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Summary of External Peer Review and

Public Comments and Disposition

This document summarizes the public and external peer review comments that the EPA’s Office of

Pollution Prevention and Toxics (OPPT) received for the draft work plan risk assessment for

trichloroethylene (TCE).  It also provides EPA/OPPT’s response to the comments received from the

public and the peer review panel.

EPA/OPPT appreciates the valuable input provided by the public and peer review panel.  The input

resulted in substantial revisions to the risk assessment.

Peer review charge questions1 are used to categorize the peer review and public comments into specific

issues related to five main themes.   

 General Issues on the Risk Assessment Document  

 Occupational Exposure Assessment

 Consumer Exposure Assessment

 Hazard and Dose‐Response Assessments

 Risk Characterization

A separate section called Other Public Comments organizes the response to those public comments that

are unrelated to the main themes listed above.

                                                            

1 These are the questions that EPA/OPPT submitted to the panel to guide the peer review process.
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General Issues on the Risk Assessment DocumentCharge question 1‐1: Please comment on whether the characterization provides a clear and logical summary of EPA’s anal

specific suggestions for improving the document.

Charge question 1‐2: Please comment on whether appropriate background information is provided and accurately charac

any other significant literature, reports, or data that would be useful to complete this characterization.

# Summary of Peer Review and Public Comments for Specific Issues Related to Charge Questions 1‐1 and 1‐2 EPA/OPPT Response

1 Document is not clear about the purpose of the risk

assessment. The document would be substantially

improved if a clear statement was made regarding the

audience and utility of the report.

EPA/OPPT has made significant revisions to the TCE risk a

the clarity of the assessment. In addition, the purpose an

described in section 1.1 of the final TCE OPPT risk assessm

2 EPA/OPPT did not assess dermal exposure to TCE for

occupational and residential scenarios; why is dermal

exposure considered less significant than inhalation

exposure?By not including dermal exposure in the exposure

assessment, exposure is likely to be underestimated.

EPA/OPPT recognizes that dermal exposure to highly vola

TCE can occur. However, based on the physical‐chemica

the scenarios described in this assessment, EPA/OPPT be

the main exposure pathway for this risk assessment. This 

underestimate total exposures resulting from the uses of 

assumption. Thus, we agree this assessment likely under

from the uses of TCE being assessed.

As stated in Section 1.3.2 of the final risk assessment, rec

experimental work supports the assumption that inhalat

exposure pathway. The dermal model described by Tibal

estimates that about 1% of TCE on the skin will be absorb

with the other 99% evaporating. Also, an experimental co

vapor exposure found that TCE and hexane had the least 

amongst a set of volatile solvents. The ratio of dermal to 

found to be 0.1 % for TCE (Kezic et al., 2000).

Citations:Kezic, S., A. C. Monster, J. Kruse, and M. M. Verberk. 200

Some Vaporous Solvents in Volunteers. International Arch

and Environmental Health, 73(6), 415‐422.

Tibaldi, R., W. ten Berge, and D. Drolet. 2014. Dermal Abs

Estimation by Ih Skinperm. J Occup Environ Hyg, 11(1), 19
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3 Can EPA/OPPT clarify why it did not include the use of TCE as

a spotting agent in its assessment?

Based on additional information provided during peer revi

revised its original assessment to include the use of TCE as 

cleaning facilities. The exposure assessment for the spotti

the occupational section 2.4 of the final TCE OPPT risk asse

Appendix H.

EPA/OPPT did not identify TCE‐based spot cleaners used 

(Section 2.5.1). It is possible that members of the genera

products intended for commercial use, but these activitie

the final TCE risk assessment.

4 For the commercial degreasing scenario, EPA’s discussion

regarding comparison of National Emissions Inventory (NEI)

and Toxics Release Inventory (TRI) data was somewhat

confusing. Can this be further clarified?

EPA/OPPT has further clarified its comparison of NEI and 

the final risk assessment includes illustrations that provid

EPA/OPPT’s assessment for the commercial degreasing s

revisions and illustrations can be found in section 2.3, Fig

Appendices E and F of the final TCE OPPT risk assessment

5 EPA did not cite the correct publication for the two‐zone

mass balance model. In addition, EPA did not reference the

publication provided by Dr. Jayjock regarding the validity of

the two‐zone mass balance model. This publication addsstrong support for using the two‐zone model to estimate

occupational exposures from commercial degreasing.

Including this reference will strongly strengthen EPA’s case forusing such a model to infer exposures. Also, this reference

supports that EPA/OPPT’s assessment is more than a

screening level assessment.

The risk assessment has been updated to cite the correct 

et al., 2009) for the two‐zone mass balance model.

In addition, EPA/OPPT updated its risk assessment to refe

provided by Dr. Jayjock during peer review.

Citation:Keil, C. B., C. E. Simmons, and A. T. Renee. 2009. Mathem

Estimating Occupational Exposure to Chemicals (2nd ed.) 

Hygiene Association (AIHA).

6 In Appendix D, a paragraph had a missing notation for the

Free Surface Area (FSA), thus causing confusion for readers.

The risk assessment has been updated to address the iss

notation for the Free Surface Area (FSA). Please note tha

draft risk assessment corresponds to Appendix G in the f

7 EPA/OPPT did not reference monitoring data to validate its

exposure estimates resulting from the use of TCE in

commercial degreasing processes. How can one have

confidence in EPA/OPPT’s estimates for occupational

exposures?

In collaboration with the Occupational Safety and Health 

relevant monitoring data specific to TCE from site survey

incorporated into the final risk assessment in section 2.3.

OSHA’s data and EPA’s assessment of it is included in the 

“OSHA IMIS TCE SAMPLES_062314v1.xlsx”.
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8 EPA/OPPT used a steady‐state assumption in estimating

airborne exposure concentrations resulting from commercial

degreasing operations. This is problematic and perhaps

simplistic for these scenarios.

In the revised risk assessment, EPA/OPPT used a transient 

balance model to estimate airborne exposure concentratio

commercial degreasing processes.

9 There does not seem to be an exhaustive effort made to

find all existing appropriate literature for the various

sections of the risk assessment.

Additional references submitted to EPA/OPPT as part of t

were incorporated if they were relevant to the assessmereferences were included relevant to the weight‐of‐evide

supporting the hazard/dose‐response assessment (Sectio

analysis for fetal cardiac malformations (Appendix N). Pl

section for the complete list of references used in the fin

10 EPA/OPPT should improve the transparency and readability

of Table F‐1 and Table 3‐19. Table F‐1 listed the hazard

values as reported in the IRIS assessment. Table 3‐19 listed

the hazard values used in the OPPT risk assessment.

