DOCUMENT-DO NOT CITE OR QUOTE 

Page 1

H

H Cl

Cl

United States Office of Chemical 

Environmental Protection Safety and Pollution 

Agency Prevention

TSCA Workplan Chemical Risk Assessment for 

Methylene Chloride:

Paint Stripping Use

CASRN: 75-09-2

December 2012

NOTICE

This document is an External Review Draft. This information is distributed solely for the 

purpose of pre-dissemination peer review under applicable information quality guidelines. It 

has not been formally disseminated by EPA. It does not represent and should not be construed 

to represent any Agency determination or policy. It is being circulated for review of its 

technical accuracy and science policy implications.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 2

Table of Contents

TABLE OF CONTENTS......................................................................................................................2

LIST OF TABLES ..................................................................................................................................4

LIST OF FIGURES.................................................................................................................................6

AUTHORS / CONTRIBUTORS / REVIEWERS ..................................................................................8

GLOSSARY OF TERMS AND ABBREVIATIONS .......................................................................................9

EXECUTIVE SUMMARY .....................................................................................................................12

CHAPTER 1: BACKGROUND AND SCOPE ...........................................................................................15

INTRODUCTION.............................................................................................................................................................15

SCOPE OF THE ASSESSMENT ............................................................................................................................................16

CHAPTER 2: SOURCES AND ENVIRONMENTAL FATE..........................................................................18

INTRODUCTION........................................................................................................................................................18

2.1. PHYSICAL AND CHEMICAL PROPERTIES OF DCM ........................................................................................................18

2.2. PRODUCTION AND USES ......................................................................................................................................19

2.2.1. Market Trends....................................................................................................................................... 19

2.2.4. Consumer Uses...................................................................................................................................... 22

2.2.4. Paint Stripping Applications .................................................................................................................. 23

2.3. ENVIRONMENTAL FATE............................................................................................................................................24

2.4. CONCLUSIONS OF ENVIRONMENTAL FATE ...................................................................................................................25

CHAPTER 3: HUMAN HEALTH RISK ASSESSMENT ..............................................................................27

INTRODUCTION........................................................................................................................................................27

3.1. HUMAN EXPOSURE ASSESSMENT ..............................................................................................................................27

3.1.1. Occupational Exposures........................................................................................................................ 27

3.1.2. Residential/Consumer Exposures.......................................................................................................... 33

3.1.3. Consumer Exposure Modeling .............................................................................................................. 33

3.1.4. Inhalation Exposure Assessment........................................................................................................... 35

3.1.5. Exposure Scenarios and Model Inputs .................................................................................................. 40

3.1.6. Summary of Model Outputs and Exposure Calculations. ...................................................................... 44

3.2. HUMAN HEALTH ASSESSMENT: HAZARD IDENTIFICATION AND DOSE-RESPONSE ................................................................46

3.2.1. Toxicokinetics and Biomonitoring ......................................................................................................... 46

3.2.2. Acute Hazard......................................................................................................................................... 47

3.2.3. Chronic Hazard...................................................................................................................................... 48

3.3. HUMAN HEALTH ASSESSMENT: DOSE-RESPONSE.........................................................................................................49

3.4. HUMAN HEALTH RISK CHARACTERIZATION................................................................................................................54

3.4.1. Risk Estimation Approach for Acute and Repeated Exposures.............................................................. 54

3.4.2. Risk Estimation Approach for Acute Exposures..................................................................................... 54

3.4.3. Risk Estimation Approach for Repeated Exposures............................................................................... 56

3.4.4. Risk Estimates for Non-Cancer Acute Inhalation Exposures in a Residential Setting ............................ 57

3.4.5. Occupational Risk Estimates for Chronic Inhalation.............................................................................. 64

3.5. DISCUSSION OF KEY SOURCES OF UNCERTAINTY AND DATA LIMITATIONS ..........................................................................65

3.5.1. Key Uncertainties and Data Limitations for Occupational Exposure Estimates..................................... 65

3.5.2. Key Uncertainties and Data Limitations for Consumer Exposure Estimates ......................................... 66

3.5.3. Uncertainties in the Hazard and Risk Assessment................................................................................. 67

3.5.4. Conclusions of Uncertainties and Limitations....................................................................................... 69

3.6. RISK CHARACTERIZATION CONCLUSIONS .....................................................................................................................69

REFERENCES ....................................................................................................................................71
DOCUMENT-DO NOT CITE OR QUOTE 

Page 3

APPENDICES ....................................................................................................................................87

APPENDIX A: SUMMARY OF ENVIRONMENTAL EFFECTS-AQUATIC TOXICITY .....................................88

APPENDIX B: INVENTORY UPDATE REPORTING RULE DATA FOR DCM...............................................90

APPENDIX C: HOUSEHOLD PRODUCTS DATA FOR DCM.....................................................................91

APPENDIX D: PAINT STRIPPING PROCESSES AND ASSOCIATED WORKER ACTIVITIES, AND FACILITY AND 

POPULATION DATA AND INFORMATION...........................................................................................93

APPENDIX E: OCCUPATIONAL EXPOSURE LITERATURE DATA ...........................................................103

APPENDIX F: RESIDENTIAL/CONSUMER EXPOSURE ASSESSMENT ...................................................120

F-1. Estimation of Emission Profiles for Paint Removers/Strippers.................................................................120

F-2. Sensitivity Analysis for Inhalation Scenarios............................................................................................125

F-3. Inhalation Exposure Scenario Inputs........................................................................................................126

F.4. Inhalation Model Outputs and Exposure Calculations.............................................................................132

F.5. MCCEM Inhalation Modeling Scenario Summaries..................................................................................139

APPENDIX G: HUMAN HEALTH TOXICITY SUMMARY ......................................................................160

APPENDIX H: HUMAN HEALTH DOSE-RESPONSE ASSESSMENT .......................................................163
DOCUMENT-DO NOT CITE OR QUOTE 

Page 4

List of Tables

Table 1-1. Primary Uses of DCM and Selection Criteria.............................................................................17

Table 2-1. Physical-Chemical Properties of DCM.a

.....................................................................................18

Table 2-2. DCM Market Trends by Use. .....................................................................................................20

Table 2-3. Major and Minor Uses of DCM. ................................................................................................21

Table 2-4. Major Uses of DCM in 2007 in the US.......................................................................................22

Table 2-5. Consumer Uses of DCM. ...........................................................................................................22

Table 2-6. Environmental Fate Characteristics of DCM, Dichloromethane.1

.............................................26

Table 3-1. Regulatory and Recommended Exposure Limits. .....................................................................28

Table 3-2. 2007 NAICS Codes Identified that Include Paint Stripping Activities........................................28

Table 3-3. Summary of Ranges of DCM Exposure Concentrations and Calculated ADCs and LADCs for 

Workers..................................................................................................................................30

Table 3-4. Summary of Number of Workers Exposed or Monitored and Total Number of Employees in 

the Monitored Facility Cited in the References Used for Each Industry................................31

Table 3-5. Consumer Exposure Scenarios for the DCM Inhalation Exposure Assessment........................40

Table 3-6. Summary of DCM Consumer Paint Stripping Scenario Descriptions and Parameters..............42

Table 3-7. Summary of Modeled DCM Concentrations to Which Consumer Users and Non-Users are 

Exposed, by Scenario. ............................................................................................................45

Table 3-8. Worker Inhalation Health Effect Reference Values Used in the Risk Assessment.a .................51

Table 3-9. Toxicological Endpoints and Approaches for Assessing Risks to DCM-Based Paint Strippers..56

Table 3-10. MOEs for CNS Effects following Acute Exposure Scenarios for Consumer/Residential Users 

and Non-Users of DCM-Based Paint Strippers.......................................................................57

Table 3-11. Acute HQs for Residential Users and Non-Users of DCM-based Paint Strippers....................59

Table 3-12. Occupational Risks for Repeated Exposures to DCM from Paint Stripping Activities.............64

Table B-1. Manufacturing and Importing Company and Site Information for DCM..................................90

Table C-1. Household Products Containing DCM from NIH’s Household Products Database...................91

Table D-1. 2007 US Economic Census Data for Painting and Wall Covering and Flooring Contractors. ...98
DOCUMENT-DO NOT CITE OR QUOTE 

Page 5

Table D-2. 2007 US Economic Census Data for Automotive Body, Paint, and Interior Repair and 

Maintenance. .........................................................................................................................98

Table D-3. 2007 US Economic Census Data for Reupholstery and Furniture Repair.................................99

Table D-4. Estimated Annual DCM Based Stripper Usage in California. ..................................................100

Table D-5. 2007 US Economic Census Data for Industry Sectors that May Engage in Art Restoration and 

Conservation Activities.........................................................................................................100

Table D-6. 2007 US Economic Census Data for Aircraft Manufacturing..................................................101

Table D-7. 2007 US Economic Census Data for Ship Building and Repairing...........................................102

Table E-1. Summary by Industry and Job Category of OSHA IMIS Data for DCM from 1992 to 2012.....106

Table E-2. Summary of Personal and Area Concentrations in a Furniture Refinishing Shop that Uses a 

Pump and Brush Stripping Technique Measured Before Engineering Controls were Added.

