the use of this product or the information contained herein. Information in
this publication is subject to change without notice. GSI Environmental Inc., disclaims any responsibility or obligation to update the information contained herein.

GSI Environmental Inc., www.gsi-net.com

-------
GSI MANN-KENDALL TOOLKIT

for Constituent Trend Analysis

Evaluation Date:

22-Sep-22



Job ID:

Five Year Review

Facility Name:

ECC



Constituent:

TCE

Conducted By:

William Clabaugh

Concentration Units:

ug/L























Sampling Point ID:

Trench 6 I I I I I I







IMS uSEl

TCE CONCENTRATION (ug/L)

1

Jun-18

1500.0













2

Dec-18

600.0













3

Jun-19

310.0













4

Dec-19

420.0













5

Jun-20

1200.0













6

Dec-20

360.0













7

Jun-21

86.0













8

Dec-21

160.0













9

Jun-22

120.0













10

















11

















12

















13

















14

















15

















16

















17

















18

















19

















20

















Coefficient of Variation:



Mann-Kendall Statistic (S):

-22 | I I I I I

Confidence Factor:

98.8% I I I I I I

Concentration Trend:

Decreasing |

Sampling Date

Notes:

1.	At least four independent sampling events per well are required for calculating the trend. Methodology is valid for 4 to 40 samples.

2.	Confidence in Trend = Confidence (in percent) that constituent concentration is increasing (S>0) or decreasing (S<0): >95% = Increasing or Decreasing;
> 90% = Probably Increasing or Probably Decreasing; < 90% and S>0 = No Trend; < 90%, S<0, and COV > 1 = No Trend; < 90% and COV < 1 = Stable.

3.	Methodology based on "MAROS: A Decision Support System for Optimizing Monitoring Plans", J.J. Aziz, M. Ling, H.S. Rifai, C.J. Newell, and J.R. Gonzales,
Groundwater, 41 (3):355-367, 2003.

DISCLAIMER: The GSI Mann-Kendall Toolkit is available "as is". Considerable care has been exercised in preparing this software product; however, no party, including without
limitation GSI Environmental Inc., makes any representation or warranty regarding the accuracy, correctness, or completeness of the information contained herein, and no such
party shall be liable for any direct, indirect, consequential, incidental or other damages resulting from the use of this product or the information contained herein. Information in
this publication is subject to change without notice. GSI Environmental Inc., disclaims any responsibility or obligation to update the information contained herein.

GSI Environmental Inc., www.gsi-net.com

-------
GSI MANN-KENDALL TOOLKIT

for Constituent Trend Analysis

Evaluation Date:
Facility Name:
Conducted By:

22-Sep-22

ECC

William Clabaugh

Job ID:
Constituent:
Concentration Units:

Five Year Review

1,2-DCE

ug/L

Sampling Point ID:

Trench 1

Trench 2

Trench 3

Trench 4

Trench 5

Trench 6

i







iifHj MM

B! SSHI^EiSI

1,2-DCE CONCENTRATION (ug/L)

1

Jun-18

3100.0

5000.0

560

220

130

3800



2

Dec-18

3900.0

1000.0

360

230

220

3200



3

Jun-19

7100.0

6100.0

660

470

420

3300



4

Dec-19

760.0

880.0

310

170

190

2900



5

Jun-20

7400.0

4300.0

460

200

160

5100



6

Dec-20

2100.0

1000.0

450

95

81

3100



7

Jun-21

25000.0

1800.0

410

170

140

2900



8

Dec-21

7900.0

820.0

770

370

360

2500



9

Jun-22

9100.0

4400.0

730

170

94

490



10

















11

















12

















13

















14

















15

















16

















17

















18

















19

















20

















Coefficient of Variation:

0.98 | 0.75 I 0.32 | 0.50 | 0.59 | 0.40

Mann-Kendall Statistic (S):

18 I -7 I 8 I -9 | -8 | -23

Confidence Factor:

96.2% | 72.8% | 76.2% | 79.2% | 76.2% | 99.1%

Concentration Trend:

Increasing Stable

No Trend Stable

Stable

Decreasing

100000

10000 ¦

U)
3

£

0)

o
c
o
o

1000

¦Trench 1
-Trench 2
-Trench 3
-Trench 4
-Trench 5
-Trench 6

09/17

04/18

10/18

05/19

12/19

06/20

01/21

07/21

02/22

08/22

Sampling Date

Notes:

1.	At least four independent sampling events per well are required for calculating the trend. Methodology is valid for 4 to 40 samples.

2.	Confidence in Trend = Confidence (in percent) that constituent concentration is increasing (S>0) or decreasing (S<0): >95% = Increasing or Decreasing;
> 90% = Probably Increasing or Probably Decreasing; < 90% and S>0 = No Trend; < 90%, S<0, and COV > 1 = No Trend; < 90% and COV < 1 = Stable.
Methodology based on "MAROS: A Decision Support System for Optimizing Monitoring Plans", J.J. Aziz, M. Ling, H.S. Rifai, C.J. Newell, and J.R. Gonzales,
Groundwater, 41 (3):355-367, 2003.

DISCLAIMER: The GSI Mann-Kendall Toolkit is available "as is". Considerable care has been exercised in preparing this software product; however, no party, including without
limitation GSI Environmental Inc., makes any representation or warranty regarding the accuracy, correctness, or completeness of the information contained herein, and no such
party shall be liable for any direct, indirect, consequential, incidental or other damages resulting from the use of this product or the information contained herein. Information in
this publication is subject to change without notice. GSI Environmental Inc., disclaims any responsibility or obligation to update the information contained herein.

GSI Environmental Inc., www.gsi-net.com

-------
GSI MANN-KENDALL TOOLKIT

for Constituent Trend Analysis

Evaluation Date:
Facility Name:
Conducted By:

22-Sep-22

ECC

William Clabaugh

Job ID:
Constituent:
Concentration Units:

Five Year Review

Vinyl Chloride

ug/L

Sampling Point ID:I Trench 1 I Trench 2

EE sum? I

B! SSHI^EiSI

VINYL CHLORIDE CONCENTRATION (ug/L)

1

Jun-18

990.0

850.0











2

Dec-18

670.0

150.0











3

Jun-19

1300.0

510.0











4

Dec-19

190.0

150.0











5

Jun-20

2400.0

960.0











6

Dec-20

880.0

140.0











7

Jun-21

6000.0

770.0











8

Dec-21

2010.0

100.0











9

Jun-22

3200.0

1700.0











10

















11

















12

















13

















14

















15

















16

















17

















18

















19

















20

















Coefficient of Variation:
Mann-Kendall Statistic (S):
Confidence Factor:
Concentration Trend:

10000

U)
3

1000 ¦

2 100 ¦

c

0)

o
c
o
o

10 ¦

¦Trench 1
-Trench 2

09/17

04/18

10/18

05/19

12/19

06/20

01/21

07/21

02/22

08/22

Sampling Date

Notes:

1.	At least four independent sampling events per well are required for calculating the trend. Methodology is valid for 4 to 40 samples.

2.	Confidence in Trend = Confidence (in percent) that constituent concentration is increasing (S>0) or decreasing (S<0): >95% = Increasing or Decreasing;
> 90% = Probably Increasing or Probably Decreasing; < 90% and S>0 = No Trend; < 90%, S<0, and COV > 1 = No Trend; < 90% and COV < 1 = Stable.
Methodology based on "MAROS: A Decision Support System for Optimizing Monitoring Plans", J.J. Aziz, M. Ling, H.S. Rifai, C.J. Newell, and J.R. Gonzales,
Groundwater, 41 (3):355-367, 2003.

DISCLAIMER: The GSI Mann-Kendall Toolkit is available "as is". Considerable care has been exercised in preparing this software product; however, no party, including without
limitation GSI Environmental Inc., makes any representation or warranty regarding the accuracy, correctness, or completeness of the information contained herein, and no such
party shall be liable for any direct, indirect, consequential, incidental or other damages resulting from the use of this product or the information contained herein. Information in
this publication is subject to change without notice. GSI Environmental Inc., disclaims any responsibility or obligation to update the information contained herein.

GSI Environmental Inc., www.gsi-net.com

-------
APPENDIX C

FIVE-YEAR REVIEW SITE INSPECTION CHECKLIST

D-l

-------
OSWERNo. 9355.7-03B-P

[This page intentionally left blank.]

D-2

-------
OSWERNo. 9355.7-03B-P

Five-Year Review Site Inspection Checklist

I. SITE INFORMATION

Site name: Envirochem Corp.

Date of inspection: 7/29/2022

Location and Region: Zionsville, IN

EPA ID: IND084259951

Agency, office, or company leading the five-year
review: USEPA

Weather/temperature:
Sunny, 73°f

Remedy Includes: (Check all that apply)
X Landfill cover/containment
X Access controls
X Institutional controls
X Groundwater pump and treatment

~	Surface water collection and treatment

~	Other

~ Monitored natural attenuation
X Groundwater containment
X Vertical barrier walls

Attachments: ~ Inspection team roster attached

~ Site map attached

II. INTERVIEWS (Check all that apply)

1. O&M site manager

Name

Interviewed ~ at site ~ at office ~ by phone Phone no.
Problems, suggestions; ~ Report attached	

Title

Date

2. O&M staff

Name	Title

Interviewed ~ at site ~ at office ~ by phone Phone no. 	

Problems, suggestions; ~ Report attached	

Date

D-3

-------
OSWERNo. 9355.7-03B-P

3. Local regulatory authorities and response agencies (i.e., State and Tribal offices, emergency response
office, police department, office of public health or environmental health, zoning office, recorder of
deeds, or other city and county offices, etc.) Fill in all that apply.

Agency	

Contact	 	 	 	

Name	Title	Date Phone no.

Problems; suggestions; ~ Report attached 	

Agency	

Contact	 	 	 	

Name Title Date Phone no.
Problems; suggestions; ~ Report attached 	

Agency	

Contact	 	 	 	

Name Title Date Phone no.
Problems; suggestions; ~ Report attached 	

Agency	

Contact	 	 	 	

Name Title Date Phone no.
Problems; suggestions; ~ Report attached 	

4. Other interviews (optional) ~ Report attached.

D-4

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OSWERNo. 9355.7-03B-P

III. ON-SITE DOCUMENTS & RECORDS VERIFIED (Check all that apply)

O&M Documents

~	O&M manual

~	As-built drawings

~	Maintenance logs
Remarks

X Readily available

~	Readily available

~	Readily available

~	Up to date ~ N/A

~	Up to date X N/A

~	Up to date X N/A

2.	Site-Specific Health and Safety Plan X Readily available X Up to date ~ N/A
~ Contingency plan/emergency response plan ~ Readily available ~ Up to date X N/A
Remarks	

3.	O&M and OSHA Training Records ~ Readily available ~ Up to date L N/A
Remarks

4. Permits and Service Agreements

~	Air discharge permit

~	Effluent discharge

~	Waste disposal, POTW

~	Other permits	

Remarks

~	Readily available

~	Readily available

~	Readily available

~	Readily available

~	Up to date

~	Up to date

~	Up to date

~	Up to date

X N/A
XN/A
XN/A
XN/A

5. Gas Generation Records

Remarks

~ Readily available

~ Up to date X N/A

6. Settlement Monument Records

Remarks

~ Readily available

~ Up to date X N/A

7. Groundwater Monitoring Records

Remarks

X Readily available

~ Up to date ~ N/A

Leachate Extraction Records

Remarks

~ Readily available ~ Up to date X N/A

9. Discharge Compliance Records

~	Air

~	Water (effluent)

Remarks

~	Readily available

~	Readily available

~	Up to date

~	Up to date

XN/A
XN/A

10. Daily Access/Security Logs

Remarks

~ Readily available

~ Up to date

XN/A

D-5

-------
OSWERNo. 9355.7-03B-P

IV. O&M COSTS

O&M Organization

~	State in-house

~	PRP in-house

~	Federal Facility in-house

~	Other

~	Contractor for State
X Contractor for PRP

~	Contractor for Federal Facility

O&M Cost Records

X Readily available X Up to date
X Funding mechanism/agreement in place
Original O&M cost estimate	

~ Breakdown attached

From

From

From

From

From

Total annual cost by year for review period if available

To

Date

To

Date

To

Date

To

Date

To

Date

Date

Date

Date

Date

Date

Total cost

Total cost

Total cost

Total cost

Total cost

~	Breakdown attached

~	Breakdown attached

~	Breakdown attached

~	Breakdown attached

~	Breakdown attached

Unanticipated or Unusually High O&M Costs During Review Period

Describe costs and reasons:

V. ACCESS AND INSTITUTIONAL CONTROLS X Applicable ~ N/A

A. Fencing

1. Fencing damaged

Remarks

~ Location shown on site map X Gates secured ~ N/A

B. Other Access Restrictions

1. Signs and other security measures

Remarks

X Location shown on site map ~ N/A

D-6

-------
OSWERNo. 9355.7-03B-P

c.

Institutional Controls (ICs)



1.

Implementation and enforcement

Site conditions imply ICs not properly implemented ~ Yes X No
Site conditions imply ICs not being fully enforced L Yes X No

Type of monitoring (e.g., self-reporting, drive by)

~	N/A

~	N/A



Frequency





Responsible party/agency





Contact





Name Title Date Phone no.



Reporting is up-to-date L Yes L No
Reports are verified by the lead agency L Yes L No

~	N/A

~	N/A



Specific requirements in deed or decision documents have been met L Yes L No
Violations have been reported L Yes L No
Other problems or suggestions: ~ Report attached

~	N/A

~	N/A



















2.

Adequacy X ICs are adequate ~ ICs are inadequate
Remarks

~ N/A













D.

General



1.

Vandalism/trespassing ~ Location shown on site map X No vandalism evident
Remarks









2.

Land use changes on site X N/A

Remarks









3.

Land use changes off site X N/A

Remarks









VI. GENERAL SITE CONDITIONS

A.

Roads X Applicable ~ N/A



1.

Roads damaged ~ Location shown on site map X Roads adequate
Remarks

~ N/A







D-7

-------
OSWERNo. 9355.7-03B-P

B. Other Site Conditions

Remarks

VII. LANDFILL COVERS X Applicable UN/A

A. Landfill Surface

1. Settlement (Low spots)

Areal extent	

Remarks

~ Location shown on site map X Settlement not evident
Depth	

2. Cracks

Lengths_
Remarks

~ Location shown on site map X Cracking not evident
Widths	 Depths	

3. Erosion

Areal extent_
Remarks

~ Location shown on site map X Erosion not evident
Depth	

4. Holes

Areal extent_
Remarks

~ Location shown on site map X Holes not evident
Depth	

5. Vegetative Cover	X Grass	X Cover properly established X No signs of stress

~ Trees/Shrubs (indicate size and locations on a diagram)

Remarks

6. Alternative Cover (armored rock, concrete, etc.) ~ N/A

Remarks

7. Bulges

Areal extent_
Remarks

~ Location shown on site map X Bulges not evident
Height	

D-8

-------
OSWERNo. 9355.7-03B-P

8.

Wet Areas/Water Damage

~	Wet areas

~	Ponding

~	Seeps

~	Soft subgrade
Remarks

X Wet areas/water damage not evident

~	Location shown on site map Areal extent

~	Location shown on site map Areal extent

~	Location shown on site map Areal extent

~	Location shown on site map Areal extent







9.

Slope Instability ~ Slides

Areal extent

Remarks

~ Location shown on site map X No evidence of slope instability







B.

Benches ~ Applicable X N/A

(Horizontally constructed mounds of earth placed across a steep landfill side slope to interrupt the slope
in order to slow down the velocity of surface runoff and intercept and convey the runoff to a lined
channel.)

1.

Flows Bypass Bench

Remarks

~ Location shown on site map ~ N/A or okay







2.

Bench Breached

Remarks

~ Location shown on site map ~ N/A or okay







3.

Bench Overtopped

Remarks

~ Location shown on site map ~ N/A or okay







C.

Letdown Channels ~ Applicable X N/A

(Channel lined with erosion control mats, riprap, grout bags, or gabions that descend down the steep side
slope of the cover and will allow the runoff water collected by the benches to move off of the landfill
cover without creating erosion gullies.)

1.

Settlement ~ Location shown on site map ~ No evidence of settlement

Areal extent Depth

Remarks







2.

Material Degradation ~ Location shown on site map ~ No evidence of degradation

Material type Areal extent

Remarks







3.

Erosion ~ Location shown on site map ~ No evidence of erosion

Areal extent Depth

Remarks







D-9

-------
OSWERNo. 9355.7-03B-P

4.

Undercutting ~ Location shown on site map ~ No evidence of undercutting

Areal extent Depth

Remarks

5.

Obstructions Type ~ No obstructions

~ Location shown on site map Areal extent

Size

Remarks

6.

Excessive Vegetative Growth Type

~	No evidence of excessive growth

~	Vegetation in channels does not obstruct flow

~	Location shown on site map Areal extent
Remarks

D.

Cover Penetrations X Applicable ~ N/A

1.

Gas Vents ~ ActivcL Passive

~	Properly secured/locked ~ Functioning ~ Routinely sampled ~ Good condition

~	Evidence of leakage at penetration ~ Needs Maintenance
XN/A

Remarks

2.

Gas Monitoring Probes

~	Properly secured/locked ~ Functioning ~ Routinely sampled ~ Good condition

~	Evidence of leakage at penetration ~ Needs Maintenance X N/A
Remarks

3.

Monitoring Wells (within surface area of landfill)

~	Properly secured/locked ~ Functioning ~ Routinely sampled ~ Good condition

~	Evidence of leakage at penetration ~ Needs Maintenance X N/A
Remarks

4.

Leachate Extraction Wells

X Properly secured/locked X Functioning ~ Routinely sampled X Good condition
~ Evidence of leakage at penetration ~ Needs Maintenance ~ N/A
Remarks: Original SVE extraction wells present. They are secured and maintained.

5.

Settlement Monuments ~ Located ~ Routinely surveyed XN/A
Remarks

D-10

-------
OSWERNo. 9355.7-03B-P

E.

Gas Collection and Treatment ~ Applicable X N/A

1.

Gas Treatment Facilities

~	Flaring ~ Thermal destruction ~ Collection for reuse

~	Good condition^ Needs Maintenance
Remarks

2.

Gas Collection Wells, Manifolds and Piping

~ Good condition^ Needs Maintenance
Remarks

3.

Gas Monitoring Facilities (e.g., gas monitoring of adjacent homes or buildings)

~ Good condition^ Needs Maintenance ~ N/A

Remarks

F.

Cover Drainage Layer X Applicable ~ N/A

1.

Outlet Pipes Inspected X Functioning ~ N/A
Remarks

2.

Outlet Rock Inspected X Functioning ~ N/A
Remarks

G.

Detention/Sedimentation Ponds ~ Applicable X N/A

1.

Siltation Areal extent Depth ~ N/A

~ Siltation not evident

Remarks

2.

Erosion Areal extent Depth
~ Erosion not evident
Remarks

3.

Outlet Works ~ Functioning ~ N/A
Remarks

4.

Dam ~ Functioning ~ N/A
Remarks

D-ll

-------
OSWERNo. 9355.7-03B-P

H. Retaining Walls

~ Applicable X N/A

1.

Deformations

Horizontal displacement

~ Location shown on site map ~ Deformation not evident
Vertical displacement



Rotational displacement
Remarks









2.

Degradation

Remarks

~ Location shown on site map ~ Degradation not evident







I. Perimeter Ditches/Off-Site Discharge X Applicable ~ N/A

1.

Siltation ~ Location shown on site map X Siltation not evident
Areal extent Depth



Remarks









2.

Vegetative Growth ~ Location shown on site map X N/A
~ Vegetation does not impede flow
Areal extent Type



Remarks









3.

Erosion

Areal extent

~ Location shown on site map X Erosion not evident
Depth



Remarks









4.

Discharge Structure

Remarks

X Functioning ~ N/A







VIII. VERTICAL BARRIER WALLS X Applicable UN/A

1.

Settlement

Areal extent

Location shown on site map X Settlement not evident
Depth



Remarks









2.

Performance Monitoring Type of monitoring Periodic
~ Performance not monitored

FrequencySemi-Annual ~ Evidence of breaching



Head differential





Remarks









D-12

-------
OSWERNo. 9355.7-03B-P

IX. GROUNDWATER/SURFACE WATER REMEDIES X Applicable ~ N/A

A.

Groundwater Extraction Wells, Pumps, and Pipelines X Applicable ~ N/A

1.

Pumps, Wellhead Plumbing, and Electrical

X Good condition^ All required wells properly operating ~ Needs Maintenance ~ N/A
Remarks

2.

Extraction System Pipelines, Valves, Valve Boxes, and Other Appurtenances

X Good condition^ Needs Maintenance
Remarks

3.

Spare Parts and Equipment

~ Readily available ~ Good condition X Requires upgrade ~ Needs to be provided
Remarks: Delays due to parts ordering has been noted in previous status reports.

B. Surface Water Collection Structures, Pumps, and Pipelines ~ Applicable X N/A

1.

Collection Structures, Pumps, and Electrical

~ Good condition^ Needs Maintenance
Remarks

2.

Surface Water Collection System Pipelines, Valves, Valve Boxes, and Other Appurtenances

~ Good condition^ Needs Maintenance
Remarks

3.

Spare Parts and Equipment

~ Readily available ~ Good condition^ Requires upgrade ~ Needs to be provided
Remarks

D-13

-------
OSWERNo. 9355.7-03B-P

C. Treatment System	~ Applicable L N/A

1.	Treatment Train (Check components that apply)

~	Metals removal	~ Oil/water separation ~ Bioremediation
X Air stripping X Carbon adsorbers

~	Filters	

~	Additive (e.g., chelation agent, flocculent)	

~	Others	

X Good condition	~ Needs Maintenance

X Sampling ports properly marked and functional

~	Sampling/maintenance log displayed and up to date
X Equipment properly identified

~	Quantity of groundwater treated annually	

~	Quantity of surface water treated annually	

Remarks: Equipment in good condition and well maintained but is past the designed operational life.
	Only one of the two treatment trains is in operation currently.	

2.	Electrical Enclosures and Panels (properly rated and functional)

~	N/A	X Good condition	~ Needs Maintenance

	Remarks:	

3.	Tanks, Vaults, Storage Vessels

~	N/A	X Good condition	~ Proper secondary containment ~ Needs Maintenance
Remarks

4. Discharge Structure and Appurtenances

~ N/A	X Good condition	~ Needs Maintenance

Remarks

5. Treatment Building(s)

~ N/A	X Good condition (esp. roof and doorways)	~ Needs repair

X Chemicals and equipment properly stored

Remarks

6. Monitoring Wells (pump and treatment remedy)

~ Properly secured/locked ~ Functioning X Routinely sampled X Good condition
X All required wells located ~ Needs Maintenance ~ N/A
	Remarks: "Monitoring wells" are the SVE trenches.	

D. Monitoring Data

1.	Monitoring Data

X Is routinely submitted on time	X Is of acceptable quality

2.	Monitoring data suggests:

X Groundwater plume is effectively contained ~ Contaminant concentrations are declining

D-14

-------
OSWERNo. 9355.7-03B-P

D. Monitored Natural Attenuation

1. Monitoring Wells (natural attenuation remedy)

~	Properly secured/locked	~ Functioning ~ Routinely sampled ~ Good condition

~	All required wells located ~ Needs Maintenance	X N/A
Remarks

X. OTHER REMEDIES

If there are remedies applied at the site which are not covered above, attach an inspection sheet describing
the physical nature and condition of any facility associated with the remedy. An example would be soil
vapor extraction.

XI. OVERALL OBSERVATIONS

A.	Implementation of the Remedy

Describe issues and observations relating to whether the remedy is effective and functioning as designed.
Begin with a brief statement of what the remedy is to accomplish (i.e., to contain contaminant plume,
minimize infiltration and gas emission, etc.).

The remedy is not operating as intended per original design. Additions to the current remedy
are ongoing, and a ROD Amendment or ESD is required.

B.	Adequacy of O&M

Describe issues and observations related to the implementation and scope of O&M procedures. In
particular, discuss their relationship to the current and long-term protectiveness of the remedy.
The IWM staff on-site has addressed issues as they occur. Downtime of O&M system has been
minor. Revision of O&M Plan is necessary to account for remedy revisions and additions.

D-15

-------
OSWERNo. 9355.7-03B-P

C.	Early Indicators of Potential Remedy Problems

Describe issues and observations such as unexpected changes in the cost or scope of O&M or a high
frequency of unscheduled repairs, that suggest that the protectiveness of the remedy may be
compromised in the future.

Equipment downtime has increased recently, both due to failures becoming more common and
increasing supply delays. A change to a proactive maintenance approach may prevent extended
downtime.

D.	Opportunities for Optimization

Describe possible opportunities for optimization in monitoring tasks or the operation of the remedy.
The treatment system is past the designed operational life, and a new system is required to
minimize downtime and maintenance.

D-16

-------
APPENDIX D

PHOTO LOG

-------

-------

-------

-------

-------

-------

-------

-------

-------

-------

-------
Photo Log Map

-------
APPENDIX E

FIGURES

-------
SITE MAP SHOWING
ADJACENT SITES

ENVIRO-CHEM SUPERFUND SITE
985 US HIGHWAY 421
ZIONSVILLE, IN

APPENDIX E
FIGURE 1

DATE: 20221013

Northside Sanitary Landfill

Third Site

>Sm™6^!si!ilEillta lis® bS!©ebB®ll^litiirsr'ari©e@a"ilRiSs!7r*&V
KlTirfiuhity T2't	'

-------
p-i- . s

•- X--

-------
APPENDIX E: FIGURE 3
SITE PLAN SHOWING
INSTITUTIONAL CONTROLS

I XVIRO-C ill VI SI'I'HRl I'M) SITE
985 S. US HIGHWAY 421
ZIONSYII I I-. INDIANA

Source: ESRI, USACE Louisville District, EPA Map: J AH; Date: 20180205

Legend

~ Support Zone - No construction or improvements allowed.

Remedial Area - No construction or improvements allowed.

Parking Area - Ingress, egress, and access to Remedial
and Support Areas allowed.

-------

-------
Legend

Groundwater Monitoring Locations

^ Sand and Gravel Monitoring Well

!	| Sand and Gravel Piezometer

^ Shallow (Till) Piezometer

~ Shallow (Till) Well

Support Zone Piezometer

A. Surface Water Sampling Location
© Waterloo Profiling Sample

" Trench Dewatering Well

Monitoring Locations Installed During
Supplemental Sampling Program

Soil Gas Monitoring Locations

A Soil Gas Point
A Temporary Soil Gas Point

	Unnamed Ditch

Extent of Clay Cover
Former Southern Concrete Pad
Extent of RCRA Cap
jgSite Boundary

Notes:

RCRA - Resource Conservation and Recovery Act

SVE - Soil Vapor Extraction

TBCW - Thin Barrier Curtain Wall

1.	Basemap site features include the fenceline, concrete pad,
RCRA cap and clay cover.

2.	Yellow highlighted symbols indicate newly installed
monitoring wells, Waterloo Profile sample locations, and
soil gas probes.

3.	Solid green line indicates where the TBCW completely
intersects the Upper Sand and Gravel unit; dashed line
indicates that the TBCW does not completely intersect the
Upper Sand and Gravel Unit.

4.	Basemap Source: ESRI, DigitalGlobe, Geoeye, Earthstar,
Geographies, CNES/Airbus DS, USDA, USGS, AEX,
Getmapping, Aerogrid, IGN, IGP, swisstopo.

100

so

100 Feet

Site Map

Enviro-Chem Superfund Site
985 South U.S. Highway 421
Zionsville, Indiana

Geosyntec^

consultants

Guelph

September 2020

Figure
5

-------
APPENDIX F

REMEDIAL GOAL TABLES

-------
1991 ROD Amendment (Table 3-1)
Site-Specific Acceptable Concentrations

Compounds

Acceptable Subsurface Water
Concentrations (|ig/L)

Acceptable Stream
Concentrations (|ig/L)

Acceptable Soil
Concentrations (|ig/kg)

Volatile Organics (VOCs):







Acetone

3,300



490

Chlorobenzene

60



10,100

Chloroform

100

15.7

2,300

1,1-Dichloroethane

0.38



5.7

1,1-Dichloroethene

7

1.85

120

Ethylebenzene

680

3,280

234,000

Methylene Chloride

4.7

15.7

20

Methyl Ethyl Ketone

170



75

Methyl Isobutyl Ketone

1,750



8,900

Tetrachloroethene

0.69

8.85

130

Toulene

2,000

3,400

238,000

1,1,1-Trichloroethane

200

5,280

7,200

1,1,2-Trichloroethane

0.61

41.8

22

Trichloroethene

5

80.7

240

Total Xylenes

440



195,000

Base Neutral/Acid Organics:







Bis(2-ethylhexyl)phthalate

2.5

50,000



Di-n-Butyl Phthalate

3,500

154,000



Diethyl Phtalate

28,000

52,100



Isophorone

8.5





Naphthalene

14,000

620



Phenol

1,400

570

9,800

Inorganics:







Antimony

14





Arsenic

50

0.0175



Barium

1,000





Beryilium

175





Cadmium

10





Chromium VI

50

11



Lead

50

10



Manganese

7,000





Nickel

150

100



Silver

50





Tin

21,000





Vandium

245





Zinc

7,000

47



Cyanide

154

5.2



Pesticides/PCBs:







Polychlorinated Biphenyls (PCBs)

0.0045

0.000079



Note: ng/L = micrograms per liter

Hg/kg = micrograms per kilogram

-------
2007 Appendix 1-1 (Table 2-1)
Site-Specific Acceptable Concentrations

Parameter

Acceptable Stream

Acceptable Soil

Concentrations (|j.g/L)

Concentrations (|j.g/kg)

Volatile Organic Compounds





Acetone



370,000

1,1-Dichloroethene



42,000

1,2-Dichloroethene (total)1

320

5,800

Ethylbenzene

3,280

160,000

Methylene chloride

15.7

1,800

Methyl ethyl ketone



250,000

Methyl isobutyl ketone



75,000

Tetrachloroethene

8.85

640

Toulene

3,400

240,000

1,1,1-Trichlorethane

5,280

280,000

1,1,2-Trichloroethane

41.8

300

Trichloroethene

80.7

82

Vinyl chloride

525

13

Xylenes (total)



170,000

Semivolatile Organic Compounds





Bis (2-ethylhexyl) phthalate

50,000



Di-n-butyl phthalate

154,000



1,2-Dichlrobenzene

763

220,000

Diethyl phthalate

52,100



Isophorone





Napthalene

620



Phenol

570

160,000

Inorganic Parameters





Antimony





Arsenic

9.2



Barium





Beryllium





Cadmium





Chromium VI

77.6



Lead

19.8



Manganese





Nickel

100



Silver





Tin





Vanadium





Zinc

123



Cyanide (total)

17.2



Polychlorinated Biphenyls





Aroclor 1016

0.5



Aroclor 1221

0.9



Aroclor 1232

0.5



Aroclor 1242

0.5



Aroclor 1248

0.5



Aroclor 1254

0.5



Aroclor 1260

0.5



Notes: |ig/L = micrograms per liter

Hg/kg = micrograms per kilogram
1. The Acceptable Stream Concentration for 1,2 Dichloroethene was changed from 7.4 |ig/L to 320
|ig/L through the April 26, 2010 Memorandum

-------
2007 Appendix Z-l (Table 2-2)
Soil Vapor Standards

Compound

Soil Vapor Standard (mg/L)

Soil Vapor Standard (ppmv)

Volatile Organic Compounds (VOCs):





Acetone

0.61

244

1,1-Dichloroethene

2

481

1,2-Dichloroethene (total)

3.7

880

Ethylbenzene

37

8,076

Methylene chloride

0.08

22

Methyl ethyl ketone

0.04

13

Methyl isobutyl ketone

0.69

159

Tetrachloroethene

0.11

16

Toluene

107

27,090

1,1,1-Trichloroethane

8.3

1,442

1,1,2-Trichloroethane

0.01

1

Trichloroethene

0.39

68

Vinyl chloride

919.2

338,808

Total Xylenes

595

130,244

Base Neutral/Acid Organics:





1,2-Dichlorobenzene

9.3

1,466

Phenol

0.005

1.3

Note: mg/L = miligrams per liter

ppmv = parts per million by volume

-------
2007 Appendix Z-l (Table 2-3)

Effluent Limits for Discharge of Treated water to Unnamed Ditch

Contaminant of Concern (COC)

Discharge Limit (iig/L)

1,1-Dichloroethane

990

1,1-Dichloroethene

2

Cis-l,2-Dichloroethene

2

Trans-l,2-Dichloroethene

2

Tetrachloroethene

5

1,1,1-Trichloroethane

200

1,1,2-Trichloroethane

42

Trichloroethene

10

Vinyl Chloride

10

bis(2-Ethylhexyl)phthalate

680

Di-n-butylphtalate

21

Diethylphtalate

7000

1,2-Dichlrobenzene

760

Napthalene

69

Phenol

570

Biological Oxygen Demand (BOD)



Summer

30 mg/L daily maximum

Winter

50 mg/L daily maximum

Note: mg/L = miligrams per liter

-------
APPENDIX G

1,1-DICHLOROETHANE
TOXICOLOGICAL PROFILE

-------
TOXICOLOGICAL PROFILE FOR
1,1 -DICHLOROETHANE

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES
Public Health Service
Agency for Toxic Substances and Disease Registry

August 2015

-------
1,1-DICHLOROETHANE

DISCLAIMER

Use of trade names is for identification only and does not imply endorsement by the Agency for Toxic
Substances and Disease Registry, the Public Health Service, or the U.S. Department of Health and Human
Services.

-------
1,1-DICHLOROETHANE

UPDATE STATEMENT

A Toxicological Profile for 1,1-Dichloroethane, Draft for Public Comment was released in April 2013.
This edition supersedes any previously released draft or final profile.

Toxicological profiles are revised and republished as necessary. For information regarding the update
status of previously released profiles, contact ATSDR at:

Agency for Toxic Substances and Disease Registry
Division of Toxicology and Human Health Sciences
Environmental Toxicology Branch
1600 Clifton Road NE
Mailstop F-57
Atlanta, Georgia 30329-4027

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1,1-DICHLOROETHANE

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1,1-DICHLOROETHANE

v

FOREWORD

This toxicological profile is prepared in accordance with guidelines* developed by the Agency for Toxic
Substances and Disease Registry (ATSDR) and the Environmental Protection Agency (EPA). The
original guidelines were published in the Federal Register on April 17, 1987. Each profile will be revised
and republished as necessary.