EPA/OPPT has made significant changes to the hazard inf

Table F‐1 and Table 3‐19 of the draft TCE OPPT risk asses

assessment, the information can be found in Table 2‐18 a

Table 2‐19 lists the lowest hazard values for different effe

OPPT assessment used to estimate risks. Table 2‐19 cont

information: exposure duration for risk analysis (acute v

organ/system, species, route of exposure, range of doses 

duration, point of departure (POD), effect, human equiva

(HEC) at the 50th, 95th and 99th percentiles, uncertainty fa

benchmark margin of exposure and the reference citatio

the complete list of oral and inhalation studies that the U

Risk Information System (IRIS) program deemed suitable response analysis.

11 Peer review comments suggested that the EPA’s Office of

Pesticides (OPP) may have empirical data that could

improve the TCE work plan risk assessment. Particularly,

indoor monitoring data for inert chemicals in consumer

pesticides might provide useful information for the TCE risk

assessment, provided that the monitoring data were for

chemical substances with similar physical‐chemical

properties.

EPA/OPPT in collaboration with the Office of Pesticide pr

OPP’s Pesticide Inert database. No exposure data that w

indoor monitoring data on TCE or surrogate chemical we

confirmed our lack of results and the improbability of fin

information that was suggested to us by the peer review

found within EPA/ OPP, it is highly likely that it is confide

information if it was submitted by a company as part of a 

under the pesticide laws, and therefore not usable in a p

Given these circumstances, EPA/OPPT believes that this e

provide useful surrogate data for refining the OPPT risk a
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12 One of the peer reviewers stated that while Section A.

Physical and Chemical Properties of TCE and Section C.

Production Volume and General Information on Uses

seemed appropriate, Section B. Environmental Fate did not

seem to be necessary or relevant to an assessment focused

on inhalation of TCE from industrial or consumer products?

The environmental fate of a substance (i.e., its transport 

the environment) can mitigate or enhance its exposure to 

environment. In the initial steps of assessing the potentia

environmental fate is considered in conjunction with its r

physical‐chemical properties to provide an understanding 

after release may impact exposure. The discussion of the 

TCE was used to help focus the assessment on the appro

(inhalation) and pathways (volatilization to air).

However, EPA/OPPT agrees with the peer reviewer that t

the environmental fate of TCE is not necessary to include 

The full discussion of the environmental fate of TCE has b

Appendix C.

13 One of the peer reviewers requested clarification of the

terms “low” and “moderate” in the conclusion of the fate

discussion below to make it less open to interpretation:

“Based on the experimental evidence and

environmental fate data available, TCE is expected

to have low bioaccumulation potential and

moderate persistence.”

In the Environmental Fate Section, EPA/OPPT addressed 

bioaccumulation/bioconcentration in aquatic organisms 

persistence. The peer reviewer appeared to interpret bio

and persistence to refer to human bioaccumulation and h

rather than bioaccumulation in aquatic organisms and en

persistence as it was intended.

EPA/OPPT agrees that the language used in the concludin

further clarification and made the following change: “Bas

evidence and environmental fate data available, TCE is ex

bioaccumulation potential in aquatic organisms

(bioconcentration/bioaccumulation factor less than 1000

persistence in the environment (environmental half‐life of 

months but less than six months) .”The revised text is fou
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Occupational Exposure AssessmentCharge question 2‐1: Please comment on the approach used, and provide any specific suggestions or recommendatioapproaches, models or information that should be considered by the Agency for improving the workplace exposure asseestimations for bystander/non‐users (e.g., women of childbearing age).

# Summary of Peer Review and Public Comments for

Specific Issues Related to Charge Question 2‐1 EPA/OPPT Response

14 EPA/OPPT did not reference monitoring data to validate its

exposure estimates resulting from the use of TCE in

commercial degreasing processes. EPA’s risk assessment

contains little actual data on exposure at small commercial

shops on which to base a robust analysis. If EPA/OPPT is going

to distinguish facilities based on their size, then more

representative data needs to be obtained before finalized the

risk assessment.

EPA/OPPT seems to indicate that its exposure estimates for

workers at commercial degreasing facilities are similar to

measured values; but EPA does not provide any monitoring

data in its risk assessment. It is important to know what TCE

workplace exposure data are available; EPA/OPPT should

include this data in the risk assessment.

EPA/OPPT should gather or identify monitoring data for TCE

exposures resulting from activities that are of concern;

exposure assumptions and models are no substitute for

exposure data. At a minimum, EPA should solicit and

welcome peer review of the TCE risk assessment from the

Consumer Product Safety Commission (CPSC) and the

National Institute for Occupational Safety and Health

(NIOSH).

EPA/OPPT did not use monitoring data to estimate workplace

exposures for the commercial degreasing scenario. Instead,

EPA chose to estimate workplace exposures based on

calculating an emission rate from degreasing operations.

Further, EPA cites Walden et al. (1989) and incorrectly states

In collaboration with OSHA, relevant monitoring data spe

This additional information has been incorporated into th

section 2.3.3 and Figure 2.2. OSHA’s data and EPA’s ass

in the supplementary file: “OSHA IMIS TCE SAMPLES_06

The National Emissions Inventory (NEI) contains data for 

Traditionally, small commercial facilities have been repre

sources; EPA/OPPT has used data for nonpoint sources to 

commercial facilities.The publication from Wadden et al. (1989) reported a to

grams of TCE per minute from an open top degreaser. S

ventilation (LEV) was used, only 2.57 grams of TCE per m

total emission) were reported as escaping into the work

data, EPA/OPPT assumed that if no LEV were used, then 

27.29 grams of TCE per minute could potentially be rele

Citation:Wadden, R. A., P. A. Scheff, and J. E. Franke. 1989. Emiss

Trichloroethylene Vapor Degreasers. American Industria

Journal, 50(9), 496‐500.
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that the emission rate ranged from 2.57 to 27.29 grams of

TCE per minute. The data from Walden et al. (1989) are for

environmental emissions that are released externally; only

9.5% of the value is emission escaping into the workplace.

EPA should not assume environmental emissions that are

released externally can be used to estimate workplace

exposures.

15 For the commercial degreasing scenario, it is not clear

whether EPA/OPPT is using the most currently available data

to estimate the number of workers exposed. It seems EPA is

using data from the 1970s or 1980s. Releases of TCE have

decreased substantially since that time. Also, workplace

practices and industrial hygiene standards have improved.

Thus, it is likely that EPA is overestimating the number of

workers and non‐users exposed.

EPA/OPPT estimates the number of workers and non‐users at

commercial degreasing facilities as 7,415 and 17,796,

respectively. But EPA/OPPT does not appear to provide any

explanation for how these estimates were obtained.

EPA/OPPT has updated the risk assessment with additio

clarify how the number of workers and non‐users was e

2.3.3 and Appendix F of the revised risk assessment).