..............................................................................................................................................113

Table E-3. Summary of Personal and Area Concentrations in a Furniture Refinishing Shop that Uses a 

Pump and Brush Stripping Technique Measured After Engineering Controls were Added to 

the Stripping Booth..............................................................................................................114

Table E-4. Summary of Personal and Area Concentrations in a Furniture Refinishing Shop that Uses a 

Pump and Brush Stripping Technique Measured After Engineering Controls were Added to 

the Stripping Booth and Wash Booth. .................................................................................115

Table F-1. US EPA (1994b) Study: Products Emissions Fit to Exponential Profile....................................120

Table F-2. Fitted Parameters to the US EPA (1994b) Study Results for the Two DCM-Containing Paint 

Strippers...............................................................................................................................123

Table F-3. Time Schedule for Brush-on Application to Chest Surface: Four Segments with Repeat 

Application. ..........................................................................................................................128

Table F-4. DCM Mass Released, by Application Target and Method.......................................................129
DOCUMENT-DO NOT CITE OR QUOTE 

Page 6

List of Figures 

Figure 2-1. Chemical Structure of Methylene Chloride. ............................................................................18

Figure 3-1. Time-varying User Personal Concentration and Maximum TWA Values for Selected Averaging 

Times......................................................................................................................................37

Figure 3-2. Time-varying Non-user Personal Concentration and Maximum TWA Values for Selected 

Averaging Times.....................................................................................................................37

Figure 3-3. Model Sensitivity Results (Percent Change from Base-case Response) for Peak One-hr TWA 

for User and Non-user............................................................................................................39

Figure 3-4. Model Sensitivity Results (Percent Change from Base-case Response) for 24-hr TWA for User 

and Non-user..........................................................................................................................39

Figure 3-5. Comparison of Acute Toxicity Values and User Exposures during Brush Application in a 

Residential Workshop. ...........................................................................................................60

Figure 3-6. Comparison of Acute Toxicity Values and User Exposures during Spray Application in a 

Residential Workshop. ...........................................................................................................62

Figure 3-7. Comparison of Acute Toxicity Values and Zone-Specific DCM Concentrations for Brush 

Application in Residential Workshop or Bathroom. ..............................................................62

Figure 3-8. Comparison of Acute Toxicity Values and Zone-Specific DCM Concentrations for Spray 

Application in Residential Workshop.....................................................................................63

Figure D-1. Typical Flow Tray for Applying Stripper to Furniture. .............................................................95

Figure D-1. Typical Water Wash Booth Used to Wash Stripper and Coating Residue from Furniture......96

Figure D-2. Example Diagram of a Dipping Tank for Furniture Stripping...................................................96

Figure F-1. Model Fit to MRI (US EPA, 1994b) Data for BIX Spray-On (Spray Application)......................122

Figure F-2. Model Fit to MRI (US EPA, 1994b) Data for Strypeeze (Brush Application). .........................123

Figure F-3. Theoretical Cumulative Mass of DCM Released for BIX Spray-On Stripper...........................124

Figure F-4. Theoretical Cumulative Mass of DCM Released for Strypeeze Stripper................................124

Figure F-5. Zone Volumes and Airflow Rates for Workshop Scenarios. ..................................................130

Figure F-6. Zone Volumes and Airflow Rates for Bathroom Scenario. ....................................................131

Figure F-7. Example of the Personal Concentration Calculation as Defined in Equation F-9. .................133
DOCUMENT-DO NOT CITE OR QUOTE 

Page 7

Figure F-8. Modeled DCM Concentrations for Scenarios 1 and 4, Stripper Application in Workshop using 

Central Parameter Values. ...................................................................................................135

Figure F-9. Modeled DCM Concentrations for Scenarios 2 and 5, Stripper Application in Workshop using 

Parameter Values selected for Upper-end User’s Exposure................................................136

Figure F-10. Modeled DCM Concentrations for Scenarios 3 and 6, Stripper Application in Workshop 

using Parameter Values Selected for Upper-End-user’s and Non-user’s Exposure.............137

Figure F-11. Modeled DCM Concentrations for Scenario 7, Brush Application in Bathroom (Simulation).

..............................................................................................................................................138

Figure H-1. Illustration of the Different AEGL Threshold Levels. .............................................................164
DOCUMENT-DO NOT CITE OR QUOTE 

Page 8

Authors / Contributors / Reviewers

The report was developed by the Office of Pollution Prevention and Toxics (OPPT), Office of 

Chemical Safety and Pollution Prevention (OCSPP). The 2012 workplan risk assessments were 

prepared based on existing data and any additional information received up to June 15, 2012.

Assessment Team

Lead: Scott Prothero, OPPT/EETD

Team: Kent Anapolle, OPPT/EETD

Judith Brown, OPPT/EETD

Iris Camacho, OPPT/RAD

Mary Dominiak, OPPT/CCD (retired)

Conrad Flessner, OPPT/EETD

Amuel Kennedy, OPPT/RAD

Doyoung Lee, OPPT/EETD

Andy Mamantov, OPPT/EETD

Justin Roberts, OPPT/EETD

Portions of this document were developed with support from:

Contractor name (contract number) Task

Abt Associates (EP-W-08-010) Production and Uses

Eastern Research Group (EP-W-10-014) Releases

Versar (EP-W-10-005) Fate, Modeling, Monitoring

SRC, Inc. (EP-W-09-027) Technical Editing

Internal Peer Reviewers

H. Kay Austin, OPPT/EETD

Stan Barone Jr., OPPT/RAD

Todd Stedeford, OPPT/RAD

External Peer Review - A peer review panel is being arranged for this influential workplan 

assessment product based upon need and following Agency peer review guidance. The format 

will be a teleconference of an ad hoc panel meeting consisting of independent experts.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 9

Glossary of Terms and Abbreviations

μg Microgram(s)

μg/m3 Microgram(s) per cubic meter

°C Degrees Celsius

°F Degrees Fahrenheit

ACGIH American Conference of Governmental Industrial Hygienists

ACH Air changes per hour

ADC Average daily concentration

AEGL Acute Exposure Guideline Level

AEGL-1 Discomfort threshold

AEGL-2 Disability threshold

AEGL-3 Death threshold

atm atmosphere(s)

ATSDR Agency for Toxic Substances and Disease Registry

BAF Bioaccumulation Factor

BCF Bioconcentration Factor

BMD Benchmark dose

BMDL10 Lower 95 percent confidence limit of the 10 percent BMD

BMDS Benchmark Dose Software

BMR Benchmark response

BW Body weight

Cal EPA California Environmental Protection Agency

CASRN Chemical Abstracts Service Registry Number

CBI Confidential business information

CDC Centers for Disease Control and Prevention

CHO Chinese hamster ovary 

CNS Central nervous system

CO Carbon monoxide

CO2 Carbon dioxide

COHb Carboxyhemoglobin

CPSC Consumer Product Safety Commission

CYP2E1 Cytochrome P450, family 2, subfamily E, polypeptide 1

DCM Dichloromethane

DEM Department of Environmental Management

DIY Do-it-yourself

DNA Deoxyribonucleic acid

DNA SSB Single stranded DNA-binding protein

DOSH Division of Occupation Safety and Health

EC European Commission

ECG Electrocardiogram

EFH Exposure Factors Handbook

EPA Environmental Protection Agency

EU European Union
DOCUMENT-DO NOT CITE OR QUOTE 

Page 10

FACE Fatality Assessment and Control Evaluation

ft Foot/feet

ft2 Square feet

FTIR Fourier transform infrared

g Gram(s)

g/cm2 Gram(s) per square centimeter

g/cm3 Grams(s) per cubic centimeter

g/ft2, g/sq ft Grams(s) per square foot

g/L Gram(s) per liter

g/minute Grams(s) per minute

g/mol Gram(s) per mole

GST Glutathione S-transferase

GWP Global warming potential

HEC Human equivalent concentration

HFC-32 Hydrofluorocarbon-32

HQ Hazard quotient

hr Hour

HVAC Heating, ventilation, and air conditioning

Koc Soil Organic Carbon Partition Coefficient

IDLH Immediately Dangerous to Life and Health

IMIS Integrated Management Information Systems

IPCC Intergovernmental Panel on Climate Change

IRIS Integrated Risk Information System

IRTA Institute for Research and Technical Assistance

IUR Inhalation Unit Risk 

IURR Inventory Update Reporting Rule

L Liter(s)

Lb(s) Pound(s)

LADC Lifetime average daily concentration

LC50 Median lethal concentration

LOAEC Lowest-observed-adverse-effect concentration

LOAEL Lowest-observed- adverse-effect level

LOEC Lowest-observed-effect concentration

MATC Maximum acceptable toxicant concentration

MCCEM Multi-Chamber Concentration and Exposure Model

mg Milligram(s)

mg/L Milligram(s) per liter

mg/m3 Milligram(s) per cubic meter

min Minute(s)

mM Milli-Molar

MMWR Morbidity and Mortality Weekly Report

MOE Margin of exposure

MRI Midwest Research Institute

MSDS Material Safety Data Sheet
DOCUMENT-DO NOT CITE OR QUOTE 

Page 11

MSU Michigan State University

NAICS North American Industry Classification System

NAS National Academy of Sciences

NESHAP National Emission Standards for Hazardous Air Pollutants

NHANES National Health and Nutrition Examination Survey

NIH National Institutes of Health

NIOSH National Institute for Occupational Safety and Health

NMP N-Methylpyrrolidone

NOAEL No-observed-adverse-effect level

NRC National Research Council

NTP National Toxicology Program

OCSPP Office of Chemical Safety and Pollution Prevention

OECD Organization for Economic Cooperation and Development

OEHHA Office of Environmental Health Hazard Assessment

OEM Original Equipment Manufacturing

OPPT Office of Pollution Prevention and Toxics

OSHA Occupational Safety and Health Administration

PBPK Physiologically Based Pharmacokinetic

PEL Permissible Exposure Limit

POD Point of departure

ppm Parts per million

REL Reference Exposure Level

RfC Reference concentration

RIA Regulatory Impact Analysis

ROH Rest of the house

SIC Standard Industry Classification

SMAC Spacecraft maximum allowable concentration

SNAP Significant New Alternatives Policy

STEL Short-Term Exposure Limit

TLV Threshold Limit Value

TRI Toxics Release Inventory

TSCA Toxic Substances Control Act

TWA Time-weighted average

UF Uncertainty factor

UFA Interspecies uncertainty factor

UFD Database deficiency uncertainty factor

UFH Intraspecies uncertainty factor

UFL LOAEL-to-NOAEL uncertainty factor

UFtotal Total uncertainty factor

UK United Kingdom

US United States

VOC Volatile organic compound

wt Weight
DOCUMENT-DO NOT CITE OR QUOTE 

Page 12

Executive Summary

Methylene chloride (dichloromethane, DCM) was assessed as part of the United States (US) 

Environmental Protection Agency’s (EPA) Existing Chemicals Management Program. EPA 

reviewed readily available information on DCM including uses, physical-chemistry, fate, 

exposures, and associated hazards to humans and the environment. 