The ATSDR toxicological profile succinctly characterizes the toxicologic and adverse health effects
information for these toxic substances described therein. Each peer-reviewed profile identifies and
reviews the key literature that describes a substance's toxicologic properties. Other pertinent literature is
also presented, but is described in less detail than the key studies. The profile is not intended to be an
exhaustive document; however, more comprehensive sources of specialty information are referenced.

The focus of the profiles is on health and toxicologic information; therefore, each toxicological profile
begins with a public health statement that describes, in nontechnical language, a substance's relevant
toxicological properties. Following the public health statement is information concerning levels of
significant human exposure and, where known, significant health effects. The adequacy of information to
determine a substance's health effects is described in a health effects summary. Data needs that are of
significance to protection of public health are identified by ATSDR.

Each profile includes the following:

(A)	The examination, summary, and interpretation of available toxicologic information and
epidemiologic evaluations on a toxic substance to ascertain the levels of significant human
exposure for the substance and the associated acute, subacute, and chronic health effects;

(B)	A determination of whether adequate information on the health effects of each substance
is available or in the process of development to determine levels of exposure that present a
significant risk to human health of acute, subacute, and chronic health effects; and

(C)	Where appropriate, identification of toxicologic testing needed to identify the types or
levels of exposure that may present significant risk of adverse health effects in humans.

The principal audiences for the toxicological profiles are health professionals at the Federal, State, and
local levels; interested private sector organizations and groups; and members of the public.

This profile reflects ATSDR" s assessment of all relevant toxicologic testing and information that has been
peer-reviewed. Staffs of the Centers for Disease Control and Prevention and other Federal scientists have
also reviewed the profile. In addition, this profile has been peer-reviewed by a nongovernmental panel
and was made available for public review. Final responsibility for the contents and views expressed in
this toxicological profile resides with ATSDR.

Patrick N. Breysse, Ph.D., CIH
Director, National Center for Environmental Health and
Agency for Toxic Substances and Disease Registry
Centers for Disease Control and Prevention

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1,1-DICHLOROETHANE

vi

"'Legislative Background

The toxicological profiles are developed under the Comprehensive Environmental Response,
Compensation, and Liability Act of 1980, as amended (CERCLA or Superfund). CERCLA section
104(i)(l) directs the Administrator of ATSDR to .. effectuate and implement the health related
authorities" of the statute. This includes the preparation of toxicological profiles for hazardous
substances most commonly found at facilities on the CERCLA National Priorities List and that pose the
most significant potential threat to human health, as determined by ATSDR and the EPA. Section
104(i)(3) of CERCLA, as amended, directs the Administrator of ATSDR to prepare a toxicological profile
for each substance on the list. In addition, ATSDR has the authority to prepare toxicological profiles for
substances not found at sites on the National Priorities List, in an effort to "... establish and maintain
inventory of literature, research, and studies on the health effects of toxic substances" under CERCLA
Section 104(i)(l)(B), to respond to requests for consultation under section 104(i)(4), and as otherwise
necessary to support the site-specific response actions conducted by ATSDR.

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1,1-DICHLOROETHANE

vii

QUICK REFERENCE FOR HEALTH CARE PROVIDERS

Toxicological Profiles are a unique compilation of toxicological information on a given hazardous
substance. Each profile reflects a comprehensive and extensive evaluation, summary, and interpretation
of available toxicologic and epidemiologic information on a substance. Health care providers treating
patients potentially exposed to hazardous substances will find the following information helpful for fast
answers to often-asked questions.

Primary Chapters/Sections of Interest

Chapter 1: Public Health Statement: The Public Health Statement can be a useful tool for educating
patients about possible exposure to a hazardous substance. It explains a substance's relevant
toxicologic properties in a nontechnical, question-and-answer format, and it includes a review of
the general health effects observed following exposure.

Chapter 2: Relevance to Public Health: The Relevance to Public Health Section evaluates, interprets,
and assesses the significance of toxicity data to human health.

Chapter 3: Health Effects: Specific health effects of a given hazardous compound are reported by type
of health effect (death, systemic, immunologic, reproductive), by route of exposure, and by length
of exposure (acute, intermediate, and chronic). In addition, both human and animal studies are
reported in this section.

NOTE. Not all health effects reported in this section are necessarily observed in the clinical
setting. Please refer to the Public Health Statement to identify general health effects observed
following exposure.

Pediatrics: Four new sections have been added to each Toxicological Profile to address child health

issues:
Chapter 1
Chapter 1
Section 3.7
Section 6.6

How Can (Chemical X) Affect Children?

How Can Families Reduce the Risk of Exposure to (Chemical X)?
Children's Susceptibility
Exposures of Children

Other Sections of Interest:

Section 3.8 Biomarkers of Exposure and Effect
Section 3.11 Methods for Reducing Toxic Effects

ATSDR Information Center

Phone: 1-800-CDC-INFO (800-232-4636) or 1-888-232-6348 (TTY)

Internet, http://www.atsdr.cdc.gov

The following additional material is available online at www.atsdr.cdc.gov:

Case Studies in Environmental Medicine—Case Studies are self-instructional publications designed to
increase primary care provider's knowledge of a hazardous substance in the environment and to
aid in the evaluation of potentially exposed patients.

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1,1-DICHLOROETHANE

viii

Managing Hazardous Materials Incidents is a three-volume set of recommendations for on-scene

(prehospital) and hospital medical management of patients exposed during a hazardous materials
incident. Volumes I and II are planning guides to assist first responders and hospital emergency
department personnel in planning for incidents that involve hazardous materials. Volume III—
Medical Management Guidelines for Acute Chemical Exposures,—is a guide for health care
professionals treating patients exposed to hazardous materials.

Fact Sheets (ToxFAOs™) provide answers to frequently asked questions about toxic substances.

Other Agencies and Organizations

The National Center for Environmental Health (NCEH) focuses on preventing or controlling disease,

injury, and disability related to the interactions between people and their environment outside the
workplace. Contact: NCEH, Mailstop F-29, 4770 Buford Highway, NE, Atlanta,
GA 30341-3724 • Phone: 770-488-7000 • FAX: 770-488-7015.

The National Institute for Occupational Safety and Health (NIOSH) conducts research on occupational
diseases and injuries, responds to requests for assistance by investigating problems of health and
safety in the workplace, recommends standards to the Occupational Safety and Health
Administration (OSHA) and the Mine Safety and Health Administration (MSHA), and trains
professionals in occupational safety and health. Contact: NIOSH, 395 E Street, S.W., Suite 9200,
Patriots Plaza Building, Washington, DC 20201 • Phone: (202) 245-0625 or 1-800-CDC-INFO
(800-232-4636).

The National Institute of Environmental Health Sciences (NIEHS) is the principal federal agency for

biomedical research on the effects of chemical, physical, and biologic environmental agents on
human health and well-being. Contact: NIEHS, PO Box 12233, 104 T.W. Alexander Drive,
Research Triangle Park, NC 27709 • Phone: 919-541-3212.

Clinical Resources

The Association of Occupational and Environmental Clinics (AOEC) has developed a network of clinics
in the United States to provide expertise in occupational and environmental issues. Contact:
AOEC, 1010 Vermont Avenue, NW, #513, Washington, DC 20005 • Phone: 202-347-4976
• FAX: 202-347-4950 • e-mail: AOEC@AOEC.ORG • Web Page: http://www.aoec.org/.

The American College of Occupational and Environmental Medicine (ACOEM) is an association of
physicians and other health care providers specializing in the field of occupational and
environmental medicine. Contact: ACOEM, 25 Northwest Point Boulevard, Suite 700, Elk
Grove Village, IL 60007-1030 • Phone: 847-818-1800 • FAX: 847-818-9266.

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1,1-DICHLOROETHANE

CONTRIBUTORS

CHEMICAL MANAGER(S)/AUTHOR(S):

Malcolm Williams, DVM, Ph.D.

Annette Ashizawa, Ph.D.

G. Daniel Todd, Ph.D.

Eugene Demchuk, Ph.D.

ATSDR, Division of Toxicology and Human Health Sciences, Atlanta, GA

Lisa Ingerman, Ph.D., DABT

Christina Coley, B.S.

Mary Kawa, M.A.

Mario Citra, Ph.D.

SRC, Inc., North Syracuse, NY

THE PROFILE HAS UNDERGONE THE FOLLOWING ATSDR INTERNAL REVIEWS:

1.	Health Effects Review. The Health Effects Review Committee examines the health effects
chapter of each profile for consistency and accuracy in interpreting health effects and classifying
end points.

2.	Minimal Risk Level Review. The Minimal Risk Level Workgroup considers issues relevant to
substance-specific Minimal Risk Levels (MRLs), reviews the health effects database of each
profile, and makes recommendations for derivation of MRLs.

3.	Data Needs Review. The Environmental Toxicology Branch reviews data needs sections to
assure consistency across profiles and adherence to instructions in the Guidance.

4.	Green Border Review. Green Border review assures the consistency with ATSDR policy.

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1,1-DICHLOROETHANE

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1,1-DICHLOROETHANE

PEER REVIEW

A peer review panel was assembled for 1,1-dichloroethane. The panel consisted of the following
members:

1. Gary Stoner, Ph.D., Department of Medicine, Division of Hematology and Oncology, Medical
College of Wisconsin, Milwaukee, Wisconsin;

2. G.A. Shakeel Ansari, Ph.D., Department of Human Biological Chemistry & Genetics and
Pathology, University of Texas Medical Branch, Galveston Texas;

3. Hermann Bolt, Ph.D., Institut fur Arbeitsphysiologie an der Universitat Dortmund (IfADo),
Leibniz Research Centre for Working Environment and Human Factors, Dortmund, Germany.

These experts collectively have knowledge of 1,1-dichloroethane's physical and chemical properties,
toxicokinetics, key health end points, mechanisms of action, human and animal exposure, and
quantification of risk to humans. All reviewers were selected in conformity with the conditions for peer
review specified in Section 104(I)(13) of the Comprehensive Environmental Response, Compensation,
and Liability Act, as amended.

Scientists from the Agency for Toxic Substances and Disease Registry (ATSDR) have reviewed the peer
reviewers' comments and determined which comments will be included in the profile. A listing of the
peer reviewers' comments not incorporated in the profile, with a brief explanation of the rationale for their
exclusion, exists as part of the administrative record for this compound.

The citation of the peer review panel should not be understood to imply its approval of the profile's final
content. The responsibility for the content of this profile lies with the ATSDR.

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1,1-DICHLOROETHANE

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1,1-DICHLOROETHANE	xiii

CONTENTS

DISCLAIMER	ii

UPDATE STATEMENT	iii

FOREWORD	v

QUICK REFERENCE FOR HEALTH CARE PROVIDERS	vii

CONTRIBUTORS	ix

PEER REVIEW	xi

CONTENTS	xiii

LIST OF FIGURES	 	xvii

LIST OF TABLES	xix

1.	PUBLIC HEALTH STATEMENT FOR 1,1-DICHLOROETHANE	1

2.	RELEVANCE TO PUBLIC HEALTH	7

2.1	BACKGROUND AND ENVIRONMENTAL EXPOSURES TO 1,1-DICHLOROETHANE

IN THE UNITED STATES	7

2.2	SUMMARY 01 HEALTH EFFECTS	7

2.3	MINIMAL RISK LEVELS (MRLs)	11

3.	HEALTH EFFECTS	13

3.1	INTRODUCTION	13

3.2	DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE	13

3.2.1	Inhalation Exposure	14

3.2.1.1	Death	14

3.2.1.2	Systemic Effects	15

3.2.1.3	Immunological and Lymphoreticular Effects	20

3.2.1.4	Neurological Effects	20

3.2.1.5	Reproductive Effects	20

3.2.1.6	Developmental Effects	20

3.2.1.7	Cancer	21

3.2.2	Oral Exposure	21

3.2.2.1	Death	21

3.2.2.2	Systemic Effects	26

3.2.2.3	Immunological and Lymphoreticular Effects	27

3.2.2.4	Neurological Effects	27

3.2.2.5	Reproductive Effects	27

3.2.2.6	Developmental Effects	27

3.2.2.7	Cancer	28

3.2.3	Dermal Exposure	29

3.2.3.1	Death	29

3.2.3.2	Systemic Effects	29

3.2.3.3	Immunological and Lymphoreticular Effects	29

3.2.3.4	Neurological Effects	29

3.2.3.5	Reproductive Effects	29

3.2.3.6	Developmental Effects	29

3.2.3.7	Cancer	29

3.3	GENOTOXICITY	31

3.4	TOXICOKINETICS	32

3.4.1 Absorption	32

3.4.1.1 Inhalation Exposure	32

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1,1-DICHLOROETHANE	xiv

3.4.1.2	Oral Exposure	32

3.4.1.3	Dermal Exposure	33

3.4.2	Distribution	33

3.4.2.1	Inhalation Exposure	33

3.4.2.2	Oral Exposure	33

3.4.2.3	Dermal Exposure	33

3.4.2.4	Other Routes of Exposure	34

3.4.3	Metabolism	34

3.4.4	Elimination and Excretion	38

3.4.4.1	Inhalation Exposure	38

3.4.4.2	Oral Exposure	38

3.4.4.3	Dermal Exposure	38

3.4.5	Physiologically Based Pharmacokinetic (PBPK)/Pharmacodynamic (PD) Models	38

3.5	MECHANISMS OF ACTION	41

3.5.1	Pharmacokinetic Mechanisms	41

3.5.2	Mechanisms of Toxicity	41

3.5.3	Animal-to-Human Extrapolations	41

3.6	TOXICITIES MEDIATED THROUGH THE NEUROENDOCRINE AXIS	41

3.7	CHILDREN'S SUSCEPTIBILITY	42

3 .8 BIOMARKERS OF EXPOSURE AND EFFECT	44

3.8.1	Biomarkers Used to Identify or Quantify Exposure to 1,1 -Dichloroethane	46

3.8.2	Biomarkers Used to Characterize Effects Caused by 1,1-Dichloroethane	46

3.9	INTERACTIONS WITH OTHER CHEMICALS	46

3.10	POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE	46

3 .11 METHODS FOR REDUCING TOXIC EFFECTS	47

3.11.1	Reducing Peak Absorption Following Exposure	47

3.11.2	Reducing Body Burden	47

3.11.3	Interfering with the Mechanism of Action for Toxic Effects	47

3.12 ADEQUACY OF THE DATABASE	48

3.12.1	Existing Information on Health Effects of 1,1-Dichloroethane	48

3.12.2	Identification of Data Needs	50

3.12.3	Ongoing Studies	55

4.	CHEMICAL AND PHYSICAL INFORMATION	57

4.1	CHEMICAL IDENTITY	57

4.2	PHYSICAL AND CHEMICAL PROPERTIES	57

5.	PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL	61

5.1	PRODUCTION	61

5.2	IMPORT/EXPORT	63

5.3	USE	63

5.4	DISPOSAL	63

6.	POTENTIAL FOR HUMAN EXPOSURE	65

6.1	OVERVIEW	65

6.2	RELEASES TO THE ENVIRONMENT	67

6.2.1	Air	68

6.2.2	Water	72

6.2.3	Soil	72

6.3	ENVIRONMENTAL FATE	72

6.3.1 Transport and Partitioning	72

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1,1-DICHLOROETHANE	xv

6.3.2 Transformation and Degradation	74

6.3.2.1	Air	74

6.3.2.2	Water	74

6.3.2.3	Sediment and Soil	75

6.4	LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT	76

6.4.1	Air	76

6.4.2	Water	80

6.4.3	Sediment and Soil	83

6.4.4	Other Environmental Media	84

6.5	GENERAL POPULATION AND OCCUPATIONAL EXPOSURE	84

6.6	EXPOSURES OF CHILDREN	87

6.7	POPULATIONS WITH POTENTIALLY HIGH EXPOSURES	87

6.8	ADEQUACY 01 THE DATABASE	88

6.8.1	Identification of Data Needs	88

6.8.2	Ongoing Studies	91

7.	ANALYTICAL METHODS	93

7.1	BIOLOGICAL MATERIALS	93

7.2	ENVIRONMENTAL SAMPLES	99

7.3	ADEQUACY OF THE DATABASE	102

7.3.1	Identification of Data Needs	102

7.3.2	Ongoing Studies	103

8.	REGULATIONS, ADVISORIES, AND GUIDELINES	105

9.	REFERENCES	109

10.	GLOSSARY	127

APPENDICES

A.	ATSDR MINIMAL RISK LEVELS AND WORKSHEETS	A-l

B.	USER'S GUIDE	B-l

C.	ACRONYMS, ABBREVIATIONS, AND SYMBOLS	C-l

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1,1-DICHLOROETHANE

xvii

LIST OF FIGURES

2-1. Health Effects for Following Inhalation Exposure to 1,1-Dichloroethane	9

2-2.	Health Effects for Following Oral Exposure to 1,1-Dichloroethane	10

3-1.	Levels of Significant Exposure to 1,1-Dichloroethane - Inhalation	18

3-2. Levels of Significant Exposure to 1,1-Dichloroethane - Oral	24

3-3. Proposed Metabolic Scheme for 1,1-Dichloroethane	37

3-4. Conceptual Representation of a Physiologically Based Pharmacokinetic (PBPK) Model for a

Hypothetical Chemical Substance	40

3 -5. Existing Information on Health Effects of 1,1 -Dichloroethane	49

6-1. Frequency of NPL Sites with 1,1-Dichloroethane Contamination	66

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1,1-DICHLOROETHANE	xix

LIST OF TABLES

3-1. Levels of Significant Exposure for 1,1-Dichloroethane - Inhalation	16

3-2. Levels of Significant Exposure for 1,1-Dichloroethane - Oral	22

3 -3. Genotoxicity of 1,1 -Dichloroethane In Vitro	30

3-4.	Production of Metabolites from 1,1-Dichloroethane with Hepatic Microsomes from
Phenobarbital-Induced Rats	36

4-1.	Chemical Identity of 1,1 -Dichloroethane	58

4-2.	Physical and Chemical Properties of 1,1-Dichloroethane	59

5-1.	Facilities that Produce, Process, or Use 1,1-Dichloroethane	62

6-1.	Releases to the Environment from Facilities that Produce, Process, or Use 1,1-Dichloroethane	69

6-2. Estimated Yearly Emissions of 1,1-Dichloroethane (mg/m2 per Year)	71

6-3. 2013 Air Monitoring Data from Air Toxics Data Ambient Monitoring Archive for

1,1 -Dichloroethane	77

6-4.	Geometric Mean and Selected Percentiles of Blood Concentrations of 1,1-Dichloroethane
(in ng/L) for the U.S. Population from the National Health and Nutrition Examination

Survey (NHANES)	85

7-1.	Analytical Methods for Determining 1,1-Dichloroethane in Biological Materials	94

7-2.	Analytical Methods for Determining 1,1-Dichloroethane in Environmental Samples	95

8-1.	Regulations, Advisories, and Guidelines Applicable to 1,1-Dichloroethane	106

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1,1-DICHLOROETHANE

1. PUBLIC HEALTH STATEMENT FOR
1,1-DICHLOROETHANE

This Public Health Statement summarizes the Division of Toxicology and Human Health Science's
findings on 1,1-dichloroethane, tells you about it, the effects of exposure, and describes what you can do
to limit that exposure.

The U.S. Environmental Protection Agency (EPA) identifies the most serious hazardous waste sites in the
nation. These sites make up the National Priorities List (NPL) and are sites targeted for long-term federal
clean-up activities. U.S. EPA has found 1,1-dichloroethane in at least 673 of the 1,699 current or former
NPL sites. The total number of NPL sites evaluated for 1,1-dichloroethane is not known. But the
possibility remains that as more sites are evaluated, the sites at which 1,1-dichloroethane is found may
increase. This information is important because these future sites may be sources of exposure, and
exposure to 1,1-dichloroethane may be harmful.

If you are exposed to 1,1-dichloroethane, many factors determine whether you'll be harmed. These
include how much you are exposed to (dose), how long you are exposed (duration), and how you are
exposed (route of exposure). You must also consider the other chemicals you are exposed to and your
age, sex, diet, family traits, lifestyle, and state of health.

WHAT IS 1,1-DICHLOROETHANE?

1,1-Dichloroethane is a colorless oily liquid with a chloroform-like odor. 1,1-Dichloroethane is a
chemical used mostly as an intermediate in the manufacture of 1,1,1-trichloroethane (1,1,1-TCE).
1,1-Dichloroethane is also used in limited amount as a solvent for cleaning and degreasing, and in the
manufacture of plastic wrap, adhesives, and synthetic fiber.

More information on the chemical and physical properties as well as the production and uses of
1,1-dichloroethane is presented in Chapters 4 and 5 of this profile.

WHERE IS 1,1-DICHLOROETHANE FOUND?

1,1-Dichloroethane can be released into the air, water, and soil at places where it is produced or used as a
solvent. The majority of the monitoring data for 1,1-dichloroethane focuses on air and water, specifically

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1,1-DICHLOROETHANE

1. PUBLIC HEALTH STATEMENT

at hazardous waste sites. Minimal data are available for concentrations of 1,1-dichloroethane measured in
soil. It is expected that the lack of available soil data is, in part, due to the rapid partitioning of
1,1 -dichloroethane to air and water from soil or sediment. 1,1 -Dichloroethane has been detected and
measured in air samples at concentrations ranging from parts per trillion (ppt) to parts per million (ppm).
In the air, 1,1-dichloroethane is slow to break down and has the potential for long-range transport.

1,1-Dichloroethane has been detected in drinking water and groundwater. 1,1-Dichloroethane does not
degrade quickly in water, but it can evaporate from the water into the air. Minimal information was found
on concentrations of 1,1-dichloroethane in soil, releases of 1,1-dichloroethane to land surfaces, or the
disposal of waste products containing 1,1-dichloroethane into landfills. 1,1-Dichloroethane released to
soil surfaces would rapidly evaporate to the air. Residual 1,1-dichloroethane remaining on soil surfaces
would be available for transport into groundwater, since it is not expected to bind to soil particulates
unless the organic content of the soil is high. Minimal information was found on the levels of
1,1-dichloroethane in other media.

In a survey of 234 table ready foods evaluated for the presence of volatile organic compounds (VOCs),
1,1-dichloroethane was not found in any of the samples. It was detected in three peanut butter samples at
levels of 1.1, 1.9, and 3.7 micrograms per kilogram (|_ig/kg): however, the compound was not found in
several other foods that were analyzed.

More information on levels of 1,1-dichorethane found in the environment is presented in Chapter 6 of this
profile.

HOW MIGHT I BE EXPOSED TO 1,1-DICHLOROETHANE?

The use of 1,1-dichloroethane as a solvent, cleaning agent, and degreaser, and its use in manufacturing of
other compounds, such as 1,1,1-TCE, may result in releases to the environment. 1,1-Dichloroethane has
been detected in ambient air and water. Exposure to 1,1-dichloroethane occurs mainly by breathing air
near contaminated areas or by drinking water contaminated with 1,1-dichloroethane. However, most
people who are exposed to 1,1-dichloroethane through air or water are exposed to very low levels, in the
range of ppm to ppt. People may be exposed to higher levels of 1,1-dichloroethane if they smoke
cigarettes or are exposed to cigarette smoke. People may also be exposed to 1,1-dichloroethane by using
consumer products that contain this compound.

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1,1-DICHLOROETHANE

1. PUBLIC HEALTH STATEMENT

Job-related exposure of 1,1-dichloroethane results from breathing in workplace air or from touching
contaminated chemicals or materials at workplaces where 1,1-dichloroethane is used. According to a
survey conducted between 1980 and 1983 by the National Institute for Occupational Safety and Health
(NIOSH), an estimated 1,957 people in the United States may have been exposed to 1,1-dichloroethane
while working. In general, people who work with 1,1-dichloroethane or live near industrial emission
sources and hazardous waste sites containing 1,1-dichloroethane are more likely to be exposed.

Additional information on levels in the environment and potential for human exposure is presented in
Chapter 6 of the toxicological profile.

HOW CAN 1,1-DICHLOROETHANE ENTER AND LEAVE MY BODY?

If you breathe air containing 1,1-dichloroethane, it will enter your body through your lungs. 1,1-Di-
chloroethane in your drinking water will enter your body through the digestive tract. We do not know
how much will be absorbed; studies with similar compounds suggested that 1,1-dichloroethane will be
rapidly and extensively absorbed.

1,1-Dichloroethane leaves your body in the breath or is broken down into other chemicals, which leave
your body in the breath or in the urine.

HOW CAN 1,1-DICHLOROETHANE AFFECT MY HEALTH?

No information is available in humans on the health effects associated with occupational or environmental
exposure to 1,1-dichloroethane. 1,1-Dichloroethane was used as an anesthetic; however, it is no longer
used for this purpose because of the heart effects that also occurred at these very high concentrations.

Kidney effects have been observed in cats exposed to 1,1-dichloroethane in air for long periods.

However, kidney effects have not been observed in other animal species following long-term inhalation
or oral exposure.

The results of a study in rats and mice suggest that 1,1-dichloroethane may cause cancer. However, the
study had several flaws and the results are not conclusive. Another long-term study of mice that drank
water containing 1,1-dichloroethane did not find cancer.

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1,1-DICHLOROETHANE

1. PUBLIC HEALTH STATEMENT

The U.S. Department of Health and Human Services (DHHS) and The International Agency for Research
on Cancer (IARC) have not evaluated the carcinogenic potential of 1,1-dichloroethane. The U.S. EPA
has determined that 1,1-dichloroethane is a possible human carcinogen.

See Chapters 2 and 3 for more information on 1,1-dichloroethane health effects.

HOW CAN 1,1-DICHLOROETHANE AFFECT CHILDREN?

This section discusses potential health effects of 1,1-dichloroethane exposure in humans from when
they're first conceived to 18 years of age, and how you might protect against such effects.

No available studies have described the effects of exposure to 1,1-dichloroethane on children or young
animals. Although we think that children would likely show the same health effects as adults, we don't
know whether children are more susceptible than are adults to 1,1-dichloroethane effects.

We don't know whether 1,1-dichloroethane can harm an unborn child. Minor skeletal problems were
observed in the fetuses of rats exposed to 1,1-dichloroethane in the air; decreases in body weight were
also observed in the mothers.

HOW CAN FAMILIES REDUCE THE RISK OF EXPOSURE TO 1,1-DICHLOROETHANE?

If your doctor finds that you have been exposed to significant amounts of 1,1-dichloroethane, ask whether
your children might also be exposed. Your doctor might need to ask your state health department to
investigate.

1,1-Dichloroethane can enter your body from air, water, or consumer products containing this substance.
Contact local drinking water authorities and follow their advice if you have any concerns about the
presence of 1,1 -dichloroethane in your tap water. 1,1 -Dichloroethane has the potential to contaminate
foods, although the levels found in food are generally low. 1,1-Dichloroethane can also be present in
groundwater and soil underneath a building or a home, resulting in above-ground vapors through vapor
intrusion (movement of vapors from groundwater or soil into air). To minimize risks associated with
breathing in contaminated vapors, ensure that the area is well ventilated. If you think that you may have
groundwater contaminated with 1,1-dichloroethane, contact your local state health department. Follow
instructions on product labels to minimize exposure to 1,1-dichloroethane. Storing these items in a shed
or an outside location may reduce exposure and decrease the impact on indoor air.

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1. PUBLIC HEALTH STATEMENT

ARE THERE MEDICAL TESTS TO DETERMINE WHETHER I HAVE BEEN EXPOSED TO
1,1-DICHLOROETHANE?

1,1-Dichloroethane and its breakdown products (metabolites) can be measured in blood and urine.
However, the detection of 1,1-dichoroethane or its metabolites cannot predict the kind of health effects
that might develop from that exposure. Because 1,1-dichloroethane and its metabolites leave the body
fairly rapidly, the tests need to be conducted within days after exposure.

For more information on the different substances formed by 1,1-dichloroethane breakdown and on tests to
detect these substances in the body, see Chapters 3 and 7.

WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE TO PROTECT
HUMAN HEALTH?

The federal government develops regulations and recommendations to protect public health. Regulations
can be enforced by law. Federal agencies that develop regulations for toxic substances include the
Environmental Protection Agency (EPA), the Occupational Safety and Health Administration (OSHA),
and the Food and Drug Administration (FDA). Recommendations provide valuable guidelines to protect
public health but cannot be enforced by law. Federal organizations that develop recommendations for
toxic substances include the Agency for Toxic Substances and Disease Registry (ATSDR) and the
National Institute for Occupational Safety and Health (NIOSH).

Regulations and recommendations can be expressed as "not-to-exceed" levels; that is, levels of a toxic
substance in air, water, soil, or food that do not exceed a critical value usually based on levels that affect
animals; levels are then adjusted to help protect humans. Sometimes these not-to-exceed levels differ
among federal organizations. Different organizations use different exposure times (an 8-hour workday or
a 24-hour day), different animal studies, or emphasize some factors over others, depending on their
mission.

Recommendations and regulations are also updated periodically as more information becomes available.
For the most current information, check with the federal agency or organization that issued the regulation
or recommendation.

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1. PUBLIC HEALTH STATEMENT

6

OSHA set a legal limit of 100 ppm 1,1-dichloroethane in workplace air averaged over an 8-hour work
day. NIOSH recommends a limit of 100 ppm 1,1-dichloroethane in workplace air averaged over a
10-hour work day.

WHERE CAN I GET MORE INFORMATION?

If you have any questions or concerns, please contact your community or state health or environmental
quality department, or contact ATSDR at the address and phone number below. ATSDR can also provide
publically available information regarding medical specialists with expertise and experience recognizing,
evaluating, treating, and managing patients exposed to hazardous substances.

•	Call the toll-free information and technical assistance number at
1-800-CDCINFO (1-800-232-4636) or

•	Write to:

Agency for Toxic Substances and Disease Registry

Division of Toxicology and Human Health Sciences

1600 Clifton Road NE

Mailstop F-57

Atlanta, GA 30329-4027

Toxicological profiles and other information are available on ATSDR's web site:
http: //www. atsdr .cdc .gov.

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2. RELEVANCE TO PUBLIC HEALTH

2.1 BACKGROUND AND ENVIRONMENTAL EXPOSURES TO 1,1-DICHLOROETHANE IN
THE UNITED STATES

The production and use of 1,1-dichloroethane as a solvent, cleaning agent, and degreaser, and in the
manufacture of 1,1,1-trichloroethane, vinyl chloride, and high vacuum rubber may result in its release to
the environment. Volatilization is expected to be high based on its vapor pressure and Henry's Law
constant. Atmospheric photooxidation occurs slowly in the environment, as does biodegradation and
hydrolysis. 1,1-Dichloroethane has high mobility in soil and has the potential to leach from surface soils
into groundwater. The bioaccumulation potential of 1,1-dichloroethane is low.

Monitoring data indicate that the general population may be exposed to 1,1-dichloroethane via inhalation
for people living near source areas, ingestion of contaminated drinking water, and use of consumer
products such as paint removers, which may contain this compound. Ingestion of food sources
contaminated with 1,1-dichloroethane is not an important exposure pathway.

A National Health and Nutrition Survey of the U.S. population in 2003-2004 screened for 1,1-dichloro-
ethane in blood from 1,367 participants (670 males and 679 females) in the age range of 20-59 years old.
The portion of the data below the limit of detection (LOD) was too high to provide valid results.

2.2 SUMMARY OF HEALTH EFFECTS

Relatively little information is available on the health effects of 1,1-dichloroethane in humans or animals.
Chlorinated aliphatics as a class are known to cause central nervous system depression and respiratory
tract and dermal irritation when humans are exposed by inhalation to sufficiently high levels. In the past,
1,1-dichloroethane was used as an anesthetic; however, this use was discontinued due to the risk of
cardiac arrhythmia induction in humans at anesthetic doses (approximately 26,000 ppm). A small number
of animal studies have examined the toxicity and carcinogenicity of 1,1-dichloroethane; these studies
have failed to conclusively identify the critical targets of toxicity. Nonneoplastic effects are limited to
renal toxicity in cats, maternal and fetal toxicity in rats, and alterations in body weight gain. Crystal
precipitations and obstruction in the renal tubule lumina and increases in serum urea and creatinine were
observed in cats exposed to 500 ppm for 13 weeks followed by a 13-week exposure to 1,000 ppm for
13 weeks. However, these effects were not observed in rats, guinea pigs, or rabbits similarly exposed to
1,1-dichloroethane, and renal effects have not been observed following gavage administration of 764 or

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1,1-DICHLOROETHANE

2. RELEVANCE TO PUBLIC HEALTH

950 mg/kg/day in rats or 2,885 or 3,331 mg/kg/day in mice 5 days/week for 78 weeks or in mice exposed
to 465 mg/kg/day 1,1-dichloroethane in drinking water for 52 weeks. Kidney effects have also been
observed in mice administered a lethal intraperitoneal injection of 1,1-dichloroethane; the effects included
increased glucose and protein in the urine and tubular swelling. The toxicological significance of the
nephrotoxicity observed in cats and the mice with regard to human health is not known given the small
number of animals tested (cats), the lack of a nephrotoxic effect in other species and in other studies
where 1,1-dichloroethane was administered orally.

The liver is the only other organ that has been examined in multiple studies; no hepatic effects have been
reported following intermediate-duration inhalation exposure of rats, guinea pigs, rabbits, or cats,
intermediate-duration oral exposure of mice, or chronic-duration exposure of rats and mice. The potential
reproductive toxicity, immunotoxicity, and neurotoxicity of 1,1-dichloroethane have not been examined
following inhalation, oral, or dermal exposure. A single developmental toxicity study reported retarded
fetal development (delayed ossification of vertebrae) in rats at 6,000 ppm (7 hours/day on gestation
days 6-15); an 11% decrease in maternal body weight gain and a decrease in maternal food consumption
were also reported at this concentration. There is inconclusive evidence that 1,1-dichloroethane may be
carcinogenic in rodents. A significant positive dose-related trend was observed for the incidence of
hemangiosarcomas and mammary adenocarcinomas in female rats, hepatocellular carcinomas in male
mice, and endometrial stromal polyps in female mice. However, only the incidence of endometrial
stromal polyps in female mice was significantly increased over the corresponding control animals.
Limitations in this study, particularly the poor survival in treated and control animals, preclude the
consideration of these results as conclusive evidence of carcinogenicity. A 52-week drinking water study,
testing much lower doses, did not find increases in the incidence of lung, liver, or kidney tumors in mice.
Based on the available carcinogenicity data for 1,1-dichloroethane and supporting data on 1,2-dichloro-
ethane, the EPA has classified 1,1-dichloroethane as a possible human carcinogen (group C). Neither the
Department of Health and Human Services nor the International Agency for Research on Cancer have
classified the carcinogenic potential of 1,1-dichloroethane.

An overview of these data is presented in Figures 2-1 and 2-2.