By using more recent data from the 2008 NEI and EPA’s 

the halogenated solvent cleaning source category (EPA, 

number of facilities (1,746), EPA/OPPT’s estimate likely 

trend in the number of facilities using TCE for degreasin

adequate order of magnitude estimate. More recent an

were not identified for the purposes of comparison.

EPA/OPPT estimated the number of workers and non‐us

to TCE based on: (1) a National Occupational Exposure 

1980s; (2) EPA’s draft generic scenario on vapor degreas

the number of small degreasing facilities as determined 

Emissions Inventory (NEI) and EPA’s 2006 risk assessme

solvent cleaning source category (EPA, 2006d).

Citation:EPA (U.S. Environmental Protection Agency). 2001a. Dra

of Vapor Degreasers. Office of Pollution Prevention and 

Engineering Branch, Washington, DC.

EPA (U.S. Environmental Protection Agency). 2006d. Ris

Halogenated Solvent Cleaning Source Category Web Site

http://yosemite.epa.gov/ee/epa/ria.nsf/vwRef/A.2006.(accessed on November 8, 2012).
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16 EPA’s draft risk assessment does not consider the impacts of

the Halogenated Solvent Cleaning National Emission

Standard for Hazardous Air Pollutants (NESHAP), which EPA

finalized in 2007. This standard limits emissions from open‐

top degreasers.

EPA/OPPT updated its risk assessment to take NESHAP e

account (see section 2.3.3, Table 2‐8, and Appendix E of 

17 The overall methodology EPA/OPPT used to estimate

emissions of TCE from commercial degreasing operations is

complex and convoluted.

EPA/OPPT has clarified its comparison of NEI and TRI da

revised risk assessment includes illustrations that provid

EPA/OPPT’s assessment for the commercial degreasing 

2.3.3, Figure 2‐1, and Appendix E of the final risk assessm

18 We downloaded the file "Facility‐Level by Pollutant" at EPA's

2008 NEI website. The total TCE emissions were 4,088,000 lb

across 2,378 facilities, which are close, but slightly less, than

the total provided by EPA (4,340,000 lb). Later in the

discussion there is a reference made to only including

emissions from facilities in one of 78 North American Industry

Classification Scheme (NAICS) codes. When we only include

the 78 NAICS codes, the emissions in the "Facility‐Level by

Pollutant" are reduced to 2,734,000 lb across 373 facilities. It

is not clear where EPA is getting the 186 TCE point sources

and 1,779 nonpoint sources. It is possible that some of the

non‐point sources are not in the facility file, but it seems that

some of them must be since there are more facilities with the

78 NAICS codes than the 186 quoted by EPA.

EPA/OPPT has updated its assessment to further clarify 

Inventory (NEI) data were used (see section 2.3.3 and Ap

assessment).In brief, EPA/OPPT used point and nonpoint source data 

These data were filtered, for example, by pollutant nam

codes (SCC), etc. After filtering the data, the number of 

facilities was estimated to be 154. Based on EPA’s 2006 

halogenated solvent cleaning source category (EPA, 200

degreasing facilities was expected to be approximately 1

small commercial degreasing facilities was estimated to 

facilities minus 154 large facilities).

Citation:EPA (U.S. Environmental Protection Agency). 2006d. Ris

Halogenated Solvent Cleaning Source Category Web Site

http://yosemite.epa.gov/ee/epa/ria.nsf/vwRef/A.2006.(accessed on November 8, 2012).

19 For the commercial degreasing scenario, EPA/OPPT provides

no indication on the relative prevalence of local exhaust

ventilation (LEV).EPA/OPPT should describe how the local exhaust ventilation

(LEV) affects the generation rate.

EPA/OPPT has adopted a scenario‐based approach for it

Thus, exposure scenarios with and without LEV have be

the relative prevalence of LEV is not known to EPA.

Based on information presented in (Wadden et al., 1989

that LEV can have an effectiveness of up to 90%. For sc

assumed to be present, the generation rate is reduced b

2.3.3 and Appendix E of the final risk assessment).
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Citation:Wadden, R. A., P. A. Scheff, and J. E. Franke. 1989. Emiss

Trichloroethylene Vapor Degreasers. American Industria

Journal, 50(9), 496‐500.

20 EPA/OPPT assumed that small commercial degreasing

facilities operate for 2 hours (hrs) a day. This is a critical

parameter; the basis for this should be fully described.

The basis for this assumption is information included in 

scenario on vapor degreasing (EPA, 2001a). This draft s

facility estimates, such as days of operation, and hours o

assumption is described in section 2.3.3 of the final risk 

that EPA/OPPT did not locate further data about facility 

parameters.

21 The free surface area (FSA) value in Table D‐1 is listed as 180

square feet. However, based on equation (5) in Appendix D,

the FSA should be 340 square feet. It appears that EPA used

the correct value of 340 square feet in its calculations, but

mistakenly listed the value as 180 square feet in the

document.

The listed FSA value has been updated to 340 square fee

Table G‐1 of the revised risk assessment).

22 EPA/OPPT should use different methods to assess workplace

exposures. For example, Drs. Jayjock and Driver both

mentioned using the Nicas model.

In the final assessment, EPA/OPPT used the Nicas mode

balance model) that Drs. Jayjock and Driver referred to; 

assess workplace exposures (see sections 2.3.3 and 2.4.2

of the revised risk assessment).

23 An understanding of actual work place practices and the

proportion of workers experiencing near field exposures is

imperative.EPA/OPPT should use a sensitivity analysis of some type to

ascertain the important parameters in the model used for

worker exposure.

In collaboration with OSHA, relevant monitoring data sp

identified and used in the assessment. A comparison be

monitoring data and the modeled results showed that t

estimates were in‐line with data from OSHA. This addit

been incorporated into the risk assessment (see section 

the final risk assessment).

EPA/OPPT agrees that work place practices information 

exposure assessment. However, such information was 

no such information was submitted to EPA/OPPT during 

period.EPA/OPPT agrees that performing a sensitivity analysis c

instances, produce useful and actionable insights. In th
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adopted a scenario‐based approach for its exposure ass

from this approach likely capture actual exposure levels 

data.

24 It is not intuitive why the number of machines found at a

large facility (which logically might be expected to have more

than one machine) can be translated to small nonpoint

sources (which logically might be expected to have only one

machine/facility). Clarification on this point would be

appreciated.

In this assessment, EPA/OPPT assumed one degreasing 

commercial operations because smaller facilities were e

degreasing units per facility than larger ones. Large facil

have 1.2 degreasing units per facility (see section 2.3.3 o

assessment).