DCM was identified because it ranked high for hazard (i.e., a probable human carcinogen) and 

high for exposure potential because it is widely used in consumer products. It has been 

detected in drinking water, indoor environments, ambient air, groundwater and soil, and 

because of these reported releases to the environment, and it was ranked high. 

DCM is volatile and does not significantly partition to solid phases. Therefore, releases of DCM 

to the environment are likely to evaporate to the atmosphere, or if released to soil, migrate to 

groundwater. DCM has been shown to biodegrade over a range of rates and environmental 

conditions and in the environment, it is moderately persistence. Measured bioconcentration 

factors for DCM suggest its bioconcentration potential is low. This assessment did not evaluate 

risks to the environment because DCM possesses moderate persistence, low bioaccumulation 

potential, and low hazard to aquatic organisms.

DCM is a quick acting and inexpensive solvent with a wide range of industrial, commercial, and 

consumer use applications such as adhesives, paint stripping, pharmaceuticals, metal cleaning, 

chemical processing, and aerosols. However, it is mainly used as a solvent, and is the primary 

ingredient in many paint stripping products. 

US demand for DCM in 2006 was estimated at 185 million pounds (lbs) with a projected 

demand of 181 million lbs for 2010. The 2006 Inventory Update Reporting Rule (IURR) indicates 

that 100 million to 500 million lbs of the chemical is produced or imported (estimated 20 

million lbs) into the US. There are only three DCM production facilities in operation in the US.

EPA assumed that direct contact or close proximity to the use (i.e., for a consumer or 

commercial application with substantial frequency or duration of exposure) would likely 

provide the highest exposures to DCM paint strippers. In either occupational or consumer 

settings, there may be significant inhalation exposure during the use of these products. In 

addition to product users, there also may be non-users or bystanders who may not come in 

direct contact with the product, but may be exposed indirectly while in a nearby area during 

product application. 

Using this rationale, EPA’s assessment focused on estimating risk(s) due to consumer and 

occupational use of paint strippers containing DCM. In the residential/ consumer scenarios 

indirect exposures to children, who could be in the vicinity of the paint strippers with 

inadequate ventilation, were also assessed. Due to DCM’s high volatility, the assessment 

covered exposure scenarios via inhalation and did not address dermal exposures because this 

route of exposure is not expected to be as significant as compared to inhalation. 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 13

For worker exposures, this assessment relied upon published exposure concentration data. 

Exposure data were found for paint stripping applications in six industry segments. While data 

were found to estimate worker exposures, EPA did not consider the available data robust 

enough to develop statistical distributions of exposure for workers. Therefore, each of the 

exposure estimates is a snapshot of the particular uses that are cited. 

EPA focused this assessment on exposures to workers employed by “small commercial shops.” 

For this assessment, EPA considered a small shop as one that employs less than 10 workers (i.e., 

the remaining facilities were considered large facilities or unassigned and were not considered 

in this assessment).

Published monitoring data for non-occupational inhalation exposures (i.e., consumer do-ityourself [DIY]) were limited to that from several experiments conducted in the US and Europe. 

No published exposure information was found for exposures to other household members (i.e., 

non-users). Of the available studies, only one US study provided sufficient information to 

estimate consumer DCM inhalation exposures. EPA used its Multi-Chamber Concentration and 

Exposure Model (MCCEM), to estimate DCM concentrations (e.g., in the room of use and the 

rest of the house; ROH), as well as to calculate potential user and non-user exposure 

concentrations.

Cancer risks were calculated for chronic worker exposure scenarios only. Cancer incidence risks 

were calculated by multiplying the chronic exposure estimates by the EPA cancer inhalation 

unit risk (IUR) value. Margins of exposure (MOE) indicate that there are occupational noncancer risks of concern associated with exposures to DCM-based paint strippers in the 

industries EPA assessed: professional contractors, aircraft paint stripping, workplace settings 

doing immersion stripping of wood, and wood and metal paint stripping. The data showed that 

the Occupational Safety and Health Administration (OSHA) Permissible Exposure Limit (PEL) and 

Short-Term Exposure Limit (STEL) were exceeded under some circumstances. The 

representativeness of the available exposure data to the broader worker populations that are 

exposed to DCM during its use in various paint stripping applications cannot be determined due 

to data and information limitations and uncertainties.

EPA’s assessment also found a potential risk of concern to people in residential environments 

where DCM vapors are released during brush-on or spray-on applications of DCM-based paint 

strippers. These findings are based on workplace air monitoring data and a modeling-based 

approach employed to estimate acute inhalation exposures to residential users and non-users.

The inhalation exposure assessment is composed of modeled exposure scenarios for which the 

inputs are based on experimental data, survey information, and a number of assumptions with 

varying degrees of uncertainty. The results are characterized as either plausible estimates of 

individual exposure, i.e., central tendency, or possibly greater than the distribution of actual 

exposures, i.e., bounding. The extent of the identified uncertainties for estimating occupational 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 14

or residential exposures is not known and could result in either larger or smaller exposure 

estimates under real world conditions. 

There is general confidence in the characterization of the hazard database for acute and chronic 

effects used for the points of departure. However there is residual uncertainty in domains of 

the hazard characterization for some outcomes. These uncertainties are drawn from concern 

for potential developmental neurotoxicity and immunological effects which are supported by 

the modes of action affecting the nervous system resulting in CNS depression and COHb

buildup and indications from acute inhalation study, specifically immunosuppressive effects 

that may be relevant for infectious diseases spread through inhalation.

In conclusion, the following consumer and worker exposure scenarios resulted in exposures 

that were of potential concern for non-cancer risks for DCM paint stripping uses: 

 Acute potential risks of concerns (i.e., neurotoxicity, generally an order of magnitude 

below acceptable margins of exposure) for consumers and bystanders for most 

scenarios.

 Chronic potential risks of concern (i.e., liver toxicity, below acceptable margin of 

exposure) and cancer (i.e., liver and lung, 1 x 10-3 to 1 x 10-6 with most above 1 x 10-4) 

potential risks of concerns for workers in almost all uses identified.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 15

Chapter 1: Background and Scope

INTRODUCTION

Methylene chloride (i.e., dichloromethane; DCM), was identified for assessment as part of the 

United States (US) Environmental Protection Agency’s (EPA) Existing Chemicals Management 

Program. EPA reviewed readily available information on DCM including: uses, physicalchemistry, fate, exposure potential, and associated hazards to humans and the environment. 

DCM is a volatile, colorless liquid with a chloroform-like, sweet odor (OSHA, 2010). It has a low 

boiling point and is moderately water soluble. DCM is used as a substitution for other solvents 

because it is non-flammable and non-explosive. Because DCM is volatile, it does not 

significantly partition to solid phases. Therefore, releases of DCM to the environment are likely 

to evaporate to the atmosphere, or if released to soil, migrate to groundwater. This substance 

has been shown to biodegrade over a range of rates and environmental conditions and is 

considered to be moderately persistence in the environment. Measured bioconcentration 

factors for DCM suggest its bioconcentration potential is low. 

DCM has been the subject of regulations by such organizations as the EPA, the Occupational 

Safety and Health Administration (OSHA), the Consumer Product Safety Commission (CPSC), 

and the European Commission (EC). This chemical is listed as a toxic (i.e., non-acute) hazardous 

waste under the Resource Conservation and Recovery Act (RCRA) (Code U080) and is listed on 

the Toxics Release Inventory (TRI) pursuant to section 313 of the Emergency Planning and 

Community Right-to-Know Act (EPCRA). CPSC issued a statement of policy (CPSC, 1987) 

regarding its decision to require labeling of consumer products that contain DCM. Labels 

indicated that inhalation of DCM vapor has caused cancer in certain laboratory animals, and the 

labels specified precautions to be taken during use by consumers. In 1997, OSHA lowered its 

permissible exposure limit (PEL) for DCM from 500 parts per million (ppm) to 25 ppm (OSHA, 

1997). EPA’s Office of Air Quality Planning and Standards issued a final rule in January 2008, 

under the National Emission Standards for Hazardous Air Pollutants (NESHAP; US EPA, 2008), 

that established national emission standards for using DCM to remove dried paint (i.e., 

including, but not limited to: paint, enamel, varnish, shellac, and lacquer) from wood, metal, 

plastic, and other substrates. The NESHAP also implemented management practices that 

minimize DCM emissions. In addition, the European Commission (EC) amended its Registration, 

Evaluation, Authorization, and Restriction of Chemical substances to incorporate restrictions for 

use of DCM in paint strippers (EC, 2010). The chemical is banned from: (1) placement on the 

market in a new product for consumers/professionals by December 2010, (2) placement on the 

market in any product for consumers/professionals by December 2011, and (3) use by 

professionals by June 2012, unless the professionals are appropriately trained and licensed.

DCM was identified because it ranked high for hazard (i.e., a probable human carcinogen and 

acute non-cancer hazard), and it ranked high for exposure potential because it is widely used in 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 16

consumer products. DCM has been detected in drinking water, indoor environments, ambient 

air, groundwater and soil, and reported releases to the environment are high (US EPA, 2012c).

SCOPE OF THE ASSESSMENT

This assessment focused on the use of DCM-based paint strippers. EPA assumed that direct 

contact or close proximity to the use (i.e., for a consumer or commercial application with 

substantial frequency or duration of exposure) would likely provide the highest exposures to 

NMP paint strippers. In either occupational or consumer settings, there may be significant 

inhalation exposure during the use of these products. In addition to product users, there also 

may be non-users or bystanders who may not come in direct contact with the product, but may 

be exposed indirectly while in a nearby area during product application. 