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1,1-DICHLOROETHANE

9

2. RELEVANCE TO PUBLIC HEALTH

Figure 2-1. Health Effects for Following Inhalation Exposure to

1,1-Dichloroethane

a11 % decrease in maternal body weight gain and increased incidence of fetuses with delayed
ossification

increased serum urea and creatinine levels, crystal precipitations and obstruction in tubule
lumina and dilatation of proximal section of renal tubules

TWA = time-weighted average

Dose (ppm)

Effects in Animals

Maternal and developmental effects in
rats3

750 (TWA)

Renal effects in catsb; no liver or kidney
effects in rats, guinea pigs, or rabbits

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1,1-DICHLOROETHANE

10

2. RELEVANCE TO PUBLIC HEALTH

Figure 2-2. Health Effects for Following Oral Exposure to 1,1-Dichloroethane

Dose (mg/kg/day)a

2,061 (males);
2,379 (females),

546 (males);
679 (females)

401 (males)

Effects in Animals

Highest no-effect level in mice following
chronic exposure

Highest no-effect level in rats following
chronic exposure

Decreases in body weight gain in rats
following 5 week exposure3

aDoses adjusted for intermittent exposure (5 days/week)

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2. RELEVANCE TO PUBLIC HEALTH

11

2.3 MINIMAL RISK LEVELS (MRLs)

Inhalation MRLs

There are limited data to derive inhalation MRLs for 1,1-dichloroethane; the database consists of two
inhalation studies. Hofmann et al. (1971) examined the potential for 1,1-dichloroethane to induce liver
and/or kidney effects in rats, guinea pigs, rabbits, and cats exposed to 500 ppm 6 hours/day, 5 days/week
for 13 weeks followed by a second 13-week exposure period to 1,000 ppm. No adverse effects were
observed in the rats, guinea pigs, or rabbits. In three of four cats, increases in serum urea and creatinine
levels and renal tubular effects (crystalline precipitates, obstruction of lumina, and dilatation) were
observed at the end of the 26-week period. Tubular degeneration and periglomerular fibrosis were also
noted; however, it is not known if this was observed in all affected cats. In a developmental toxicity
study (Schwetz et al. 1974), decreases in maternal body weight gain and decreases in maternal food
consumption were observed in rats exposed to 3,800 or 6,000 ppm 1,1-dichloroethane on gestation
days 6-15 (7 hours/day); the magnitude of the decrease in weight gain was 8 and 11%, respectively.
Increases in the incidence of fetuses with delayed ossification of sternebrae were also observed at
6,000 ppm. No other developmental effects, including alterations in fetal resorptions, fetal growth, or
incidences of gross or soft tissue anomalies, were observed.

These studies examined a limited number of end points and there is a great deal of uncertainty regarding
the primary targets of toxicity following inhalation exposure. The lowest adverse effect level that has
been identified is 750 ppm (time-weighted average) for renal effects in cats following a 26-week exposure
(Hofmann et al. 1971). However, this effect has not been corroborated in other species following
inhalation (Hofmann et al. 1971) or oral (Klaunig et al. 1986; NCI 1977) exposure. Additionally, it is not
known if cats are a good model for 1,1-dichloroethane-induced crystal formation and tubular damage and
there is uncertainty regarding the threshold concentration for these renal effects due to the exposure
protocol, which involved increasing the exposure concentration mid-way through the study. Both
maternal and fetal growth retardation were observed at 6,000 ppm in an acute-duration study; however, it
is not known if systemic or neurological effects would occur at lower concentrations. 1,1-Dichloroethane
has anesthetic properties at fairly high concentrations (approximately 26,000 ppm) (Miller et al. 1965), a
concentration also associated with cardiac arrhythmias (Reid and Muianga 2012). It is not known if
exposure to lower concentrations would also result in central nervous system depressive effects or
cardiotoxic effects because these end points have not been examined. Uncertainties associated with

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2. RELEVANCE TO PUBLIC HEALTH

12

identification of the most sensitive target and the associated concentration-response relationships,
precludes deriving inhalation MRLs for 1,1-dichloroethane.

Oral MRLs

Two studies have examined the oral toxicity of 1,1-dichloroethane following intermediate- or chronic-
duration exposure. No lung, liver, or kidney effects were observed in mice exposed to doses as high as
465 mg/kg/day 1,1-dichloroethane in drinking water for 52 weeks (Klaunig et al. 1986); no other potential
targets were examined. Similarly, no nonneoplastic effects were noted in major tissues and organs of rats
and mice administered 1,1-dichloroethane in corn oil 5 days/week for 78 weeks (NCI 1977). The highest
doses tested were 764 and 950 mg/kg/day, respectively, in male and female rats and 2,885 and
3,331 mg/kg/day, respectively, in male and female mice. A 6-week study found decreases in body weight
gain (>16%) in male rats administered 562 mg/kg/day and female rats administered 1,780 mg/kg/day
1,1-dichloroethane 5 days/week in corn oil (NCI 1977). No additional information was reported, and the
cause of the decreased weight gain is not known. The chronic-duration rat study did not find significant
alterations in body weight gain at higher concentrations in the male rats. Thus, the oral studies have not
identified a target of toxicity, precluding the derivation of oral MRLs for 1,1-dichloroethane.

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1,1-DICHLOROETHANE

13

3. HEALTH EFFECTS

3.1	INTRODUCTION

The primary purpose of this chapter is to provide public health officials, physicians, toxicologists, and
other interested individuals and groups with an overall perspective on the toxicology of
1,1-dichloroethane. It contains descriptions and evaluations of toxicological studies and epidemiological
investigations and provides conclusions, where possible, on the relevance of toxicity and toxicokinetic
data to public health.

A glossary and list of acronyms, abbreviations, and symbols can be found at the end of this profile.

3.2	DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE

To help public health professionals and others address the needs of persons living or working near
hazardous waste sites, the information in this section is organized first by route of exposure (inhalation,
oral, and dermal) and then by health effect (death, systemic, immunological, neurological, reproductive,
developmental, genotoxic, and carcinogenic effects). These data are discussed in terms of three exposure
periods: acute (14 days or less), intermediate (15-364 days), and chronic (365 days or more).

Levels of significant exposure for each route and duration are presented in tables and illustrated in
figures. The points in the figures showing no-observed-adverse-effect levels (NOAELs) or lowest-
observed-adverse-effect levels (LOAELs) reflect the actual doses (levels of exposure) used in the studies.
LOAELs have been classified into "less serious" or "serious" effects. "Serious" effects are those that
evoke failure in a biological system and can lead to morbidity or mortality (e.g., acute respiratory distress
or death). "Less serious" effects are those that are not expected to cause significant dysfunction or death,
or those whose significance to the organism is not entirely clear. ATSDR acknowledges that a
considerable amount of judgment may be required in establishing whether an end point should be
classified as a NOAEL, "less serious" LOAEL, or "serious" LOAEL, and that in some cases, there will be
insufficient data to decide whether the effect is indicative of significant dysfunction. However, the
Agency has established guidelines and policies that are used to classify these end points. ATSDR
believes that there is sufficient merit in this approach to warrant an attempt at distinguishing between
"less serious" and "serious" effects. The distinction between "less serious" effects and "serious" effects is
considered to be important because it helps the users of the profiles to identify levels of exposure at which
major health effects start to appear. LOAELs or NOAELs should also help in determining whether or not

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3. HEALTH EFFECTS

the effects vary with dose and/or duration, and place into perspective the possible significance of these
effects to human health.

The significance of the exposure levels shown in the Levels of Significant Exposure (LSE) tables and
figures may differ depending on the user's perspective. Public health officials and others concerned with
appropriate actions to take at hazardous waste sites may want information on levels of exposure
associated with more subtle effects in humans or animals (LOAELs) or exposure levels below which no
adverse effects (NOAELs) have been observed. Estimates of levels posing minimal risk to humans
(Minimal Risk Levels or MRLs) may be of interest to health professionals and citizens alike.

3.2.1 Inhalation Exposure

Very little information is available regarding the health effects of 1,1-dichloroethane following inhalation
exposure in humans or animals. 1,1-Dichloroethane was used in the past as an anesthetic at a pressure of
0.026 atm, which is approximately equivalent to a concentration of 105,000 mg/m3 (26,000 ppm) (Miller
et al. 1965). This use was discontinued when it was discovered that this compound induced cardiac
arrhythmias at anesthetic doses (Reid and Muianga 2012).

Table 3-1 and Figure 3-1 describe the health effects observed in laboratory animals associated with
inhalation exposure levels at varying time and exposure durations.

3.2.1.1 Death

No studies were located regarding death in humans following inhalation exposure to 1,1-dichloroethane.
In a review paper, Smyth (1956) reported that no deaths were observed in rats exposed to 4,000 ppm for
8 hours, but an 8-hour exposure to 16,000 ppm was lethal. It has been reported in the early literature that
the lethal exposure level of 1,1-dichloroethane in mice was 17,500 ppm (Reid and Muianga 2012). These
values were reported in a secondary source and it is therefore impossible to assess their validity.
Subchronic intermittent exposure to 500 ppm of 1,1-dichloroethane for 13 weeks followed by 1,000 ppm
of 1,1-dichloroethane for an additional 13 weeks was not lethal to rats, rabbits, guinea pigs, or cats
(Hofmann et al. 1971).

The highest NOAEL values for death in each species and duration category are recorded in Table 3-1 and
plotted in Figure 3-1.

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3. HEALTH EFFECTS

3.2.1.2 Systemic Effects

No studies were located regarding respiratory, gastrointestinal, hematological, musculoskeletal, or
dermal/ocular effects in humans or animals following inhalation exposure to 1,1-dichloroethane.

Cardiovascular Effects. A cardiostimulatory effect resulting in arrhythmias prompted the
discontinuance of the use of 1,1-dichloroethane as an anesthetic in humans (Reid and Muianga 2012).

This effect was noted at the relatively high dose used to induce anesthesia (0.026 atm, which is
approximately equivalent to 105,000 mg/m3, or 26,000 ppm) (Miller et al. 1965). No studies were located
regarding cardiovascular effects in animals following inhalation exposure to 1,1-dichloroethane.

Hepatic Effects. No studies were located regarding hepatic effects in humans following inhalation
exposure to 1,1-dichloroethane. Rats, rabbits, guinea pigs, and cats experienced no change in serum
alanine aminotransferase or aspartate aminotransferase activity after intermittent 6-hour inhalation
exposure to 500 ppm 1,1-dichloroethane for 13 weeks followed by 13 weeks of exposure 6 hours/day to
1,000 ppm 1,1-dichloroethane (Hofmann et al. 1971). Furthermore, no treatment-related histopatho-
logical lesions were noted in the livers of these animals after this 26-week exposure regimen. Six days
after termination of a 10-day exposure to 6,000 ppm 1,1-dichloroethane (7 hours/day), a slight but
statistically significant increase in relative liver weight (26% higher than controls) was observed in female
Sprague-Dawley rats (Schwetz et al. 1974). However, there was no increase in aspartate amino-
transferase activity over control values, and no changes in the gross appearance of the liver were noted at
necropsy in these animals; the slight increase in liver weight was not considered adverse.

Renal Effects. No studies were located regarding renal effects in humans following inhalation
exposure to 1,1-dichloroethane. Renal injury was apparent in cats intermittently exposed 6 hours/day to
1,000 ppm 1,1-dichloroethane for 13 weeks following 13 weeks of intermittent exposure to 500 ppm
1,1-dichloroethane (Hofmann et al. 1971). Serum urea and creatinine were increased in these animals.
One cat was so severely affected that it had to be removed from the study. Histopathological lesions in
the kidney tubules (including crystalline precipitates and dilation) were noted in three of four cats at
necropsy; renal tubular degenerations without preliminary lumen displacement and periglomerular
fibrosis and tubule destruction were also observed. The ill health of these animals was also manifest by a
progressive decrease in body weight. Rats, rabbits, and guinea pigs similarly exposed to 1,1-dichloro-
ethane exhibited no adverse effects.

-------
Table 3-1 Levels of Significant Exposure to 1,1-Dichloroethane - Inhalation

Key to Species
Figure (Strain)

Exposure/
Duration/
Frequency
(Route)

LOAEL

System

NOAEL
(PPm)

Less Serious
(PPm)

Serious
(PPm)

Reference
Chemical Form

Comments

ACUTE EXPOSURE

Systemic

1

Rat

(Sprague-
Dawley)

Developmental

2 Rat

(Sprague-
Dawley)

7 hr/d
10 d

7 hr/d
Gd 6-15

Hepatic

6000 F

3000 F

6800 F (Increased incidence of
delayed ossification)

Schwetz et al. 1974

Schwetz et al. 1974

INTERMEDIATE EXPOSURE

Systemic

Rat

(Sprague-
Dawley)

6 hr/d
5 d/wk
26 wk

Hepatic

750

Hofmann et al. 1971
1,1-DCE

Renal
Bd Wt

750
750

Gn Pig

(Firbright-

White)

6 hr/d
5 d/wk
26 wk

Hepatic

750

Hofmann et al. 1971
1,1-DCE

Renal
Bd Wt

750
750

Rabbit
(Brunte)

6 hr/d
5 d/wk
26 wk

Hepatic

750

Hofmann et al. 1971
1,1-DCE

Renal

750

Bd Wt

750

-------
Table 3-1 Levels of Significant Exposure to 1,1-Dichloroethane - Inhalation

(continued)

Exposure/ LOAEL
Duration/		

Key to Species Frequency	NOAEL Less Serious	Serious	Reference

Figure (Strain) ^ ^	System (ppm)	(ppm)	(ppm)	Chemical Form

Cat
(NS)

6 hr/d
5 d/wk
26 wk

Hepatic

750

Hofmann et al. 1971
1,1-DCE

Renal

750 (crystal precipitation and
obstruction in tubule
lumina)

Bd Wt	750

Comments

a The number corresponds to entries in Figure 3-1.

Bd Wt = body weight; d = day(s); F = Female; Gd = gestational day; Gn pig = guinea pig; hr = hour(s); LOAEL = lowest-observed-adverse-effect level; NOAEL =
no-observed-adverse-effect level; NS = not specified; wk = week(s)

-------
Figure 3-1 Levels of Significant Exposure to 1,1 -Dichloroethane - Inhalation

Acute (<14 days)

Systemic	^

ppm ——



10000

0

1

I-

o

73

o

I
>

Cl2r

;ir

J2r

CO

I
m
>

O
—I

w

1000

r-Rat	~ Cancer Effect Level-Animals

•	LOAEL, More Serious-Animals

*	LOAEL, Less Serious-Animals
NOAEL - Animals

~ Cancer Effect Level-Humans
A LOAEL, More Serious-Humans
^ LOAEL, Less Serious-Humans
NOAEL - Humans

¦ LD50/LC50
Minimal Risk Level
for effects
other than
Cancer

00

-------
Figure 3-1 Levels of Significant Exposure to 1,1-Dichloroethane - Inhalation (Continued)

Intermediate (15-364 days)

Systemic













36c 4g 3r 5h Cl6c 4g 3r 5h 6c 4g 3r 5h

c-Cat
r-Rat
h-Rabbit
g-Guinea Pig

•	Cancer Effect Level-Animals

•	LOAEL, More Serious-Animals

•	LOAEL, Less Serious-Animals
ONOAEL - Animals

~ Cancer Effect Level-Humans
A LOAEL, More Serious-Humans
4 LOAEL, Less Serious-Humans
ANOAEL - Humans

ILD50/LC50
Minimal Risk Level
for effects
„ other than
Cancer

-------
1,1-DICHLOROETHANE

3. HEALTH EFFECTS

3.2.1.3 Immunological and Lymphoreticular Effects

No studies were located regarding immunological effects in humans or animals after inhalation exposure
to 1,1-dichloroethane.

3.2.1.4 Neurological Effects

Since 1,1-dichloroethane was once used as a gaseous anesthetic, it can be inferred that it causes central
nervous system depression upon acute exposure. No information is available on the long-term neurologic
effects of inhaled 1,1-dichloroethane in humans.

No studies were located regarding neurologic effects in animals after inhalation exposure to 1,1-dichloro-
ethane.

3.2.1.5 Reproductive Effects

No studies were located regarding developmental effects in humans or animals following inhalation
exposure to 1,1 -dichloroethane.

3.2.1.6 Developmental Effects

No studies were located regarding reproductive effects in humans following inhalation exposure to
1,1 -dichloroethane.

One study examined the developmental toxic potential of 1,1-dichloroethane following inhalation
exposure. No alterations in litter size, fetal resorptions, fetal growth, or incidences of gross or soft tissue
anomalies were observed in the offspring of Sprague-Dawley rats exposed to 3,800 or 6,000 ppm

7 hours/day on gestation days 6-15 (Schwetz et al. 1974). A significant increase in the incidence of
fetuses with delayed ossification of sternebrae was observed at 6,000 ppm. Maternal food consumption
and body weight were significantly reduced in the treated animals during the exposure period but returned
to normal by day 21 of gestation; on gestation day 3, dams in the 3,800 and 6,000 ppm groups weighed

8 and 11% less than controls, respectively. No other adverse effects were noted in the dams. Based on
the observed effects, the LOAEL value for the developmental toxicity of 1,1-dichloroethane in rats was
6,000 ppm; the NOAEL was 3,800 ppm. These values are listed in Table 3-1 and plotted in Figure 3-1.

-------
1,1-DICHLOROETHANE

3. HEALTH EFFECTS

3.2.1.7 Cancer

No studies were located regarding cancer in humans or animals after inhalation exposure to 1,1-dichloro-
ethane.

3.2.2 Oral Exposure

Two studies were located that investigated the health effects associated with oral exposure to 1,1-di-
chloroethane in rats and mice (Klaunig et al. 1986; NCI 1977). With the exception of body weight
depression observed in one subchronic range-finding study, neither one provided any conclusive evidence
of adverse toxic effects associated with oral exposure to 1,1-dichloroethane.

Table 3-2 and Figure 3-2 describe the health effects observed in laboratory animals associated with oral
exposure levels at varying time and exposure durations. No MRLs to humans for adverse effects (other
than cancer) were calculated for the oral route of exposure because of the limited database.

3.2.2.1 Death

No studies were located regarding death in humans following oral exposure to 1,1-dichloroethane.

Secondary sources report the following oral LD50 values in rats: 725 mg/kg (Lewis 2004) and 14.1 g/kg
(Archer 1978). Since these values were obtained from secondary sources, no details were available to
assess the quality of these data. Survival was poor in both treated and control rats and mice in the chronic
bioassay conducted by the National Cancer Institute (NCI 1977), but a significant dose-related trend for
mortality was noted in the male rats and mice. The deaths could not be attributed to cancer or any other
non-neoplastic lesions, although pneumonia was observed in a large percentage of the rats, and this was
thought to be related to the increased mortality (NCI 1977).

The highest NOAEL values and all reliable LOAEL values for death in each species and duration
category are recorded in Table 3-2 and plotted in Figure 3-2.

-------
Table 3-2 Levels of Significant Exposure to 1,1 -Dichloroethane - Oral

Key to Species
Figure (Strain)

Exposure/
Duration/
Frequency
(Route)

LOAEL

NOAEL Less Serious
System (mg/kg/day) (mg/kg/day)

Serious
(mg/kg/day)

Reference
Chemical Form

Comments

INTERMEDIATE EXPOSURE

Death

1 Rat

(Osborne-
Mendel)

5	d/wk

6	wk
(GO)

3160 F (2/5 rats died)

NCI 1977
1,1-DCE

2	Mouse
(B6C3F1)

Systemic

3	Rat
(Osborne-
Mendel)

5	d/wk

6	wk
(GO)

5	d/wk

6	wk
(GO)

Bd Wt

562 M (16% decreased body
weight gain)

5620 (4/10 deaths)

1000 M (29% decreased body
weight gain)

NCI 1977
1,1-DCE

NCI 1977
1,1-DCE

Mouse	daily

(B6C3F1) 52 wk
(W)

Resp

Hepatic
Renal
Bd Wt

465 M

465 M
465 M
465 M

Mouse
(B6C3F1)

5	d/wk

6	wk
(GO)

Bd Wt

2885 M

Klaunig et al. 1986
1,1-DCE

NCI 1977
1,1-DCE

-------
Table 3-2 Levels of Significant Exposure to 1,1 -Dichloroethane - Oral

(continued)

Exposure/
Duration/

LOAEL

Key to Species Frequency

Figure (Strain)

(Route)

NOAEL Less Serious
System (mg/kg/day) (mg/kg/day)

Serious
(mg/kg/day)

Reference
Chemical Form

Comments

CHRONIC EXPOSURE

Systemic

6 Rat	5 d/wk

(Osborne-	78 wk

Mendel)	(GO)

7 Mouse	5 d/wk

(B6C3F1) 78 wk
(GO)

Resp

764 M

Cardio

764 M

Hemato

764 M

Musc/skel

764 M

Hepatic

764 M

Renal

764 M

Endocr

764 M

Dermal

764 M

Bd Wt

764 M

Resp

2885 M

Cardio

2885 M

Gastro

2885 M

Musc/skel

2885 M

Hepatic

2885 M

Renal

2885 M

Endocr

2885 M

Dermal

2885 M

Bd Wt

2885 M

NCI 1977
1,1-DCE

NCI 1977
1,1-DCE

a The number corresponds to entries in Figure 3-2.

Bd Wt = body weight; Cardio = cardiovascular; d = day(s); Endocr = endocrine; F = Female; Gastro = gastrointestinal; (GO) = gavage in oil; Hemato = hematological; hr = hour(s);
LOAEL = lowest-observed-adverse-effect level; M = male; Musc/skel = musculoskeletal; NOAEL = no-observed-adverse-effect level; NS = not specified; Resp = respiratory; (W) =
drinking water; wk = week(s)

-------
Figure 3-2 Levels of Significant Exposure to 1,1-Dichloroethane - Oral

Intermediate (15-364 days)

mg/kg/day
10000

Systemic

^ <#£>



•2n

»1r

--'5m

1000

•3r

»3r

4m 4m 4m 4m

0

1
r~
O
XJ

o

I
>

O)

X
m
>

o

—i
C/)

100

r-Rat

~ Cancer Effect Level-Animals

~ Cancer Effect Level-Humans

¦ LD50/LC50

m-Mouse

• LOAEL, More Serious-Animals

A LOAEL, More Serious-Humans

Minimal Risk Level

• LOAEL, Less Serious-Animals

^ LOAEL, Less Serious-Humans

for effects



NOAEL - Animals

"NOAEL - Humans

^ other than







Cancer

N)
4^

-------
Figure 3-2 Levels of Significant Exposure to 1,1-Dichloroethane - Oral (Continued)

Chronic (>365 days)

Systemic

&	^ ^	^j>6

#

O
X
r~
O
XJ

o

X
>

- 7m - 7m - 7m

- 7m - 7m - 7m - 7m - 7m - 7m

O)

x
m
>

1000

O
—i

w

6r 6r

6r 6r 6r 6r 6r 6r 6r

100

r-Rat	~Cancer Effect Level-Animals

m-Mouse	• LOAEL, More Serious-Animals

• LOAEL, Less Serious-Animals
' ;NOAEL- Animals

~ Cancer Effect Level-Humans
A LOAEL, More Serious-Humans
A LOAEL, Less Serious-Humans
ANOAEL - Humans

ILD50/LC50
Minimal Risk Level
for effects
x other than
Cancer

-------
1,1-DICHLOROETHANE

3. HEALTH EFFECTS

3.2.2.2 Systemic Effects

No studies were located regarding systemic effects in humans following oral exposure to 1,1-dichloro-
ethane.

There were no treatment-related histopathological changes in the liver, kidneys, or other tissues of the rats
examined in the NCI (1977) study. Similarly, no histopathological alterations were noted in the liver,
kidneys, or lungs of male mice that ingested relatively high levels of 1,1-dichloroethane in drinking water
(up to 2500 mg/L) for 52 weeks (Klaunig et al. 1986).

Respiratory Effects. No histological alterations were observed in the lungs of mice exposed to
465 mg/kg/day 1,1-dichloroethane in drinking water for 52 weeks (Klaunig et al. 1986). Similarly, no
significant alterations in respiratory tract lesions were observed in rats or mice chronically exposed to
1,1-dichloroethane for 78 weeks (NCI 1977). The highest gavage doses were 764 and 950 mg/kg/day
(5 days/week) in male and female rats, respectively, and 2,885 and 3,331 mg/kg (5 days/week) in male
and female mice, respectively.

Cardiovascular Effects. The NCI (1977) chronic-duration gavage study did not find significant
alterations in the incidence of lesions in the cardiovascular system.

Gastrointestinal Effects. No gastrointestinal effects were reported in rats or mice administered
gavage doses of 1,1-dichloroethane for 78 weeks (NCI 1977).

Hematological Effects. No histological alterations were observed in hematological tissues in rats or
mice chronically exposed to 1,1-dichloroethane (NCI 1977); however, the study did not examine the
potential for alterations in erythrocyte or leukocyte counts or hemoglobin levels.

Musculoskeletal Effects. No musculoskeletal alterations were reported in the NCI (1977) chronic
study of rats and mice.

Hepatic Effects. No nonneoplastic alterations were observed in mice exposed to 465 mg/kg/day via
drinking water for 52 weeks (Klaunig et al. 1986) or in rats or mice administered 764/950 mg/kg/day or

-------
1,1-DICHLOROETHANE

3. HEALTH EFFECTS

2,885/3,331 mg/kg/day 1,1-dichloroethane, respectively, viagavage 5 days/week for 78 weeks (NCI
1977).

Renal Effects. Intermediate-duration drinking exposure of mice (Klaunig et al. 1986) or chronic
gavage administration to rats and mice (NCI 1977) did not result in significant alteration in the occurrence
of renal lesions.

Endocrine Effects. No histological alterations in endocrine tissues were observed in rats or mice
chronically administered 1,1-dichloroethane (NCI 1977).

Dermal Effects. No dermal effects were noted in rats or mice administered 1,1-dichloroethane for
78 weeks (NCI 1977).

Ocular Effects. No eye damage was noted in rats or mice following chronic administration of
1,1-dichloroethane (NCI 1977).

Body Weight Effects. Administration of doses as high as 562 mg/kg/day in male rats and
1,780 mg/kg/day in female rats 5 days/week for 6 weeks resulted in decreases in body weight gain
(>16%) (NCI 1977); no alterations in body weight were observed in mice similarly exposed to doses as
high as 10,000 mg/kg/day (NCI 1977). This study did not find significant decreases in body weight gain
following 78 weeks of exposure (5 days/week) to 764 and 950 mg/kg/day, respectively, in male and
female rats and 2,885 and 3,331 mg/kg/day, respectively, in male and female mice (NCI 1977).

Similarly, no alterations in body weight gain were observed in mice exposed to 465 mg/kg/day in
drinking water for 52 weeks (Klaunig et al. 1986).

No studies were located regarding the following health effects in humans or animals following oral
exposure to 1,1 -dichloroethane:

3.2.2.3 Immunological and Lymphoreticular Effects

3.2.2.4 Neurological Effects

3.2.2.5 Reproductive Effects

3.2.2.6 Developmental Effects

-------
1,1-DICHLOROETHANE

3. HEALTH EFFECTS

3.2.2.7 Cancer

No studies were located regarding carcinogenic effects in humans following oral exposure to
1,1-dichloroethane. The results of the bioassay conducted by NCI (1977) suggest carcinogenic effects
induced by 1,1-dichloroethane in rats and mice. A significant positive dose-related trend was observed
for the incidence of hemangiosarcomas and mammary adenocarcinomas in female rats, hepatocellular
carcinoma in male mice, and endometrial stromal polyps in female mice. However, only the incidence of
endometrial stromal polyps in female mice exposed to 3,331 mg/kg/day, 5 days/week was significantly
increased over the corresponding control animals. When only male mice surviving at least 52 weeks were
examined, there was a significant increase in the incidence of hepatocellular carcinomas in the
2,885 mg/kg/day group. There are several limitations to this study. Survival was poor in both treated and
control animals, thereby limiting the validity of these results. Although survival was significantly lower
in the exposed groups, it is not clear that the increase in mortality was treatment-related. Furthermore,
there were no other treatment-related effects on body weight, clinical signs, or the incidence of non-
neoplastic lesions. Because of the high mortality in both the treated and control animals, the authors
concluded that not enough animals survived to be at risk for late-developing tumors. Thus, though the
results of this bioassay suggest that 1,1-dichloroethane is carcinogenic to rats and mice, the evidence is
not conclusive.

The carcinogenicity of 1,1-dichloroethane was also examined in mice exposed to 155 or 465 mg/kg/day
of the compound in the drinking water for 52 weeks (Klaunig et al. 1986). A two-stage carcinogenesis
protocol was also employed in this study to assess the ability of 1,1-dichloroethane to act as a tumor
promoter. Neither 1,1-dichloroethane-treated animals initiated with diethylnitrosamine (DENA) or
animals treated with 1,1-dichloroethane without initiation showed a significant increase in the incidence
of lung or liver tumors over their corresponding controls. However, the conclusion that 1,1 -dichloro-
ethane is not a tumor promoter may not be entirely justified since a maximal response was observed in
terms of tumor incidence in the DENA-alone-treated mice (100% tumor incidence at 52 weeks).
Therefore, an increase in the incidence of liver tumors due to 1,1-dichloroethane following DENA
initiation, if it existed, could not have been detected. Furthermore, since measurement of water
consumption and replenishment were only done once a week, there was no way to determine the extent, if
any, evaporation contributed to loss of the test chemical and affected the reported level of exposure.
However, precautions were taken to minimize the loss of test chemical during the 1-week period; amber
bottles with Teflon stoppers and double sipper tubes were used. Since 1,1-dichloroethane is a volatile

-------
1,1-DICHLOROETHANE

3. HEALTH EFFECTS

chemical, this may present a limitation to the interpretation of results obtained from drinking water
administration.

The difference in results (e.g., induction of liver tumors) between the NCI (1977) and Klaunig et
al. (1986) studies may be due to the method of administration, vehicle, and/or doses used. The
pharmacokinetics of 1,1-dichloroethane may vary considerably when administered in drinking water ad
libitum over a week as compared to bolus doses given in corn oil. Evidence obtained with carbon
tetrachloride indicates that corn oil likely acts as a reservoir in the gut to delay and diminish the systemic
absorption of the lipophilic chemical, while such a chemical is probably rapidly absorbed when ingested
in water (Kim et al. 1990a, 1990b). Furthermore, the doses given to mice by gavage were approximately
6 times higher than the drinking water concentrations. Sufficient information is not available to assess the
contributions of these factors to the apparently disparate responses.

Milman et al. (1988) examined the carcinogenic potential of 1,1-dichloroethane in initiation and
promotion assays. In partially hepatectomized Osborne-Mendel rats receiving a single gavage dose of
700 mg/kg 1,1-dichloroethane in corn oil followed by dietary exposure to phenobarbitol for 7 weeks,
there were no alterations in gamma-glutamyltranspeptidase (GGT)-altered foci. However, in the
promotion assay in which partially hepatecomized Osborne-Mendel rats received an intraperitoneal dose
of diethylnitrosamine followed by gavage administration of 700 mg/kg 1,1-dichloroethane in corn oil
5 days/week for 7 weeks, there was an increase in the total number of GGT-altered foci.

3.2.3 Dermal Exposure

No studies were located regarding the following health effects in humans or animals after dermal
exposure to 1,1-dichloroethane:

3.2.3.1 Death

3.2.3.2 Systemic Effects

3.2.3.3 Immunological and Lymphoreticular Effects

3.2.3.4 Neurological Effects

3.2.3.5 Reproductive Effects

3.2.3.6 Developmental Effects

3.2.3.7 Cancer

-------
1,1-DICHLOROETHANE

30

3. HEALTH EFFECTS

Table 3-3. Genotoxicity of 1,1-Dichloroethane In Vitro

Results

Species (test system)

End point

With Without
activation activation Reference

Prokaryotic organisms:

Salmonella typhimuriu,m strains Gene mutation
TA97, TA98, TA100, and TA102
(Ames assay)

S. typhimurium, strains TA1535, Gene mutation
TA1537, TA1538, TA98, and
TA100 (Ames assay)

S. typhimurium, strains TA1537, Gene mutation
TA98, TA100, and TA1535
(dessicator assay; vapor exposure)

S. typhimurium, strains TA1535, Gene mutation
TA98, and TA100 (Ames assay;
dessicator)

Eukaryotic organisms:

Saccharomyces cerevisiae D7 Gene mutation
Mammalian cells

Syrian hamster embryo (cell	DNA viral

transformation assay; vapor	transformation

exposure)

Osborne-Mendel rat and B6C3F1
mouse hepatocytes
BALB/C-3T3 (cell transformation
assay; exposure in sealed
chamber)

BALB/C-3T3 (cell transformation
assay; exposure in sealed
chamber)

Chinese hamster lung fibroblasts Chromosomal
(chromosomal aberration assay; aberrations
exposure in sealed chamber)

No data +

on

DNA repair	No data +

Cell transformation No data

Cell transformation No data

Nohmi et al. 1986
Simmon et al. 1977
Riccio et al. 1983
Milman et al. 1988

Bronzetti et al. 1987
Hatch et al. 1983

Milman et al. 1988
Tu et al. 1985

Milman et al. 1998

Matsuoka et al.
1998)

— = negative result; + = positive result; ± = weakly positive

-------
1,1-DICHLOROETHANE

3. HEALTH EFFECTS

3.3 GENOTOXICITY

A limited number of studies have examined the genotoxicity of 1,1-dichloroethane. No studies were
located regarding in vivo genotoxic effects in humans. The genotoxic potential of 1,1-dichloroethane has
been investigated in vitro in bacteria, fungus, and mammalian systems; the results of these studies are
summarized in Table 3-3. 1,1-Dichloroethane did not result in an increase in reverse mutations in
Salmonella typhimurium strains with or without metabolic activation in Ames assays (Nohmi et al. 1985;
Simmon et al. 1977). In contrast, Riccio et al. (1983, as reported in an abstract) and Milman et al. (1988)
reported positive mutagenic alterations in S. typhimurium exposed to 1,1-dichloroethane vapor in a
desiccator assay in the presence and absence of S9 mix. Negative findings for mutagenicity were
observed in Saccharomyes cerevisiae exposed to 1,1-dichloroethane, with or without metabolic activation
(Bronzetti et al. 1987).

Similarly, negative genotoxicity results have been observed in mammalian cell assays. In vitro exposure
to 1,1-dichloroethane did not induce increases in cell transformations in BALB/C-3T3 cells (Milman et al.
1988; Tu et al. 1985) or chromosomal aberrations in Chinese hamster lung fibroblasts (Matsuoka et al.
1998). However, an increase in Simian adenovirus (SA7)-induced transformations was observed in
Syrian hamster embryo cells (Hatch et al. 1983) and an increase in DNA repair was found in hepatocytes
from Osborne-Mendel rats and B6C3F1 mice (Milman et al. 1988).