25 For the commercial degreasing scenario, I found the

inhalation model choice, model inputs and treatment of the

industrial inhalation scenario to be well done with the

possible exception of the “typical ventilation” rate. The only

questionable variable in my opinion is the use of 3,000 cubic

feet per minute (cfm) as the “typical value” for general

ventilation in an industrial room. My experience has been

that industrial rooms without special exhaust will be

ventilated in a range of 2 to 5 air changes per hr.

Based on this input and additional published sources, EP

range for the air exchange parameter to 2 to 15 air exch

scenario‐based exposure assessment (see Appendix G a

risk assessment).
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Consumer Exposure AssessmentCharge question 3‐1: Please comment on the approach used and provide any specific suggestions or recommendations fo

approaches, models, or information (e.g., information on duration and number of user events) that could be considered by 

developing the exposure assumptions and estimates for the hobbyist degreaser and clear protective coating spray uses, an

bystander/non‐users (e.g., children, women of childbearing age).

# Summary of Peer Review and Public Comments for Specific Issues Related to Charge Question 3‐1 EPA/OPPT Response

26 Panelists and the general public commented on the use of

the Consumer Exposure Model (CEM) to calculate

exposures for the consumer use scenarios. Some

commenters felt that the Multi‐ Chamber Concentration

and Exposure Model (MCCEM) or other models (e.g.,

Nicas2) should be used as well. Some commenters also

suggested the use of probabilistic methods (e.g. Monte

Carlo).

In the final assessment, EPA/OPPT retained the current c

model to estimate exposure levels for the residential sce

data for TCE did not support the use of MCCEM or other 

Those models rely on more complex input data to gener

It should be noted that many of the inhalation models u

engines to generate exposure concentrations. For exam

properties distinguishing MCCEM from CEM is the ability 

chamber studies into MCCEM to replace the empirical m

evaporation rates in CEM. Running additional models w

input data, when many use similar 2 box models for the 

will not yield significant improvements to the consumer 

Models like Nicas2 that include personal breathing zone 

likely increase the exposure to consumers by accounting 

concentrations near users of aerosol products. This adde

be important for assessments where further refinement 

but in this assessment risk exists without the more refin

consumers.Given the current uncertainty in the input parameters a

may correspond to real user behavior, appropriate input 

available for probabilistic exposure modeling.
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27 Panelists and the general public commented on the

absence of indoor monitoring data within the consumer

exposure assessment.

EPA/OPPT did not find monitoring studies related to the 

products containing TCE. Indoor air concentrations have 

final risk assessment in section 2.5.4.2 and a list of refere

concentrations is in the supplemental material entitled “

Measured TCE Concentrations in Indoor Air”. The only 

those related to TCE exposures from vapor intrusion or s

general household levels of volatile organic compounds 

are not expected to represent the concentrations that m

use of products containing TCE under the scope of this a

28 Panelists and the general public suggested describing the

consumer exposure assessment as screening level. A

Panelist recommended using the Westat survey data to

provide further information on consumer behavior

patterns and the collection of mass used during product

use data.

The exposure assessment is not a theoretical bounding a

case assessment. Collection of new data or measureme

of the workplan assessment process.

The TCE assessment did not use the screening level para

the defaults in the EFAST2 modeling software. A hypoth

created based on professional judgment due to a lack of 

the products in the assessment. EPA/OPPT has not foun

source of consumer use information for these products. 

the hypothetical consumer use behavior patterns were m

but the household parameters used in the modeling we

median values e.g. air exchange rate.

The Westat survey data have been added to the final ass
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29 The public commented on the back calculation used to

generate 24‐hr time averaged exposure numbers for the

consumer exposure portion of the exposure assessment.

One reviewer seemed to think the assessment was based

on a single peak value from the CEM run.

The CEM module calculates potential acute dose rates (A

of the simulated home. This dose rate involves summing 

multiple small intervals which are based on the concent

in the home and the breathing rate and body mass of th

The back calculation removed the parameters describing 

characteristics of the users in different age groups (e.g. b

weight) from the acute dose rate and converted it to the 

experienced by either the user or a bystander over a 24‐

CEM output also discusses a peak concentration for the 

this value was not used in the risk assessment because it 

10‐second interval within the entire simulation and is m

model diagnostics. Additional information about the co

concentrations (ppm) is found in Appendix J.

30 Peer reviewers and the public submitted comments

expressing confusion regarding how CEM calculated

emission rates of TCE and on how mixtures of chemicals

may affect the evaporation rates. Commenters expressed

a desire for further transparency on the model parameter

selection within EFAST in the main body of the document.

In the absence of measured data for emission of TCE in r

chamber studies for the selected products, EPA/OPPT us

to estimate the evaporation rates of solvents from a sur

is based on an exponential decay model and is not const

of use or the 24‐hr period used to calculate the air conce

are exposed to. Further explanation for this calculation, 

and information on the model parameters in general ha

exposure section 2.5 and Appendix I.

31 Commenters were unsure of the meaning of some fate

parameters and the need for a fate section.

The persistence and bioaccumulation scores were based 

considerations and were mainly present as part of the ju

performing an ecological assessment. An overview of th

and releases of TCE can be found in the main body of th

particularly section 2.2. The rest of the information has 

Appendix C.

32 Peer reviewers requested further information on the peer

review of the CEM model.

EPA/OPPT has posted the peer review documentation fo

http://www.epa.gov/oppt/exposure/pubs/efastqa.htm.

33 Peer reviewers requested that the technical presentation

be more contiguous within the main body of the

document.

More information on the exposure assessment has been 

supplementary documents to the main body of the risk a

particular in section 2.5.3.
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34 Public and peer reviewers requested the collection of

experimental data to increase the certainty of the

exposure assessment. Requested data included mass of

TCE emitted during use, chamber study data, personal

breathing zone monitoring, and indoor air measurements

to validate user and bystander exposures.

Data collection requests are outside the scope of OPPT W

assessment process, which rely on data and models that 

EPA/OPPT requested that outside parties submit data th

workplan chemical risk assessments with the agency, bu

received data that would augment the TCE consumer ex

35 A peer reviewer suggested expanding the age level for

users of the TCE consumer products.

EPA/OPPT believes that users of these products will gen

however it is possible that teenagers or younger children 

the same room with the user while engaging in arts and 

degreasing.The current exposure assessment can be expanded to al

levels by using the indoor air concentrations estimates f

products. Data are not available for any consumer use p

estimated indoor air concentrations would be applied to 

36 Peer reviewers suggested that CEM undergo model

validation CEM has undergone a peer review and some limited vali

37 Peer reviewers requested that a sensitivity analysis be

performed for the exposure assessment.