EPA’s assessment focused on estimating the quantitative risk(s) due to occupational and 

residential use of paint strippers containing DCM. Occupational exposures include possible 

direct exposures to workers who may use these products at work, in training, or other 

situations. In the residential/consumer scenarios indirect exposures to individuals, who could 

be in the vicinity of the paint strippers with inadequate ventilation, also were assessed. These

types of exposure scenarios for small commercial shop workers and consumers (including 

“DIYs”) are addressed in this assessment.

EPA understands that exposures that result from large-scale industrial operations are generally 

monitored and well controlled. In small commercial or consumer settings, users may not 

adhere to the same types of controls. Thus, large-scale manufacturing exposure scenarios are 

not addressed in this risk assessment. EPA focused this assessment on exposures to workers 

employed by “small commercial shops.” For the purpose of this assessment, EPA considered a 

small shop as one that employs less than 10 workers (i.e., the remaining facilities were 

considered large facilities or were unassigned and were not considered in this assessment). 

Due to its high volatility, dermal exposure is of less concern to EPA than other routes of 

exposure. Its rapid evaporation suggests that the most likely route of exposure is via

inhalation; therefore, the risk assessment focused on inhalation exposures to commercial 

workers and consumers.

EPA focused the assessment on DCM use in paint stripping. Other uses beyond paint stripping 

were not covered in the risk assessment. Table 1-1 shows the primary uses of DCM and the 

rationale for their inclusion or exclusion for this risk assessment. Narrowing of the scope 

required exclusion of some uses based on comparative judgments on potential exposure (e.g.,

percent content relative to potential exposure) among the primary uses identified.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 17

Table 1-1. Primary Uses of DCM and Selection Criteria.

Use Category

Percent 

DCM 

Content

Population

Exposeda Considered in this Assessment?

Adhesives 60-100 Small commercial shop 

workers, consumers 

(including “DIYs”); 

industrial workers

No – Relatively narrower range of removal 

applications and likely lower exposure levels 

compared to paint stripping. Information 

indicates that many of the adhesive uses are in 

adhesive removers.

Paint stripping 25-100 Small commercial shop 

workers, consumers 

(including “DIYs”); 

industrial workers

Yes – Relatively high percent content range, 

broad range of stripping and removal applications 

(automotive, furniture, marine, wall paint, similar 

coating removal).

Pharmaceuticals N/Ab Industrial workers No – Industrial use settings which are generally 

believed to be better controlled and monitored.

Metal cleaning 15-40 Small commercial shop 

workers, consumers 

(including “DIYs”); 

industrial workers

No – Small market percentage (7 percent) and 

likely lower exposure levels compared to paint 

stripping.

Chemical 

processing

N/Ab Industrial workers No – Industrial use settings which are generally 

believed to be better controlled and monitored.

Aerosols 

(propellant use)

<25 Small commercial shop 

workers, consumers 

(including “DIYs”); 

industrial workers

No – Relatively low percent content range, small 

market percentage (5 percent), and likely lower 

exposure levels compared to paint stripping.

Polyurethane 

foam

N/Ab Industrial workers No – Industrial use settings which are generally 

believed to be better controlled and monitored.

a

For the purposes of this assessment, consumers are defined as non-commercial/non-industrial users of products 

containing DCM. Commercial workers are defined as persons employed in a commercial enterprise providing 

salable goods or services. Examples of a commercial enterprise include, but are not limited to, commercial and 

residential cleaning services, painting companies, carpet installers, commercial and residential repair and 

refurbishing companies, and automotive painting and repair shops.

a

For these industrial applications, the percent of DCM content is expected to be at or near 100 percent.

Ecological impacts of DCM also were considered, but were ruled out, during EPA’s problem 

formulation and scoping process. The aquatic toxicity of DCM for fish, aquatic invertebrates, 

and aquatic plants is low based on the Office of Pollution Prevention and Toxics (OPPT) criteria 

described in the TSCA Work Plan Chemicals Methods Document (US EPA, 2012b, 1992b) and the 

Classification Criteria for Environmental Toxicity and Fate of Industrial Chemicals (US EPA, 

1992b). Appendix A contains a summary of the aquatic toxicity studies considered in the 

evaluation of environmental hazards of DCM. Because of its low hazard observed in aquatic 

toxicity studies, EPA did not evaluate risks to the environment from DCM.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 18

Chapter 2: Sources and Environmental Fate

INTRODUCTION

To assess the environmental risks of dichloromethane (DCM), a firm understanding of the 

physical and chemical properties, sources related to production and uses, and fate in the 

environment is important. These topics are introduced in Chapter 2 and discussed in relation to 

the risk characterization in Chapter 3.

2.1. PHYSICAL AND CHEMICAL PROPERTIES OF DCM

The chemical structure for DCM is shown in Figure 2-1.

Figure 2-1. Chemical Structure of Methylene Chloride.

DCM is a volatile (vapor pressure = 351.8 Torr at 25 °C), colorless liquid with a chloroform-like, 

sweet odor (OSHA, 2010). DCM is low boiling (39.8 °C ) and moderately water soluble (13.7 g/L 

at 20 °C), but more dense than water (1.33 g/cm3 at 20 °C). DCM is used as a substitution for 

other solvents because it is non-flammable and non-explosive. DCM also is not readily 

oxidizable (CRC, 2001; IUCLID, 2000; Merck, 2001). Table 2-1 shows common physical-chemical 

properties for DCM. 

Table 2-1. Physical-Chemical Properties of DCM.

a

Molecular formula CH2Cl2

Molecular weight 84.93

Physical form Colorless liquid; sweet, pleasant odor resembling chloroform

Melting point -95 °C

Boiling point 39.7 °C

Vapor pressure 351.8 mmHg at 25 °C

Log KOW 5.3 ("slow stirring" method); 5.9 @ 25 °C (measured; OECD 117)

Water solubility 13.7 g/L at 20 °C

Density 1.33 g/cm3 at 20 °C

Flash point none

a IUCLID, 2000

H

H Cl

Cl
DOCUMENT-DO NOT CITE OR QUOTE 

Page 19

2.2. PRODUCTION AND USES

DCM is mainly used as a solvent, usually at concentrations ranging from 20 to 90 percent, and is 

the primary ingredient in many paint stripping products (Mannsville, 1999). It is a quick acting 

and inexpensive solvent with a wide range of industrial, commercial, and consumer uses, which 

include: solvent for vapor degreasing; paint/varnish removers; electronics; resin cleaners; 

adhesives; tablet coatings; process solvent for cellulose acetate; butyl rubber; cleaning solvent; 

plastics processing; blowing agent in polyurethane foams; propellant for paint aerosols; 

refrigerant; heat-transfer fluid; extraction solvent for industrial applications and food; color 

diluents for foods; and food packaging adhesives (Ash, 2009). It also has several minor uses, 

especially as an extraction solvent for spice oleoresins and hops, and for the removal of caffeine 

from coffee. It is approved as an extraction solvent for these uses by the Food and Drug 

Administration, although most decaffeinators no longer use DCM due to concerns over 

residuals (ATSDR, 2000). 

2.2.1. MARKET TRENDS

Use of DCM as a solvent in a number of sectors has been declining steadily since the mid-1980s 

due to increasing government regulation (i.e., both federal and state), and environmental, 

consumer, and worker exposure concerns (ICIS, 2007; US EPA, 2006b, 1994a, 1991). These 

regulations include: a lower Occupational Safety and Health Administration’s (OSHA’s) 

Permissible Exposure Limit (PEL) in 1997,; CPSC required warning labels on all products 

containing more than 1 percent of DCM in 1988; NIOSH listed DCM as a potential carcinogen; 

and new OSHA standards required facilities using DCM to use vapor control equipment by 2000 

(ICIS, 2007). 

In 1984, there were four domestic producers of DCM selling around 501 million lbs. In 2000, 

there were three domestic manufacturers with five DCM plants in the US (Cal EPA, 2000). 

Currently, there are only two manufacturers in the US with a total of three plants in operation. 

DCM use has declined in several areas in recent years for various reasons, including the OSHA’s 

reduction in the PEL in 1997 (US EPA, 2010b). Table 2-2 presents DCM market trends by use. 

Based on current estimations, use of DCM is expected to increase in only one category, DCM as 

feedstock in the production of a refrigerant, hydrofluorcarbon-32 (HFC-32).
DOCUMENT-DO NOT CITE OR QUOTE 

Page 20

Table 2-2. DCM Market Trends by Use.

DCM Use Use Trend Background

Paint stripper Decreasing • OSHA’s 1997 reduced PEL for paint removal in furniture 

refinishing operations resulted in new equipment costs 

(especially for small shops), which led to a reduction of 

DCM use as a paint strippera

• Consumer Product Safety Commission (CPSC) warning 

labels on consumer DIY products has also resulted in less 

furniture refinishing usea

• The aircraft industry has replaced DCM paint stripping on 

commercial and military planes with non-chemical stripping 

processes because new technology in chemical processing 

has resulted in less of a need for DCMa

• Use of substitutes like high-boiling ketones, glycol ethers, 

and N-methylpyrrolidone (NMP) has been increasingb

Metal cleaner and 

degreaser

Decreasing • Lower OSHA PEL resulted in reduced DCM usea

Aerosol products Decreasing • CPSC labeling requirements have led most aerosol 

manufacturers to eliminate DCM use, but it is still 

somewhat useda

Foam adhesives Decreasing • EPA’s 2007 Flexible Polyurethane Foam Production and 

Fabrication National Emission Standards for Hazardous Air 

Pollutants (NESHAP) required a reduction in use of DCMa

• Lower OSHA PEL has steered many foam manufacturers 

into using non-DCM adhesives due to the cost of 

compliance with the PELa

Feedstock in production 

of refrigerant HFC-32

Increasing • Expected to grow because HFC-32 is an EPA Significant New 

Alternatives Policy (SNAP) replacement chemical for HFC22a

• Fluorocarbon production accounts for less than 10 percent 

of DCM usea

Sources: aUS EPA (2010b). b

Mannsville (1999).