In an in vivo study by Colacci et al. (1985), 1,1-dichloroethane (98% purity) was found covalently bound
to nucleic acids and proteins from liver, lung, kidney, and stomach of male rats and mice 22 hours
following a single intraperitoneal injection of approximately 1.2 mg/kg. In vitro binding of
1,1-dichloroethane to nucleic acids and proteins was mediated by liver P-450 dependent microsomal
mixed function oxidase system. Glutathione-S-transferase (GSH) shifted the equilibrium of the
enzymatic reaction and thereby decreased binding, presumably by reducing the amount of toxic
metabolite available for binding to macromolecules. On the other hand, phenobarbitone increased
binding by increasing cytochrome P-450 activity, thus generating more toxic metabolites available for
binding to macromolecules. Presumably, the metabolites generated from P-450 enzymatic action on
1,1-dichloroethane bind to cellular macromolecules. Lung microsomes were weakly effective whereas
kidney and stomach microsomal fractions were ineffective. Therefore, the binding to macromolecules of
various organs detected in vivo may have been due to a stable hepatic metabolite that was circulated to
reach extrahepatic organs. Pretreatment with phenobarbitone enhanced the binding to DNA, microsomal
RNA and proteins while addition of glutathione-s-transferase to the microsomal systems caused

-------
1,1-DICHLOROETHANE

3. HEALTH EFFECTS

suppression of binding. Because only radioactivity was measured it is difficult to determine whether the
(imole bound represents 1,1-dichloroethane or its metabolite(s). However, the fact that binding is
enhanced with induction of P-450 suggests that it represents the metabolite(s). Thus, GSH appears to
play a detoxification role in the metabolism of 1,1-dichloroethane. The fact that 1,1-dichloroethane binds
to nucleic acid suggests that it may have a potential to produce mutation in a mammalian system.

3.4 TOXICOKINETICS
3.4.1 Absorption

3.4.1.1 Inhalation Exposure

No studies were located in humans or animals regarding the absorption of inhaled 1,1-dichloroethane.
However, its use as a gaseous anesthetic agent in humans provides evidence of its absorption.
Furthermore, the volatile and lipophilic nature of 1,1-dichloroethane favors pulmonary absorption.
Structurally related chlorinated aliphatics and gaseous anesthetics are known to be rapidly and extensively
absorbed from the lung. The total amount absorbed from the lungs will be directly proportional to the
concentration in inspired air, the duration of exposure, the blood/air partition coefficient of
1,1-dichloroethane, its solubility in tissues, and the individual's ventilation rate and cardiac output. One
of the most important factors controlling pulmonary absorption is the blood/air partition coefficient of the
chemical. The concentration of the chemical and the duration of exposure are also important
determinants of the extent of systemic absorption.

It is known that an isomer of 1,1-dichloroethane, 1,2-dichloroethane, is well-absorbed following
inhalation exposure. However, the blood/air partition coefficient for 1,2-dichloroethane is approximately
4 times that of 1,1-dichloroethane. This suggests that 1,1-dichloroethane would not be absorbed into the
blood from air as readily as 1,2-dichloroethane, but it will still be well absorbed from the lung (Sato and
Nakajima 1987).

3.4.1.2 Oral Exposure

No studies were located that quantitated the absorption of ingested 1,1-dichloroethane in humans or
animals. However, when 700 mg [14C]-l,l-dichloroethane/kg was orally administered to rats and mice,
absorption was evidenced by the presence of radiolabel in expired air and the presence of radiolabeled

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3. HEALTH EFFECTS

metabolites in urine, although there was no quantitative assessment made of the extent or rate of
absorption (Mitoma et al. 1985).

3.4.1.3 Dermal Exposure

No studies were located regarding the absorption of 1,1-dichloroethane in humans or animals following
dermal exposure. However, Reid and Muianga (2012) reported evidence that 1,1-dichloroethane
penetrates the skin. 1,1-Dichloroethane was applied to the shaved abdominal skin of rabbits that were
fitted with masks to prevent inhalation of the compound. Exhaled air from the rabbits was passed into
pure alcohol, and the presence of halogen was tested by flaming a copper wire introduced into it. The
green color observed after 1 hour indicated that the halogen ion was absorbed into the bloodstream,
although no quantitative assessment of the extent or rate of absorption was possible.

3.4.2 Distribution

3.4.2.1 Inhalation Exposure

No studies were located in humans or animals regarding the distribution of 1,1-dichloroethane following
inhalation exposure. However, since this chemical was once used as a gaseous anesthetic, it can be
assumed that it is distributed to the central nervous system as well as to the other tissues of the body.
Tissue uptake of halocarbons such as 1,1-dichloroethane is governed by the affinity of each tissue for the
lipophilic chemical (i.e., the higher the lipid content of a tissue, the greater its uptake of 1,1-dichloro-
ethane) (Sato and Nakajima 1987).

3.4.2.2 Oral Exposure

No studies were located regarding the distribution of 1,1-dichloroethane following oral exposure in
humans or animals.

3.4.2.3 Dermal Exposure

No studies were located regarding the distribution of 1,1-dichloroethane following dermal exposure in
humans or animals.

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3.4.2.4 Other Routes of Exposure

Rats and mice were intraperitoneally injected with 1.2 mg [14C]-l,l-dichloroethane/kg and sacrificed
22 hours later. 1,1-Dichloroethane was covalently bound to proteins, RNA, and DNA of liver, kidney,
lung, and stomach. The extent of binding was greatest in the tissue proteins and least in the DNA.
Binding to rat and mouse DNA was greatest in the stomach and liver, respectively (Colacci et al. 1985).
Although distribution of 1,1-dichloroethane very likely occurs to other tissues, the liver, kidney, lung, and
stomach were the only tissues analyzed in this study.

3.4.3 Metabolism

The metabolism of 1,1-dichloroethane has not been extensively characterized. In vivo studies of the
metabolism of 1,1-dichloroethane in humans and animals are very limited. Elucidation of 1,1-dichloro-
ethane's metabolic scheme to date is primarily based on in vitro studies. In general, the identification of
specific metabolites and the monitoring of enzyme activities indicate that the biotransformation of
1,1-dichloroethane is mediated by hepatic microsomal cytochrome P-450 system.

In rats and mice orally administered 700 or 1,800 mg/kg, respectively, 1,1-dichloroethane (5 days/week
for 4 weeks followed by a single dose of radiolabelled 1,1-dichloroethane), most of the radiolabel was
detected in expired air; the investigators assumed that this was parent compound (Mitoma et al. 1985).
Forty-eight hours after oral administration, 7.4 and 29.3% of the radiolabel was detected in the urine,
carcass, or expired carbon dioxide. The investigators assumed that this represented metabolized
1,1-dichloroethane; however, only radiolabel was measured in the carcass. It is likely that the ingested
radiolabeled 1,1-dichloroethane underwent first-pass extraction by the liver. It is possible that high doses
used in this study exceeded the capacity of the animals to metabolize 1,1-dichloroethane. The
radiolabeled compound that was not excreted unchanged in the expired air was probably largely
metabolized in the liver, followed by subsequent redistribution of labeled metabolites to other organs
prior to their excretion.

An in vitro study demonstrated cytochrome P450 metabolism of 1,1-dichloroethane. McCall et al. (1983)
demonstrated 1,1-dichloroethane binding to hepatic microsomal cytochrome P450 from rats; as compared
to microsomes from untreated rats, cytochrome P450 binding was 2.25 times higher, per mole of
cytochrome, in microsomes from phenobarbital-stimulated rats. Administration of (3-naphthaflavone had
no effect on the extent of 1,1-dichloroethane binding to cytochrome P450 binding. In vitro exposure of
hepatic microsomal to 1,1-dichloroethane also stimulated NADPH oxidation. The rate and extent of

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1,1-dichloroethane metabolism was increased 6.3 times in the hepatic microsomes of rats that were
induced by chronic ethanol consumption (Sato et al. 1980).

Metabolism of 1,1-dichloroethane by hepatic microsomes resulted in the production of acetic acid as the
major metabolite and 2,2-dichloroethanol, mono-, and dichloroacetic acid as minor metabolites
(Table 3-4) (McCall et al. 1983). On the basis of these results, pathways for the metabolism of
1,1-dichloroethane were proposed (Figure 3-3). The initial steps in the metabolism of 1,1-dichloroethane
were proposed to involve cytochrome P-450-dependent hydroxylations at either carbon. Hydroxylation at
C-l would result in the production of an unstable alpha-haloalcohol, which can lose HC1 to yield acetyl
chloride. An alternative, but less favorable reaction, would be a chlorine shift to yield chloroacetyl
chloride. These acyl chlorides can react with water to generate free acids or react with cellular
constituents. Hydroxylation at C-2 would produce 2,2-dichloroethanol, which would undergo subsequent
oxidation to dichloroacetaldehyde and dichloroacetic acid (McCall et al. 1983).

Chloroethanes have been shown to undergo dechlorination by an enzyme system that is similar to the
hepatic microsomal mixed function oxidase system (Van Dyke and Wineman 1971). Dechlorination was
inducible by phenobarbital and required oxygen and NADPH. However, dechlorination also required a
factor from the cytosolic fraction of the liver homogenate for optimal dechlorinating activity. In terms of
structural requirements, dechlorination was enhanced if the carbon atom containing the chlorine had only
one hydrogen. In a microsomal incubation, 13.5% of the 36C1 of 1,1-dichloroethane was enzymatically
removed after 30 minutes, while <0.5% of the 36C1 of 1,2-dichloroethane was removed (Van Dyke and
Wineman 1971).

Under hypoxic conditions, 1,1-dichloroethane gives rise to free radicals. However, its ability to develop
free radicals is much less when compared to other chlorinated hydrocarbons like trichloroethane and
carbon tetrachloride. It has been suggested that these free radicals possess the potential to induce toxic
and carcinogenic effects. There is no correlation between the ease of free radical activation, covalent
binding formation, or carcinogenic potency (Tomasi et al. 1984).

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36

Table 3-4. Production of Metabolites from 1,1-Dichloroethane with Hepatic
Microsomes from Phenobarbital-lnduced Rats

Metabolites

Metabolic production3

(nmoles/mg microsomal protein/20 minutes)

Acetic acid

179 (15)

2,2-Dichloroethane

0.12 (0.02)

Chloroacetic acid

0.22 (0.08)

Dichloroacetic acid

0.048 (0.005)

Chloroacetaldehyde

<0.07 (0.03)

aValues represent means (standard deviation) for determinations in triplicate on three to five separate preparations of
hepatic microsomes.

Source: McCall et al. 1983

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Figure 3-3.

3. HEALTH EFFECTS

Proposed Metabolic Scheme for 1,1-Dichloroethane

37

ci2hcch3

P450 (C-2)

ci2hcch2oh

2,2-dichloroethanol

CLHCCH 	

2 II

O

dichloroacetaldehyde

- CLHCC-OH

2 II

O

dichloroacetic acid

P450
(0-1)

[HOCI2CCH3]
alpha-haloalcohol

chlorine
shift

[CICH2CCI]
O

chloroacetyl
chloride

H20

O

CICH2COH

-HCI

monochloroacetic
acid

-HCI	H20

[cicch3] 	*-ch3cooh

II	-HCI

O	acetic

acetyl	acid

chloride

Source: McCall et al. 1983

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3.4.4 Elimination and Excretion

3.4.4.1 Inhalation Exposure

No empirical data on the elimination of excretion of 1,1-dichloroethane in humans or animals were
identified. Sato and Nakajima (1987) predicted that 59% of inhaled 1,1-dichloroethane would be
metabolized and excreted in the urine and 41% would be eliminated in expired air.

3.4.4.2 Oral Exposure

Mitoma et al. (1985) examined excretion of 1,1-dichloroethane in rats and mice administered
1,1-dichloroethane via gavage 700 or 1,800 mg/kg, respectively, 5 days/week for 4 weeks followed by a
single dose of radiolabeled 1,1-dichloroethane. In the rats, 86% of the administered dose was excreted in
expired air 5% expired as carbon dioxide and 0.9% was detected in the urine. In mice, 70% was excreted
in expired air, 25% was expired as carbon dioxide, and 1.6% was detected in urine. Because rats and
mice were administered different doses, a determination cannot be made as to whether the differences in
excretion and metabolism are due to species differences or are a reflection of different doses.

3.4.4.3 Dermal Exposure

No studies were located in humans or animals regarding excretion of 1,1-dichloroethane following dermal
exposure

3.4.5 Physiologically Based Pharmacokinetic (PBPK)/Pharmacodynamic (PD) Models

Physiologically based pharmacokinetic (PBPK) models use mathematical descriptions of the uptake and
disposition of chemical substances to quantitatively describe the relationships among critical biological
processes (Krishnan et al. 1994). PBPK models are also called biologically based tissue dosimetry
models. PBPK models are increasingly used in risk assessments, primarily to predict the concentration of
potentially toxic moieties of a chemical that will be delivered to any given target tissue following various
combinations of route, dose level, and test species (Clewell and Andersen 1985). Physiologically based
pharmacodynamic (PBPD) models use mathematical descriptions of the dose-response function to
quantitatively describe the relationship between target tissue dose and toxic end points.

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PBPK/PD models refine our understanding of complex quantitative dose behaviors by helping to
delineate and characterize the relationships between: (1) the external/exposure concentration and target
tissue dose of the toxic moiety, and (2) the target tissue dose and observed responses (Andersen and
Krishnan 1994; Andersen et al. 1987). These models are biologically and mechanistically based and can
be used to extrapolate the pharmacokinetic behavior of chemical substances from high to low dose, from
route to route, between species, and between subpopulations within a species. The biological basis of
PBPK models results in more meaningful extrapolations than those generated with the more conventional
use of uncertainty factors.

The PBPK model for a chemical substance is developed in four interconnected steps: (1) model
representation, (2) model parameterization, (3) model simulation, and (4) model validation (Krishnan and
Andersen 1994). In the early 1990s, validated PBPK models were developed for a number of
toxicologically important chemical substances, both volatile and nonvolatile (Krishnan and Andersen
1994; Leung 1993). PBPK models for a particular substance require estimates of the chemical substance-
specific physicochemical parameters, and species-specific physiological and biological parameters. The
numerical estimates of these model parameters are incorporated within a set of differential and algebraic
equations that describe the pharmacokinetic processes. Solving these differential and algebraic equations
provides the predictions of tissue dose. Computers then provide process simulations based on these
solutions.

The structure and mathematical expressions used in PBPK models significantly simplify the true
complexities of biological systems. If the uptake and disposition of the chemical substance(s) are
adequately described, however, this simplification is desirable because data are often unavailable for
many biological processes. A simplified scheme reduces the magnitude of cumulative uncertainty. The
adequacy of the model is, therefore, of great importance, and model validation is essential to the use of
PBPK models in risk assessment.

PBPK models improve the pharmacokinetic extrapolations used in risk assessments that identify the
maximal (i.e., the safe) levels for human exposure to chemical substances (Andersen and Krishnan 1994).
PBPK models provide a scientifically sound means to predict the target tissue dose of chemicals in
humans who are exposed to environmental levels (for example, levels that might occur at hazardous waste
sites) based on the results of studies where doses were higher or were administered in different species.
Figure 3-4 shows a conceptualized representation of a PBPK model.

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3. HEALTH EFFECTS

40

Figure 3-4. Conceptual Representation of a Physiologically Based
Pharmacokinetic (PBPK) Model for a
Hypothetical Chemical Substance

Inhaled chemical	]	|	*¦ Exhaled chemical

Chemicals
contacting skin

Note: This is a conceptual representation of a physiologically based pharmacokinetic (PBPK) model for a
hypothetical chemical substance. The chemical substance is shown to be absorbed via the skin, by inhalation, or by
ingestion, metabolized in the liver, and excreted in the urine or by exhalation.

Source: adapted from Krishnan and Andersen 1994

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If PBPK models for 1,1-dichloroethane exist, the overall results and individual models are discussed in
this section in terms of their use in risk assessment, tissue dosimetry, and dose, route, and species
extrapolations.

No PBPK models were identified for 1,1-dichloroethane.

3.5 MECHANISMS OF ACTION

3.5.1 Pharmacokinetic Mechanisms

No information was identified on the pharmacokinetic mechanisms of action of 1,1-dichloroethane.

3.5.2 Mechanisms of Toxicity

There are limited data to identify the critical targets of 1,1 -dichloroethane toxicity or to elucidate the
mode of action for the observed effects.

3.5.3 Animal-to-Human Extrapolations

The inhalation study by Hofmann et al. (1971) found species differences in the renal toxicity of
1,1-dichloroethane. Crystalline precipitations and tubular obstruction were observed in cats, but not in
rats, rabbits, or guinea pigs. There are insufficient data to determine whether this would also be a relevant
end point in humans and whether humans would be as sensitive to this effect as cats.

3.6 TOXICITIES MEDIATED THROUGH THE NEUROENDOCRINE AXIS

Recently, attention has focused on the potential hazardous effects of certain chemicals on the endocrine
system because of the ability of these chemicals to mimic or block endogenous hormones. Chemicals
with this type of activity are most commonly referred to as endocrine disruptors. However, appropriate
terminology to describe such effects remains controversial. The terminology endocrine disruptors,
initially used by Thomas and Colborn (1992), was also used in 1996 when Congress mandated the EPA to
develop a screening program for "...certain substances [which] may have an effect produced by a
naturally occurring estrogen, or other such endocrine effect[s]...". To meet this mandate, EPA convened a
panel called the Endocrine Disruptors Screening and Testing Advisory Committee (EDSTAC), and in
1998, the EDSTAC completed its deliberations and made recommendations to EPA concerning endocrine
disruptors. In 1999, the National Academy of Sciences released a report that referred to these same types

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of chemicals as hormonally active agents. The terminology endocrine modulators has also been used to
convey the fact that effects caused by such chemicals may not necessarily be adverse. Many scientists
agree that chemicals with the ability to disrupt or modulate the endocrine system are a potential threat to
the health of humans, aquatic animals, and wildlife. However, others think that endocrine-active
chemicals do not pose a significant health risk, particularly in view of the fact that hormone mimics exist
in the natural environment. Examples of natural hormone mimics are the isoflavinoid phytoestrogens
(Adlercreutz 1995; Livingston 1978; Mayr et al. 1992). These chemicals are derived from plants and are
similar in structure and action to endogenous estrogen. Although the public health significance and
descriptive terminology of substances capable of affecting the endocrine system remains controversial,
scientists agree that these chemicals may affect the synthesis, secretion, transport, binding, action, or
elimination of natural hormones in the body responsible for maintaining homeostasis, reproduction,
development, and/or behavior (EPA 1997). Stated differently, such compounds may cause toxicities that
are mediated through the neuroendocrine axis. As a result, these chemicals may play a role in altering,
for example, metabolic, sexual, immune, and neurobehavioral function. Such chemicals are also thought
to be involved in inducing breast, testicular, and prostate cancers, as well as endometriosis (Berger 1994;
Giwercman et al. 1993; Hoel et al. 1992).

No studies were located regarding endocrine disruption in [humans and/or animals] after exposure to
1,1 -dichloroethane.

No in vitro studies were located regarding endocrine disruption of 1,1-dichloroethane.
3.7 CHILDREN'S SUSCEPTIBILITY

This section discusses potential health effects from exposures during the period from conception to
maturity at 18 years of age in humans, when all biological systems will have fully developed. Potential
effects on offspring resulting from exposures of parental germ cells are considered, as well as any indirect
effects on the fetus and neonate resulting from maternal exposure during gestation and lactation.

Relevant animal and in vitro models are also discussed.

Children are not small adults. They differ from adults in their exposures and may differ in their
susceptibility to hazardous chemicals. Children's unique physiology and behavior can influence the
extent of their exposure. Exposures of children are discussed in Section 6.6, Exposures of Children.

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Children sometimes differ from adults in their susceptibility to hazardous chemicals, but whether there is
a difference depends on the chemical (Guzelian et al. 1992; NRC 1993). Children may be more or less
susceptible than adults to health effects, and the relationship may change with developmental age
(Guzelian et al. 1992; NRC 1993). Vulnerability often depends on developmental stage. There are
critical periods of structural and functional development during both prenatal and postnatal life, and a
particular structure or function will be most sensitive to disruption during its critical period(s). Damage
may not be evident until a later stage of development. There are often differences in pharmacokinetics
and metabolism between children and adults. For example, absorption may be different in neonates
because of the immaturity of their gastrointestinal tract and their larger skin surface area in proportion to
body weight (Morselli et al. 1980; NRC 1993); the gastrointestinal absorption of lead is greatest in infants
and young children (Ziegler et al. 1978). Distribution of xenobiotics may be different; for example,
infants have a larger proportion of their bodies as extracellular water, and their brains and livers are
proportionately larger (Altman and Dittmer 1974; Fomon 1966; Fomon et al. 1982; Owen and Brozek
1966; Widdowson and Dickerson 1964). The fetus/infant has an immature (developing) blood-brain
barrier that past literature has often described as being leaky and poorly intact (Costa et al. 2004).
However, current evidence suggests that the blood-brain barrier is anatomically and physically intact at
this stage of development, and the restrictive intracellular junctions that exist at the blood-CNS interface
are fully formed, intact, and functionally effective (Saunders et al. 2008, 2012).

However, during development of the blood-brain barrier, there are differences between fetuses/infants and
adults which are toxicologically important. These differences mainly involve variations in physiological
transport systems that form during development (Ek et al. 2012). These transport mechanisms (influx and
efflux) play an important role in the movement of amino acids and other vital substances across the
blood-brain barrier in the developing brain; these transport mechanisms are far more active in the
developing brain than in the adult. Because many drugs or potential toxins may be transported into the
brain using these same transport mechanisms—the developing brain may be rendered more vulnerable
than the adult. Thus, concern regarding possible involvement of the blood-brain barrier with enhanced
susceptibility of the developing brain to toxins is valid. It is important to note however, that this potential
selective vulnerability of the developing brain is associated with essential normal physiological
mechanisms; and not because of an absence or deficiency of anatomical/physical barrier mechanisms.

The presence of these unique transport systems in the developing brain of the fetus/infant is intriguing; as
it raises a very important toxicological question as to whether these mechanisms provide protection for
the developing brain or do they render it more vulnerable to toxic injury. Each case of chemical exposure

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should be assessed on a case-by-case basis. Research continues into the function and structure of the
blood-brain barrier in early life (Kearns et al. 2003; Saunders et al. 2012; Scheuplein et al. 2002).

Many xenobiotic metabolizing enzymes have distinctive developmental patterns. At various stages of
growth and development, levels of particular enzymes may be higher or lower than those of adults, and
sometimes unique enzymes may exist at particular developmental stages (Komori et al. 1990; Leeder and
Kearns 1997; NRC 1993; Vieira et al. 1996). Whether differences in xenobiotic metabolism make the
child more or less susceptible also depends on whether the relevant enzymes are involved in activation of
the parent compound to its toxic form or in detoxification. There may also be differences in excretion,
particularly in newborns who have a low glomerular filtration rate and have not developed efficient
tubular secretion and resorption capacities (Altman and Dittmer 1974; NRC 1993; West et al. 1948).
Children and adults may differ in their capacity to repair damage from chemical insults. Children also
have a longer remaining lifetime in which to express damage from chemicals; this potential is particularly
relevant to cancer.

Certain characteristics of the developing human may increase exposure or susceptibility, whereas others
may decrease susceptibility to the same chemical. For example, although infants breathe more air per
kilogram of body weight than adults breathe, this difference might be somewhat counterbalanced by their
alveoli being less developed, which results in a disproportionately smaller surface area for alveolar
absorption (NRC 1993).

Information on children's susceptibility to the toxic effects of 1,1-dichloroethane is limited to a
developmental toxicity study in rats (Schwetz et al. 1974) that found an increase in the incidence of
delayed ossifications in the fetuses of dams exposed to 6,000 ppm 1,1-dichloroethane on gestation
days 6-15. An in vitro study (Andrews et al. 2002; only available as an abstract) utilizing rat whole
embryo cultures reported eye defects in at 17.9 mM; this concentration also reported in 35%
embryolethality.

3.8 BIOMARKERS OF EXPOSURE AND EFFECT

Biomarkers are broadly defined as indicators signaling events in biologic systems or samples. They have
been classified as markers of exposure, markers of effect, and markers of susceptibility (NAS/NRC
1989).

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The National Report on Human Exposure to Environmental Chemicals provides an ongoing assessment
of the exposure of the U.S. population to environmental chemicals using biomonitoring. This report is
available at http://www.cdc.gov/exposurereport/. The biomonitoring data for 1,1-dichloroethane from
this report is discussed in Section 6.5. A biomarker of exposure is a xenobiotic substance or its
metabolite(s) or the product of an interaction between a xenobiotic agent and some target molecule(s) or
cell(s) that is measured within a compartment of an organism (NAS/NRC 1989). The preferred
biomarkers of exposure are generally the substance itself, substance-specific metabolites in readily
obtainable body fluid(s), or excreta. However, several factors can confound the use and interpretation of
biomarkers of exposure. The body burden of a substance may be the result of exposures from more than
one source. The substance being measured may be a metabolite of another xenobiotic substance (e.g.,
high urinary levels of phenol can result from exposure to several different aromatic compounds).
Depending on the properties of the substance (e.g., biologic half-life) and environmental conditions (e.g.,
duration and route of exposure), the substance and all of its metabolites may have left the body by the
time samples can be taken. It may be difficult to identify individuals exposed to hazardous substances
that are commonly found in body tissues and fluids (e.g., essential mineral nutrients such as copper, zinc,
and selenium). Biomarkers of exposure to 1,1-dichloroethane are discussed in Section 3.8.1.

Biomarkers of effect are defined as any measurable biochemical, physiologic, or other alteration within an
organism that, depending on magnitude, can be recognized as an established or potential health
impairment or disease (NAS/NRC 1989). This definition encompasses biochemical or cellular signals of
tissue dysfunction (e.g., increased liver enzyme activity or pathologic changes in female genital epithelial
cells), as well as physiologic signs of dysfunction such as increased blood pressure or decreased lung
capacity. Note that these markers are not often substance specific. They also may not be directly
adverse, but can indicate potential health impairment (e.g., DNA adducts). Biomarkers of effects caused
by 1,1-dichloroethane are discussed in Section 3.8.2.

A biomarker of susceptibility is an indicator of an inherent or acquired limitation of an organism's ability
to respond to the challenge of exposure to a specific xenobiotic substance. It can be an intrinsic genetic or
other characteristic or a preexisting disease that results in an increase in absorbed dose, a decrease in the
biologically effective dose, or a target tissue response. If biomarkers of susceptibility exist, they are
discussed in Section 3.10, Populations That Are Unusually Susceptible.

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3.8.1 Biomarkers Used to Identify or Quantify Exposure to 1,1-Dichloroethane

As summarized in Section 6.5, 1,1-dichloroethane was not detected in blood samples collected from the
National Health and Nutrition Examination Survey (2003-2004). No other biomarkers that could be used
to identify or quantify exposure to 1,1-dichloroethane were identified.

3.8.2 Biomarkers Used to Characterize Effects Caused by 1,1-Dichloroethane

1,1-Dichloroethane was used as an anesthetic in the early part of the 20th century (Konietzko 1984; Reid
and Muianga 2012). No information was available on blood levels associated with anesthesia or the
occurrence of anesthesia-induced cardiac arrhythmias.

3.9 INTERACTIONS WITH OTHER CHEMICALS

No information was located regarding toxic interactions of 1,1-dichloroethane with other xenobiotics.
Evidence exists to indicate that 1,1-dichloroethane is detoxified by glutathione (Colacci et al. 1985).

Thus, it is likely that other substances that deplete glutathione stores such as other chlorinated
hydrocarbons (e.g., 1,1-dichloroethene and 1,2-dichloroethane), acetaminophen, and bromobenzene may
enhance the toxicity of 1,1-dichloroethane. Substances that alter the activity of the microsomal enzymes
that are responsible for the metabolism of 1,1-dichloroethane may also affect the toxicity of this chemical.
For example, it has been shown that ethanol increases the metabolism of 1,1-dichloroethane in vitro (Sato
et al. 1980).

3.10 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE

A susceptible population will exhibit a different or enhanced response to 1,1-dichloroethane than will
most persons exposed to the same level of 1,1-dichloroethane in the environment. Reasons may include
genetic makeup, age, health and nutritional status, and exposure to other toxic substances (e.g., cigarette
smoke). These parameters result in reduced detoxification or excretion of 1,1-dichloroethane, or
compromised function of organs affected by 1,1-dichloroethane. Populations who are at greater risk due
to their unusually high exposure to 1,1-dichloroethane are discussed in Section 6.7, Populations with
Potentially High Exposures.

No populations unusually susceptible to 1,1-dichloroethane or chlorinated ethanes in general have been
identified. NIOSH (1978) has identified the following individuals as possibly being at increased risk

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from exposure to 1,1-dichloroethane: (1) individuals with skin disease because of the purported dermal
irritant effects induced by 1,1-dichloroethane; (2) individuals with liver disease because of the role of this
organ in the biotransformation and detoxification of xenobiotics such as 1,1-dichloroethane;
(3) Individuals with impaired renal function because of the limited evidence that 1,1-dichloroethane is
nephrotoxic in animals; and (4) individuals with chronic respiratory disease because of the purported
respiratory irritant effects induced by 1,1-dichloroethane. Although there are no data to substantiate this,
additional populations that may be unusually susceptible to 1,1-dichloroethane include children and the
elderly because of immature or compromised metabolic capabilities, and phenobarbital or alcohol
consumers because of the ability of these substances to alter the activity of the cytochrome P-450 system.

It should be noted that no reliable data were found regarding dermal or respiratory irritant effects of
1,1 -dichloroethane.

3.11 METHODS FOR REDUCING TOXIC EFFECTS

This section will describe clinical practice and research concerning methods for reducing toxic effects of
exposure to 1,1-dichloroethane. However, because some of the treatments discussed may be experimental
and unproven, this section should not be used as a guide for treatment of exposures to 1,1-dichloroethane.
When specific exposures have occurred, poison control centers and medical toxicologists should be
consulted for medical advice. No texts providing specific information about treatment following
exposures to 1,1-dichloroethane were identified.

3.11.1 Reducing Peak Absorption Following Exposure

No information specific to 1,1-dichloroethane was identified.

3.11.2 Reducing Body Burden

No information specific to 1,1-dichloroethane was identified.

3.11.3 Interfering with the Mechanism of Action for Toxic Effects

The mechanisms of toxicity have not been identified for 1,1-dichloroethane.

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1,1-DICHLOROETHANE

3. HEALTH EFFECTS

3.12 ADEQUACY OF THE DATABASE

Section 104(I)(5) of CERCLA, as amended, directs the Administrator of ATSDR (in consultation with the
Administrator of EPA and agencies and programs of the Public Health Service) to assess whether
adequate information on the health effects of 1,1-dichloroethane is available. Where adequate
information is not available, ATSDR, in conjunction with the National Toxicology Program (NTP), is
required to assure the initiation of a program of research designed to determine the health effects (and
techniques for developing methods to determine such health effects) of 1,1-dichloroethane.

The following categories of possible data needs have been identified by a joint team of scientists from
ATSDR, NTP, and EPA. They are defined as substance-specific informational needs that if met would
reduce the uncertainties of human health assessment. This definition should not be interpreted to mean
that all data needs discussed in this section must be filled. In the future, the identified data needs will be
evaluated and prioritized, and a substance-specific research agenda will be proposed.

3.12.1 Existing Information on Health Effects of 1,1-Dichloroethane

The existing data on health effects of inhalation, oral, and dermal exposure of humans and animals to
1,1-dichloroethane are summarized in Figure 3-5. The purpose of this figure is to illustrate the existing
information concerning the health effects of 1,1-dichloroethane. Each dot in the figure indicates that one
or more studies provide information associated with that particular effect. The dot does not necessarily
imply anything about the quality of the study or studies, nor should missing information in this figure be
interpreted as a "data need". A data need, as defined in ATSDR's Decision Guide for Identifying
Substance-Specific Data Needs Related to Toxicological Profiles (Agency for Toxic Substances and
Disease Registry 1989), is substance-specific information necessary to conduct comprehensive public
health assessments. Generally, ATSDR defines a data gap more broadly as any substance-specific
information missing from the scientific literature.

Figure 3-5 graphically depicts the information that currently exists on the health effects of
1,1-dichloroethane. The literature reviewed concerning the health effects of 1,1-dichloroethane in
humans consisted solely of an anecdotal report describing the occurrence of cardiac arrhythmias when
this compound was used as a gaseous anesthetic. Chlorinated aliphatics as a class are known to cause
central nervous system depression, and respiratory tract and dermal irritation when humans are exposed

-------
1,1-DICHLOROETHANE

3. HEALTH EFFECTS

Figure 3-5. Existing Information on Health Effects of 1,1-Dichloroethane

Inhalation

Oral

Dermal

Human

Inhalation
Oral
Dermal

Animal

• Existing Studies

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1,1-DICHLOROETHANE

3. HEALTH EFFECTS

by inhalation to sufficiently high levels. It has been inferred that 1,1-dichloroethane causes these effects,
but no reliable data were found that verified this activity.

The database for the health effects of 1,1-dichloroethane in experimental animals is lacking, and the
studies reviewed consisted primarily of one subchronic inhalation study, one inhalation developmental
toxicity study, and two oral chronic bioassays. No information is available on the effects of
1,1-dichloroethane following dermal exposure. The limited information available in animals suggests that
1,1-dichloroethane may be nephrotoxic, fetotoxic, and possibly carcinogenic. The data also indicate that
1,1-dichloroethane is considerably less toxic than 1,2-dichloroethane and the tetrachlorinated aliphatics.

3.12.2 Identification of Data Needs

Acute-Duration Exposure. No reliable information is available on the effects of acute exposure to
1,1-dichloroethane in humans. Information on the lethality of 1,1-dichloroethane following inhalation or
oral exposure of animals comes from secondary sources (Archer 1978; Smyth 1956). One study
examined the nonlethal toxicity of 1,1-dichloroethane following inhalation exposure (Schwetz et al.
1974); this study reported decreases in maternal weight gain and delayed ossification in the fetuses.
Because the potential systemic toxicity of 1,1-dichloroethane has not been evaluated following acute
inhalation or dermal exposure, the database was not considered adequate for derivation of acute-duration
inhalation or oral MRLs for 1,1-dichloroethane.

Since the chlorinated aliphatics in general are known to cause central nervous system depression and
irritation of respiratory and ocular mucosal epithelium following single high-level exposures, more
information on the effects of acute-duration exposures to 1,1-dichloroethane by all routes would be useful
to assess more fully the acute hazards of this chemical.