The mass of product used per event would be a highly se

based on professional judgments created through repea

However when weighing the relative importance of othe

important to remember that all of the consumer behavi

parameters for the consumer behavior are hypothetical

sensitivity analysis to incorrectly identify certain parame

important than they would be if survey data were availa

For example, the current assumption is that the user spe

of use (i.e., a utility room). This parameter choice leads 

in the importance of the emission rate of TCE to the roo

rate would still lead to exposure of all of the emitted TC

analysis of the current parameters would perhaps falsely 

emission rate from the surface of use was relatively unim

consumer behavior pattern information would be neede

analysis would be useful, and such information has not b
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38 A panel member commented that the model runs may

have not correctly used the data from the most recent

exposure factors handbook for the weight and breathing

rates of the members of different age groups.

The default exposure values cited in the EFAST2 docume

publically available model preceded those recently publ

Exposure Factors Handbook (EFH). EPA/OPPT did not us

EFAST2, but instead relied on the exposure values publis

This has been clarified in section 2.5.3 and in Appendix I.

39 A panelist commented that product compositions would

vary over time leading to inaccurate chronic exposure

calculations.

The chronic exposure numbers are generated by default 

not used in the TCE risk assessment. They are only includ

since they are generated by CEM for all model runs.

40 Peer reviewers asked for a determination of the exposed

population from these consumer products.

EPA/OPPT did not find exposed population data nor rece

public comment period for the draft TCE risk assessmen

address this point. The workplan assessments are based 

This information would not affect the calculated exposu

users and bystanders.
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Hazard and Dose‐Response AssessmentsCharge question 4‐1: Please comment on the strengths and weaknesses of evaluating different endpoints based on expos

acute versus chronic).

Charge question 4‐2: Please comment on the strengths and weaknesses of using multiple values for each type of adverse 

Charge question 4‐3: PBPK modeling was employed in the 2011 IRIS assessment for route‐to‐route extrapolation to develo

inhalation value from oral studies, some of which involved endpoints not studied or reported in inhalation studies. OPPT su

used in the IRIS assessment. However, OPPT did not use PBPK‐derived human‐equivalent concentrations from oral studies 

risk assessment, because OPPT focused on a narrow set of TCE consumer uses (e.g., degreasing and arts/crafts uses) that a

therefore, OPPT’s draft risk assessment relied only on inhalation exposure studies that directly mimicked inhalation exposu

both adults and developmental life stages. Please comment on whether the 2011 IRIS assessment's PBPK‐derived inhalatiostudies should be used in the final OPPT risk assessment.

#

Summary of Peer Review and Public Comments for

Specific Issues Related to

Charge Questions 4‐1, 4‐2 and 4‐3

EPA/OPPT Response

41 It was suggested that EPA/OPPT needed to conduct a

systematic evaluation of the quality of each toxicological

study used in the TCE risk assessment. The final TCE OPPT

risk assessment should have a discussion of the study

quality criteria used in the study evaluation, as well as a

discussion of the strengths and limitations of the studies

selected as the basis for hazard values.

Some peer reviewers and public commenters criticized

EPA/OPPT for using studies that had deficiencies and were

not used in the IRIS’ non‐cancer dose‐response assessment

for deriving candidate RfCs.

Some peer reviewers and public commenters suggested that

the selection of the hazard value should be based on the

“best” study that represents the health effects domain (or

endpoint) based on the assessment of study

integrity/quality. This “best” study should be selected

instead of using a range of hazard values within a specific

endpoint.

The final TCE risk assessment relies on the non‐cancer an

that were published in the latest Toxicological Review for 

U.S. EPA’s Integrated Risk Information System (IRIS) in 20

TCE IRIS assessment].The U.S. EPA’s IRIS assessment represents the latest haza

analysis for TCE that EPA has completed to date. The TCE 

a systematic weight‐of‐evidence (WOE) approach, the lat

information and physiologically‐based pharmacokinetic m

develop hazard and dose‐response assessments for TCE’s 

carcinogenic health effects resulting from lifetime oral or 

The strengths and limitations of the data set for cancer a

can be found in the TCE IRIS assessment.

Development of TCE’s hazard and dose‐response assessm

principles set forth by the various risk assessment guideli

National Research Council and the U.S. EPA (see Appendi

assessment). Primary, peer‐reviewed literature identifie

2010 was also included where that literature was determ

the assessment.
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One peer reviewer recommended reviewing the data set

available for each endpoint and determining whether the

data are adequate to describe the qualitative and dose‐

response elements of the endpoint.

The TCE IRIS assessment identified the most suitable non

dose‐response analysis by health effects domain (i.e., live

toxicity, neurotoxicity, immunotoxicity, reproductive toxi

developmental toxicity). A list of these studies are found 

final TCE OPPT risk assessment. EPA/OPPT relied on the 

hazard values (i.e., human equivalent concentration or H

or chronic non‐cancer risks for the specific TCE uses (see 

Table 2‐18 in the final TCE OPPT assessment).

42 The draft risk assessment did not provide information about

how the PBPK modeling was used to develop the non‐cancer

hazard values (i.e., HECs).

EPA/OPPT added new language in the risk assessment ex

modeling approach and HEC derivation. The information 

sections 2.6.1.2.2 and 2.6.1.4. A comprehensive discussio

model can be found in the TCE IRIS assessment.

43 EPA/OPPT should use both inhalation and oral studies that

the TCE IRIS assessment evaluated when deriving the

inhalation RfC. The TCE IRIS assessment used

physiologically‐based pharmacokinetic (PBPK) modeling to

do route‐to‐route extrapolation.

The final TCE OPPT risk assessment used the oral and inh

TCE IRIS assessment evaluated in the non‐cancer dose‐re

EPA/OPPT relied on the point of departures (PODs) that t

identified for the most suitable studies for dose‐response 

were categorized by health effects domains (i.e., liver tox

neurotoxicity, immunotoxicity, reproductive toxicity, and 

toxicity). These studies are listed in Appendix L of the fin

assessment. The studies with the lowest hazard values (i

concentration or HECs) were used to estimate acute or c

for the specific TCE uses (see section 2.6.1.2.2 and Table 

OPPT assessment).

44 Some panelists and public commenters indicated that the

developmental toxicity studies cannot be used to derive

hazard values for single exposures. The developmental

toxicity studies reported adverse effects that resulted from

repeated exposures to TCE and thus they should not be

used to estimate acute risks.

In addition, there were also public and peer review

comments objecting to the use of the developmental

toxicity studies by Johnson et al. (2003, 2005) for estimatingacute or chronic non‐cancer risks due to methodological and

replicability issues.

EPA/OPPT used developmental toxicity data to evaluate t

acute exposures based on EPA’s long standing policy that 

within a critical window of development may induce dev

discussed in the EPA’s Guidelines for Developmental Tox

(http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=

acknowledges that this is a health‐protective policy that 

acute risks.

Developmental effects, including fetal cardiac defects, m

maternal exposure to TCE. Chick embryo and oral develo

including those reported by the Johnson et al. studies (se

below), have reported cardiac malformations after expos
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incidence of congenital cardiac malformation has been re

studies from the same laboratory group and has been sh

Moreover, studies with TCE metabolites have also induce

developmental oral toxicity studies.