US consumption of DCM declined from a high of approximately 540 million lbs in the mid-1980s 

to approximately 160 million lbs currently (US EPA, 2010b). US demand for DCM in 2006 was 

estimated at 185 million lbs by industry sources with a projected demand of 181 million lbs for 

2010 (ICIS, 2007; HSIA, 2008). The 2006 non-confidential business information (CBI) Inventory 

Update Reporting Rule (IURR) indicates that 100 million to 500 million lbs of the chemical is 

produced or imported into the US (US EPA, 2006a). DCM imports were estimated at 20 million 

lbs in 2006 (ICIS, 2007), so the production volume of DCM makes up 80 to 96 percent of the 

market share depending on the high or low estimates of total production and imports. Only 

The Dow Chemical Company (one facility) and Occidental Chemical Corporation (i.e., two
DOCUMENT-DO NOT CITE OR QUOTE 

Page 21

facilities) manufacture DCM in the US. Between these two companies, there are only three 

DCM production facilities remaining in operation in the US (US EPA, 2010b).

In terms of environmental releases, according to data from the EPA’s 2010 Toxics Release 

Inventory (TRI), 292 facilities reported a total of 4.8 million lbs of on- and off-site disposal or 

other releases of DCM (US EPA, 2011a). 

Table 2-3 presents the major and minor uses of DCM, as well as the potential benefits of using 

DCM in different industries.

Table 2-3. Major and Minor Uses of DCM.

Major Usesa Minor Usesa Overall Benefits

• Paint removal

• Formulated products

• Adhesives

• Aerosol propellant

• Metal cleaner and degreaser

• Chemical processor for 

polycarbonate resins and cellulose 

triacetate (photographic film)

• Flexible polyurethane foam 

manufacturing

• Feedstock in the production of the 

refrigerant, hydrofluorocarbon-32 

(HFC-32)

• Extraction solvent for 

oils, waxes, fats, 

spices, and hops

• Tablet coating for 

pharmaceuticals

• Low flammabilityb

• Non-corrosive to many substratesb

• Strong solvency propertiesb

• No flash point under normal use 

conditions and can be used to 

reduce the flammability of other 

substancesc

• Does not contribute significantly to 

atmospheric pollution through the 

formation of smog, to depletion of 

the ozone layer, or to global 

warmingc

• Lower costs

Sources: aHSIA (2008); US EPA (2006a); Dow (1999); (Aerias, 2012). b

Mannsville (1999). c

HSIA (2010).

As recently as the 1980s, approximately 50 percent of the total DCM market was made up of

paint stripping products (Mannsville, 1999). Industry sources stated 40 percent of the domestic 

DCM market was made up of paint strippers in 2006 (HSIA, 2008). However, the most recent 

industry figures indicate paint stripping products now only make up 25 percent of the domestic 

market for DCM (Table 2-4). These figures coupled with an overall decline in the demand for 

DCM suggest manufactures may be substituting other solvents for DCM in their paint stripping 

products. Because the data are too recent, EPA cannot determine at this point if this is a real 

trend. The estimates for DCM use in 2007 are shown in Table 2-4. The percentages of DCM use 

by application type are based on production volume for use in domestic products. 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 22

Table 2-4. Major Uses of DCM in 2007 in the US.

Major Uses Percent of DCM Consumed in 2007 in End Products

Adhesives 37

Paint stripping 25

Pharmaceuticals 10

Metal cleaning 7

Chemical processing 7

Aerosols 5

Polyurethane foam blowing 5

Miscellaneous 4

Source: ICIS (2007).

2.2.4. CONSUMER USES

DCM has a number of TSCA consumer uses. The 2006 IURR data indicated that DCM is used in 

the following commercial/consumer use categories: paints and coatings, adhesives and 

sealants, and “other” (US EPA, 2006a) (Appendix B). The National Institutes of Health (NIH)

Household Products Database currently lists 49 products containing DCM, in concentrations 

ranging from one to 100 percent. The products are divided almost evenly between aerosol and 

liquid formulations (with one in granular form) (NIH, 2012).

DCM uses addressed by other agencies (i.e., non TSCA regulations) have changed over time. 

Once an ingredient in aerosol cosmetic products, such as hairsprays, in concentrations ranging 

from 10 to 25 percent, DCM was banned as an ingredient from all cosmetic products in 1989

(FDA, 1989). It no longer is used in hair sprays or cosmetic products (Cal EPA, 2000). Table 2-5 

presents the major consumer uses of DCM.

Table 2-5. Consumer Uses of DCM.

Consumer Uses

Paint strippers • Paint thinnersa

• Paint removers and strippersb

• Varnish removersb

• Graffiti removersb

Aerosol applications • Aerosol paintsc

• Automotive productsc

• Spray shoe polisha

• Rust removersa

• Primersa

Cleaners/protectors • Water repellant/protectorsa

• Spot removersa

• Wood floor and panel cleanersa
DOCUMENT-DO NOT CITE OR QUOTE 

Page 23

Table 2-5. Consumer Uses of DCM.

Consumer Uses

• Specialized electronic cleaners (for TV, VCR, razor, etc.)

a

• Wood stainsa

• Transmission cleanersa

• Battery terminal protectora

• Brake quieter/cleanera

• Gasket removersa

Adhesives • Contact cementa

• Super gluesa

• Spray adhesivesa

• Adhesive removers (general purpose, tile and wallpaper)a

Miscellaneous • Silicone lubricants (excluding automotive)a

• Outdoor water repellantsa

• Gasket removersa

• Herbicidesb

Sources: aNIH (2005). b

NIH (2012). c

Mannsville (1999).

2.2.4. PAINT STRIPPING APPLICATIONS

DCM is considered the best chemical stripper that is effective on the widest range of cured 

coatings from the widest variety of substrates (Mannsville, 1999). The major applications for 

DCM-based paint strippers include use on Original Equipment Manufacturing (OEM), field 

maintenance stripping, and home improvement and repair. Most of these users purchase paint 

stripper from a formulator who mixes the DCM with other chemicals to achieve the desired 

product (SRRP, 1992). For industrial use, paint strippers are typically 70 to 90 percent DCM by 

weight. Household paint strippers for consumer use are typically 60 to 80 percent (US EPA, 

1993; see also: Appendix C).

Several studies have been conducted to evaluate the extent of DCM use in paint stripping. In 

2008, EPA estimated that a total of 39,000 establishments perform surface coating operations, 

including paint stripping, motor vehicle, mobile equipment, and miscellaneous activities.

Specifically, EPA estimated that about 3,000 of these facilities were paint stripping shops. Of 

these 3,000 facilities, 2,000 used paint strippers containing ≤ 2,000 lbs of DCM, while 1,000 

facilities used products containing > 2000 lbs of the chemical (US EPA, 2010b).
DOCUMENT-DO NOT CITE OR QUOTE 

Page 24

2.3. ENVIRONMENTAL FATE

The environmental fate of a compound is important to understanding potential exposures to its 

specific environmental media (e.g., water, sediment, soil, plants) and impact on target 

organisms of concern. Releases of DCM to soil can volatilize from soil surfaces or migrate 

through soil and contaminate groundwater.

DCM has high mobility in soil. It is not readily biodegradable, but biodegrades at varying rates 

under both aerobic and anaerobic conditions. The rate of hydrolysis is negligible. The high 

vapor pressure and Henry’s Law constant, 2.19 × 10-3 atm-m3

/mole, indicate DCM has a 

tendency to partition to the atmosphere. DCM is not expected to undergo photooxidation in 

the atmosphere and is considered moderately persistent and has low bioaccumulation 

potential (OECD SIAP 2011, National Institute of Technology and Evaluation, 2002, EPA, 2012; 

Federal Register. 1999). Due to its volatility, DCM enters the atmosphere where it reacts slowly 

enough to undergo atmospheric transport and act as a greenhouse gas. DCM has been 

reported to the Intergovernmental Panel on Climate Change (IPCC) as a global warming 

potential (GWP) chemical with a value of 8.7 (i.e., or approximately 8.7 times more heat 

absorptive than carbon dioxide (CO2)) GWP (IPCC Fourth Assessment Report, 2007). This 

section summarizes current knowledge of the transport, persistence, bioaccumulation, and 

bioconcentration of DCM in the environment including biological and abiotic reactions and 

environmental distribution.

Fate in Air. If released to the atmosphere, DCM is expected to exist solely in the vapor-phase 

based on its vapor pressure. Vapor-phase DCM is degraded slowly in air by reaction with 

photochemically produced hydroxyl radicals. The half-life of this reaction is approximately 107 

days. Thus, it is considered persistent in the atmosphere and subject to transport.

Fate in Water. When released to water, DCM is not expected to adsorb to suspended solids 

and sediment in the water column based upon its soil organic carbon partition coefficient (Koc)

value. The rate of volatilization is expected to be high based on a Henry’s Law constant of 2.19 

× 10-3 atm-m3

/mole. A volatilization half-life of 21 minutes was measured for DCM when 

stirred in distilled water in a laboratory beaker at 25 oC (Dilling et al. 1975). The volatilization 

half-life increased to over 90 minutes when the solution was not stirred. The rate of hydrolysis 

under environmental conditions is expected to be negligible. The hydrolysis half-life reported at 

neutral pH, is approximately 18 months at 25 o

C (Dilling et al. 1975). Biodegradation is 

expected to occur slowly under aerobic conditions, but may degrade more rapidly in anaerobic 

waters. A half-life of 11 days was reported for DCM in a 2 month laboratory study using 

bacteria isolated from an anaerobic aquifer as inoculum (Hazardous Substance Databank 

(HSDB, 2012). A half-life of 108 days was observed for DCM in contaminated groundwater 

under methanogenic conditions (HSDB, 2012). Bioconcentration factor (BCF) values ranging 

from 2.0 to 5.4 were measured for DCM in carp over a 6 week incubation period at an initial 

concentration of 0.25 mg/L (National Institute of Technology and Evaluation 2002). 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 25

BCF values of <6.4 to 40.0 were observed when the concentration was 0.025 mg/L. Based on 

the BCF study, DCM is not expected to bioconcentrate significantly in aquatic organisms. 