Intermediate-Duration Exposure. No reliable information is available on the effects of repeated
exposure in humans. Limited information is available on the effects of repeated inhalation and oral
exposures to 1,1-dichloroethane in animals. The studies reviewed indicate that 1,1-dichloroethane is
possibly nephrotoxic, but this effect has only been demonstrated at high doses in cats, but not in rats,
guinea pigs, or rabbits (Hofmann et al. 1971). No other toxic effects have been attributed to
1,1-dichloroethane following intermediate-duration inhalation exposures in animals. The lack of
supporting toxicity or mechanistic data precluded using this study as the basis on an intermediate-duration
inhalation MRL. More information on the systemic effects of repeated-dose exposures in animals,

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1,1-DICHLOROETHANE

3. HEALTH EFFECTS

particularly by the inhalation route since this is the most likely route of human exposure, would be useful
to determine whether nephrotoxic effects observed in one study are an actual result of exposure to
1,1-dichloroethane, to determine if 1,1-dichloroethane reacts like other chlorinated aliphatics (e.g., causes
neurotoxicity and liver toxicity), and to more fully assess potential human health hazards from repeated
exposure to 1,1-dichloroethane. Two studies have examined the intermediate-duration oral toxicity of
1,1-dichloroethane. In a limited reported study, NCI (1977) found alterations in body weight gain in rats,
but not mice, administered 1,1-dichloroethane for 6 weeks. In the second study, no adverse effects were
observed in mice exposed to 1,1-dichloroethane in drinking water for 52 weeks (Klaunig et al. 1986).
Additional oral studies are needed to identify sensitive targets of toxicity and establish dose-response
relationships. Dermal studies are also necessary to evaluate the toxicity of this compound.

Chronic-Duration Exposure and Cancer. No information is available on the effects of chronic
exposure to 1,1-dichloroethane in humans. No chronic-duration inhalation or dermal exposure studies
were identified. In chronic-duration oral exposure studies in rats and mice (NCI 1977), no nonneoplastic
alterations were observed. Without information on the targets of toxicity and dose-response relationships,
inhalation and oral MRLs cannot be derived. Additional chronic toxicity studies particularly by the
inhalation route would be useful to fully assess potential human health hazard from long-term exposure to
1,1 -dichloroethane.

Two bioassays were reviewed that investigated the potential carcinogenic effect of 1,1-dichloroethane by
the oral route of exposure in animals. One study provided suggestive evidence of carcinogenicity, but
because there was poor survival in this study and the statistical significance of the cancer incidence is
uncertain, the results could not be considered conclusive (NCI 1977). The other bioassay yielded
negative results for 1,1-dichloroethane (Klaunig et al. 1986). Given the limitations (high mortality)
present in the NCI (1977) study and the observations that 1,1-dichloroethane possibly forms DNA
adducts and metabolizes to free radicals, more information obtained from well-conducted carcinogenicity
studies would be useful to assess more fully the carcinogenic potential of 1,1-dichloroethane in humans
and animals. Studies conducted by the inhalation route would be useful.

Genotoxicity. The genotoxic potential of 1,1-dichloroethane has been investigated in in vitro assays;
in vivo genotoxicity studies are necessary to evaluate the genotoxic potential of this chemical. In general,
these studies provide suggestive evidence that 1,1-dichloroethane is not genotoxic. 1,1-Dichloroethane
has been observed to enhance cell transformation in Syrian hamster embryo cells (Hatch et al. 1983) and
results suggest that 1,1-dichloroethane or a metabolite can bind to cellular macromolecules such as DNA

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1,1-DICHLOROETHANE

3. HEALTH EFFECTS

(Colacci et al. 1985). More information on the genotoxic effects of 1,1-dichloroethane in animals both in
vitro and in vivo would be useful to resolve the discrepancies in the present data and to assess the
genotoxic hazard of this chemical in humans.

Reproductive Toxicity. No information on the reproductive effects of 1,1-dichloroethane in humans
or animals is available. Reproductive toxicity studies in animals would be useful particularly by the
inhalation route since this is the most likely route of human exposure.

Developmental Toxicity. No information on the developmental effects of 1,1-dichloroethane in
humans is available. One study was located that investigated the developmental effects of inhaled
1,1-dichloroethane in animals (Schwetz et al. 1974). The results from this study indicated that
1,1-dichloroethane is fetotoxic in rats, causing retarded fetal development (i.e., delayed ossification of the
vertebrae) in the presence of decreases in maternal food consumption and body weight gain.

Additionally, well-conducted developmental toxicity studies on 1,1-dichloroethane, particularly by the
inhalation route since this is the most likely route of human exposure, would be useful to verify the data
from the single study that suggest this compound may cause adverse developmental effects.

Immunotoxicity. No information is available on the immunotoxic effects of 1,1-dichloroethane in
humans or animals. Immunotoxicity studies in animals, particularly by the inhalation route since this is
the most likely route of human exposure, would be useful to assess the potential risk for
1,1-dichloroethane-induced adverse immunologic effects in humans.

Neurotoxicity. Chlorinated aliphatics as a class are known to cause central nervous system depression
in humans exposed by inhalation to sufficiently high levels. 1,1-Dichloroethane can also cause this effect,
evidenced by its former use as an anesthetic. However, no reliable data were found that indicated a
threshold level for this effect. No data (behavioral, histopathological, neurochemical, or
neurophysiological) are available on possible neurotoxic effects of long-term low level exposures to
1,1-dichloroethane. More information on potential short- and long-term neurotoxic effects of inhaled
1,1-dichloroethane would be useful to determine whether this compound can produce neurotoxic effects
following low-level, long-term exposures, and to determine the threshold exposure level for
1,1-dichloroethane-induced central nervous system depression.

Epidemiological and Human Dosimetry Studies. No epidemiological studies were located on
1,1-dichloroethane. Well-controlled epidemiological studies of people living in close proximity to areas

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1,1-DICHLOROETHANE

3. HEALTH EFFECTS

where 1,1-dichloroethane contamination of surface water and groundwater or air is known to have
occurred, people living near hazardous waste sites, and of occupationally exposed people could add to the
limited database and clarify health effects in humans induced by 1,1-dichloroethane. However, while this
information would be useful, it is unlikely that it could be easily obtained from occupational studies.
Other short-chain halogenated hydrocarbons are usually encountered in the same facilities where
1,1-dichloroethane is manufactured or used, thus confounding the results obtained in such a study.

Biomarkers of Exposure and Effect. For high exposure to 1,1-dichloroethane, the levels of this
compound in the blood, urine, and breath may be used for biomarkers of exposure. However, these
methods should be more sensitive and quantitative. The formation of DNA adducts has been suggested,
and if they do occur in vivo, they may serve to identify long-term exposure to 1,1-dichloroethane. The
development of methods for detecting metabolites in the fluids and tissue of humans is needed to indicate
1,1-dichloroethane exposure.

Biomarkers of effect would be useful for identifying 1,1-dichloroethane-specific injury (e.g.,
hepatotoxicity, renal toxicity, neurotoxicity) for short-, intermediate-, and long-term exposure. Presently,
no biomarkers of effect are available; however, DNA adducts may be useful for indicating
carcinogenicity in animals or humans following chronic exposure to 1,1-dichloroethane.

Absorption, Distribution, Metabolism, and Excretion. Studies of the toxicokinetics of
1,1-dichloroethane are very limited. Much of the information regarding the disposition of 1,1-dichloro-
ethane is based on indirect evidence. Toxicokinetic data are useful for providing information on
mechanisms of toxicity and can often support findings of toxicity studies.

Absorption of 1,1-dichloroethane occurs following exposure via all routes. The presence of a
1,1-dichloroethane metabolite in urine and expired air and its binding to tissue macromolecules provide
evidence of its absorption. Studies regarding the direct analysis of the extent and rate of
1,1-dichloroethane absorption are lacking and would provide useful information on the potential health
hazards associated with exposure to 1,1-dichloroethane via inhalation of contaminated air or ingestion of
contaminated water.

Studies in humans and animals regarding tissue distribution of 1,1-dichloroethane are not available. Its
lipophilicity suggests that the compound would be well absorbed and distributed to tissues according to
their lipid content. Binding studies conducted in rats following intraperitoneal injection indicate that

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1,1-DICHLOROETHANE

3. HEALTH EFFECTS

1,1-dichloroethane localizes in the liver, kidney, lung, and stomach. However, analysis has been limited
to these tissues. Distribution studies using routes of administration relevant to human exposure
(inhalation, oral) would provide useful information on potential target organs of 1,1-dichloroethane-
induced toxicity in humans.

Characterization of 1,1-dichloroethane's metabolism relies heavily on in vitro data. These studies reveal
that the biotransformation process is mediated by cytochrome P-450 with hepatic microsomes being the
most effective. Identification of products in these microsomal studies allows for the prediction of
metabolic pathways. However, exposure to 1,1-dichloroethane under in vivo conditions may alter
substrate availability and consequently alter the metabolic scheme. In vivo studies would provide a better
understanding of the rate and extent of 1,1-dichloroethane metabolism and a more realistic perspective of
its metabolic fate. This information would allow more accurate prediction of the potential of
1,1-dichloroethane to induce toxic effects, and aid in devising methods to detoxify exposed persons.

Studies regarding the excretion of 1,1-dichloroethane by humans were not available. One study was
located in animals regarding the extent or rate of 1,1-dichloroethane excretion. Studies monitoring levels
in blood and excretion would be useful to estimate pharmacokinetic parameters.

Comparative Toxicokinetics. The absorption, distribution, metabolism, and excretion data for
1,1-dichloroethane are all derived from animal studies. It is likely that human disposition would follow a
scheme similar to that found in animals, but this conclusion is highly speculative. However, similar
results obtained in vivo across several animal species would provide supportive evidence for the
assumption that 1,1-dichloroethane is handled in a similar manner in humans.

Methods for Reducing Toxic Effects. Limited information regarding methods for reducing the
toxic effects of 1,1-dichloroethane were identified. Additional information regarding the toxicity of
1,1-dichloroethane is needed prior to research on mitigating the toxicity of this compound.

Children's Susceptibility. Data needs relating to both prenatal and childhood exposures, and
developmental effects expressed either prenatally or during childhood, are discussed in detail in the
Developmental Toxicity subsection above.

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1,1-DICHLOROETHANE

3. HEALTH EFFECTS

55

No data were identified on children's susceptibility to the toxic effects of 1,1-dichloroethane and whether
there are toxicokinetic differences in the metabolism of this chemical between adults and children. As
noted previously, one developmental toxicity study (Schwetz et al. 1974) reported altered fetal growth.

Child health data needs relating to exposure are discussed in Section 6.8.1, Identification of Data Needs:
Exposures of Children.

3.12.3 Ongoing Studies

No ongoing studies sponsored by NIH, NTP, or EPA were identified for 1,1-dichloroethane.

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1,1-DICHLOROETHANE

3. HEALTH EFFECTS

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1,1-DICHLOROETHANE	57

4. CHEMICAL AND PHYSICAL INFORMATION

4.1	CHEMICAL IDENTITY

The synonyms, and identification numbers for 1,1-dichloroethane are listed in Table 4-1.

4.2	PHYSICAL AND CHEMICAL PROPERTIES

Important physical and chemical properties of 1,1-dichloroethane are listed in Table 4-2.

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1,1-DICHLOROETHANE	58

4. CHEMICAL AND PHYSICAL INFORMATION

Table 4-1. Chemical Identity of 1,1-Dichloroethane

Characteristic

Information3

Reference

Chemical name
Synonym(s)

Registered trade name(s)
Chemical formula
Chemical structure

Identification numbers:
CAS registry
NIOSH RTECS
EPA hazardous waste
OHM/TADS

DOT/UN/NA/IMDG shipping

HSDB

NCI

1,1-Dichloroethaneb

Alpha,alpha-dichloroethane; asymmetrical dichloroethane;
S-dichloroethene; Dutch oil; ethane, 1,1-dichloro-; ethylidene
chloride; ethylidene dichloride; 1,1-ethylidene dichloride0
No data
C2H4CI2b

CI H
I I
CI—C-C-H
I I
H H

75-34-3b
KI0175000
U076
No data

DOT 2362; UN 2362; IMO 3.2
64

C04535d

aAII information obtained from HSDB 2012, except where noted
bO'Neil etal. 2006
cArcher 1978; Weiss 1986
dChemlDPIus Lite 2012

CAS = Chemical Abstracts Service; DOT/UN/NA/IMDG = Department of Transportation/United Nations/North
America/International Maritime Dangerous Goods Code; EPA = Environmental Protection Agency;

HSDB = Hazardous Substances Data Bank; NCI = National Cancer Institute; NIOSH = National Institute for
Occupational Safety and Health; OHM/TADS = Oil and Hazardous Materials/Technical Assistance Data System;
RTECS = Registry of Toxic Effects of Chemical Substances

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1,1-DICHLOROETHANE

59

4. CHEMICAL AND PHYSICAL INFORMATION

Table 4-2. Physical and Chemical Properties of 1,1-Dichloroethane

Property

Information

Reference

Molecular weight
Color

Physical state
Melting point
Boiling point
Density at 20 °C
Odor

Odor threshold:

Water
Air
Solubility:

Water at 20 °C
Organic solvents

Partition coefficients:

Log Kow
Log Koc
Vapor pressure at 25 °C
Henry's law constant at 24 °C

Autoignition temperature
Flashpoint
Flammability limits
Conversion factors

Explosive limits

98.97
Colorless
Oily liquid
-96.9 °C
57.3 °C
1.175 g/cm3

Aromatic ethereal; chloroform-like
No data

120 ppm; 200 ppm

0.55 g/100 g
Miscible with oxygenated and chlorinated
solvents

1.79
1.48

230 mmHg
5.62x10"3 atm-m3/mol
5.51x10-3 atm-m3/mol
457.8 °C

Closed cup -12 °C; open cup 14 °C

Lower 5.4%; upper 11.4%

1 ppm x 4.05 = 1 mg/m3

1 mg/m3 x 0.25 = 1 ppm

Lower explosive limit: 5.6%; moderate

explosion hazard when exposed to heat or

flame

HSDB2012

O'Neil et al. 2006
HSDB2012
O'Neil etal. 2006
HSDB2012

Verschueren 1983

HSDB2012

HSDB2012

HSDB2012

HSDB2012

HSDB2012

Chen et al. 2012

HSDB2012

HSDB2012

HSDB2012

HSDB2012

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4. CHEMICAL AND PHYSICAL INFORMATION

This page is intentionally blank.

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1,1-DICHLOROETHANE

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL

5.1 PRODUCTION

Table 5-1 lists the number of facilities in each state that manufacture or process 1,1-dichloroethane, the
activities and uses, and the range of maximum amounts of 1,1-dichloroethane that are stored on site. The
data listed in Table 5-1 are derived from the Toxics Release Inventory (TRI13 2014). Based on the TRI
information from 2013, there are 19 facilities that produce or process 1,1-dichloroethane in the United
States. The TRI data should be used with caution since only certain types of facilities were required to
report. This is not an exhaustive list.

1,1-Dichloroethane is produced commercially through the reaction of hydrogen chloride and vinyl
chloride at 20-55 °C in the presence of an aluminum, ferric, or zinc chloride catalyst (HSDB 2012).

Other production methods include the direct chlorination of ethane, addition of hydrogen chloride to
acetylene, the reaction of ethylene and chlorine in the presence of calcium chloride, and the reaction of
phosphorus chloride and acetaldehyde (HSDB 2012). 1,1-Dichloroethane can also be produced as a
byproduct during the manufacture of chloral, as a byproduct in the production of vinyl chloride via
ethylene oxychlorination (HSDB 2012; Marshall 2003), and as an intermediate in the production of
1,1,1-trichloroethane by thermal or photochemical chlorination of vinyl chloride (Cowfer 2006). It has
been reported that 1,1-dichloroethane often occurs as an unwanted byproduct in numerous chlorination
and oxychlorination processes of C2 hydrocarbons (HSDB 2012).

Information regarding the production volume of 1,1-dichloroethane in the United States is not reported in
SRI Directory of Chemical Producers (SRI 2011). Additionally, no data are reported for U.S. production
volume in the Hazardous Substance Data Bank (HSDB 2012).

Data from the Chemical Data Reporting (CDR) information system indicates that three companies within
the United States manufactured or imported 1,1-dichloroethane (EPA 2014a). The Dow Chemical
Company reported 0 pounds/year for imported and exported data, confidential business information (CBI)
for manufactured data, 0 pounds/year for volume used on site and 'CBI' for past production volume data.
1,1-Dichloroethane is reported to be used as an intermediate, a substance used to form another compound
by the Dow Chemical Company. The Shin Etsu Company reports 'withheld' for imported data,

1,844,512 pounds/year for exported data, 'withheld' for manufactured data, 2,629,704 pounds/year for
volume used on site data, and 2,959,696 pounds/year for past production volume data (EPA 2014a). The

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1,1-DICHLOROETHANE

62

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL

Table 5-1. Facilities that Produce, Process, or Use 1,1-Dichloroethane





Minimum

Maximum





Number of

amount on site

amount on site



State3

facilities

in pounds'5

in pounds'5

Activities and usesc

KY

1

10,000

99,999

1, 3, 6

LA

9

0

9,999,999

1,2, 3, 4, 5, 6, 8, 12, 13

NY

1

100

999

12

OH

1

1,000

9,999

12

SC

1

100

999

12

TX

6

1,000

999,999

1,2, 3, 5, 6, 8, 12, 13, 14

aPost office state abbreviations used.

bAmounts on site reported by facilities in each state.

cActivities/Uses:

1.	Produce

2.	Import

3.	Onsite use/processing

4.	Sale/Distribution

5.	Byproduct

6.	Reactant

7.	Formulation Component

8.	Article Component

9.	Repackaging

10.	Chemical Processing Aid

11.	Manufacturing Aid

12.	Ancillary/Other Uses

13.	Manufacturing Impurity

14.	Process Impurity

Source: TRI13 2014 (Data are from 2013)

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1,1-DICHLOROETHANE

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL

Shin Etsu Company reports use of 1,1-dichloroethane as 'not reasonably known or ascertainable.' The
national production volume ranged between 1,000,000 and 10,000,000 pounds/year. There are no data
reported for consumer products or consumer uses.

According to EPA Inventory Update Rule (IUR) records, in 2006, two companies in the United States
produced 1,1-dichloroethane in 2006: Oxy Vinyls in La Porte, Texas and The Dow Chemical Company
in Plaquemine, Louisiana (EPA 2010). Both of these companies manufactured 1,1-dichloroethane
primarily to be used as an intermediate, a substance used to form another compound. Production volume
data were not provided for each specific company. Aggregated national production volumes reported in
2006 were in the range of 500,000-
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1,1-DICHLOROETHANE 64

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL

Consultation with environmental regulatory agencies is advised (HSDB 2012; Marshall 2003; NIOSH
1978).

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

6.1 OVERVIEW

1,1-Dichloroethane has been identified in at least 673 of the 1,699 hazardous waste sites that have been
proposed for inclusion on the EPA National Priorities List (NPL) (HazDat 2007). However, the number
of sites evaluated for 1,1-dichloroethane is not known. The frequency of these sites can be seen in
Figure 6-1.

1,1-Dichloroethane has been identified in at least 400 of the 1,760 proposed (51), final (1,323), and
deleted (386) hazardous waste sites listed on the EPA Superfund NPL under the synonym
1,1-dichloroethene (CASRN: 75-34-3) and at least 26 of the 1,760 EPA Superfund NPL sites under the
synonym ethylidene dichloride (CASRN: 75-34-3) (EPA 2015c; NLM 2015). However, the number of
sites evaluated for 1,1-dichloroethane is not known.

1,1-Dichloroethane in the environment is mainly related to the production, storage, consumption,
transport, and disposal of 1,1-dichloroethane used as a chemical intermediate, solvent, finish remover, and
degreaser. 1,1-Dichloroethane may occur in the environment as a biodegradation product of
1,1,1-trichloroethane. In addition, 1,1-dichlrooethane was reported as a constituent in the gaseous
emissions of cigarette smoke. Releases from industrial processes are almost exclusively to the
atmosphere. Releases of the compound to surface waters and soils are expected to partition rapidly to the
atmosphere through volatilization. Hydrolysis, photolysis, and biodegradation do not appear to be
important processes in determining the environmental fate of 1,1-dichloroethane. It has been detected at
generally low levels in ambient air, surface water, groundwater, drinking water, and human breath.
Concentrations in environmental media are greatest near source areas (e.g., industrial point sources,
hazardous waste sites).

The main route of human exposure to 1,1-dichloroethane is through inhalation of 1,1-dichloroethane in
ambient or workplace air. Estimates of populations potentially exposed to 1,1-dichloroethane in
workplace environments in the 1980s ranged from 715 to 1,957 workers (EPA 2001c). Ingestion of
contaminated drinking water may also be an important route of exposure for populations living near
industrial facilities and hazardous waste sites. Boman and Maibach (1996) concluded that exposure to
skin results in very little absorption due to the compound's volatility; in addition, the concentration levels
greatly diminish in properly ventilated areas.

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

Figure 6-1. Frequency of NPL Sites with 1,1-Dichloroethane Contamination

Derived from HazDat

Derived from

Frequency
of

NPL Sites

11-3
~4-6
¦7-9

~ 10-14

~ 17-28
¦ 50-62

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

6.2 RELEASES TO THE ENVIRONMENT

The Toxics Release Inventory (TRI) data should be used with caution because only certain types of
facilities are required to report (EPA 2005). This is not an exhaustive list. Manufacturing and processing
facilities are required to report information to the TRI only if they employ 10 or more full-time
employees; if their facility is included in Standard Industrial Classification (SIC) Codes 10 (except 1011,
1081, and 1094), 12 (except 1241), 20-39, 4911 (limited to facilities that combust coal and/or oil for the
purpose of generating electricity for distribution in commerce), 4931 (limited to facilities that combust
coal and/or oil for the purpose of generating electricity for distribution in commerce), 4939 (limited to
facilities that combust coal and/or oil for the purpose of generating electricity for distribution in
commerce), 4953 (limited to facilities regulated under RCRA Subtitle C, 42 U.S.C. section 6921 et seq.),
5169, 5171, and 7389 (limited S.C. section 6921 et seq.), 5169, 5171, and 7389 (limited to facilities
primarily engaged in solvents recovery services on a contract or fee basis); and if their facility produces,
imports, or processes >25,000 pounds of any TRI chemical or otherwise uses >10,000 pounds of a TRI
chemical in a calendar year (EPA 2005).

Of the 21,526 TRI facilities reporting nationwide, 1,1-dichloroethane (CASRN: 75-34-3), has been
reported in 0 onsite TRI releases for the reporting year 2013. Of these TRI facilities reporting
nationwide, 1,1-dichloroethane, under the synonym ethylidene dichloride (CASRN: 75-34-3), has been
reported in 18 onsite TRI releases for the reporting year 2013 (NLM 2015).

Section 112 of the Clean Air Act (CAA) lists 1,1-dicloroethane as one of 188 hazardous air pollutants
(HAPs) known to cause or suspected of causing cancer or other serious human health effects or ecosystem
damage (EPA 2000). EPA's National Emission Inventory (NEI) database contains data regarding sources
that emit criteria air pollutants and their precursors, and HAPs for the 50 United States, Washington DC,
Puerto Rico, and the U.S. Virgin Islands (prior to 1999, criteria pollutant emission estimates were
maintained in the National Emission Trends [NET] database and HAP emission estimates were
maintained in the National Toxics Inventory [NTI] database). The NEI database derives emission data
from multiple sources including: state and local environmental agencies; the TRI database; computer
models for on-road and off-road emissions; databases related to EPA's Maximum Achievable Control
Technology (MACT) programs to reduce emissions of hazardous air pollutants. Using composite data
from the NTI database from 1990 to 1993, it was estimated that the annual emissions of 1,1-dichloro-
ethane in the United States was approximately 274 tons per year during that time frame (EPA 2000).

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

Data downloaded from the 2005 NEI indicated that the total emission of 1,1-dichloroethane was
approximately 387 tons, with the biggest source arising from point source waste disposal (EPA 2012c).

There are no known natural sources of 1,1-dichloroethane. It has been reported that 1,1,1-trichloroethane
is rapidly biodegraded in anaerobic methanogenic environments, such as those found in landfills, to form
1,1-dichloroethane as the major product, with slow, yet complete anaerobic degradation of 1,1-dichloro-
ethane to carbon dioxide also indicated (deBest et al. 1997; van Eekert et al. 1999; Vogel and McCarty
1987). 1,1,1-Trichloroethane occurs in the environment as a result of accidental spills, industrial
manufacturing, and use processes. Laboratory studies designed to elucidate the degradation reactions of
chloroethenes and chloroethanes have been described by Hallen et al. (1986) and Vogel and McCarty
(1987). Hallen et al. (1986) observed that dechlorination reactions appear to be reversible, and
chlorinated ethanes can be converted to chlorinated ethenes. Releases of 1,1-dichloroethane to the
environment are a result of industrial manufacturing use processes and from the degradation of
1,1,1-trichloroethane. Additional sources of environmental release are fugitive emissions from storage,
distribution, and disposal; use as an extraction solvent and fumigant or insecticide spray and in paints,
varnish, and paint removers; as a constituent of medicines and stone, clay, and glass products; and in ore
floatation (EPA 2001c; Infante and Tsongas 1982).

6.2.1 Air

Estimated releases of 20,972 pounds (-9.51 metric tons) of 1,1-dichloroethane to the atmosphere from
19 domestic manufacturing and processing facilities in 2013, accounted for about 90.1% of the estimated
total environmental releases from facilities required to report to the TRI (TRI13 2014). These releases are
summarized in Table 6-1.

Emissions to the atmosphere comprise >98% of all releases of 1,1-dichloroethane to the environment
(TRI 102012). 1,1 -Dichloroethane released in the production of 1,1,1 -trichloroethane accounts for about
52% of the atmospheric releases, with the production of 1,2-dichloroethane accounting for about 35%.
Pellizzari (1982) reported the presence of low levels of 1,1-dichloroethane in ambient air of the Baton
Rouge industrial area and at the Kin-Buc waste disposal site outside Edison, New Jersey. Eitzer (1995)
observed low levels of 1,1-dichloroethane (<1 (.ig/nr1) in at least one of eight municipal solid waste sites
sampled in the United States.

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

Table 6-1. Releases to the Environment from Facilities that Produce, Process, or

Use 1,1-Dichloroethanea

Reported amounts released in pounds per yearb

Total release

State0

RFd

Air®

Waterf

UI9

Landh

Other'

On-sitej

Off-sitek

On- and off-site

20,612

20,692

20,703

297

2,200

2,498

Total

20,972

2,200

23,254

23,275

aThe TRI data should be used with caution since only certain types of facilities are required to report. This is not an

exhaustive list. Data are rounded to nearest whole number.

bData in TRI are maximum amounts released by each facility.

cPost office state abbreviations are used.

dNumber of reporting facilities.

eThe sum of fugitive and point source releases are included in releases to air by a given facility.

'Surface water discharges, waste water treatment-(metals only), and publicly owned treatment works (POTWs) (metal

and metal compounds).

gClass I wells, Class ll-V wells, and underground injection.

hResource Conservation and Recovery Act (RCRA) subtitle C landfills; other onsite landfills, land treatment, surface
impoundments, other land disposal, other landfills.

'Storage only, solidification/stabilization (metals only), other off-site management, transfers to waste broker for
disposal, unknown

'The sum of all releases of the chemical to air, land, water, and underground injection wells.
kTotal amount of chemical transferred off-site, including to POTWs.

RF = reporting facilities; Ul = underground injection

Source: TRI13 2014 (Data are from 2013)

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

Approximately 52,000 kg of 1,1-dichloroethane are released to the atmosphere by privately owned
treatment work facilities (POTWs) each year (EPA 1980).

In 2002, air emissions from point, area, and mobile sources in the Great Lakes region were calculated.
Data from Illinois, Indiana, Michigan, Minnesota, New York, Ontario, Pennsylvania, and Wisconsin were
evaluated. Total emissions of 1,1-dichloroethane in the Great Lakes region were calculated to be
27,110 pounds from point sources and 1,360 pounds from area sources. All states reported only point
source emissions for the compound with the exception of Minnesota, which reported 341 pounds from
point sources and 1,360 pounds from area sources. Ontario and Illinois accounted for the majority of the
emissions (41 and 33%, respectively). The other states each accounted for 1-9% of the emissions (Great
Lakes Commission 2006).

1,1-Dichloroethane was detected with the VOCs emanating from a low-level radioactive waste disposal
facility at the U.S. Geological Survey (USGS) Amargosa Desert Research Site in Nevada (Baker et al.
2012). The study quantified VOCs being emitted over an 11-year period and estimated the yearly vertical
diffusive flux of the detected VOCs to the atmosphere. Concentrations decreased as the distance from the
site increased. Samples taken at the site contained 29.9, 33.6, and 66 mg dichloroethane/m2 per year,
while samples taken 100 m from the site along the north south transect contained 2.8, 3.6, and 9.7 mg
dichloroethane/m2 per year in 2001, 2003, and 2005 respectively. At distances of 200 and 300 m,
concentrations were reported as 0.0 mg dichloroethane/m2 for 2001, 2003, and 2005. Table 6-2
summarizes the estimates obtained from locations along the north-south transect at distances of 0-400 m
from the facility.

Emissions from six commercial cigarette brands were examined in a chamber study; five cigarettes per
brand were smoked for approximately 6 minutes (Wang et al. 2012). The amount of 1,1-dichloroethane
emitted during smoking ranged between 51 and 110 (ig/cigarette. The average concentration of
1,1-dichloroethane during smoking ranged from 12 to 26 (.ig/nr1 and the average concentration during the
post-smoking period ranged from 7.9 to 17 |_ig/m3.

In 2011, 1,1-dichloroethane was detected in the gaseous emissions of a commercial poultry farm in
Poland (Witkowska 2013). The farm consisted of five buildings that had mechanical ventilation systems.
Measurements were taken over the turkey's rearing period, from week 4 to 19. The average
concentrations detected in the turkey houses at week 4, 7, 10, and 13 were 1.15±0.55, 1,08±0.82,

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1,1-DICHLOROETHANE 71

6. POTENTIAL FOR HUMAN EXPOSURE

Table 6-2. Estimated Yearly Emissions of 1,1-Dichloroethane (mg/m2 per Year)

Distance from landfill (m)

2001

2003

2005

29.9

33.6

22.6

31.8

51.5

18.4

17.9

Not reported

16.4

Not reported

100

2.8

3.6

9.7

150

Not reported

0.1

Not reported

200

0.0

300

0.0

400

0.0

Not reported

Source: Baker et al. 2012

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

1.57±0.45, and 1.33±0.55 ppm, respectively. Reported concentrations for week 16 and 19 were
0.00 ppm.

6.2.2 Water

Estimated releases of 82 pounds (-0.037 metric tons) of 1,1-dichloroethane to surface water from
15 domestic manufacturing and processing facilities in 2013, accounted for <1% of the estimated total
environmental releases from facilities required to report to the TRI (TRI13 2014). This estimation
includes surface water discharges, waste water treatment (metal only), and POTWs (metal and metal
compounds) (TRI13 2014). These releases are summarized in Table 6-1.

Industrial releases of 1,1-dichloroethane to surface waters are minor in comparison to releases to the
atmosphere. Industrial processes involving the use of 1,1-dichloroethane as a chemical intermediate or
cleaning solvent are believed to be the largest sources of surface water releases. Young et al. (1983)
reported 1,1-dichloroethane in the primary, secondary, and final effluents from municipal wastewater
treatment plants. Approximately 1,000 kg of 1,1-dichloroethane are discharged in effluent from POTWs
each year (EPA 1980).

6.2.3 Soil

Estimated releases of 21 pounds (-0.009 metric tons) of 1,1-dichloroethane to soils from eight domestic
manufacturing and processing facilities in 2013, accounted for <0.01% of the estimated total
environmental releases from facilities required to report to the TRI (TRI13 2014). An additional 2,200
pounds (-1.0 metric tons), constituting about 9.46% of the total environmental emissions, were released
via underground injection (TRI13 2014). These releases are summarized in Table 6-1.

Little information was found regarding releases of 1,1-dichloroethane to soils. Approximately 4,000 kg
of 1,1-dichloroethane from POTWs are dispersed on land each year as sludge (EPA 1980).

6.3 ENVIRONMENTAL FATE
6.3.1 Transport and Partitioning

Releases of 1,1-dichloroethane to the environment as a result of industrial activity are expected to be
primarily to the atmosphere (see Section 6.2). 1,1-Dichloroethane released to the atmosphere may be

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

transported long distances before being washed out in precipitation. For example, Pearson and
McConnell (1975) attributed the presence of chlorinated organic compounds, including 1,1-dichloro-
ethane, in upland waters to long-range aerial transport and deposition in precipitation. EPA (1982b)
discussed the atmospheric fate of 1,1-dichloroethane in the Gulf Coast area, where there is a high
percentage of cloudy days. Increased atmospheric losses due to washout in frequent, heavy rains could
occur, although much of the 1,1-dichloroethane could be revolatilized. Dichloroethanes released in this
area could be transported north by the prevailing winds to populated areas before significant
photochemical degradation could occur.

Cupitt (1980), however, considered the loss of 1,2-dichloroethane from the atmosphere by dissolution
into rain drops or adsorption onto aerosols insignificant compared with loss from chemical degradation
based on mathematical calculations. Since 1,1-dichloroethane has higher volatility and lower aqueous
solubility than the 1,2-isomer, physical removal of 1,1-dichloroethane from the atmosphere would be
even less likely to be important. Pellizzari et al. (1979) measured actual concentrations of airborne
contaminants in the vicinity of known emission sources of 1,1-dichloroethane, making aerial transport the
logical source of downwind concentrations.

The Henry's law constant value for 1,1-dichloroethane (5.5 lxlO 3 atm-m3/mol) suggests that it should
partition rapidly to the atmosphere. The evaporation half-life depends on a number of factors; wind speed
and mixing conditions of the receiving waters are particularly important. Dilling et al. (1975) and Dilling
(1977) estimated a volatilization half-life of 22 minutes for 1,1-dichloroethane present at 1 ppm
concentration in an open water column held at 25 °C and stirred at 200 rpm. Under these conditions, 90%
of the compound was removed within 109 minutes. Volatilization half-lives determined in the laboratory
are related to actual environmental situations by a correction factor that takes into account the oxygen re-
aeration rate ratio. The re-aeration rate ratio has been determined to be 0.55 for 1,1-dichloroethane
(Cadena et al. 1984). Using the values of Mabey et al. (1982) for oxygen re-aeration rates in ponds and
rivers (0.19 and 0.96 day"1, respectively), the evaporation half-life of 1,1-dichloroethane is estimated to be
approximately 5 times longer for ponds than for rivers (>1 day for river water and >6 days for pond
water).