A recent erratum (Johnson, 2014) and subsequent evalua

developmental toxicity data reaffirmed that the Johnson 

adequate to use in hazard identification and dose‐respon

(Appendix N). As explained in the TCE IRIS assessment, w

studies have limitations, there is insufficient reason to di

especially when the findings are analyzed in combination 

and mechanistic evidence.

A summary of the weight of e

TCE‐related fetal cardiac defects is provided in section 2.6

of the final TCE OPPT risk assessment. The comprehensiv

the developmental toxicity data, including fetal cardiac te

discussed in the TCE IRIS assessment and expanded in thi

(Appendix N).

Thus, EPA/OPPT has incorporated the Johnson et al. stud

assessment (see Tables

2‐18,

2‐31 to

2‐35; sections 2.7.2 

Citations:

Dawson, B., P. Johnson, S. Goldberg, and J. Ulreich. 1990

of Trichloroethylene and Dichloroethylene in

a Mammalia

American College of Cardiology, 16(5), 1304‐1309. (as cit

Dawson, B., P. Johnson, S. Goldberg, and J. Ulreich. 1993

of Halogenated Hydrocarbon‐Contaminated Drinking Wa

American College of Cardiology, 21(6), 1466‐1472. (as cit

Johnson, P., S. Goldberg, S. Mays, and B. Dawson. 2005. C

Trichloroethylene Contamination in Maternal Drinking W

Heart Development in the Rat. Environmental Health Per

cited in EPA, 2011e).

Johnson, P. D. 2014. Erratum: Erratum for Johnson Et Al. 

Perspect 113: A18 (2005)]. Environmental Health Perspec

10.1289/ehp.122‐A94.
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Johnson, P. D., S. J. Goldberg, M. Z. Mays, and B. V. Daws

Trichloroethylene Contamination in Maternal Drinking W

Heart Development in the Rat. Environmental Health Per

292. (as cited in EPA, 2011e).

45 PBPK‐derived HECs from developmental toxicity studies

should not be used in the OPPT’s risk assessment of TCE.

The TCE PBPK model does not model pregnancy or gestation

and as such the internal doses are based on dose‐metrics

that are not considering developmental effects in the fetus.

Typically the placenta is expected to lower exposure to the

fetus by 2 to 10‐fold. Since a key concern is developmental

toxicity, that should be considered. Comparison of

benchmarks derived from oral and inhalation routes can

provide useful insight.

The TCE PBPK model did not incorporate a pregnancy com

model to estimate the internal dose of TCE in the develo

maternal dose metric was used as surrogate for the fetal 

assumption has been noted in section 2.6.1.4 and Table 2

OPPT risk assessment. Also, the uncertainties related to 

metrics for the developing fetus have been discussed in s

TCE OPPT risk assessment.

46 EPA/OPPT inappropriately uses the Healy et al. (1982) study

for the acute inhalation exposures, as the Healy et al study

does not report dose‐response data.

The TCE IRIS assessment identified Healy et al. (1987) as 

developmental toxicity studies (see Appendix L of the fina

assessment). Among all of the developmental toxicity stu

L, EPA/OPPT selected the study reporting the lowest haza

which in this case was the Johnson et al. (2003) study and 

47 Peer reviewers noted that the Forand et al. (2012) study was

cited in the EPA’s presentation to the TCE peer review panel

as a supporting study for the association between TCE

exposure and fetal cardiac malformations in humans. Two

panelists requested to review the study. One of the

reviewers requested to do a review by an independent

scientist.

The Forand et al., (2012) is a small retrospective cohort s

among New York residents in a TCE contaminated area v

study provides evidence for an association between mate

and cardiac defects. The study observed an elevated ris

defects (adjusted rate ratios of 2.15; 95% confidence inte

conotruncal defects compared to no exposure (adjusted 

95% confidence internal: 1.58 ‐ 15.24).

EPA conducted an internal review of the Forand et al. stu

the study findings were consistent with other human epi

have observed cardiac malformations in children exposed 

EPA/OPPT incorporated a brief summary of the study and 

2.6.2.3.6 of the final TCE OPPT risk assessment. Section 2

summary of the human data supporting the effects in the 

prenatal exposure to TCE as well as a summary of the we

analysis supporting the association between TCE exposur
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teratogenesis. Appendix N contains the weight‐of‐eviden

cardiac malformations following TCE exposure.

Citation:Forand, SP; Lewis‐Michl, EL; Gomez, MI. (2012). Adverse 

maternal exposure to trichloroethylene and tetrachloroe

vapor intrusion in New York State. Environ Health Perspe

48 The selection of the HEC99 for the dose‐response

assessment is overly conservative. EPA/OPPT shouldexplore using another HEC at a different percentile. Several

panelists indicated that the document did not articulate why

the HEC99 was the best choice compared to other values at

different percentiles. The panelists also could not

understand the uncertainty around the chosen HEC and the

appropriateness of the lower bound 99th percentile across

the various dose‐response relationships considered.

EPA/OPPT used the HEC50, HEC95 or HEC99 estimates repo

assessment, which represent the 50th, 95th or 95th percen

uncertainty and variability distribution of human internal 

The HEC50 was interpreted as being the concentration of 

there is 50% likelihood that a randomly selected individu

dose less than or equal to the internal dose POD (idPOD) 

The HEC95 and HEC99 were interpreted as being the conce

for which there is 95% and 99% likelihood, respectively, 

selected individual will have an internal dose less than or 

derived from the rodent study.

The TCE IRIS assessment preferred the HEC99 for the non‐

analysis because the HEC99 was interpreted to be protect

individual. EPA/OPPT supported the interpretation of the 

the TCE IRIS assessment. Hence,HEC99‐based risk estimat

assessment over those estimated from the HEC50 and HEC

preference, the OPPT’s risk assessment also includes risk 

HEC50 and HEC95 values to provide a sense of the differen

median, the 95% and 99% confidence bound for the com

variability. Calculations of HEC50/95 and HEC50/99 ratios ge

fold difference for the various studies identified in Table 

was the study reporting kidney effects (NTP, 1998) that s

and HEC50/99 ratios (i.e., 5‐9‐fold) due to uncertainties in 

dose estimates. In contrast, HEC95 values were similar to 

HEC95/99 ratios showing a 1.3‐1.5 fold difference.

Section 2.6.1.4 describes the range of HEC percentiles use

assessment as well as the ratio comparison among the H

percentile values. Sections 2.7.2 and 2.7.3.2 present the 

cancer risk estimates, respectively, for the range of HEC p
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Citation:NTP (National Toxicology Program). 1988. Toxicology and 

of Trichloroethylene (CAS No. 79‐01‐6) in Four Strains of R

Marshall, Osborne‐Mendel‐‐Gavage Studies). U.S. Depart

Human Services, Public Health Service, National Institute

Triangle Park, NC. (as cited in EPA, 2011e).