Fate in Soil/Sediment. Based on its low soil organic carbon partitioning coefficient (Koc) of 25, 

DCM is likely to possess high mobility in soils and may be expected to leach from soils into 

groundwater (ATSDR 2000). DCM present at 100 mg/L achieved 13 percent of its theoretical 

biochemical oxygen demand (BOD) using an activated sludge inoculum at 30 mg/L and the 

modified MITI (i.e., Ministry of International Trade and Industry) test (OECD 301C) over the 

course of a 4 week incubation period and is not readily biodegradable (National Institute of 

Technology and Evaluation, 2002). DCM was shown to degrade under aerobic conditions in 

static culture screening studies that used domestic wastewater amended with yeast as 

inoculum (Tabak et al. 1981). Complete loss of DCM was observed within 7 days in the static 

culture tests; however, up to 25% of the loss could have arisen from volatilization. These 

studies suggest that given its low affinity for soil and potential to grade somewhat slowly, DCM 

will be mobile in soils and persist long enough to migrate to groundwater. 

Bioconcentration and Persistence. Bioconcentration and persistence are qualitatively 

characterized according to the criteria set forth in EPA’s TSCA New Chemical Premanufacture 

Notification Program (PMN) (Federal Register (FR), 1999). Though biodegradation tests of this 

substance found it not readily biodegradable, there is evidence to support that metabolism 

occurs under both aerobic and anaerobic conditions. Measured BCF values, indicate that DCM 

does not bioconcentrate.

2.4. CONCLUSIONS OF ENVIRONMENTAL FATE

DCM is volatile and does not significantly partition to solid phases. Therefore, releases of DCM 

to the environment are likely to evaporate to the atmosphere, or if released to soil, migrate to 

groundwater. It has been shown to biodegrade over a range of rates and conditions and is 

considered to be moderately persistence in the environment. Measured bioconcentration 

factors for DCM suggest its bioconcentration potential is low. Table 2-6 provides a summary of 

the environmental fate information for DCM. 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 26

Table 2-6. Environmental Fate Characteristics of DCM, Dichloromethane.1

Property Value

CASRN 79-09-2

Photodegradation Half-life 107 days (measured)

Hydrolysis Half-life 18 months (measured)

Biodegradation 13 % in 28 days (not readily biodegradable)2

Bioconcentration Factor 

(BCF)

BCF = 2.0 to 5.4 (measured in carp)2;

BCF = <6.4 to 40.0 (measured in carp)2

BAF = 2.6 (estimated)3

Log Koc 1.4 (measured)3

Fugacity

(Level III Model)3

Air (%)

Water (%)

Soil (%)

Sediment (%)

43.8

45.0

11.0

0.1

Persistence4 Moderate

Bioaccumulation4 Low

1 OECD SIAP. 2011. OECD HPV Chemicals Programme. Dichloromethane. Available online at 

http://webnet.oecd.org/hpv/ui/SponsoredChemicals.aspx as of March 19, 2012. 2 NITE (National Institute of Technology and Evaluation). 2002. Biodegradation and Bioaccumulation of the 

Existing Chemical Substances under the Chemical Substances Control Law. Available online from: 

http://www.safe.nite.go.jp/english/kizon/KIZON_start_hazkizon.html as of March 19, 2012. 3 U.S. EPA. 2012. Estimation Programs Interface SuiteTM for Microsoft® Windows, v4.10. U.S. Environmental 

Protection Agency, Washington, DC, USA. Available online at 

http://www.epa.gov/opptintr/exposure/pubs/episuitedl.htm as of March 19, 2012. 4 Federal Register. 1999. Category for Persistent, Bioaccumulative, and Toxic New Chemical Substances. Federal 

Register 64, Number 213 (November 4, 1999) pp. 60194–60204.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 27

Chapter 3: Human Health Risk Assessment 

INTRODUCTION

EPA reviewed readily available information on the chemistry, uses, sources, fate, exposure and 

hazard of DCM to humans and the environment. The review of this information helped focus 

the scope of this risk assessment. This chapter has five major sections: (1) Human Exposure 

Assessment, (2) Hazard Identification and Dose-Response Assessment, (3) Human Health 

Characterization, and (4) Discussion of Key Sources of Uncertainty and Data Limitations.

3.1. HUMAN EXPOSURE ASSESSMENT

This assessment focused on the use of DCM-based paint strippers. EPA assumed that direct

contact or close proximity to the use (i.e., for a consumer or commercial application with 

substantial frequency or duration of exposure) would likely provide the highest exposures to 

DCM paint strippers. In either occupational or consumer settings, there may be inhalation 

exposure during the product use. In addition to product users, there also may be non-users or 

bystanders who may not come in direct contact with the product, but may be exposed 

indirectly while in a nearby area during product application. 

For quantifying risks, estimates were provided for inhalation exposures to workers and 

residential consumers who use DCM-based paint strippers, and for inhalation exposures to 

residential non-users, who may be indirectly exposed. 

3.1.1. OCCUPATIONAL EXPOSURES

This section summarizes the available information on occupational exposure monitoring data 

and regulatory and non-regulatory occupational exposure limits to DCM for the primary 

industries where DCM is used in paint stripping applications. 

Recommended worker exposure limits have been established for DCM. A summary of the 

values established by OSHA, the National Institute for Occupational Safety and Health (NIOSH), 

and the American Conference of Governmental Industrial Hygienists (ACGIH) is provided in 

Table 3-1. Additional background on processes, respiratory protection, and facilities and 

worker populations are presented in Appendix D. OSHA amended the regulatory occupational 

exposure limits for DCM effective April 10, 1997. The amendments included reducing the PEL, 

reducing and changing the averaging time of the Short-Term Exposure Limit (STEL), adding an 

action level, and removing the ceiling limit (OSHA, 1997a). The pre-1997 limits are included 

here to provide context when analyzing exposure data measured on or before 1997. 

Workplaces may consider these levels when instituting respiratory protections.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 28

Table 3-1. Regulatory and Recommended Exposure Limits.

Source Limit Type Exposure Limit

OSHA PEL (1997 and forward) PEL (8-hr TWA) 25 ppm

STEL (15-minute TWA) 125 ppm

Action Level (8-hr TWA) 12.5 ppm

OSHA PEL (pre-1997) PEL (8-hr TWA) 500 ppm

Ceiling 1,000 ppm

STEL (5-minute average in any 2-hr period) 2,000 ppm

NIOSH exposure limitsa IDLH 2,300 ppm

REL Ca

ACGIH TLV 8-hr TWA 50 ppm

a

IDLH values are based on effects that might occur from a 30-minute exposure; REL notation Ca is for a potential 

occupational carcinogen, and the NIOSH Pocket Guide website has detailed policy recommendations for chemicals 

with Ca notations (NIOSH, 2011b).

IDLH = Immediately Dangerous to Life and Health; TLV = Threshold Limit Value; TWA = time-weighted average

Source: OSHA (1997a).

Because a variety of industries include paint stripping among their business activities, an effort 

was made to determine and characterize these industries, especially for the “small commercial 

shops” of interest to EPA. The terms for commercial, industrial, and small (i.e., in terms of 

employees per employer) often are difficult to distinguish, particularly as related to exposure 

data. EPA reviewed the published literature and evaluated the 2007 North American Industry

Classification System (NAICS) codes to determine industries that likely included paint stripping 

activities presented in Table 3-2.

Table 3-2. 2007 NAICS Codes Identified that Include Paint Stripping Activities.

2007 NAICSa 2007 NAICS Title Rationale for Inclusion of NAICS with Paint Stripping 

Activities

238320 Painting and wall 

covering contractors

US Census reports an index entry of “Paint and wallpaper 

stripping” (US Census, 2007a).

238330 Flooring contractors US Census reports index entries of “Floor laying, scraping, 

finishing, and refinishing” and “Resurfacing hardwood 

flooring” (US Census, 2007a). NIOSH (1993) cites the paint 

stripping of flooring by a wood flooring and restoration 

company (NIOSH, 1993).

811121 Automotive body, paint, 

and interior repair and 

maintenance

NAICS code 811121 is identified as the NAICS code for 

automobile refinishing per the Organisation for Economic 

Co-operation and Development (OECD) Coating Application via

Spray-Painting in the Automotive Refinishing Industry ESD 

(OECD, 2010).

811420 Reupholstery and US Census reports index entries of “Furniture refinishing 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 29

furniture repair shops” and “Restoration and repair of antique furniture” (US 

Census, 2007a).

711510 Independent artists, 

writers, and performers

US Census reports index entries of “Painting restorers, 

independent” and “Conservators (i.e., art, artifact restorers), 

independent” (US Census, 2007a). Research has shown art 

conservation to use paint strippers based on DCM or, 

preferably, NMP (Wollbrinck, 1993).

712110 Museums Research has shown art conservation to use paint strippers 

based on DCM or, preferably, NMP (Wollbrinck, 1993).

336411 Aircraft manufacturing US Census reports an index entry of “Aircraft rebuilding (i.e., 

restoration to original design specifications)” (US Census, 

2007a). Paint removal during the restoration process may use 

DCM- or NMP-based paint strippers.