Little information was found regarding partitioning of 1,1-dichloroethane from the water column onto
sediments. According to DeWulf et al. (1996), 1,1-dichloroethane does not really accumulate on marine
sediment and it will therefore not be an important sink for this compound. Analogs of the compound (i.e.,
dichloromethane, trichloromethane, and 1,1,1-trichloroethane) have not been found to concentrate

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

selectively onto sediments (Dilling et al. 1975; Pearson and McConnell 1975). The Koc values for these
compounds are similar to the Koc for 1,1-dichloroethane; therefore, partitioning to sediment from the
water column is not likely to be an important environmental fate process for 1,1-dichloroethane.

1,1-Dichloroethane released to land surfaces in spills would rapidly volatilize to the atmosphere, but
1,1-dichloroethane remaining on soil surfaces would be available for transport into groundwater, since the
compound does not sorb to soil particulates unless the organic content of the soil is high. Experimentally
derived Koc values for a silt loam soil also indicate that little sorption of 1,1-dichloroethane to low organic
content soil is expected. Goodin and Webber (1992) conducted studies of several volatile organic
compounds (VOCs), including 1,1-dichloroethane, to determine their fate in soils. It was determined that
the compounds were lost from the soils mainly by volatilization, with first-order disappearance half-lives
ranging from 1 to 949 hours. Wilson et al. (1981) found that although 50% of the applied 1,1-dichloro-
ethane volatilized to the atmosphere, the remainder percolated rapidly through a sandy soil, suggesting
ready availability to groundwater transport processes.

Gossett et al. (1983) analyzed the tissues of several species of aquatic organisms for 1,1-dichloroethane
near the discharge of the Los Angeles County waste water treatment plant. The concentration of
1,1-dichloroethane in the effluent was 3.5 ppb; however, none was found in the animal tissues (detection
limit of 0.3-0.5 ppb). These results may be evidence that the potential for 1,1-dichloroethane to
bioconcentrate is low in aquatic organisms. An estimated bioconcentration factor of 5 indicates that
bioconcentration would be low (HSDB 2012).

6.3.2 Transformation and Degradation

6.3.2.1 Air

In the atmosphere, 1,1-dichloroethane is oxidized by reaction with hydroxyl radicals. The rate constant
for the vapor-phase reaction is 2.74xl0~13 cm3/molecule-second at 25 °C (HSDB 2012). The residence
time of the compound in the atmosphere has been estimated to be 49 days (HSDB 2012).

6.3.2.2 Water

1,1-Dichloroethane in surface water is expected to be lost to the atmosphere through volatilization before
undergoing any significant chemical or biological degradation. The hydrolytic half-life of 1,1-dichloro-
ethane at pH 7 and 25 °C has been estimated to be 60 years (Jeffers et al. 1989).

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

As summarized in Klecka et al. (1990), 1,1-dichloroethane is produced by biodegradation of
1,1,1-trichloroethane in groundwater. Further degradation could also occur. In the absence of oxygen
and in the presence of anaerobic, methane-producing bacteria, halocarbons are transformed by reductive
dehydrohalogenation in a step-wise manner: 1,1,1 -trichloroethane —> 1,1 -dichloroethane —> chloroethane.
van Eeker et al. (1999) reported 31.1% anaerobic degradation of 1,1-dichloroethane to mainly
chloroethane (14.5%) in living sludge after 25 days. Under aerobic conditions, Tabak et al. (1981)
reported about 50% degradation of 1,1-dichloroethane by unadapted microorganisms isolated from
municipal waste water inoculum after 7 days, which was increased to 78% degradation by adapted
organisms in the same time period. 1,1-Dichloroethane has been reported to be resistant to biological
degradation by bacteria isolated from shallow aquifer aerobic groundwater after 8-16 weeks incubation
(Wilson etal. 1983).

Data from landfill sites with a documented contamination history were examined by Cline and Viste
(1985). They observed that 1,1-dichloroethane was detected in groundwater at sites where the compound
had not been handled or disposed of and concluded that 1,1-dichloroethane had been produced by
anaerobic degradation of other compounds present, particularly 1,1,1-trichloroethane. Washington and
Cameron (2001) used well monitoring data, from a landfill with a contamination history, to calculate a
degradation rate constant for 1,1-dichloroethane. Under sulfate-reducing conditions at 10 °C, the rate
constant was found to be 6.0xl0~3 L/day with a half-life of 115 days.

6.3.2.3 Sediment and Soil

1,1-Dichloroethane in soils is expected to volatilize to the atmosphere or be transported to groundwater
before undergoing significant abiotic transformation; the compound is not expected to sorb to soils of low
organic content. As in surface waters, direct photolysis of 1,1-dichloroethane on soil surfaces is not
expected. The rate of biodegradation of 1,1-dichloroethane in soils is unknown. In subsurface soil, the
loss of 1,1-dichloroethane through biodegradation is expected to be insignificant (Wilson et al. 1983).
The biodegradation half-life of 1,1,1-trichloroethane under anaerobic conditions has been reported to be
about 16 days, whereas the half-life of 1,1-dichloroethane has been reported to be >30-60 days (Wood et
al. 1985).

Hamonts et al. (2012) monitored chlorinated aliphatic hydrocarbons, such as 1,1-dichloroethane, in
groundwater that discharges into the Zenne River over a 21-month period. The Zenne River had been

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

previously continuously contaminated with municipal sewage containing chlorinated aliphatic
hydrocarbons. The study also evaluated microbial reductive dechlorination occurring under anaerobic
conditions in the river sediments. Microbial degradation of 1,1-dichloroethane was evident in the
riverbed locations in which Dehalobactor spp. was detected; however, in the absence of this
microorganism, 1,1-dichloroethane did not appear to degrade.

6.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT

Reliable evaluation of the potential for human exposure to 1,1-dichloroethane depends in part on the
reliability of supporting analytical data from environmental samples and biological specimens.
Concentrations of 1,1-dichloroethane in unpolluted atmospheres and in pristine surface waters are often
so low as to be near the detection limits of analytical methods. In reviewing data on 1,1-dichloroethane
levels monitored or estimated in the environment, it should also be noted that the amount of chemical
identified analytically is not necessarily equivalent to the amount that is bioavailable. The analytical
methods available for monitoring 1,1-dichloroethane in a variety of environmental media are detailed in
Chapter 7.

1,1-Dichloroethane has been detected in ambient urban and rural air, in waste gas generated from garbage
dumps, and in surface water, groundwater, and drinking water. Quantitative concentration information is
presented in the following sections by environmental medium.

6.4.1 Air

The Air Quality System (AQS) database is EPA's repository of criteria air pollutants and hazardous air
pollutants (HAPs) containing monitoring data from over 2,600 monitoring sites across the United States.
Detailed AQS ambient air monitoring data from 2013 for 1,1-dichloroethane are summarized in Table 6-3
(http://www.epa.gOv/ttnamtil/toxdat.html#data*). Data for other years are available as zipped Microsoft
Access database files that may be accessed directly from the EPA website. In general, the average
concentration of the samples for 1,1-dichloroethane in outdoor air was approximately 0.02 (ig/m3. The
highest reported concentration (4.4 (ig/m3) occurred in one sample from Kentucky. The second highest
reported concentration (0.83 (ig/m3) also occurred in one sample from Kentucky. The third highest
reported concentration (0.81 (ig/m3) was detected in 173 samples from Ohio. Rhode Island had the
largest number of samples with detectable concentrations, 836 samples, that ranged in concentration from
0.004 to 0.12 |ig/m3. The 24-hour average concentration of 1,1-dichloroethane in outdoor air ranged from

-------
1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

Table 6-3. 2013 Air Monitoring Data from Air Toxics Data Ambient Monitoring

Archive for 1,1-Dichloroethane

State3 Number of samples Concentration range (|jg/m3)

AK 61 0

AZ 104 0

CO 61 0

FL 32 0.0081-0.18

FL 376 0

GA 237 0

IA 87 0

IL 180 0

IN 28 0.04

IN 442 0

KY 33 0.044-4.4

KY 467 0

MA 141 0.004-0.0081

MA 25 0

ME 36 0.016-0.4

ME 244 0

Ml 2 0.34-0.35

Ml 329 0

MN 1 0.004

MN 1,008 0

MO 61 0

MS 121 0

NC 437 0

NJ 1 0.045

NJ 239 0

NY 238 0.004-0.47

NY 483 0

OH 173 0.81

OH 243 0

OK 303 0

PA 27 0.04-0.12

PA 274 0

Rl 836 0.004-0.012

Rl 42 0

SC 118 0

TX 6 0.04-0.2

TX 2,355 0

UT 52 0

VA 89 0

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

Table 6-3. 2013 Air Monitoring Data from Air Toxics Data Ambient Monitoring

Archive for 1,1-Dichloroethane

State3

Number of samples

Concentration range (|jg/m3)

140

aPost office state abbreviations used.
Source: EPA 2015b

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

approximately 0.008 to 3.5.4 |ig/m3 (0.001-1.09 ppb). The analytical methods had detection limits that
ranged between 0.0081 and 3.4 |ig/m3 (EPA, 2015b).

1,1-Dichloroethane was not seen at a detection limit of 5 ppt in ambient rural air samples taken in
southeastern Washington state (Grimsrud and Rasmussen 1975). It has been found at higher
concentrations in ambient air samples from urban areas of the United States. EPA (1983b) tabulated
atmospheric levels at urban, rural, and industrial sites across the United States and reported a median
concentration of 55 ppt. Pellizzari (1982) reported the detection of low levels (unspecified
concentrations) of the compound in the vicinity of the Baton Rouge industrial area. EPA (1983a)
reported that the average concentration of the compound in the air of seven urban locations in 1980-1981
ranged from 0.1 to 1.5 ppb. It has also been detected in samples of ambient air collected in the vicinity of
hazardous waste disposal sites, such as the Kin-Buc site near Edison, New Jersey, at a level of 23 |ig/m3
(5.68 ppm) (Pellizzari 1982). EPA (1978) tabulated analytical results for 1,1-dichloroethane in the
ambient air of various locations generally in close proximity to industrial plants, including Magna, Utah
(0.082 ppb); Iberville, Louisiana (0.12 ppm); Deer Park, Texas (0.14 ppb); and Baton Rouge (0.058 ppb)
and Geismar, Louisiana (0.14 ppb).

Barkley et al. (1980) found no 1,1-dichloroethane in the ambient air surrounding nine houses bordering
the old Love Canal. Gupta et al. (1984) found 1,1-dichloroethane at higher levels indoors (mean
concentration of 3.2 ppb) than outdoors (not detected) in residences in suburban Knoxville, Tennessee,
and concluded that there must be a source of the compound inside the home. Possible sources were not
identified except to suggest building materials or chlorinated water.

Air monitoring data from 22 tire fire incidents across the United States were evaluated. 1,1-Dichloro-
ethane was detected at low levels in the vicinity of several of the fires. It was noted that the source may
be from something other than the burning tires (EPA 1993).

Air was monitored over a 3-week period at the Fresh Kills Landfill of Staten Island, New York. The
overall air emission rate for 1,1-dichloroethane was 0.216 g/second (EPA1996a).

In 1994, 1,1-dichloroethane was not detected in six spatial sites around the Columbus metro area.
Detection limits of the analysis were 0.05 ppb (Spicer 1996).

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

In 1996, Mohamed et al. (2002) monitored VOCs in air at 13 urban locations in the United States for
1 year. Monitoring sites were located in Louisiana, Texas, Vermont, and New Jersey. TRI reporting
facilities near the monitoring sites ranged from 0 to 38 facilities. 1,1-Dichloroethane was detected at all
13 of the monitoring stations at levels <1 ppb by volume (ppbv). The detection limit of the analytical
method was <0.5 ppbv.

1,1-Dichloroethane was detected in the headspace of five out of eight household bleach products at levels
ranging from 0.7 to 176 |_ig/m3. It was concluded that the compound was formed by the reaction of
hypochlorite and the organic matter of the product's additives. In addition, 1,1-dichloroethane levels of
indoor air increased during the use of bleach products, from 0.004-0.01 (.ig/nr1 before use, to 0.01-
0.62 (ig/m3 during use, and then to 0.01-0.29 (.ig/nr1 after use (Odabasi 2008).

From February to December 2009, 1,1-dichloroethane was detected in ambient air samples from four sites
in Seoul, Korea (Jong Ro, Yang Jae, Gwang Jin, and Gang Seo) at concentrations of 0.04-0.18, 0.03-
0.08, 0.04-0.15, and 0.04-0.32 ppb, respectively (Kim et al. 2012).

6.4.2 Water

. The compound has been found in samples of urban runoff from Long Island, New York, and Eugene,
Oregon, at concentrations of 1.5 and 3 ppb, respectively (Cole et al. 1984). Coniglio et al. (1980)
summarized groundwater monitoring data obtained by numerous state agencies and reported that
1,1-dichloroethane was found in 18% of the wells tested, with a maximum concentration of 11,330 ppb.
They cautioned that the state data may have been biased since the monitoring was generally conducted by
the states in areas where contamination was suspected. However, 1,1-dichloroethane has been detected in
groundwater sampled during random testing of water supplies (see further discussion).

Finished water supplies obtained from groundwater sources were tested by EPA for contaminants. It was
reported that up to 10.8% of 158 nonrandom sample sites from across the United States contained
detectable levels of 1,1-dichloroethane. The maximum concentration was 4.2 ppb (Westrick et al. 1984).

Drinking water samples from a number of urban and rural locations in the United States have been
reported to be contaminated with 1,1-dichloroethane. Unspecified levels of the compound have been
detected in drinking water samples taken from Philadelphia (Suffet et al. 1980). Private drinking water
wells in Wisconsin were found to contain unspecified levels of 1,1-dichloroethane in 11 of 617 wells

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

surveyed (Krill and Sonzogni 1986). Concentrations of 1-3 ppb were reported in four public well water
supplies in Iowa (EPA 1985).

Groundwater samples taken from 178 hazardous waste disposal sites were found to contain 1,1-dichloro-
ethane at 18% frequency (Plumb 1987), with an average concentration of 0.31 ppm and a maximum
concentration of 56.1 ppm (Yang and Rauckman 1987). Using the STORET database, Staples et al.
(1985) reported median concentrations of <0.1 ppb in 8,716 samples of ambient water (3% detectable
values), <1.0 ppb in 1,375 effluent samples (5% detectable values), <5.0 ppb in 354 sediment samples
(0.6% detectable values), and <0.05 ppb in 94 biota samples (no detectable values).

Nine shallow groundwater samples contained 1,1-dichloroethane with a maximum concentration of
2.2 |ig/L. in 5.3% of 208 urban wells sampled in the United States (Kolpin et al. 1997).

1,1-Dichloroethane was detected above background levels in groundwater beneath Savannah River Site's
Interim Sanitary Landfill. Several wells at the site were sampled twice each in 2005. The site was in
operation from 1992 to 1998 (DOE2005).

The Aerojet-General Corporation reports that 1,1-dichloroethane is present as a groundwater contaminant
just outside Sacramento, California, in varying concentrations in several separate domestic and industrial
well water samples and test borings. Additionally, a 1996 study indicated the presence of the compound
in groundwater from the Glassboro region of Southern New Jersey at a detection frequency of 5% and a
concentration of >0.1 |ig/L (HSDB 2012).

The Solid Waste Management Unit 12 in South Carolina was in use from the 1970s until 1981. In
September 1999, water sampled from an excavation hole that contained a leaking underground storage
tank (UST) contained 1,1-dichloroethane at a concentration of 84,300 |ig/L. Monitoring efforts of wells
surrounding the site from August 2000 to November 2007 detected 1,1-dichloroethane as a consistent
contaminant in the groundwater. Groundwater samples from August 2001 indicated that the highest
concentrations of contaminants in groundwater were near the UST, indicating that it was the source area.
Maximum measured concentrations of 1,1-dichloroethane of 155,000 |ig/L were found at that time.
Natural and engineered remediation efforts have contributed to the irregular decline of contaminants. On
the northern side of the facility, concentrations of 1,1-dichloroethane in groundwater at one of the wells
declined from >100 |ig/L in 2000 to approximately 20-30 |ig/L in 2003, remained relatively unchanged in
2003-2005, and declined in 2006-2007 (USGS 2006b).

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

The National Water Quality Assessment Program (NAWQA) evaluated 3,496 wells nationwide for the
presence of VOCs from 1985 to 2001. 1,1-Dichloroethane had an overall detection frequency of 0.86% at
an assessment level of 0.2 j^ig/L: a detection frequency of 0.17% at an assessment level of 1 j^ig/L: and a
detection frequency of 0.029% at an assessment level of 5 (ig/L. The compound was also detected as a
mixture with 1,1,1-trichloroethane in 0.71% of the samples (USGS 2006a). According to the report, there
were 30 detections of 1,1-dichloroethane in 3,496 aquifer samples. More specifically, 7 detections
occurred in 2,400 domestic well samples, 22 detections occurred in 1,096 public well samples,
20 detections occurred in 847 urban area shallow groundwater samples, and 1 detection occurred in
723 agricultural area shallow groundwater samples. Reported concentrations ranged from approximately
0.007 to 9 (ig/L, with the bulk of the samples falling in the range of 0.02-0.2 (ig/L (USGS 2006a).

1,1-Dichloroethane was detected in 2.3% of 130 groundwater well samples at a maximum concentration
of 0.6 (ig/L (Bi et al. 2012). Samples were collected during 2008 and 2009 from five alluvial plains in
East China considered to be susceptible to contamination from human activities.

From May 3, 1999 through October 23, 2000, random samples from 954 water sources across the United
States were collected. The sources included 579 groundwater and 375 surface water samples.
1,1-Dichloroethane was detected in 11 groundwater samples at levels between 0.1 and 10 (ig/L (USGS
2003a).

Shallow groundwaters underlying areas of residential and commercial use in Salt Lake Valley, Utah were
analyzed for VOCs such as 1,1-dichloroethane using monitoring wells at 30 separate sites (USGS 2003b).
1,1-Dichloroethane was detected in one of the samples, at an estimated concentration of 0.03 (ig/L (below
the laboratory reporting level of 0.07(.ig/L).

1,1-Dicholorethane was one of the primary VOCs detected in several water quality studies from the Snake
River Plain aquifer conducted between 1987 and 2005 (USGS 2010a). In April 2007, the USGS National
Water Quality Laboratory analyzed perched groundwater samples from well USGS 92 at the Radioactive
Waste Management Complex in the Snake River Plain aquifer and 1,1-dichloroethane was detected at a
concentration of 0.8 (ig/L (USGS 2010a).

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

The CALEPA (2003) analysis of 13,347 California groundwater sources of drinking water found
1,1-dichloroethane in 68 samples, ranging from 0.51 to 30 ppb. 1,1-Dichloroethane was not found in any
of the 754 surface water sources of drinking water sampled.

Samples from 2,948 wells across the United States were sampled between 1985 and 1995. The sources
consisted of both drinking water and non-drinking water in 406 urban wells and 2,542 rural wells. The
detection frequency of 1,1-dichloroethane was 6.4% in urban wells and 0.7% in rural wells. Reported
concentrations were approximately 0.2-60 (ig/L with a median of approximately 0.45 (ig/L, and
approximately 0.2-8 (ig/L with a median of about 0.7 (ig/L, respectively (Squillace et al. 1999).

VOCs were examined in 30 public water supply wells in the Columbia aquifer in Delaware (USGS
2010c). In 2000, 1,1-dichloroethane was detected 6 times at concentrations ranging from 0.015 to
0.149 (ig/L and in 2008, the chemical was detected 4 times at concentrations of <0.04-0.135 (ig/L.

Active wells were resampled in a study by the Source Water Assessment and Protection Program from
August through November 2008. Twenty-two of the original wells and 8 similar wells were sampled.
The range of detected concentrations remained the same; however, the number of detections decreased by
1 for both years.

The USGS assessed the quality of source water from public supply wells in the United States from 1993
to 2007 (USGS 2010d). 1,1-Dichloroethane was detected in 7.7% of 832 samples, and 1.4% of the
samples contained >0.2 j^ig/L (USGS 2010b). The maximum concentration of 1,1-dichloroethane
detected was 4.878 (ig/L.

6.4.3 Sediment and Soil

Very little information was found on the ambient concentrations of 1,1-dichloroethane in soil, or on the
current disposal of waste products containing the compound in landfills. 1,1-Dichloroethane was
detected, yet not quantified, in soil samples of Love Canal, New York. At a detection limit of 0.5 ppb,
1,1-dichloroethane was not detected in sediment of the submarine outfall region of the Los Angeles
County (Joint Water Pollution Control Plant [JWPCP]) municipal waste water treatment plant (HSDB
2012). The compound has more commonly been detected in ambient air and groundwater samples taken
at hazardous waste sites, and it is expected that the lack of available soil monitoring data is at least in part
due to rapid partitioning of 1,1-dichloroethane released to soils to these other media.

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

Soil gas was monitored forthe U.S. Army from October 2010 until September 2011 in Fort Gordon,
Georgia (USGS 2012). Soil-gas samplers were installed at three former fuel-dispensing stations in order
to assess organic soil-gas contaminants for the Resource Conservation and Recovery Act Part B
Hazardous Waste Permit process. There were 55 samplers at one site, 30 samplers at a second site, and
39 samplers at a third site. 1,1-Dichloroethane was reported as not detected in all samples and the method
detection limit was 0.02 (ig (USGS 2012).

6.4.4 Other Environmental Media

Little information was found on the levels of 1,1-dichloroethane in other media. Ferrario et al. (1985)
measured 33 ppb wet weight of 1,1-dichloroethane in oysters from Lake Pontchartrain near New Orleans,
Louisiana; however, 1,1-dichloroethane was not detected in two types of clams. Kallonen et al. (1985)
detected 1,1-dichloroethane in the effluent gases of burning polyester fiber fill. Data on concentrations in
human breath are presented in Section 6.5. 1,1-Dichloroethane was not found in any samples in a survey
of 234 table-ready foods evaluated for the presence of VOCs (Heikes et al. 1995). Page and Lacroix
(1995) found 1,1-dichloroethane in three peanut butter samples at levels of 1.1, 1.9,and3.7 j^ig/kg:
however, the compound was not found in several other foods that were analyzed.

6.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE

The greatest source of exposure to 1,1-dichloroethane for most of the U.S. population is inhalation of the
compound in contaminated air, especially near source areas. Another potential route of human exposure
is ingestion of the compound in contaminated drinking water, and use of consumer products that may
contain 1,1-dichloroethane. The general population may also be exposed through inhalation of cigarette
smoke (Wang et al. 2012). Occupational exposure to 1,1-dichloroethane may occur via inhalation or
dermal contact at workplaces where it is produced or used (HSDB 2012).

The Fourth National Report on Human Exposures to Environmental Chemicals, published and updated by
the Centers for Disease Control and Prevention (CDC 2015), reported data for 1,1-dichlorethane from the
National Health and Nutrition Examination Survey (NHANES) for the survey years 2003-2004 and
2005-2006. These data are summarized in Table 6-4. Blood concentrations of 1,1-dichloroethane for
male and female participants of ages 12->60 years and various ethnicities were reported. Concentrations
of 1,1-dichloroethane in all categories for all NHANES survey years were below the detection limit of the
method (0.01 (ig/L) (CDC 2015).

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

Table 6-4. Geometric Mean and Selected Percentiles of Blood Concentrations of
1,1-Dichloroethane (in ng/L) for the U.S. Population from the National Health and

Nutrition Examination Survey (NHANES)

Geometric Selected percentiles (95% CI)

Survey mean
years (95% CI)

50th

75th

90th

95th

Sample
size

Total

2003-2004 *a

60 years

2005-2006 *

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

The National Occupational Exposure Survey (NOES), conducted by NIOSH from 1981 to 1983, indicated
that 1,957 workers, including 272 women, were potentially exposed to 1,1-dichloroethane in the
workplace (NOES 1990). The exposed workers were employed in the chemical and allied products and
business service industries, as chemical technicians; plumbers, pipefitters, and steamfitters; supervisors in
production occupations; electricians; machinists; chemical engineers; and welders and cutters. The
estimates were based on direct observation by the surveyor of the actual use of the compound.

NIOSH (1978) noted that there was a large potential for exposure to 1,1-dichloroethane in the workplace
during its use as a dewaxer of mineral oils, extractant for heat-sensitive substances, or fumigant, and in
the manufacture of vinyl chloride and high-vacuum rubber and silicon grease.

The EPA (1982a) and Wallace et al. (1982) conducted a study of the levels of 1,1-dichloroethane in the
inhaled and exhaled air and drinking water of college students in Texas and North Carolina. Low levels
(<0.49 ppb) of 1,1-dichloroethane were found in the personal air quality monitors of the Texas students,
whose campus bounded a petrochemical manufacturing area, but none was detected in the exhaled breath
samples. 1,1-Dichloroethane was not detected in the breathing zone air of the North Carolina students.

Barkley et al. (1980) found a trace of 1,1-dichloroethane in the expired breath of one resident whose
home bordered the old Love Canal, but none was detected in ambient air. Wallace et al. (1984) found a
trace of 1,1-dichloroethane in the expired breath and drinking water of one resident of New Jersey).

Assuming a median ambient air level of 55 pptv reported by EPA (1983b) and a theoretical average
inhalation of 20 m3 air/day, the average inhalation exposure to 1,1-dichloroethane for an individual in the
United States is estimated at 4 (ig/day.

Buckley et al. (1997) reported the detection of 1,1-dichlorethane in 1 of 16 blood samples at a
concentration of 0.01 (ig/L. 1,1-Dichloroethane was detected in <10% of blood samples from
1,000 people between the years 1988 and 1994 (Needham et al. 1995). In October 2001, Edelman et al.
(2003) analyzed blood and urine samples from World Trade Center firefighters for VOCs, including
1,1-dichloroethane; detection of the compound was insignificant. A National Health and Nutrition
Survey of the U.S. population in 2003-2004 screened for 1,1-dichloroethane in blood samples at a limit
of detection (LOD) concentration of 0.01 ng/mL (CDC 2015). The samples were taken from
1,367 participants in the age range of 20-59 years old, about half females (n=679) and half males
(n=670). The survey included Mexican Americans (n=267), non-Hispanic blacks (n=300), and non-

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

Hispanic whites (n=695). The portion of the data below the LOD for 1,1-dichloroethane was too high to
provide valid results (CDC 2015).

6.6 EXPOSURES OF CHILDREN

This section focuses on exposures from conception to maturity at 18 years in humans. Differences from
adults in susceptibility to hazardous substances are discussed in Section 3.7, Children's Susceptibility.

Children are not small adults. A child's exposure may differ from an adult's exposure in many ways.
Children drink more fluids, eat more food, breathe more air per kilogram of body weight, and have a
larger skin surface in proportion to their body volume. A child's diet often differs from that of adults.
The developing human's source of nutrition changes with age: from placental nourishment to breast milk
or formula to the diet of older children who eat more of certain types of foods than adults. A child's
behavior and lifestyle also influence exposure. Children crawl on the floor, put things in their mouths,
sometimes eat inappropriate things (such as dirt or paint chips), and spend more time outdoors. Children
also are closer to the ground, and they do not use the judgment of adults to avoid hazards (NRC 1993).

There are no exposure studies or body burden measurements of 1,1-dichloroethane in children.
1,1-Dichloroethane has been detected in air, as discussed in Section 6.4.1, and inhalation of contaminated
air likely represents the greatest route of potential exposure for children. 1,1-Dichloroethane has also
been detected in drinking water, and therefore, ingestion of contaminated water is a possible source of
exposure. Dichloroethane (isomer not specified) has been detected in human milk (Urusova 1953);
however, these data are not current.

6.7 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES

Human exposure to 1,1-dichloroethane is expected to be highest among certain occupational groups (e.g.,
chemical and allied products industry workers) and members of the general population living in the
vicinity of industrial point emission sources (EPA 2001c) and hazardous waste sites. The compound has
been detected in both ambient air and water in low concentrations, with substantially higher
concentrations in localized areas around industrial and disposal sites. No information was found
regarding the number of people potentially exposed around hazardous waste sites.

Smokers are exposed to higher concentrations of 1,1-dichloroethane than nonsmokers. Emissions from
cigarette smoke can contain between 51 and 110 p.g 1,1-dichloroethane/cigarette (Wang et al. 2012). The

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

average concentration of 1,1-dichloroethane at the onset of smoking and 60 minutes after smoking ranges
from 7.9 to 26 (ig/m3. In addition, nonsmokers who are in close proximity to cigarette smoke are
susceptible to higher exposure concentrations.

6.8 ADEQUACY OF THE DATABASE

Section 104(i)(5) of CERCLA, as amended, directs the Administrator of ATSDR (in consultation with the
Administrator of EPA and agencies and programs of the Public Health Service) to assess whether
adequate information on the health effects of 1,1-dichloroethane is available. Where adequate
information is not available, ATSDR, in conjunction with NTP, is required to assure the initiation of a
program of research designed to determine the health effects (and techniques for developing methods to
determine such health effects) of 1,1-dichloroethane.

6.8.1 Identification of Data Needs

Physical and Chemical Properties. The physical/chemical properties of 1,1-dichloroethane are
sufficiently well characterized to enable assessment of the environmental fate of this compound.

Production, Import/Export, Use, Release, and Disposal. According to the Emergency
Planning and Community Right-to-Know Act of 1986, 42 U.S.C. Section 11023, industries are required
to submit substance release and off-site transfer information to the EPA. The TRI, which contains this
information for 2013, became available in October of 2014. This database is updated yearly and should
provide a list of industrial production facilities and emissions.

Based on its industrial use, 1,1-dichloroethane is primarily released to the atmosphere, and humans are
potentially exposed to this chemical through the inhalation or ingestion of contaminated air or water.
However, because the data available on production, import, export, use, and disposal are limited, it is
difficult to estimate whether or not the potential for human exposure to 1,1-dichloroethane may be
substantial. Data concerning the production and use of 1,1-dichloroethane both within the United States

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

and worldwide are extremely limited. Information regarding possible disposal methods, criteria, and
regulations are available; however, the present criteria may undergo revision in the near future.
Information on current production levels, quantities imported and exported, proportions allocated to
various uses, and proportions and efficiencies associated with differing modes of disposal is limited. This
information would be useful in identifying potential sources and levels of exposure, thus enabling
identification of exposed populations.

Environmental Fate. Releases from industrial processes are almost exclusively to the atmosphere,
and releases of the compound to surface waters and soils are expected to partition rapidly to the
atmosphere through volatilization. 1,1-Dichloroethane released to the atmosphere may be transported
long distances before being washed out in precipitation. Although 1,1-dichloroethane released to land
surfaces in spills would rapidly volatilize to the atmosphere, the 1,1-dichloroethane remaining on soil
surfaces would be available for transport into groundwater. The atmospheric residence time of
1,1-dichloroethane is about 44 days. The dominant removal mechanism is reaction with hydroxyl free
radicals. Hydrolysis and biodegradation do not appear to be important processes in the environmental
fate of this compound. Data are lacking on the partitioning of 1,1-dichloroethane from the water column
onto sediments. Additional information on the atmospheric transformation and on the rate of
biodegradation of 1,1-dichloroethane in soils would be useful in the determination of its environmental
fate.

Bioavailability from Environmental Media. Data are incomplete on the bioavailability of
1,1-dichloroethane from environmental media. Animal data on 1,1-dichloroethane exposure via
inhalation and oral administration in drinking water suggest that the compound is bioavailable following
inhalation of ambient air and ingestion of drinking water. Additional information on the bioavailability of
1,1-dichloroethane from air, water, soil, and sediment would be useful in determining actual risks
associated with exposure to environmental levels of 1,1-dichloroethane.

Food Chain Bioaccumulation. The information located on the potential for bioconcentration of
1,1-dichloroethane in plants, aquatic organisms, or animals is limited. An analysis of animal tissues from
several species of aquatic organisms near the discharge of a waste water treatment plant did not detect
1,1-dichloroethane in the animal tissues, although the compound was found in the effluent. However,
1,1-dichloroethane has been detected in oysters (33 ppb wet weight). An estimated bioconcentration
potential of <1 from the K0„ suggests that bioconcentration would not be expected. Very little
information was found regarding the biomagnification of 1,1-dichloroethane among food chain trophic

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

levels. Additional information on bioconcentration and biomagnification would be useful in determining
whether food chain bioaccumulation is an important source of human exposure.

Exposure Levels in Environmental Media. Reliable monitoring data for the levels of
1,1-dichloroethane in contaminated media at hazardous waste sites are needed so that the information
obtained on levels of 1,1-dichloroethane in the environment can be used in combination with the known
body burden of 1,1-dichloroethane to assess the potential risk of adverse health effects in populations
living in the vicinity of hazardous waste sites.

Limited information is available regarding ambient concentrations of 1,1-dichloroethane in soils. Based
on a median ambient air level reported in 1982, the average inhalation exposure to 1,1-dichloroethane for
an individual in the United States has been estimated to be 4 (ig/day. The information on foodstuffs is
limited to the detection of 1,1-dichloroethane in oysters (33 ppb wet weight). Additional site-specific
concentration data for ambient air, drinking water, soil, and biota would be helpful in estimating potential
exposure of the general population as well as populations in the vicinity of hazardous waste sites.

Exposure Levels in Humans. Although relatively recent estimates of the size of the population
occupationally exposed to 1,1-dichloroethane are available from NIOSH, monitoring data on workplace
exposures are generally limited, with a few observations about 1,1-dichloroethane included in detailed
studies of 1,2-dichloroethane. A study of the levels of 1,1-dichloroethane in the inhaled and exhaled air
and drinking water of college students in Texas and North Carolina found low levels (<0.49 ppb) of
1,1-dichloroethane in the personal air quality monitors of the Texas students, whose campus bounded a
petrochemical manufacturing area, but none in samples of their exhaled breath. Additional information
on the availability of biomarkers that could be used to indicate human exposure to 1,1-dichloroethane
would be helpful.

This information is necessary for assessing the need to conduct health studies on these populations.

Exposures of Children. A data need has been identified to conduct body burden studies of
1,1-dichloroethane in children. Measurements of 1,1-dichloroethane in blood samples for a population of
adults was conducted in 2003-2004 as part of the National Health and Nutrition Examination Survey
(CDC 2015). Most of the samples were below the detection limit of 0.01 ng/mL. Similar results among a
group of children would demonstrate that exposure to 1,1-dichloroethane is low for both children and
adults.

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

Child health data needs relating to susceptibility are discussed in Section 3.12.2, Identification of Data
Needs: Children's Susceptibility.