49 HEC99 values are questionable since they are 2 to 10,000‐

fold lower than the corresponding POD value. When the

difference between the benchmark from an animal study

and the HEC99 is >100 it suggests that additional UFs are not

necessary. Moreover, differences of 1000‐fold or more call

into question the underlying assumptions that produced

these hypothetical differences. For example, when

endpoints are similar (neurotoxicity or reproductive toxicity)

for animals and humans, the ratio of POD to HEC are < 100‐

fold between species. So what underlying assumptions

make the ratio of BMDL to HEC99 > 10,000 for kidney

effects?

EPA/OPPT disagrees with the way the HEC99 values were 

animal POD values. The TCE PBPK model predicted huma

concentration (HEC) that would be expected to induce th

toxic effect as the experimental animal species concentra

dose metrics at the target tissue. On the other hand, the 

external air concentration of TCE obtained from the anim

beginning of a low‐dose extrapolation in the non‐cancer 

Thus, it is not appropriate to compare the animal POD wi

percentiles because the HECs are based on measures of i

extrapolated from rodent to humans, whereas the animathe external air concentration.

50 EPA/OPPT inappropriately used the HEC99 to support

excluding dermal exposures. Several panelists criticized that

the HEC “can provide a counterweight to not considering

dermal exposure.”

EPA/OPPT deleted this argument from the final risk asses

the PBPK model for TCE lacks a dermal compartment tha

dermal risk estimation via route‐to‐route extrapolation o

dermal and inhalation exposures.

51 Neurotoxic endpoints should be used when evaluating the

chronic risks at the workplace setting. The occupational

risks were assessed using renal, immune and reproductive

endpoints. Neurotoxicity was not included.

EPA/OPPT agrees with this comment. Inclusion of the ne

for chronic non‐cancer risk estimation is presented in sec

also considered other endpoints (i.e., developmental tox

immunotoxicity, reproductive toxicity, liver toxicity) whe

occupational non‐cancer risks of TCE exposures.

52 EPA/OPPT incorrectly described TCE as a “probable human

carcinogen”.

EPA/OPPT agrees with this comment. The U.S. EPA’s IRIS 

TCE as a human carcinogen by all routes. The correct cla

sections 1.3.4 and 2.6.1.2.1 of the final TCE OPPT risk ass

53 EPA/OPPT did not provide empirical data supporting the

assumption that minimal buildup of TCE would be expected

This assumption was supported by PBPK simulations pres

and 2‐25. In these simulations, the TCE PBPK model was 

at the 50th and 99th percentile for the cardiac malforma
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in humans exposed to TCE in an intermittent basis based on

product usage assumptions.

chronic (steady‐state) or intermittent (occupational) expo

different exposure durations (i.e., 1 day, 3 weeks, 9 mont

HEC at the 50th and 99th percentile did not show signific

compared to the HECs for the other exposure durations (

months) under continuous and intermitted exposures to 

from the PBPK simulations showed that the assumption (

buildup of TCE in the body between exposure events) is r

final TCE OPPT risk assessment. This explanation has bee

section 2.6.1.4 of the final risk assessment.

54 EPA/OPPT did not discuss the physiological TCE levels

associated with the acute exposures assessed in the

document.

The TCE PBPK model can be used to estimate the interna

(“physiological TCE levels) associated with the acute expo

within the scope of the OPPT risk assessment. The mode

internal doses when calculating the 24‐hr human equival

(HECs) for specific health effects domains. EPA/OPPT use

(HEC50, HEC95, or HEC99) for developmental effects to esti

comparing the HECs with the acute exposure concentrati

consumer exposure assessment (i.e., 24‐hr exposure leve

55 EPA/OPPT incorrectly adjusted the exposure duration and

frequency for the hazard values. This resulted in hazard

values that did not match the exposure of the persons for

whom the assessment was being conducted. Selection of

the appropriate time‐averaging period, relevant to each

endpoint selected from reliable studies is criticallyimportant for deciding what exposure (absorbed dose)

metric should be used for risk estimate derivation.

For example, the POD hazard values were adjusted in the

IRIS program to continuous exposure (i.e., 24‐hr HECs).

Thus, worker exposure estimates need to be adjusted from

8‐hr to 24‐hr estimates.

For chronic risks, the daily exposure should be put into an

annual (chronic) average exposure and compared to the

chronic hazard benchmark.

Also, neurotoxicity and developmental toxicity endpoints

may, or may not be appropriate for comparison to acute /

EPA/OPPT used 24‐hr exposure estimates to estimate acu

made time adjustments to the exposure estimates, when 

them with the 24‐hr HECs. For instance, the 8‐hr worker 

were adjusted to 24 hrs for acute exposures. Average da

(ADCs) or lifetime average daily concentrations (LADCs) w

used for the non‐cancer or cancer chronic risk calculation

that the consumer exposure estimates for TCE were not a

were expressed as 24‐hr time averaged indoor air concen

2.3.3 and 2.4.2 of the final TCE OPPT risk assessment pre

were used to adjust the worker estimates to 24‐hrs.

The final TCE OPPT risk assessment considered the body 

toxicity data, including the recent developmental neuroto

et al. 2012 and 2013), but only estimated acute risks for d

based on the cardiac defect findings reported by the John

comment #44). Acute risks for neurotoxic effects as repo

(1994) were dropped in the final assessment because the 

inhalation study did not involve an acute/short‐term exp

instance, Arito et al. (1994) exposed rats to TCE for 8 hrs/ 

for 6 weeks.
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peak potential inhalation exposure/dose estimates,

depending on the time to effect. Although developmental toxicity studies are of a repeat‐d

policy is that a single exposure within a critical window o

induce developmental effects. EPA/OPPT acknowledges 

protective policy that may overestimate the acute risks. 

further information about the selection of fetal cardiac d

endpoint for the acute risk estimates.

Citations:Arito, H., M. Takahashi, and T. Ishikawa. 1994. Effect of S

Exposure to Low‐Level Trichloroethylene on Heart Rate a

in Freely Moving Rats. Sangyo Igaku/Japanese Journal of 

(Japan), 36(1), 1‐8. (as cited in 2011 TCE IRIS assessment)

Blossom, S. J., S. Melnyk, C. A. Cooney, K. M. Gilbert, and 

Postnatal Exposure to Trichloroethylene Alters Glutathio

Methylation Potential, and Neurotrophin Expression in th

Hippocampus. Neurotoxicology, 33(6), 1518‐1527.