336611 Ship building and 

repairing

US Census NAICS definition includes shipyards involved in the 

construction of ships as well as “their repair and conversion 

and alteration” (US Census, 2007a). Any paint removal 

activities during repair, conversion, and alteration may use 

DCM- or NMP-based paint strippers.

a

NAICS codes were identified by performing general internet searches to identify workplace-related activities that 

involve paint stripping, and searching the US Census 2007 NAICS website for keywords related to paint stripping, 

including those determined from the general internet search, such as “refinish,” “stripping,” “paint,” “restorer,” 

and “conservator” (US Census, 2007a).

Published monitoring studies were used to estimate occupational exposures to DCM. 

Additionally, inhalation exposure data from OSHA and state health inspections were obtained 

from the OSHA’s Integrated Management Information System (IMIS) database. Appendix H 

presents a detailed discussion of these data. These studies formed the basis from which EPA 

calculated Average Daily Concentrations (ADCs) and lifetime average daily concentrations 

(LADCs) from eight-hr time-weighted average (TWA) exposures, using Equation 3-1 (Eq; US EPA, 

2009) to assess the risks to workers from these exposures. The ADC or LADC is equivalent to EC 

in the equation below with the substitution of the appropriate AT value.

Eq. (3-1)

where:

ADC = exposure concentration (mg/m3

);

C = contaminant concentration in air (mg/m3

);

ED = exposure duration (hrs/day; default: 8);

EF = exposure frequency (days/year; default: 250);

WY= working years per lifetime (years; ADC and LADC: 40 years); and

AT= averaging time (lifetime in years × 365 days/years × 24 hrs/day; ADC: 40 years; LADC: 70 

years, which is used to match the years used to calculate EPA’s cancer inhalation unit 

risk [IUR]).
DOCUMENT-DO NOT CITE OR QUOTE 

Page 30

A summary of the identified exposure concentrations and the calculated ADCs and LADCs for 

several of the exposed populations are provided in Table 3-3. In comparison to more detailed 

literature sources, OSHA IMIS data were not included in this summary except where noted 

because of the high degree of uncertainty and questionable relevancy of these data to paint 

stripping with DCM-containing products. EPA determined that the available datasets were not 

amenable to developing statistical distributions of all exposures in the specified industries. 

Therefore, each of the exposure estimates represents a snapshot of the particular cases studied 

and may not be representative of the broader worker populations that are exposed to DCM 

during its use in various paint stripping applications. Despite these limitations, these data show 

that the OSHA PEL and STEL are exceeded under some circumstances.

Table 3-3. Summary of Ranges of DCM Exposure Concentrations and Calculated ADCs and LADCs for 

Workers.

Industry Number 

of Studies

Time Range 

of Studies

Range of TaskBased, Short-Term, 

or Peak Exposure 

Concentrations 

(mg/m3

)

a

Range of 8-hr

TWA Exposure 

Concentrations 

(mg/m3

)

b

ADC 

(mg/m3

)

c

LADC 

(mg/m3)

c

Professional 

contractors

4 1990-1998 130-14,100

(37-4,063 ppm)

– – –

1 1981 – 60-2,980

(17-859 ppm)

14-680 7.8-390

Bathtub 

refinishing

1 2003-2008 6,940-7,565

(2,000-2,180 ppm)

– – –

Automotive 

refinishing

1 2004 250–416

(72-120 ppm)

– – –

1 2004 – 90-416

(26-120 ppm)

21-95 12-54

Furniture 

refinishing

5 1990-2007 24-3,814

(7-1,099 ppm)

– – –

4 1991-2007 – 2.4-1,270

(0.7-366 ppm)

0.55-290 0.32-170

Art restoration 

and 

conservationd

1 2005 – 2

(0.58 ppm)

0.46 0.26

Aircraft paint 

stripping

4 1977-pre199938-5,400

(11-1,556 ppm)

– – –

4 1994-2002 – 86-3,802

(25-1,096 ppm)

20-870 11-500

Ship paint 

stripping

1 1980 215

(62 ppm)

– – –
DOCUMENT-DO NOT CITE OR QUOTE 

Page 31

Table 3-3. Summary of Ranges of DCM Exposure Concentrations and Calculated ADCs and LADCs for 

Workers.

Industry Number 

of Studies

Time Range 

of Studies

Range of TaskBased, Short-Term, 

or Peak Exposure 

Concentrations 

(mg/m3

)

a

Range of 8-hr

TWA Exposure 

Concentrations 

(mg/m3

)

b

ADC 

(mg/m3

)

c

LADC 

(mg/m3)

c

Unspecified 

workplace 

setting: 

immersion 

stripping of 

wood

Unknown 1980-1994 – 35-7,000

(10-2,017 ppm)

8.0-1,600 4.6-910

Unspecified 

workplace 

setting: wood 

and metal 

paint stripping

1 1980 – 633-1,017

(182-293 ppm)

150-230 83-130

a

These exposures include task-based exposures averaged over a time period of <8 hrs, short-term (i.e., STEL) exposures, and 

peak exposures.

b

These exposures include 8-hr TWA exposures that were either directly measured or calculated from shorter time frame 

exposures by the study authors.

c

Calculated Average Daily Concentration (ADC) and Lifetime-Average Daily Concentrations (LADC) are only calculated from 8-hr

TWA exposures; see Equation 3-1. d

The data point provided for this industry was obtained from OSHA IMIS. No other literature data were obtained.

Note: Airborne concentration conversion factor for DCM is 3.47 mg/m3 per ppm (NIOSH, 2011a).

-- indicates no data found.

The data presented in Table 3-3 were obtained from the cited studies in Table 3-4, which 

summarizes the number of workers monitored or exposed in the respective studies and the 

total number of employees at the facility.

Table 3-4. Summary of Number of Workers Exposed or Monitored and Total Number of Employees in 

the Monitored Facility Cited in the References Used for Each Industry.

Industry Reference* Number of Workers 

Exposed or Monitored

Total Number of 

Employees in Facility

Professional contractors TNO (1999) Unknowna Unknown

US EPA (1994b) N/A N/A

Bathtub refinishingb CDC (2012b, a); 

MSU/MIFACE (2011)

1 1

Lofgren et al. (2010) 1 Unknown

Automotive refinishing Enander et al. (2004) 1 14

Furniture refinishing NIOSH (1992) 5 Unknown

Grevenkamp (2007) 1 18
DOCUMENT-DO NOT CITE OR QUOTE 

Page 32

Table 3-4. Summary of Number of Workers Exposed or Monitored and Total Number of Employees in 

the Monitored Facility Cited in the References Used for Each Industry.

Industry Reference* Number of Workers 

Exposed or Monitored

Total Number of 

Employees in Facility

McCammon et al. (1991) 14c Unknown

NIOSH (1991) 1 Unknown

NIOSH (1990) 1 1

TNO (1999) Unknown Unknown

Art restoration and 

conservation

OSHA (2012) 1 Unknown

Aircraft paint stripping IARC (2010); TNO (1999); 

EU (2007a); Vincent et al.

(1994)

Unknown Unknown

Ship paint stripping IARC (2010) 8 Unknown

Unspecified workplace 

setting

TNO (1999) Unknown Unknown

*Study details are provided in Appendix E. a

Unknown (i.e., not specified in the reference). b

For bathtub refinishing, "facility" refers to the job site where the refinisher was working at the time of the 

monitoring or at the time the fatality occurred. c

For this particular study, a total of 14 workers were monitored over a total of five furniture stripping shops, which 

averages to 2.8 workers monitored per facility.

Using the limited information identified, EPA could not estimate the current total number of 

workers in the potentially exposed populations. Knowing the sizes of exposed populations 

provides perspective on how prevalent the effects may be. By way of comparison, more recent 

OSHA data on the numbers of facilities and workers in the wood furniture stripping industry 

indicate that the current total number of workers exposed to DCM appear fewer than the 

7,872 estimated in the mid-1990s (Appendix D).

When identifying “small commercial shops,” the available data provide information that may 

allow some generalizations about the relative sizes of facilities/shops that fit this category. EPA 

combined the facility and population data from Appendix D and the average number of 

employees per facility to generally categorize the industries included in this assessment into the 

following classifications:

• Small shops could generally be expected to include (< 10 workers) professional 

contractors (i.e., including bathtub refinishers), automotive refinishers, furniture 

refinishers, and independent art restorers;

• Larger facilities (> 10 workers) could generally be expected to include facilities that strip 

paint from aircraft and ships; and 

• The exposures labeled Unspecified Workplace Setting cannot be classified into either 

small shop or larger facilities.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 33

Because these size distinctions are simple generalizations that may not be entirely applicable to 

the exposure data in the industry categories identified, the exposure estimates from all of the 

industries were considered in the risk characterization presented later in this chapter.

3.1.2. RESIDENTIAL/CONSUMER EXPOSURES

DCM was selected for further assessment based on its high hazard (i.e., due to liver toxicity and 

cancer risks) and its numerous uses in consumer products, EPA assessed the exposure route

with the greatest potential for consumer exposure to DCM. This section provides estimates of

inhalation exposures for residential users and other residential occupants (bystanders) during 

the use of paint-stripper products containing DCM. In the absence of sufficient measured data 

on consumer exposures, inhalation exposures were calculated for current use patterns using a 

model-based approach. Specifically, the EPA’s Multi-Chamber Concentration and Exposure 

Model (MCCEM) was utilized to predict airborne concentrations of DCM in various consumeruse scenarios (US EPA, 2010a). 

3.1.3. CONSUMER EXPOSURE MODELING 

Input Parameters. The parameters needed to support EPA’s modeling effort to estimate 

consumer inhalation exposure and the input values used for different exposure scenarios and 

their rationale are described in this section. 

The MCCEM model requires input of several chemical-specific parameters. EPA identified

published data for current product characteristics, use patterns, exposure factors, and air 

concentrations to develop appropriate scenarios and for modeling input parameters. A limited 

number of relevant sources were identified; however, the majority of these were over a decade 

old. All sources were compared to quality criteria, e.g., currency, scope, accuracy/reliability, 

transparency, clarity, and completeness of the information provided. 