Exposure Registries. No exposure registries for 1,1-dichloroethane were located. This substance is
not currently one of the compounds for which a sub-registry has been established in the National
Exposure Registry. The substance will be considered in the future when chemical selection is made for
sub-registries to be established. The information that is amassed in the National Exposure Registry
facilitates the epidemiological research needed to assess adverse health outcomes that may be related to
exposure to this substance.

6.8.2 Ongoing Studies

No ongoing studies regarding sponsored by NIH or EPA were identified for 1,1-dichloroethane.

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1,1-DICHLOROETHANE

6. POTENTIAL FOR HUMAN EXPOSURE

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1,1-DICHLOROETHANE

7. ANALYTICAL METHODS

The purpose of this chapter is to describe the analytical methods that are available for detecting,
measuring, and/or monitoring 1,1-dichloroethane, its metabolites, and other biomarkers of exposure and
effect to 1,1-dichloroethane. The intent is not to provide an exhaustive list of analytical methods. Rather,
the intention is to identify well-established methods that are used as the standard methods of analysis.
Many of the analytical methods used for environmental samples are the methods approved by federal
agencies and organizations such as EPA and the National Institute for Occupational Safety and Health
(NIOSH). Other methods presented in this chapter are those that are approved by groups such as the
Association of Official Analytical Chemists (AOAC) and the American Public Health Association
(APHA). Additionally, analytical methods are included that modify previously used methods to obtain
lower detection limits and/or to improve accuracy and precision.

The analytical methods used to quantify 1,1-dichloroethane in biological and environmental samples are
summarized below. Table 7-1 lists the applicable analytical methods used for determining 1,1-dichloro-
ethane in biological fluids and tissues, and Table 7-2 lists the methods used for determining 1,1-dichloro-
ethane in environmental samples.

7.1 BIOLOGICAL MATERIALS

The determination of trace levels of 1,1-dichloroethane in biological tissues and fluids has been restricted
to gas chromatography (GC) equipped with mass spectrometry (MS) or flame ionization detection (FID).

Work conducted by Cramer and co-workers (1988) showed that 1,1-dichloroethane can be detected at
nanogram per liter (ppt) levels in whole human blood using a dynamic headspace analyzer and GC/MS
technique. A disadvantage of the GC/MS technique is that only limited mass scanning can be employed
to obtain better sensitivity of target VOCs at ppt levels. This is because of the inherent differences in
sensitivity between the full-scan MS and the limited mass scanning MS techniques (Cramer et al. 1988).

Uehori et al. (1987) developed a retention index in GC to screen and quantify VOCs in blood. A dynamic
headspace analyzer and GC/FID with retention indices were employed for the detection of 1,1-dichloro-
ethane at nanogram levels. Uehori et al. (1987) noted that this method is simple and reliable, and requires
little or no sample preparation.

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1,1-DICHLOROETHANE 94

7. ANALYTICAL METHODS

Table 7-1. Analytical Methods for Determining 1,1-Dichloroethane in Biological

Materials

Analytical

Sample

Percent

Sample matrix

Preparation method

method

detection limit

recovery

Reference

Blood

Vaporize blood sample in a

GC/FID

ng range

No data

Uehori et al.

headspace vial and inject into

1987

GC column

Whole blood

Purge-and-trap on Tenax

GC/MS

100 ng/L

76-110

Cramer et

adsorbent

al. 1988

Blood and urine

Heat biological sample;

GC/MS

No data

Barkley et

purge-and-trap volatile

al. 1980

compounds on Tenax GC

adsorbent

Whole blood

Collect by venipuncture, store

GC/MS

0.013 ppb

102-118

Ashley et al.

cold; inject sample into purge-

1992

and-trap apparatus

Breath

Collect human breath sample

GC/MS

Not detected

No data

Barkley et

by means of a spirometer and

al. 1980

analyze

Breath

Collect human breath sample

GC/MS

Not reported

No data

Raymer et

by means of a spirometer and

al. 1990

analyze

FID = flame ionization detector; GC = gas chromatography; MS = mass spectrometry

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1,1-DICHLOROETHANE

7. ANALYTICAL METHODS

Table 7-2. Analytical Methods for Determining 1,1-Dichloroethane in

Environmental Samples

Sample
matrix

Preparation method

Analytical Sample Percent

method detection limit recovery Reference

Groundwater,
aqueous
sludges,
caustic
liquors, soils,
sediments
Groundwater,
surface water,
waste water

Groundwater

Purge-and-trap (EPA
method 624) or direct
injection (EPA Method
5030)

Purge-and-trap on
absorbent

GC/MS

GC with
HECD

GC/MS

4.7 |jg/L 59-155% EPA 1994a (Method

(groundwater; 8240B), 2015a

5 jjg/kg
(soil/sediment)

0.002 jjg/L 47-132 EPA 1994b (Method

8010B)

Lopez-Avila et al.
1987a

Groundwater Purge-and-trap on

absorbent
Groundwater Purge-and-trap on
and soil absorbent

Drinking water Heat water sample;

purge-and-trap volatile
compounds on Tenax
GC absorbent
Drinking water Pass sample through
XAD-2 macroreticular
resin and extract
continuously with ether

Drinking water Purge-and-trap water
sample

Drinking water Extract sample in

hexane and analyze
Drinking water Purge-and-trap on
Tenax absorbent
Drinking water Purge-and-trap water
sample

Drinking water Purge-and-trap water
sample

Water (river; Inject 1 ml_ into flow
sea) injection analysis

system

Wastewater Collect water sample
through a permeation
cell membrane and
direct into GC

0.0001- <±5

0.02 jjg/sample relative
standard
deviation

GC/FID-FID No data No data Driscoll et al. 1987

GC/EICD-FID Water=0.1- 83-102 Lopez-Avila 1987b
0.9 jjg/L;
soil=1 —5 |jg/L

GC/MS Not detected No data Barkley et al. 1980

GC/MS

<1 |jg/L

No data Suffet et al. 1986

GC/MS 0.2 jjg/L

GC-EICD <1 jjg/L
GC-EICD-FID <1 jjg/L
GC/EICD 80 jjg/L

No data

>75

GC/EICD-FID 0.1-0.5 jjg/L No data
MIMS/ITD 0.2 ppb No data

Otson and Chan
1987

Otson and Chan

Otson and Williams

1982

Comba and Kaiser

1983

Kingsley et al. 1983

Bauer and Solyom
1994

GC/FID |jg/L (ppb) <6 relative Blanchard and
range standard Hardy 1986

deviation

-------
1,1-DICHLOROETHANE

7. ANALYTICAL METHODS

Table 7-2. Analytical Methods for Determining 1,1-Dichloroethane in

Environmental Samples

Sample
matrix

Preparation method

Analytical Sample Percent

method detection limit recovery Reference

Wastewater Collect sample through GC/FID
a permeation cell
membrane; adsorb onto
charcoal; extract with
carbon disulfide
Waste water Purge-and-trap (EPA GC/MS
(municipal method 601) with direct
and industrial aqueous injection; the
discharges) trap is backflushed and
heated to desorb
compounds onto column

Waste water Purge-and-trap (EPA GC/MS
(municipal method 624); the trap is
and industrial backflushed and heated
discharges) to desorb compounds
onto column

Waste water Purge-and-trap with GC/MS
isotopic dilution (EPA
method 1624); stable
isotopes are added; the
trap is backflushed and
heated to desorb
compounds onto column

Purge-and-trap on GC/MS
adsorbent

Purge and trap water GC/AED
sample

Purge-and-trap on GC/ECD
charcoal absorbent;
extract with carbon
disulfide

Collect air sample on GC/MS
Tenax adsorbent;
vaporize thermally and
analyze

Collect air particulates GC/MS
on a glass fiber filter and
Tenax GC adsorbent;
extract with MeOH
pentane

Air (ambient) Adsorb air sample onto GC/FID
charcoal tube; extract
with carbon disulfide

Waste water
and sludge
Drinking,
ground, and
surface water
Air (ambient)

Air (ambient)

74- No data Blanchard and

16,800 jjg/L Hardy 1985

0.07 |jg/L 47-132 EPA 2001 a

4.7 (j/L

10 |jg/L

No data

0.001 ppm
range

23 |jg/m3

59-155 EPA 1999, 2015a

Labeled EPA 2001b

compound

recovery:

23-191

No data Giabbaie et al. 1983

0.17 |jg/L No data Silgoner et al. 1997

No data

Bruner et al. 1978

No data Pellizari 1982

Not detected No data Barkley et al. 1980

ppm range No data NIOSH 2003

(method 1003)

-------
1,1-DICHLOROETHANE

7. ANALYTICAL METHODS

Table 7-2. Analytical Methods for Determining 1,1-Dichloroethane in

Environmental Samples

Sample

Analytical

Sample

Percent

matrix

Preparation method

method

detection limit recovery

Reference

Air (space

Dehydrohalogenate air

GC/MS

0.5-4.0 ppm

No data

Spain et al. 1985

cabin)

sample with lithium

hydroxide and analyze

Air (high

Collect vapor sample in

Portable

25 ppm

0.998

Barsky et al. 1985

humidity

a Tedlargas bag

organic vapor

correlation

atmosphere)

analyzer with

coefficient

PID

Air

Air collected in cooled

GC/IMS

No data

Simpson et al. 1996

trap; heated upon

injection

Air (ambient)

Collection on

Capillary

0.71 ppbv

Oliver et al. 1996

multiadsorbent traps;

GC/MS

automated

preconcentration

Air

Sample collected on

GC/PID/EICD

0.1 ppb

Maeda et al. 1998

Tenax GC/carboxene

1000 trap, separated by

capillary column

Various food

Food containing >70%

GC/ECD-

ng/g range

-70

Daft 1988

(e.g., dairy

fat: dissolve sample in

EICD

products,

isooctane and shake;

meat,

cleanup on florisil

vegetables,

column

and soda)

Various food

Cold liquid (4 °C) and

SD/PT/GC

0.003 |jg/kg

95.2

Page and Lacroix

(e.g., fruit

aqueous flour-based

1995

juices, soda,

samples injected;

coffees,

plunge sampling tube or

cream, peanut

needle into dry/viscous

butter, and

foods for injection;

butter)

steam distillation; purge

and trap

Compound

Prepare dilute solution

GC/PID

20 pg

No data

Jerpe and Davis

formulation

of sample in MeOH;

1987

introduce into

headspace trap

Fish tissue

Add water to fish

GC/MS

0.01 |jg/g

Easley et al. 1981

sample; homogenize

and extract

ultrasonically; purge-

and-trap on adsorbent

Fish tissue

Freeze fish sample;

GC/MS

No data

Hiatt 1983

homogenize in liquid

equipped with

nitrogen; distill in

fused-silica

vacuum

capillary

column

-------
1,1-DICHLOROETHANE

7. ANALYTICAL METHODS

Table 7-2. Analytical Methods for Determining 1,1-Dichloroethane in

Environmental Samples

Sample
matrix

Preparation method

Analytical Sample Percent
method detection limit recovery

Reference

Fish tissue Warm sample; purge- GC/FID
and-trap volatiles on
activated carbon
adsorbent; extract with
carbon disulfide
Fish tissue Edible tissue and liver GC/EICD
homogenized in blender;
organic-free water and
standard added; vial
sealed and placed in
ultrasonic bath; purge
and trap

Whole fish Freeze fish sample and GC/MS

homogenize; add MeOH equipped with
and extract fused-silica

ultrasonically; purge- capillary
and-trap on adsorbent column
Fish and Add water containing GC/MS
sediment acrolein and acrylonitrile
to sample; freeze
sample; extract in
vacuum

No data

-32

Reinert et al. 1983

5 pg/g

115±25

Roose and
Brinkman 1998

7.5x10"4 |jg/g 6.2 relative Dreisch and
standard Munson 1983
deviation

0.025 |jg/g Sediment Hiatt 1981
matrix 101;
fish matrix
90

AED = atomic emission detection; ECD = electron captive detector; EICD = electrolytic conductivity detector;
FID = flame ionization detector; GC = gas chromatography; HECD = Hall electrolytic conductivity detector; IMS = ion
mobility spectrometry; ITD = ion trap detector; MIMS = membrane introduction mass spectrometry; MS = mass
spectrometry; PID = photoionization detector; PT = purge-and-trap; SD = steam distillation

-------
1,1-DICHLOROETHANE

7. ANALYTICAL METHODS

Gas purging-and-trapping on a Tenax GC adsorbent and GC/MS technique has been employed by
Barkley et al. (1980) and Ashley et al. (1992) for the determination of trace levels of volatile halogenated
compounds (including 1,1-dichloroethane) in water, human blood, and urine.

7.2 ENVIRONMENTAL SAMPLES

A GC equipped with an appropriate detector is the most frequently used analytical technique for
determining the concentrations of 1,1-dichloroethane in air, water, soil, fish, dairy products, and various
foods. Volatile organic compounds in environmental samples may exist as complex mixtures or at very
low concentrations (ppt to ppb range). Subsequently, the GC technique must be supplemented by some
method of sample preconcentration. The EPA updated Method 624 with revised quality control
frequencies and improved internal standards and surrogates (EPA 2015a). GC columns were changed
from packed columns to open tubular capillary columns in order to increase resolution and decrease
losses due to adsorption.

Gas purging-and-trapping is the generally accepted method for the isolation, concentration, and
determination of VOCs in water and various environmental samples (Bellar et al. 1979; EPA 1994a,
1994b, 1996b, 1999, 2001a, 2001b; Lopez-Avila et al. 1987a, 1987b; Page and Lacroix 1995; Reding
1987; Wylie 1988). This method appears to be most adaptable for use with almost any GC detector—
MS, FID, electron capture detector (ECD), and electrolytic conductivity detector (EICD). In addition, the
method offers an important preliminary separation of highly volatile compounds from often highly
complex samples prior to GC analysis. Detection limits at <1 |ig 1,1-dichloroethane/L of sample have
been achieved by this method (Dreisch and Munson 1983; Kingsley et al. 1983; Lopez-Avila et al. 1987a,
1987b; Otson and Williams 1982). Page and Lacroix (1995) successfully coupled purge-and-trap
procedures with steam distillation collection methods to yield an analytical method, for various foods,
with a detection limit of 0.003 j^ig/kg for 1,1-dichloroethane. Bruner et al. (1978) employed purge-and-
trap technique on charcoal adsorbent and GC/ECD for determination at ppt levels of volatile halo organic
compounds in air. A major problem is that some of the halocarbons in the atmosphere are present as
ultra-trace impurities in highly pure commercial inert gases. Subsequently, these impurities may interfere
with the quantitative and qualitative analysis of 1,1-dichloroethane in environmental samples.

A purge-and-trap method with cryogenic trapping (cryofocusing) for concentrating VOCs from water
samples into the headspace, for analysis by capillary GC, was described by Pankow and Rosen (1988).
The purge-and-trap technique offers advantages over other techniques in that it allows easy isolation and

-------
1,1-DICHLOROETHANE

7. ANALYTICAL METHODS

100

concentration of target compounds, which reduces interference, thereby improving overall limits of
detection and recovery of sample (Otson and Chan 1987). Among the other advantages of the purge-and-
trap technique with cryofocusing are its simplicity and therefore its reliability; the low background
contamination since no sorbent traps are needed; and the relatively short time of sample analysis (Pankow
and Rosen 1988). Roose and Brinkman (1998) capitalized on these techniques to analyze fish samples in
a rapid, selective, and sensitive manner. An automated GC system with dual multi-adsorbent traps was
successfully operated in a mobile laboratory to collect and analyze ambient air samples. The system
continuously collects air samples, uses a pre-concentration approach (cryofocusing), and recovers
analytes using thermal desorption. The detection limit for 1,1-dichloroethane was reported as 0.71 ppbv
(Oliver etal. 1996).

Purge-and-trap techniques have been successfully coupled with atomic emission detection (AED) for the
analysis of water (Silgoner et al. 1997). Solutes eluting from the GC are atomized in a microwave-
induced plasma, and individual wavelengths are measured using a photodiode array. The detection limit
of this method for 1,1-dichloroethane is 0.17 (ig/L. While some improvement is still needed, the purge-
and-trap technique coupled with AED offers some advantages over other methods. Dynamic headspace
analyzer GC has been used for the analysis and identification of 1,1-dichloroethane in water and fish
tissue (Comba and Kaiser 1983; Mehran et al. 1986; Otson and Williams 1982; Reinert et al. 1983;). The
analytic sample is placed in a sealed flask connected to the headspace analyzer, which is directly
interfaced with the injection port of the GC system. This arrangement allows for a greater proportion of
compound contained in a sample to be analyzed. Detection limits of <1 |ig 1,1-dichloroethane/L water
and <1 |ig 1,1-dichloroethane/g fish tissue were achieved (Mehran et al. 1986; Otson and Williams 1982;
Reinert et al. 1983; Trussel et al. 1983). A disadvantage of this technique is that the inherent volatility of
the halo organic compounds gives rise to an excessive foaming in the headspace system, thereby forming
low yields and causing interference with the GC quantification. The typical yield of 1,1-dichloroethane
was approximately 32% (Reinart et al. 1983). The authors indicated that use of an antifoaming agent
such as silicone surfaces greatly reduced the foam, but extraneous chromatographic components and peak
masking problems were encountered.

Bauer and Solyom (1994) and Wong et al. (1995) reported that membrane introduction mass spectrometry
(MIMS) offers measurements of trace-level organics in environmental media, including polluted
seawater, without sample preparation, using a non-porous silicon membrane. A detection limit of 0.2 ppb
was reported for 1,1-dichloroethane (Bauer and Solyom 1994).

-------
1,1-DICHLOROETHANE

7. ANALYTICAL METHODS

101

Pellizzari (1982) initiated the development and evaluation of trace levels of VOCs in industrial and
chemical waste disposal sites. Ambient air samples were collected by a sampler equipped with Tenax GC
adsorbent cartridges. Compounds were thermally removed from the adsorbent and analyzed by capillary
GC/MS. The detection limit was at the (.ig/nr1 level (Pellizzari 1982).

Simpson et al. (1996) developed a method that has potential for on-site monitoring of vapor-phase
organics in air. GC is coupled with ion mobility spectrometry to offer high sensitivity and the ability to
operate at ambient pressure. While a detection limit for 1,1-dichloroethane was not reported, detection
limits for several other EPA priority pollutants ranged from 0.05 to 140 pg/second. Maeda et al. (1998)
also investigated analytical methods that may be applied to on-site monitoring techniques of HAPs. The
analytical methods that they employed included a Tenax GC and Carboxene 1000 trap, followed by
capillary separation and either photo ionization detector (PID) or EICD detection methods. The detection
limit of the system was reported as 0.1 ppb. Another method for sampling and analyzing VOCs in air is
proposed to have some advantages for use in field situations and may provide satisfactory results. The
method uses teraglyme as a sample enrichment tool and employs purge-and-trap methods along with
GC/MS (Huybrechts et al. 2001).

Blanchard and Hardy (1985, 1986) developed a method that allows for continuous monitoring or
intermittent analysis of volatile organic priority pollutants in environmental media. The method is based
on permeation of VOCs through a silicone polycarbonate membrane from wastewater sample matrix, into
an inert gas stream and directed into a capillary GC/FID via a sampling loop (Blanchard and Hardy 1986).
Advantages of this procedure are that it is simple, it does not require time-consuming preconcentration
steps, and it can be used either in the field or in the laboratory.

The liquid-liquid extraction procedure provides a simple, rapid, screening method for semiquantitative
determination of 1,1-dichloroethane in aqueous samples containing limited number of VOCs. It is less
effective for aqueous samples containing large numbers of VOCs. Furthermore, interference from the
organic (hexane) extraction solvent makes it more difficult to identify completely all compounds (Otson
and Williams 1981). GC/EICD was employed by Otson and Williams (1981) for the detection of trace
amounts (<1 |ig/L of sample) of 1,1-dichloroethane in drinking water.

Daft (1988) employed a photoionization detector and an electrolytic conductivity detector connected in
series to a capillary GC to detect 1,1-dichloroethane at ng/g levels in fumigants and industrial chemical
residues of various foods (e.g., dairy products, meat, vegetables, and soda). Typically, foods were

-------
1,1-DICHLOROETHANE

7. ANALYTICAL METHODS

102

extracted with isooctane and injected in GC column for analysis. However, foods containing lipid and fat
were subjected to further clean-up on micro-florisil column prior to GC analysis.

A procedure was developed by Hiatt (1983) and Dreisch and Munson (1983) to identify and quantify
1,1-dichloroethane in fish tissue samples by GC/MS, employing a fiised-silica capillary column (FSCC)
and vacuum distillation (extraction). An advantage of the vacuum extraction is that the system does not
require elevated temperatures or the addition of reagents, which could produce unwanted degradation
products (Hiatt 1981). The FSCC provides a more attractive approach than packed column for
chromatographic analysis of VOCs, because FSCC can be heated to a higher-temperature (350 °C) than
that recommended for packed column thereby improving the resolution (at the ng/g level) of compounds
at a lesser retention time. A physical limitation for compounds that can be detected, however, is that the
vapor pressure of the compounds must be >0.78 torr (approximately 50 °C) in the sample chamber (Hiatt
1983).

7.3 ADEQUACY OF THE DATABASE

7.3.1 Identification of Data Needs

Methods for Determining Biomarkers of Exposure and Effect. Reliable methods are available
for detecting and quantifying 1,1-dichloroethane in the tissues and body fluids of humans. GC/MS or
GC/FID has been employed to detect 1,1-dichloroethane at nanogram to picogram levels in blood and
tissue samples of humans. No additional analytical methods for determining trace levels of 1,1-dichloro-

-------
1,1-DICHLOROETHANE

7. ANALYTICAL METHODS

103

ethane in the blood of humans are needed. Also, no detection limits for detecting 1,1-dichloroethane in
urine samples by GC/MS were indicated by Barkley et al. (1980). Therefore, additional research and
development of sensitive and selective methods for detecting and quantifying the levels of
1,1-dichloroethane and its metabolites in the tissues and urine of humans would be useful. If methods
were available, it would assist investigators in determining whether specific levels of 1,1-dichloroethane
found in the tissues/fluids of exposed persons correlate with any adverse health effects.

Methods for Determining Parent Compounds and Degradation Products in Environmental
Media. Analytical methods are available to detect 1,1-dichloroethane in environmental samples.
Purge-and-trap or direct injection followed by analysis with GC/ECD and GC/MS have been used to
detect and quantify 1,1-dichloroethane in water samples at ppt and ppb levels (methods 5030, 8240,
8010B [EPA 1994a, 1994b, 1996b]; method 601, 624, 1624 [EPA 1999, 2001a, 2001b]). GC equipped
with FID, PID, or EICD has also been used to detect and quantify 1,1-dichloroethane in air, water, milk,
vegetables, and fish at ppb levels NIOSH (method 1003 [NIOSH 2003]). No additional analytical
methods for determining trace levels of 1,1-dichloroethane in environmental media are needed.

7.3.2 Ongoing Studies

No ongoing studies regarding sponsored by NIH or EPA were identified for 1,1-dichloroethane.

-------
1,1-DICHLOROETHANE 104

7. ANALYTICAL METHODS

This page is intentionally blank.

-------
1,1-DICHLOROETHANE

105

8. REGULATIONS, ADVISORIES, AND GUIDELINES

MRLs are substance specific estimates, which are intended to serve as screening levels, are used by
ATSDR health assessors and other responders to identify contaminants and potential health effects that
may be of concern at hazardous waste sites.

No inhalation or oral MRLs were derived for 1,1-dichloroethane.

The EPA (IRIS 2002) has not derived an oral reference dose (RfD) or an inhalation reference
concentration (RfC) for 1,1-dichloroethane.

1,1-Dichloroethane appears on the list of chemicals in "The Emergency Planning and Community Right-
to-Know Act of 1986" and has been assigned a reportable quantity (RQ) limit of 1,000 pounds (EPA
2014e). The RQ represents the amount of a designated hazardous substance which, when released to any
environmental media, must be reported to the appropriate authority.

The international and national regulations, advisories, and guidelines regarding 1,1-dichloroethane in air,
water, and other media are summarized in Table 8-1.

-------
1,1-DICHLOROETHANE

106

8. REGULATIONS, ADVISORIES, AND GUIDELINES

Table 8-1. Regulations, Advisories, and Guidelines Applicable to

1,1-Dichloroethane

Agency

Description

Information

Reference

INTERNATIONAL
Guidelines:

IARC
WHO

NATIONAL
Regulations and
Guidelines:
a. Air
ACGIH
AIHA
DOE

EPA

NIOSH

OSHA

b. Water
EPA

Carcinogenicity classification
Air quality guidelines
Drinking water quality guidelines

No data
No data
No data3

TLV (8-hour TWA)

ERPGs

PAC-1 and PAC-2b
PAC-3b
AEGLs
NAAQS

REL (10-hour TWA)

IDLH

PEL (8-hour TWA) for general industry
PEL (8-hour TWA) for construction
PEL (8-hour TWA) for shipyards

Designated as hazardous substances in No data
accordance with Section 311(b)(2)(A) of
the Clean Water Act

Drinking water standards and health No data
advisories

Master Testing List Yesd

National primary drinking water No data

standards

National recommended water quality No data
criteria: human health for the
consumption of

Reportable quantities of hazardous No data
substances designated pursuant to
Section 311 of the Clean Water Act

IARC 2015
WHO 2010
WHO 2011

100 ppm
No data
160 ppm
4,000 ppm
No data
No data

100 ppm (400 mg/m3)c
3,000 ppm

100 ppm (400 mg/m3)
100 ppm (400 mg/m3)
100 ppm (400 mg/m3)

ACGIH 2014
AIHA 2014
DOE 2012a

EPA 2014b
EPA 2012b
NIOSH 2015

OSHA 2013
29 CFR 1910.1000,
Table Z-1
OSHA 2014a
29 CFR 1926.55,
Appendix A
OSHA 2014b
29 CFR 1915.1000

EPA 2013a
40 CFR 116.4

EPA 2012a

EPA 2014c
EPA 2009

EPA 2013b

EPA 2013c
40 CFR 117.3

-------
1,1-DICHLOROETHANE

107

8. REGULATIONS, ADVISORIES, AND GUIDELINES

Table 8-1. Regulations, Advisories, and Guidelines Applicable to

1,1-Dichloroethane

Agency

Description

Information

Reference

NATIONAL (cont.)

c. Food
FDA

d. Other
ACGIH
EPA

NTP

EAFUSe

Carcinogenicity classification
Carcinogenicity classification
RfC
RfD

Identification and listing of hazardous
waster

Inert pesticide ingredients in pesticide
products

Superfund, emergency planning, and
community right-to-know

Designated CERCLA hazardous
substance and reportable quantity

Effective date of toxic chemical
release reporting
Extremely hazardous substances
and its threshold planning quantity

TSCA chemical lists and reporting
periods

Effective date
Reporting date
TSCA health and safety data reporting
Effective date
Reporting date
Carcinogenicity classification

No data

A4f
C9

No data
No data
U076

No data

1,000 poundsh

01/01/1994

No data

03/11/1994
05/10/1994

06/01/1987
06/01/1997
No data

FDA 2013

ACGIH 2014
IRIS 2002

EPA 2013e
40 CFR 261,
Appendix VIII
EPA 2014d

EPA 2014e
40 CFR 302.4

EPA 2014f
40 CFR 372.65
EPA 2013d
40 CFR 355,
Appendix A
EPA 2014g
40 CFR 712.30

EPA 2014h
40 CFR 716.120

NTP 2014

aln view of the very limited database on toxicity and carcinogenicity, the Guidelines concluded that no guideline value
for 1,1-dichloroethane should be proposed.

bDefinitions of PAC terminology are available from U.S. Department of Energy (DOE 2012b).
cNIOSH recommends that 1,1-dichloroethane be treated in the workplace with caution because of its structural
similarity to the four chloroethanes (ethylene dichloride, hexachloroethane, 1,1,2,2-tetrachloroethane, and
1,1,2-trichloroethane) shown to be carcinogenic in animals.

d1,-Dichloroethane was recommended to the MTL by the EPA's Office of Water and Office of Drinking Water in 1990
and was later removed in 1995. The initial chemical testing program was for prechronic toxicity (14-28 day) and
subchronic toxicity (90 day) health effects.

eThe EAFUS list of substances contains ingredients added directly to food that FDA has either approved as food
additives or listed or affirmed as GRAS.
fA4: not classifiable as a human carcinogen
gC: possible human carcinogen

designated CERCLA hazardous substance pursuant to Section 307(a)of the Clean Water Act, Section 112 of the
Clean Air Act, and Section 3001 of RCRA.

-------
1,1-DICHLOROETHANE 108

8. REGULATIONS, ADVISORIES, AND GUIDELINES

Table 8-1. Regulations, Advisories, and Guidelines Applicable to

1,1-Dichloroethane

Agency Description Information Reference

ACGIH = American Conference of Governmental Industrial Hygienists; AEGL = acute exposure guideline levels;

AIHA = American Industrial Hygiene Association; CERCLA = Comprehensive Environmental Response,
Compensation, and Liability Act; CFR = Code of Federal Regulations; DOE = Department of Energy;

EAFUS = Everything Added to Food in the United States; EPA = Environmental Protection Agency;

ERPG = emergency response planning guidelines; FDA = Food and Drug Administration; GRAS = Generally
Recognized As Safe; IARC = International Agency for Research on Cancer; IDLH = immediately dangerous to life or
health; IRIS = Integrated Risk Information System; MTL = Master Testing List; NAAQS = National Ambient Air Quality
Standards; NIOSH = National Institute for Occupational Safety and Health; NTP = National Toxicology Program;
OSHA = Occupational Safety and Health Administration; PAC = Protective Action Criteria; PEL = permissible
exposure limit; RCRA = Resource Conservation and Recovery Act; REL = recommended exposure limit;
RfC = inhalation reference concentration; RfD = oral reference dose; TLV = threshold limit values; TSCA = Toxic
Substances Control Act; TSD = treatment, storage, and disposal; TWA = time-weighted average; WHO = World
Health Organization

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1,1-DICHLOROETHANE

109

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10. GLOSSARY

Absorption—The taking up of liquids by solids, or of gases by solids or liquids.

Acute Exposure—Exposure to a chemical for a duration of 14 days or less, as specified in the
Toxicological Profiles.

Adsorption—The adhesion in an extremely thin layer of molecules (as of gases, solutes, or liquids) to the
surfaces of solid bodies or liquids with which they are in contact.

Adsorption Coefficient (Koc)—The ratio of the amount of a chemical adsorbed per unit weight of
organic carbon in the soil or sediment to the concentration of the chemical in solution at equilibrium.

Adsorption Ratio (Kd)—The amount of a chemical adsorbed by sediment or soil (i.e., the solid phase)
divided by the amount of chemical in the solution phase, which is in equilibrium with the solid phase, at a
fixed solid/solution ratio. It is generally expressed in micrograms of chemical sorbed per gram of soil or
sediment.

Benchmark Dose (BMD)—Usually defined as the lower confidence limit on the dose that produces a
specified magnitude of changes in a specified adverse response. For example, a BMDio would be the
dose at the 95% lower confidence limit on a 10% response, and the benchmark response (BMR) would be
10%. The BMD is determined by modeling the dose response curve in the region of the dose response
relationship where biologically observable data are feasible.

Benchmark Dose Model—A statistical dose-response model applied to either experimental toxicological
or epidemiological data to calculate a BMD.

Bioconcentration F actor (BCF)—The quotient of the concentration of a chemical in aquatic organisms
at a specific time or during a discrete time period of exposure divided by the concentration in the
surrounding water at the same time or during the same period.

Biomarkers—Broadly defined as indicators signaling events in biologic systems or samples. They have
been classified as markers of exposure, markers of effect, and markers of susceptibility.

Cancer Effect Level (CEL)—The lowest dose of chemical in a study, or group of studies, that produces
significant increases in the incidence of cancer (or tumors) between the exposed population and its
appropriate control.

Carcinogen—A chemical capable of inducing cancer.

Case-Control Study—A type of epidemiological study that examines the relationship between a
particular outcome (disease or condition) and a variety of potential causative agents (such as toxic
chemicals). In a case-controlled study, a group of people with a specified and well-defined outcome is
identified and compared to a similar group of people without outcome.

Case Report—Describes a single individual with a particular disease or exposure. These may suggest
some potential topics for scientific research, but are not actual research studies.

Case Series—Describes the experience of a small number of individuals with the same disease or
exposure. These may suggest potential topics for scientific research, but are not actual research studies.

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Ceiling Value—A concentration of a substance that should not be exceeded, even instantaneously.

Chronic Exposure—Exposure to a chemical for 365 days or more, as specified in the Toxicological
Profiles.

Cohort Study—A type of epidemiological study of a specific group or groups of people who have had a
common insult (e.g., exposure to an agent suspected of causing disease or a common disease) and are
followed forward from exposure to outcome. At least one exposed group is compared to one unexposed
group.

Cross-sectional Study—A type of epidemiological study of a group or groups of people that examines
the relationship between exposure and outcome to a chemical or to chemicals at one point in time.

Data Needs—Substance-specific informational needs that if met would reduce the uncertainties of human
health assessment.

Developmental Toxicity—The occurrence of adverse effects on the developing organism that may result
from exposure to a chemical prior to conception (either parent), during prenatal development, or
postnatally to the time of sexual maturation. Adverse developmental effects may be detected at any point
in the life span of the organism.

Dose-Response Relationship—The quantitative relationship between the amount of exposure to a
toxicant and the incidence of the adverse effects.

Embryotoxicity and Fetotoxicity—Any toxic effect on the conceptus as a result of prenatal exposure to
a chemical; the distinguishing feature between the two terms is the stage of development during which the
insult occurs. The terms, as used here, include malformations and variations, altered growth, and in utero
death.

Environmental Protection Agency (EPA) Health Advisory—An estimate of acceptable drinking water
levels for a chemical substance based on health effects information. A health advisory is not a legally
enforceable federal standard, but serves as technical guidance to assist federal, state, and local officials.

Epidemiology—Refers to the investigation of factors that determine the frequency and distribution of
disease or other health-related conditions within a defined human population during a specified period.

Genotoxicity—A specific adverse effect on the genome of living cells that, upon the duplication of
affected cells, can be expressed as a mutagenic, clastogenic, or carcinogenic event because of specific
alteration of the molecular structure of the genome.

Half-life—A measure of rate for the time required to eliminate one half of a quantity of a chemical from
the body or environmental media.

Immediately Dangerous to Life or Health (IDLH)—The maximum environmental concentration of a
contaminant from which one could escape within 30 minutes without any escape-impairing symptoms or
irreversible health effects.

Immunologic Toxicity—The occurrence of adverse effects on the immune system that may result from
exposure to environmental agents such as chemicals.