Blossom, S. J., C. A. Cooney, S. B. Melnyk, J. L. Rau, C. J. Sw

Wessinger. 2013. Metabolic Changes and DNA Hypometh

Are Associated with Behavioral Alterations in Mice Expos

Postnatally. Toxicology and Applied Pharmacology, 269(3

Johnson, P. D., S. J. Goldberg, M. Z. Mays, and B. V. Daws

Trichloroethylene Contamination in Maternal Drinking W

Heart Development in the Rat. Environmental Health Per

292. (as cited in 2011 TCE IRIS assessment).
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Risk CharacterizationCharge question 5‐1: Please comment on the strengths and weaknesses of the MOE approach used to estimate the chron

the workplace exposures; including non‐users.

Charge question 5‐2: Please comment on the strengths and weaknesses of the MOE approach used to estimate the acute 

including non‐users (e.g., children, women of childbearing age). Specifically, please comment on the decision to limit the an

exposures without residual concern between events (i.e., once/week for users of the clear protective coating spray, and tw

degreaser users).

Charge question 5‐3: Please comment on the use of a uniform benchmark MOE of 30 rather than a benchmark MOE equa

Uncertainty Factors for each study as identified in the 2011 US EPA IRIS assessment for TCE.

#

Summary of Peer Review and Public Comments for

Specific Issues Related to

Charge Questions 5‐1, 5‐2, and 5‐3

EPA/OPPT Response

56 Some peer reviewers and public commenters suggested

using the endpoint/study‐specific uncertainty factors (UFs)

reported in the TCE IRIS assessment as the benchmark MOE.

Some peer review and public comments noted that the UFs

associated with the PBPK‐derived HEC99 were not

appropriate. One reviewer said that the UFs associated with

the PBPK‐derived HEC99 must be revised for acute

exposures.

EPA/OPPT revised the benchmark MOEs to reflect the en

UFs identified in the IRIS assessment for the PBPK‐derive

associated with specific non‐cancer effects domains. Tab

endpoint/study‐specific UFs by study/effects domain tha

benchmark MOEs for the acute and chronic non‐cancer r

57 EPA/OPPT provided an inadequate explanation for not

using the RfC values and hazard quotients (HQ)

calculations in the EPA/OPPT draft risk assessment for

TCE.

EPA/OPPT used margin of exposures (MOEs) to presen

estimates for different adverse endpoints identified to 

different exposure scenarios. For this reason, MOEs w

single HQ risk estimate based on the inhalation RfC. T

applicable for chronic exposures, although can be used 

exposure under certain circumstances. This issue was 

2.6.1.2.2 of the TCE OPPT risk assessment.

58 EPA/OPPT used a risk metric (i.e., MOEs) that did not

account for differences that occur in susceptibility between

humans and animals nor within animals or humans.

The differences between human and animals or within an

captured in the UFs that were used as the benchmark MO

study/endpoint, a variety of UFs were used (Section 2.7.1

 Interspecies UF

 Intraspecies UF
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 Subchronic to chronic UF LOAEL to NOAEL UF;

59 Peer review and public comments criticized the cancer risk

level of 1 x 10‐5 that the assessment used to interpret the

cancer risks and suggested to use 1 x 10‐4.

EPA/OPPT reported the occupational cancer risks for thre

different scenarios and uses: 1 x 10‐4, 1 x 10‐5, and 1 x 10

and Figures 2‐6 and 2‐7).

60 The MOE approach does not quantitatively characterize the

uncertainty in the estimated risk. The fact that the MOE is

reduced to the use of two numbers, the hazard value and

the exposure value, regardless of how they were obtained,

does not provide a quantitative assessment of how much

we can rely on that estimated risk. This issue could be

addressed, by incorporating in the MOE a metric to

characterize the uncertainty in the hazard value and/or the

exposure value, for instance calculating the MOE with

different possible values of both, the hazard and the

exposure, under different scenarios to understand the

impact in the obtained MOE. An empirical variance of the

MOE would explain how variable the MOE would be, and

sensitivity analysis would explain how sensitive the MOE is

to how the exposure and the hazard are obtained under

different scenarios of interest. Comparing the MOE to just a

benchmark number, 30 in this case, is questionable, in

particular when there is no assessment of the variability and

uncertainty in the MOE.

The comment is implying that EPA/OPPT should conduct 

assessment. EPA/OPPT focused on feasible refinements 

hazard/dose‐response assessment based on the available 

Thus, a probabilistic risk assessment was not developed.

The final risk assessment estimates non‐cancer risks for v

endpoints based on the PBPK‐derived hazard values (HEC

These HECs captured the 50th, 95th or 95th percentile of th

uncertainty and variability distribution of human internal 

See comment #48

Charge question 5‐4: Please comment on whether the document has adequately described the uncertainties and data l

methodology used to assess risks to allow the EPA to reduce risks to human health from TCE. Please comment on wheth

presented in a transparent manner.

# Summary of Peer Review and Public Comments for Specific Issues Related to Charge Question 5‐4 EPA/OPPT Response

61 How can one have confidence in EPA’s estimates for

occupational exposures? EPA did not reference monitoring

data to validate its exposure estimates resulting from the

use of TCE in commercial degreasing processes.

In collaboration with OSHA, relevant monitoring data spe

identified. EPA/OPPT incorporated this additional inform

of the final risk assessment.

62 EPA/OPPT has not adequately described data limitations

and uncertainties associated to the exposure, hazard/dose

response, and risk characterization assessments. In

EPA/OPPT has expanded upon and further refined the Un

Limitations section. See section 2.8 of the final TCE OPPT 
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addition, variability and uncertainty were treated the

same in some of the discussion in the Uncertainty

section.
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Other Public Comments

# Summary of Other Public Comments EPA/OPPT Response

63 Public commenters indicated that EPA is adequately

regulating TCE under the Clean Air Act (CAA). Does that

pertain to the exposure scenarios described in the

assessment?

Appendix B of the final risk assessment provides a sum

regulatory history of TCE in the U.S. EPA, including reg

The National Emission Standards for Hazardous Air Pol

an example of such regulation under CAA. OPPT’s risk 

NESHAP emission limits into account and characterized 

for specific TCE uses covered under the Toxic Substanc

64 It was stated that the assessment was based on exposure

data that predated regulations on vapor degreasing. Is

this true? If so, how would more recent values affect the

risk assessment?

EPA/OPPT’s exposure assessment for vapor degreasing 

data from the 2008 National Emissions Inventory (NEI) 

Release Inventory (TRI). Further, EPA/OPPT updated it

take NESHAP emission limits into account.

65 Some public comments criticized EPA/OPPT for using

modeled rather than measured exposure data.

EPA/OPPT acknowledges that it is not always possible 

data for the purposes of risk assessment and that valid

be used for the purposes of estimating potential expos