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Immunological Effects—Functional changes in the immune response.

Incidence—The ratio of individuals in a population who develop a specified condition to the total
number of individuals in that population who could have developed that condition in a specified time
period.

Intermediate Exposure—Exposure to a chemical for a duration of 15-364 days, as specified in the
Toxicological Profiles.

In Vitro—Isolated from the living organism and artificially maintained, as in a test tube.
In Vivo—Occurring within the living organism.

Lethal Concentration(LO) (LClo)—The lowest concentration of a chemical in air that has been reported
to have caused death in humans or animals.

Lethal Concentration^*)) (LCso)—A calculated concentration of a chemical in air to which exposure for
a specific length of time is expected to cause death in 50% of a defined experimental animal population.

Lethal Dose(LO) (LDl0)—The lowest dose of a chemical introduced by a route other than inhalation that
has been reported to have caused death in humans or animals.

Lethal Dose(so) (LD50)—The dose of a chemical that has been calculated to cause death in 50% of a
defined experimental animal population.

Lethal Time(so) (LT50)—A calculated period of time within which a specific concentration of a chemical
is expected to cause death in 50% of a defined experimental animal population.

Lowest-Observed-Adverse-Effect Level (LOAEL)—The lowest exposure level of chemical in a study,
or group of studies, that produces statistically or biologically significant increases in frequency or severity
of adverse effects between the exposed population and its appropriate control.

Lymphoreticular Effects—Represent morphological effects involving lymphatic tissues such as the
lymph nodes, spleen, and thymus.

Malformations—Permanent structural changes that may adversely affect survival, development, or
function.

Minimal Risk Level (MRL)—An estimate of daily human exposure to a hazardous substance that is
likely to be without an appreciable risk of adverse noncancer health effects over a specified route and
duration of exposure.

Modifying Factor (MF)—A value (greater than zero) that is applied to the derivation of a Minimal Risk
Level (MRL) to reflect additional concerns about the database that are not covered by the uncertainty
factors. The default value for a MF is 1.

Morbidity—State of being diseased; morbidity rate is the incidence or prevalence of disease in a specific
population.

Mortality—Death; mortality rate is a measure of the number of deaths in a population during a specified
interval of time.

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Mutagen—A substance that causes mutations. A mutation is a change in the DNA sequence of a cell's
DNA. Mutations can lead to birth defects, miscarriages, or cancer.

Necropsy—The gross examination of the organs and tissues of a dead body to determine the cause of
death or pathological conditions.

Neurotoxicity—The occurrence of adverse effects on the nervous system following exposure to a
chemical.

No-Observed-Adverse-Effect Level (NOAEL)—The dose of a chemical at which there were no
statistically or biologically significant increases in frequency or severity of adverse effects seen between
the exposed population and its appropriate control. Effects may be produced at this dose, but they are not
considered to be adverse.

Octanol-Water Partition Coefficient (Kow)—The equilibrium ratio of the concentrations of a chemical
in /7-octanol and water, in dilute solution.

Odds Ratio (OR)—A means of measuring the association between an exposure (such as toxic substances
and a disease or condition) that represents the best estimate of relative risk (risk as a ratio of the incidence
among subjects exposed to a particular risk factor divided by the incidence among subjects who were not
exposed to the risk factor). An OR of greater than 1 is considered to indicate greater risk of disease in the
exposed group compared to the unexposed group.

Organophosphate or Organophosphorus Compound—A phosphorus-containing organic compound
and especially a pesticide that acts by inhibiting cholinesterase.

Permissible Exposure Limit (PEL)—An Occupational Safety and Health Administration (OSHA)
allowable exposure level in workplace air averaged over an 8-hour shift of a 40-hour workweek.

Pesticide—General classification of chemicals specifically developed and produced for use in the control
of agricultural and public health pests.

Pharmacokinetics—The dynamic behavior of a material in the body, used to predict the fate
(disposition) of an exogenous substance in an organism. Utilizing computational techniques, it provides
the means of studying the absorption, distribution, metabolism, and excretion of chemicals by the body.

Pharmacokinetic Model—A set of equations that can be used to describe the time course of a parent
chemical or metabolite in an animal system. There are two types of pharmacokinetic models: data-based
and physiologically-based. A data-based model divides the animal system into a series of compartments,
which, in general, do not represent real, identifiable anatomic regions of the body, whereas the
physiologically-based model compartments represent real anatomic regions of the body.

Physiologically Based Pharmacodynamic (PBPD) Model—A type of physiologically based dose-
response model that quantitatively describes the relationship between target tissue dose and toxic end
points. These models advance the importance of physiologically based models in that they clearly
describe the biological effect (response) produced by the system following exposure to an exogenous
substance.

Physiologically Based Pharmacokinetic (PBPK) Model—Comprised of a series of compartments
representing organs or tissue groups with realistic weights and blood flows. These models require a

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10. GLOSSARY

131

variety of physiological information: tissue volumes, blood flow rates to tissues, cardiac output, alveolar
ventilation rates, and possibly membrane permeabilities. The models also utilize biochemical
information, such as air/blood partition coefficients, and metabolic parameters. PBPK models are also
called biologically based tissue dosimetry models.

Prevalence—The number of cases of a disease or condition in a population at one point in time.

Prospective Study—A type of cohort study in which the pertinent observations are made on events
occurring after the start of the study. A group is followed over time.

qi*—The upper-bound estimate of the low-dose slope of the dose-response curve as determined by the
multistage procedure. The qi* can be used to calculate an estimate of carcinogenic potency, the
incremental excess cancer risk per unit of exposure (usually |ig/L for water, mg/kg/day for food, and
|ig/m3 for air).

Recommended Exposure Limit (REL)—A National Institute for Occupational Safety and Health
(NIOSH) time-weighted average (TWA) concentration for up to a 10-hour workday during a 40-hour
workweek.

Reference Concentration (RfC)—An estimate (with uncertainty spanning perhaps an order of
magnitude) of a continuous inhalation exposure to the human population (including sensitive subgroups)
that is likely to be without an appreciable risk of deleterious noncancer health effects during a lifetime.
The inhalation reference concentration is for continuous inhalation exposures and is appropriately
expressed in units of mg/m3 or ppm.

Reference Dose (RfD)—An estimate (with uncertainty spanning perhaps an order of magnitude) of the
daily exposure of the human population to a potential hazard that is likely to be without risk of deleterious
effects during a lifetime. The RfD is operationally derived from the no-observed-adverse-effect level
(NOAEL, from animal and human studies) by a consistent application of uncertainty factors that reflect
various types of data used to estimate RfDs and an additional modifying factor, which is based on a
professional judgment of the entire database on the chemical. The RfDs are not applicable to
nonthreshold effects such as cancer.

Reportable Quantity (RQ)—The quantity of a hazardous substance that is considered reportable under
the Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA). Reportable
quantities are (1) 1 pound or greater or (2) for selected substances, an amount established by regulation
either under CERCLA or under Section 311 of the Clean Water Act. Quantities are measured over a
24-hour period.

Reproductive Toxicity—The occurrence of adverse effects on the reproductive system that may result
from exposure to a chemical. The toxicity may be directed to the reproductive organs and/or the related
endocrine system. The manifestation of such toxicity may be noted as alterations in sexual behavior,
fertility, pregnancy outcomes, or modifications in other functions that are dependent on the integrity of
this system.

Retrospective Study—A type of cohort study based on a group of persons known to have been exposed
at some time in the past. Data are collected from routinely recorded events, up to the time the study is
undertaken. Retrospective studies are limited to causal factors that can be ascertained from existing
records and/or examining survivors of the cohort.

Risk—The possibility or chance that some adverse effect will result from a given exposure to a chemical.

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10. GLOSSARY

132

Risk Factor—An aspect of personal behavior or lifestyle, an environmental exposure, or an inborn or
inherited characteristic that is associated with an increased occurrence of disease or other health-related
event or condition.

Risk Ratio—The ratio of the risk among persons with specific risk factors compared to the risk among
persons without risk factors. A risk ratio greater than 1 indicates greater risk of disease in the exposed
group compared to the unexposed group.

Short-Term Exposure Limit (STEL)—The American Conference of Governmental Industrial
Hygienists (ACGIH) maximum concentration to which workers can be exposed for up to 15 minutes
continually. No more than four excursions are allowed per day, and there must be at least 60 minutes
between exposure periods. The daily Threshold Limit Value-Time Weighted Average (TLV-TWA) may
not be exceeded.

Standardized Mortality Ratio (SMR)—A ratio of the observed number of deaths and the expected
number of deaths in a specific standard population.

Target Organ Toxicity—This term covers a broad range of adverse effects on target organs or
physiological systems (e.g., renal, cardiovascular) extending from those arising through a single limited
exposure to those assumed over a lifetime of exposure to a chemical.

Teratogen—A chemical that causes structural defects that affect the development of an organism.

Threshold Limit Value (TLV)—An American Conference of Governmental Industrial Hygienists
(ACGIH) concentration of a substance to which most workers can be exposed without adverse effect.
The TLV may be expressed as a Time Weighted Average (TWA), as a Short-Term Exposure Limit
(STEL), or as a ceiling limit (CL).

Time-Weighted Average (TWA)—An allowable exposure concentration averaged over a normal 8-hour
workday or 40-hour workweek.

Toxic Dose(5o> (TD50)—A calculated dose of a chemical, introduced by a route other than inhalation,
which is expected to cause a specific toxic effect in 50% of a defined experimental animal population.

Toxicokinetic—The absorption, distribution, and elimination of toxic compounds in the living organism.

Uncertainty Factor (UF)—A factor used in operationally deriving the Minimal Risk Level (MRL) or
Reference Dose (RfD) or Reference Concentration (RfC) from experimental data. UFs are intended to
account for (1) the variation in sensitivity among the members of the human population, (2) the
uncertainty in extrapolating animal data to the case of human, (3) the uncertainty in extrapolating from
data obtained in a study that is of less than lifetime exposure, and (4) the uncertainty in using lowest-
observed-adverse-effect level (LOAEL) data rather than no-observed-adverse-effect level (NOAEL) data.
A default for each individual UF is 10; if complete certainty in data exists, a value of 1 can be used;
however, a reduced UF of 3 may be used on a case-by-case basis, 3 being the approximate logarithmic
average of 10 and 1.

Xenobiotic—Any chemical that is foreign to the biological system.

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A-1

APPENDIX A. ATSDR MINIMAL RISK LEVELS AND WORKSHEETS

The Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA) [42 U.S.C.
9601 et seq.], as amended by the Superfund Amendments and Reauthorization Act (SARA) [Pub. L. 99-
499], requires that the Agency for Toxic Substances and Disease Registry (ATSDR) develop jointly with
the U.S. Environmental Protection Agency (EPA), in order of priority, a list of hazardous substances most
commonly found at facilities on the CERCLA National Priorities List (NPL); prepare toxicological
profiles for each substance included on the priority list of hazardous substances; and assure the initiation
of a research program to fill identified data needs associated with the substances.

The toxicological profiles include an examination, summary, and interpretation of available toxicological
information and epidemiologic evaluations of a hazardous substance. During the development of
toxicological profiles, Minimal Risk Levels (MRLs) are derived when reliable and sufficient data exist to
identify the target organ(s) of effect or the most sensitive health effect(s) for a specific duration for a
given route of exposure. An MRL is an estimate of the daily human exposure to a hazardous substance
that is likely to be without appreciable risk of adverse noncancer health effects over a specified duration
of exposure. MRLs are based on noncancer health effects only and are not based on a consideration of
cancer effects. These substance-specific estimates, which are intended to serve as screening levels, are
used by ATSDR health assessors to identify contaminants and potential health effects that may be of
concern at hazardous waste sites. It is important to note that MRLs are not intended to define clean-up or
action levels.

MRLs are derived for hazardous substances using the no-observed-adverse-effect level/uncertainty factor
approach. They are below levels that might cause adverse health effects in the people most sensitive to
such chemical-induced effects. MRLs are derived for acute (1-14 days), intermediate (15-364 days), and
chronic (365 days and longer) durations and for the oral and inhalation routes of exposure. Currently,
MRLs for the dermal route of exposure are not derived because ATSDR has not yet identified a method
suitable for this route of exposure. MRLs are generally based on the most sensitive chemical-induced end
point considered to be of relevance to humans. Serious health effects (such as irreparable damage to the
liver or kidneys, or birth defects) are not used as a basis for establishing MRLs. Exposure to a level
above the MRL does not mean that adverse health effects will occur.

MRLs are intended only to serve as a screening tool to help public health professionals decide where to
look more closely. They may also be viewed as a mechanism to identify those hazardous waste sites that

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1,1-DICHLOROETHANE

APPENDIX A

A-2

are not expected to cause adverse health effects. Most MRLs contain a degree of uncertainty because of
the lack of precise toxicological information on the people who might be most sensitive (e.g., infants,
elderly, nutritionally or immunologically compromised) to the effects of hazardous substances. ATSDR
uses a conservative (i.e., protective) approach to address this uncertainty consistent with the public health
principle of prevention. Although human data are preferred, MRLs often must be based on animal studies
because relevant human studies are lacking. In the absence of evidence to the contrary, ATSDR assumes
that humans are more sensitive to the effects of hazardous substance than animals and that certain persons
may be particularly sensitive. Thus, the resulting MRL may be as much as 100-fold below levels that
have been shown to be nontoxic in laboratory animals.

Proposed MRLs undergo a rigorous review process: Health Effects/MRL Workgroup reviews within the
Division of Toxicology and Human Health Sciences, expert panel peer reviews, and agency-wide MRL
Workgroup reviews, with participation from other federal agencies and comments from the public. They
are subject to change as new information becomes available concomitant with updating the toxicological
profiles. Thus, MRLs in the most recent toxicological profiles supersede previously published levels.
For additional information regarding MRLs, please contact the Division of Toxicology and Human
Health Sciences, Agency for Toxic Substances and Disease Registry, 1600 Clifton Road NE, Mailstop
F-57, Atlanta, Georgia 30329-4027.

MRLs were not derived for 1,1-dichloroethane, as discussed in Section 2.3.

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1,1-DICHLOROETHANE

B-1

APPENDIX B. USER'S GUIDE

Chapter 1

Public Health Statement

This chapter of the profile is a health effects summary written in non-technical language. Its intended
audience is the general public, especially people living in the vicinity of a hazardous waste site or
chemical release. If the Public Health Statement were removed from the rest of the document, it would
still communicate to the lay public essential information about the chemical.

The major headings in the Public Health Statement are useful to find specific topics of concern. The
topics are written in a question and answer format. The answer to each question includes a sentence that
will direct the reader to chapters in the profile that will provide more information on the given topic.

Chapter 2

Relevance to Public Health

This chapter provides a health effects summary based on evaluations of existing toxicologic,
epidemiologic, and toxicokinetic information. This summary is designed to present interpretive, weight-
of-evidence discussions for human health end points by addressing the following questions:

1. What effects are known to occur in humans?

2. What effects observed in animals are likely to be of concern to humans?

3. What exposure conditions are likely to be of concern to humans, especially around hazardous
waste sites?

The chapter covers end points in the same order that they appear within the Discussion of Health Effects
by Route of Exposure section, by route (inhalation, oral, and dermal) and within route by effect. Human
data are presented first, then animal data. Both are organized by duration (acute, intermediate, chronic).
In vitro data and data from parenteral routes (intramuscular, intravenous, subcutaneous, etc.) are also
considered in this chapter.

The carcinogenic potential of the profiled substance is qualitatively evaluated, when appropriate, using
existing toxicokinetic, genotoxic, and carcinogenic data. ATSDR does not currently assess cancer
potency or perform cancer risk assessments. Minimal Risk Levels (MRLs) for noncancer end points (if
derived) and the end points from which they were derived are indicated and discussed.

Limitations to existing scientific literature that prevent a satisfactory evaluation of the relevance to public
health are identified in the Chapter 3 Data Needs section.

Interpretation of Minimal Risk Levels

Where sufficient toxicologic information is available, ATSDR has derived MRLs for inhalation and oral
routes of entry at each duration of exposure (acute, intermediate, and chronic). These MRLs are not
meant to support regulatory action, but to acquaint health professionals with exposure levels at which
adverse health effects are not expected to occur in humans.

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1,1-DICHLOROETHANE

APPENDIX B

B-2

MRLs should help physicians and public health officials determine the safety of a community living near
a chemical emission, given the concentration of a contaminant in air or the estimated daily dose in water.
MRLs are based largely on toxicological studies in animals and on reports of human occupational
exposure.

MRL users should be familiar with the toxicologic information on which the number is based. Chapter 2,
"Relevance to Public Health," contains basic information known about the substance. Other sections such
as Chapter 3 Section 3.9, "Interactions with Other Substances," and Section 3.10, "Populations that are
Unusually Susceptible" provide important supplemental information.

MRL users should also understand the MRL derivation methodology. MRLs are derived using a
modified version of the risk assessment methodology that the Environmental Protection Agency (EPA)
provides (Barnes and Dourson 1988) to determine reference doses (RfDs) for lifetime exposure.

To derive an MRL, ATSDR generally selects the most sensitive end point which, in its best judgement,
represents the most sensitive human health effect for a given exposure route and duration. ATSDR
cannot make this judgement or derive an MRL unless information (quantitative or qualitative) is available
for all potential systemic, neurological, and developmental effects. If this information and reliable
quantitative data on the chosen end point are available, ATSDR derives an MRL using the most sensitive
species (when information from multiple species is available) with the highest no-observed-adverse-effect
level (NOAEL) that does not exceed any adverse effect levels. When a NOAEL is not available, a
lowest-observed-adverse-effect level (LOAEL) can be used to derive an MRL, and an uncertainty factor
(UF) of 10 must be employed. Additional uncertainty factors of 10 must be used both for human
variability to protect sensitive subpopulations (people who are most susceptible to the health effects
caused by the substance) and for interspecies variability (extrapolation from animals to humans). In
deriving an MRL, these individual uncertainty factors are multiplied together. The product is then
divided into the inhalation concentration or oral dosage selected from the study. Uncertainty factors used
in developing a substance-specific MRL are provided in the footnotes of the levels of significant exposure
(LSE) tables.

Chapter 3

Health Effects

Tables and Figures for Levels of Significant Exposure (LSE)

Tables and figures are used to summarize health effects and illustrate graphically levels of exposure
associated with those effects. These levels cover health effects observed at increasing dose
concentrations and durations, differences in response by species, MRLs to humans for noncancer end
points, and EPA's estimated range associated with an upper- bound individual lifetime cancer risk of 1 in
10,000 to 1 in 10,000,000. Use the LSE tables and figures for a quick review of the health effects and to
locate data for a specific exposure scenario. The LSE tables and figures should always be used in
conjunction with the text. All entries in these tables and figures represent studies that provide reliable,
quantitative estimates of NOAELs, LOAELs, or Cancer Effect Levels (CELs).

The legends presented below demonstrate the application of these tables and figures. Representative
examples of LSE Table 3-1 and Figure 3-1 are shown. The numbers in the left column of the legends
correspond to the numbers in the example table and figure.

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1,1-DICHLOROETHANE

APPENDIX B

B-3

LEGEND

See Sample LSE Table 3-1 (page B-6)

(1) Route of Exposure. One of the first considerations when reviewing the toxicity of a substance

using these tables and figures should be the relevant and appropriate route of exposure. Typically
when sufficient data exist, three LSE tables and two LSE figures are presented in the document.
The three LSE tables present data on the three principal routes of exposure, i.e., inhalation, oral,
and dermal (LSE Tables 3-1, 3-2, and 3-3, respectively). LSE figures are limited to the inhalation
(LSE Figure 3-1) and oral (LSE Figure 3-2) routes. Not all substances will have data on each
route of exposure and will not, therefore, have all five of the tables and figures.

(2) Exposure Period. Three exposure periods—acute (less than 15 days), intermediate (15-

364 days), and chronic (365 days or more)—are presented within each relevant route of exposure.
In this example, an inhalation study of intermediate exposure duration is reported. For quick
reference to health effects occurring from a known length of exposure, locate the applicable
exposure period within the LSE table and figure.

(3) Health Effect. The major categories of health effects included in LSE tables and figures are
death, systemic, immunological, neurological, developmental, reproductive, and cancer.
NOAELs and LOAELs can be reported in the tables and figures for all effects but cancer.
Systemic effects are further defined in the "System" column of the LSE table (see key number
18).

(4) Key to Figure. Each key number in the LSE table links study information to one or more data
points using the same key number in the corresponding LSE figure. In this example, the study
represented by key number 18 has been used to derive a NOAEL and a Less Serious LOAEL
(also see the two "18r" data points in sample Figure 3-1).

(5) Species. The test species, whether animal or human, are identified in this column. Chapter 2,
"Relevance to Public Health," covers the relevance of animal data to human toxicity and
Section 3.4, "Toxicokinetics," contains any available information on comparative toxicokinetics.
Although NOAELs and LOAELs are species specific, the levels are extrapolated to equivalent
human doses to derive an MRL.

(6) Exposure Frequency/Duration. The duration of the study and the weekly and daily exposure

regimens are provided in this column. This permits comparison of NOAELs and LOAELs from
different studies. In this case (key number 18), rats were exposed to "Chemical x" via inhalation
for 6 hours/day, 5 days/week, for 13 weeks. For a more complete review of the dosing regimen,
refer to the appropriate sections of the text or the original reference paper (i.e., Nitschke et al.
1981).

(7) System. This column further defines the systemic effects. These systems include respiratory,
cardiovascular, gastrointestinal, hematological, musculoskeletal, hepatic, renal, and
dermal/ocular. "Other" refers to any systemic effect (e.g., a decrease in body weight) not covered
in these systems. In the example of key number 18, one systemic effect (respiratory) was
investigated.

(8) NOAEL. A NOAEL is the highest exposure level at which no harmful effects were seen in the
organ system studied. Key number 18 reports a NOAEL of 3 ppm for the respiratory system,
which was used to derive an intermediate exposure, inhalation MRL of 0.005 ppm (see
footnote "b").

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1,1-DICHLOROETHANE

APPENDIX B

B-4

(9) LOAEL. A LOAEL is the lowest dose used in the study that caused a harmful health effect.
LOAELs have been classified into "Less Serious" and "Serious" effects. These distinctions help
readers identify the levels of exposure at which adverse health effects first appear and the
gradation of effects with increasing dose. A brief description of the specific end point used to
quantify the adverse effect accompanies the LOAEL. The respiratory effect reported in key
number 18 (hyperplasia) is a Less Serious LOAEL of 10 ppm. MRLs are not derived from
Serious LOAELs.

(10) Reference. The complete reference citation is given in Chapter 9 of the profile.

(11) CEL. A CEL is the lowest exposure level associated with the onset of carcinogenesis in
experimental or epidemiologic studies. CELs are always considered serious effects. The LSE
tables and figures do not contain NOAELs for cancer, but the text may report doses not causing
measurable cancer increases.

(12) Footnotes. Explanations of abbreviations or reference notes for data in the LSE tables are found
in the footnotes. Footnote "b" indicates that the NOAEL of 3 ppm in key number 18 was used to
derive an MRL of 0.005 ppm.

LEGEND

See Sample Figure 3-1 (page B-7)

LSE figures graphically illustrate the data presented in the corresponding LSE tables. Figures help the
reader quickly compare health effects according to exposure concentrations for particular exposure
periods.

(13) Exposure Period. The same exposure periods appear as in the LSE table. In this example, health
effects observed within the acute and intermediate exposure periods are illustrated.

(14) Health Effect. These are the categories of health effects for which reliable quantitative data
exists. The same health effects appear in the LSE table.

(15) Levels of Exposure. Concentrations or doses for each health effect in the LSE tables are
graphically displayed in the LSE figures. Exposure concentration or dose is measured on the log
scale "y" axis. Inhalation exposure is reported in mg/m3 or ppm and oral exposure is reported in
mg/kg/day.

(16) NOAEL. In this example, the open circle designated 18r identifies a NOAEL critical end point in
the rat upon which an intermediate inhalation exposure MRL is based. The key number 18
corresponds to the entry in the LSE table. The dashed descending arrow indicates the
extrapolation from the exposure level of 3 ppm (see entry 18 in the table) to the MRL of

0.005 ppm (see footnote "b" in the LSE table).

(17)

CEL. Key number 38m is one of three studies for which CELs were derived. The diamond
symbol refers to a CEL for the test species-mouse. The number 38 corresponds to the entry in the
LSE table.

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1,1-DICHLOROETHANE

APPENDIX B

B-5

(18) Estimated Upper-Bound Human Cancer Risk Levels. This is the range associated with the upper-
bound for lifetime cancer risk of 1 in 10,000 to 1 in 10,000,000. These risk levels are derived
from the EPA's Human Health Assessment Group's upper-bound estimates of the slope of the
cancer dose response curve at low dose levels (qi*).

(19) Key to LSE Figure. The Key explains the abbreviations and symbols used in the figure.

-------

SAMPLE

Table 3-1. Levels of Significant Exposure to [Chemical x] - Inhalation

Exposure

Key to frequency/ NOAEL

figure3 Species duration System (ppm)

LOAEL (effect)

Less serious
(ppm)

Serious (ppm)

Reference

INTERMEDIATE EXPOSURE

I-

0
m

1
>

—>

Systemic

Rat

13 wk

5 d/wk

6 hr/d

CHRONIC EXPOSURE
Cancer

Resp

10 (hyperplasia)

Nitschke et al. 1981

>
"D
"D

m
z
o
X

Rat

Mouse

18 mo
5 d/wk
7 hr/d

89-104 wk

5 d/wk

6 hr/d

79-103 wk

5 d/wk

6 hr/d

20 (CEL, multiple
organs)

10 (CEL, lung tumors,
nasal tumors)

10 (CEL, lung tumors,
hemangiosarcomas)

Wong et al. 1982

NTP 1982

12 —> a The number corresponds to entries in Figure 3-1.

b Used to derive an intermediate inhalation Minimal Risk Level (MRL) of 5x10 3 ppm; dose adjusted for intermittent exposure and divided
by an uncertainty factor of 100 (10 for extrapolation from animal to humans, 10 for human variability).

-------
SAMPLE

Figure 3-1. Levels of Significant Exposure to [Chemical X] - Inhalation

Acute (<14 days)

Systemic

H >

[iT]—~ppm

10000
1000 —
100-
10 —

1—
0.1-
0.01-
0.001-
0.0001-
0.00001—
0.000001
0.0000001—'

-Of

Iff

11 r

12r

Ol7h
®15h

®14r

3 18r
—~ Ol8r

Oi6r

Intermediate (15-364 days)
Systemic

\o#

fir

J* ^ J*

•32r (J35h
*31r ®33h

Q37h

^38m

~39m ^40m

®34r

036g

"Doses represent the lowest dose tested per study that produced a tumorigenic
response and do not imply the existence of a threshold for the cancer end point.

1a4
icr5
1a6
10"7-1

k-Monkey
g-Guinea Pig
r-Rat
IvRabbit
m-Mouse

Cancer Effect Level-Animals
®LOAEL. More Serious-Animals
(JLOAEL. Less Serious-Animals
OnOAEL-Animals

Minimal Risk Level
for effects
other than
Cancer

Estimated ^—
Upper-Bound
Human Cancer
Risk Levels

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1,1-DICHLOROETHANE

APPENDIX B

This page is intentionally blank.

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1,1-DICHLOROETHANE

C-1

APPENDIX C. ACRONYMS, ABBREVIATIONS, AND SYMBOLS

ACGIH

American Conference of Governmental Industrial Hygienists

ACOEM

American College of Occupational and Environmental Medicine

ADI

acceptable daily intake

ADME

absorption, distribution, metabolism, and excretion

AED

atomic emission detection

AFID

alkali flame ionization detector

AFOSH

Air Force Office of Safety and Health

ALT

alanine aminotransferase

AML

acute myeloid leukemia

AOAC

Association of Official Analytical Chemists

AOEC

Association of Occupational and Environmental Clinics

alkaline phosphatase

APHA

American Public Health Association

AST

aspartate aminotransferase

atm

atmosphere

ATSDR

Agency for Toxic Substances and Disease Registry

AWQC

Ambient Water Quality Criteria

BAT

best available technology

BCF

bioconcentration factor

BEI

Biological Exposure Index

BMD/C

benchmark dose or benchmark concentration

BMDx

dose that produces a X% change in response rate of an adverse effect

BMDLx

95% lower confidence limit on the BMDx

BMDS

Benchmark Dose Software

BMR

benchmark response

BSC

Board of Scientific Counselors

centigrade

CAA

Clean Air Act

CAG

Cancer Assessment Group of the U.S. Environmental Protection Agency

CAS

Chemical Abstract Services

CDC

Centers for Disease Control and Prevention

CEL

cancer effect level

CELDS

Computer-Environmental Legislative Data System

CERCLA

Comprehensive Environmental Response, Compensation, and Liability Act

CFR

Code of Federal Regulations

curie

confidence interval

ceiling limit value

CLP

Contract Laboratory Program

centimeter

CML

chronic myeloid leukemia

CPSC

Consumer Products Safety Commission

CWA

Clean Water Act

DHEW

Department of Health, Education, and Welfare

DHHS

Department of Health and Human Services

DNA

deoxyribonucleic acid

DOD

Department of Defense

DOE

Department of Energy

DOL

Department of Labor

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1,1-DICHLOROETHANE

APPENDIX C

C-2

DOT Department of Transportation

DOT/UN/ Department of Transportation/United Nations/

NA/IMDG North America/Intergovernmental Maritime Dangerous Goods Code

DWEL drinking water exposure level

ECD electron capture detection
ECG/EKG electrocardiogram

EEG electroencephalogram

EEGL Emergency Exposure Guidance Level

EPA Environmental Protection Agency

F Fahrenheit

Fi first-filial generation

FAO Food and Agricultural Organization of the United Nations

FDA Food and Drug Administration

FEMA Federal Emergency Management Agency

FIFRA Federal Insecticide, Fungicide, and Rodenticide Act

FPD flame photometric detection

fpm feet per minute

FR Federal Register

FSH follicle stimulating hormone

g gram

GC gas chromatography

gd gestational day

GLC gas liquid chromatography

GPC gel permeation chromatography

HPLC high-performance liquid chromatography

HRGC high resolution gas chromatography

HSDB Hazardous Substance Data Bank

IARC International Agency for Research on Cancer

IDLH immediately dangerous to life and health

ILO International Labor Organization

IRIS Integrated Risk Information System

Kd adsorption ratio

kg kilogram

kkg metric ton

Koc organic carbon partition coefficient

Kow octanol-water partition coefficient

L liter

LC liquid chromatography

LC50 lethal concentration, 50% kill

LClo lethal concentration, low

LD50 lethal dose, 50% kill

LDlo lethal dose, low

LDH lactic dehydrogenase

LH luteinizing hormone

LOAEL lowest-observed-adverse-effect level

LSE Levels of Significant Exposure

LT50 lethal time, 50% kill

m meter

MA trans, trans-muconic acid

MAL maximum allowable level

mCi millicurie

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APPENDIX C

C-3

MCL maximum contaminant level

MCLG maximum contaminant level goal

MF modifying factor

MFO mixed function oxidase

mg milligram

mL milliliter

mm millimeter

mmHg millimeters of mercury

mmol millimole

mppcf millions of particles per cubic foot

MRL Minimal Risk Level

MS mass spectrometry

NAAQS National Ambient Air Quality Standard

NAS National Academy of Science

National Air Toxics Information Clearinghouse

NATO North Atlantic Treaty Organization

NCE normochromatic erythrocytes

NCEH National Center for Environmental Health

NCI National Cancer Institute

ND not detected

NFPA National Fire Protection Association

ng nanogram

NHANES National Health and Nutrition Examination Survey

NIEHS National Institute of Environmental Health Sciences

NIOSH National Institute for Occupational Safety and Health

NIOSHTIC NIOSH's Computerized Information Retrieval System

NLM National Library of Medicine

nm nanometer

nmol nanomole

NOAEL no-observed-adverse-effect level

NOES National Occupational Exposure Survey

NOHS National Occupational Hazard Survey

NPD nitrogen phosphorus detection

NPDES National Pollutant Discharge Elimination System

NPL National Priorities List

NR not reported

NRC National Research Council

NS not specified

NSPS New Source Performance Standards

NTIS National Technical Information Service

NTP National Toxicology Program

ODW Office of Drinking Water, EPA

OERR Office of Emergency and Remedial Response, EPA

OHM/TADS Oil and Hazardous Materials/Technical Assistance Data System

OPP Office of Pesticide Programs, EPA

OPPT Office of Pollution Prevention and Toxics, EPA

OPPTS Office of Prevention, Pesticides and Toxic Substances, EPA

OR odds ratio

OSHA Occupational Safety and Health Administration

OSW Office of Solid Waste, EPA

OTS Office of Toxic Substances

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APPENDIX C

C-4

Office of Water

OWRS

Office of Water Regulations and Standards, EPA

PAH

polycyclic aromatic hydrocarbon

PBPD

physiologically based pharmacodynamic

PBPK

physiologically based pharmacokinetic

PCE

polychromatic erythrocytes

PEL

permissible exposure limit

picogram

PHS

Public Health Service

PID

photo ionization detector

pmol

picomole

PMR

proportionate mortality ratio

ppb

parts per billion

ppm

parts per million

ppt

parts per trillion

PSNS

pretreatment standards for new sources

RBC

red blood cell

REL

recommended exposure level/limit

RfC

reference concentration

RfD

reference dose

RNA

ribonucleic acid

reportable quantity

RTECS

Registry of Toxic Effects of Chemical Substances

SARA

Superfund Amendments and Reauthorization Act

SCE

sister chromatid exchange

SGOT

serum glutamic oxaloacetic transaminase

SGPT

serum glutamic pyruvic transaminase

SIC

standard industrial classification

SIM

selected ion monitoring

SMCL

secondary maximum contaminant level

SMR

standardized mortality ratio

SNARL

suggested no adverse response level

SPEGL

Short-Term Public Emergency Guidance Level

STEL

short term exposure limit

STORET

Storage and Retrieval

TD50

toxic dose, 50% specific toxic effect

TLV

threshold limit value

TOC

total organic carbon

TPQ

threshold planning quantity

TRI

Toxics Release Inventory

TSCA

Toxic Substances Control Act

TWA

time-weighted average

uncertainty factor

U.S.

United States

USD A

United States Department of Agriculture

USGS

United States Geological Survey

VOC

volatile organic compound

WBC

white blood cell

WHO

World Health Organization

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C-5

APPENDIX C

greater than

greater than or equal to

equal to

less than

less than or equal to

0/
/o

percent

alpha

beta

gamma

delta

(im

micrometer

microgram

cancer slope factor

negative

positive

(+)

weakly positive result

(-)

weakly negative result

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