EPA used published values for DCM-containing products currently available for consumer 

purchase (Brown, 2012) to determine reasonable percentage of DCM in products and product 

densities. Other resources providing information on product characteristics included: (1) the

NIH’s Household Products Database; (2) MSDSs; and, (3) Product Labels and Technical Data 

Sheets. Information was collected from available product labels or Technical Data Sheets for 

approximately half of the products listed in Brown (2012). 

 

EPA identified published air monitoring data from the consumer use(s) of DCM paint strippers

from two comprehensive US experimental studies. One study was conducted by the US EPA 

(1994b) and the other was conducted by the Consumer Product Safety Commission (CPSC) in 

1986 (as cited in US EPA, 1996; Riley et al., 2000). Both studies were over 15 years old; the 

usefulness of the CPSC study was limited because the original source was not available for 

quality criteria evaluation. Limited results and experimental parameters were obtained from 

the CPSC study, US EPA (1996), and Riley et al. (2000).
DOCUMENT-DO NOT CITE OR QUOTE 

Page 34

EPA also reviewed a European Commission (EC, 2004) study that described chamber 

experiments performed in the EU in 2003. A standard scenario was monitored and other 

scenarios reported in this study that estimated changes in air concentration based on variations 

in surface area, ventilation, surface orientation, exposure duration, and product amount; only 

air concentrations for the standard scenario were measured. However, this study had several 

limitations to its utility for the current assessment including: (1) too little information to 

confirm model parameters, study design, or results; (2) lack of information on , study design of 

and product formulation or percent DCM in the test products; (3) the presence of vapor 

retardants, which not typical in US products; (4) the ventilation rate was high for indoor rooms 

unless mechanical ventilation is used (e.g., a fan venting directly outdoors); and, (5) differences 

in typical US room size (i.e., US room sizes may be larger).

Exposure factor information was identified from a variety of sources, including the Exposure 

Factors Handbook (EFH; EPA, 2011c) which provides recent information on generic exposure 

factors (e.g., body weights, body part surface areas, house volumes, and house ventilation 

rates) as well as for specific use of paint strippers (i.e., use amounts, frequencies, durations as 

presented in Westat (1987) and Abt (1992)).

EPA utilized some information on paint stripper use patters by Riley (2001). This study 

provides relevant data on paint strippers and is the most current use-pattern survey available 

for paint strippers. This single-site survey was not specific to the use of DCM paint strippers, 

was based on a small sample size (n=20), and utilized participant recall of product-use behavior. 

Other information, not specific to paint strippers but used to identify input parameters for the 

inhalation modeling, such as interzonal air flows and air exchange, rates, was obtained from 

published sources including EPA (1995b) and Matthews et al. (1989). 

Rationale for a Modeling-Based Approach. Complete air monitoring data for the consumer use 

of paint strippers containing DCM are only available from EPA (1994b). In that study, chamber 

experiments were conducted for five paint stripping products, including two paint-stripping 

products containing DCM. The two DCM products were: 1) a spray-on product containing 80 to 

85 percent DCM; and, 2) a brush-on product containing >10 percent DCM. It is unclear why US 

EPA (1996) doesn’t discuss a third product in the study that also contained DCM; however, 

DCM was not listed as an ingredient, nor were air monitoring results provided for the product. 

An advantage of this study is that it used US products and provided sufficient descriptions of 

the study design and results. However, the experimental data cannot be used directly to assess 

residential inhalation exposures in this assessment because the values for the required 

exposure factors, (e.g., room/house volume, airflow rates, and surface area of object) do not 

reflect the range of possible residential values. Additionally, the experiments were conducted 

in a one-room chamber and, thus, do not provide concentrations for areas of the house other 

than the treatment room. The study was useful, however, in determining product application 

rates (i.e., in g/ft2 and g/min) and in estimating the fraction of applied chemical mass that 

ultimately was released to the indoor air, as described in more detail in Appendix F, F-1.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 35

Estimation of Emission Profiles for Paint Removers/Strippers. EPA identified other air 

monitoring studies for consumer paint strippers using DCM-containing products, including the 

previously described European Commission (EC) study (EC, 2004) and a study conducted in the 

Netherlands by van Veen et al. (2002). The EC (2004) study is the most current experimental 

study conducted for paint strippers. However, one of its main limitations was the failure to 

provide the raw data in the report. Thus, the overall findings of the EC study could not be 

verified. Additionally, the study may not be representative of use patterns and DCM-containing 

products in the US. The van Veen et al. (2002) study provided useful information related to this 

task; however, the study was conducted on a small scale and, as with the EC (2004) study, the 

exposure scenario assessed did not represent well use patterns in the US.

3.1.4. INHALATION EXPOSURE ASSESSMENT

Methodology. Inhalation exposure to DCM emitted during paint stripper application and 

associated scraping was modeled using the MCCEM which is ideally suited to this application. It 

provides for modeling of “incremental source” emissions, whereby a product is applied at a 

constant rate and the emission rate of the chemical in each instantaneously applied segment is 

assumed to decline exponentially over time. Depending on the type of applied product, either 

one or two exponential expressions may be needed to characterize the declining emission rate. 

From an analysis of chamber tests conducted in US EPA (1994b) (see Appendix F, F-1.

Estimation of Emission Profiles for Paint Removers/Strippers), it was determined that a singleexponential expression was appropriate for paint strippers with DCM as a primary ingredient.

The selection of exposure scenarios for the inhalation exposure assessment was guided in part 

by the outcome of a sensitivity analysis to determine which parameters used in the model have 

the most influence over the results of the assessment. Changing those values for various 

combinations of parameters will generate a wide range of plausible exposure scenarios and can 

increase the level of confidence in the model results. The methods for and results of this 

analysis are described immediately below.

Sensitivity Analysis. The types of factors that can be varied in MCCEM include the following:

• The configuration of the structure (residence in this case) being modeled, including the 

number of zones, volume of each zone, airflow rates between each zone and outdoors, 

and airflow rates between zones (i.e., interzonal airflow rates);

• The quantity of DCM emitted from the applied product and the time-varying emission 

rate, which are related to: (1) the type and area of surface being stripped; (2) the type of 

application (e.g., brush-on vs. spray-on); and (3) the rate at which the product is applied 

to the surface; and

• Locations during and after stripping of: (1) the user(s)—the individual(s) applying the 

product, and (2) the non-user(s)—other individual(s) present in the house who are not 

involved in the paint-stripping activity and, by assumption, are located in a house zone 

other than the one in which the paint-stripping activity is taking place.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 36

The sensitivity analysis was conducted using an approach that has been termed a “nominal 

range sensitivity analysis” (Frey and Patil, 2002). With this approach, a “base case” is defined

first, typically consisting of central values for each model input. Next, the inputs are varied—

one at a time—and the model response (i.e., average or peak concentrations to which 

individuals are exposed) is noted. The “index of sensitivity” is the magnitude of change in 

model response, typically expressed as a percent change from that of the base case. Details on 

this approach are in Appendix F, F-2. Sensitivity Analysis for Inhalation Scenarios.

The time required to apply and scrape the paint stripper, including the wait time between 

applying and scraping, is about an hr, according to Abt (1992) . Consequently, the model was 

run for a 24-hr period to capture all or most of the declining indoor-air concentrations following 

the episode of product use.

For this assessment, the relevant exposure measures include the maximum or peak TWA 

concentrations for certain averaging periods (i.e., one, 10, and 30 minutes and one, four, and 

eight hrs) in addition to the 24-hr TWA value. Time-varying concentrations that the user and 

non-user could be exposed to are shown in Figures 3-1 and 3-2 along with the maximum TWA 

values and the corresponding time periods for selected averaging times. All the exposure 

measures as described were included for the formal model runs; but only the maximum one-hr 

and the 24-hr TWA were used for the sensitivity analysis.

The base case for the sensitivity analysis was formed using central values for the various inputs, 

as follows:

• House volume of 492 m3 (corresponds to a 36 ft × 30 ft, two-story house with 8-ft 

ceiling);

• Workshop (area of product use) volume of 54 m3 (corresponds to a 20 ft × 12 ft 

room with 8-ft ceiling) and an indoor-outdoor airflow rate of 68 m3/hr (expected 

value for a room with multiple open windows);

• Airflow rate of 197 m3/hr for the ROH, assuming windows closed, corresponding to 

an air exchange rate of 0.45 ACH;

• Brush-on application with a target surface area of 10 ft2

; 

• Applied product mass of 900 g (90 g/ft2

) and emitted (released to indoor air) DCM 

mass of 148.5 g, assuming a DCM weight fraction of 0.5 in the product and a release 

fraction of 0.33; and,

• User located in workshop during application and scraping periods but in ROH during 

wait periods between applying/scraping and after completion of all 

applying/scraping.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 37

Figure 3-1. Time-varying User Personal Concentration and Maximum TWA Values for Selected 

Averaging Times.

Figure 3-2. Time-varying Non-user Personal Concentration and Maximum TWA Values for Selected 

Averaging Times.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 38

The sensitivity results for two exposure measures, peak one-hr TWA and 24-hr TWA are 

displayed in Figures 3-3 and 3-4, respectively. For both measures, and for both the user and the 

non-user, the change in model output for changing chemical mass is 75 percent, indicative of a 

linear and proportional response. For the user, the model response is highly sensitive to 

location during the wait period between applying and scraping (i.e., user stays in workshop vs.

moves to ROH). The model response is somewhat sensitive to the ROH air exchange rate with 

outdoors (ROH ACH) for the non-user, but not for the user. As a result of the sensitivity 

analysis, EPA determined that the chosen modeling scenarios should include some variations in 

each of these three factors to address greater model sensitivity.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 39

Figure 3-3. Model Sensitivity Results (Percent Change from Base-case Response) for Peak One-hr TWA 

for User and Non-user.

Figure 3-4. Model Sensitivity Results (Percent Change from Base-case Response) for 24-hr TWA for 

User and Non-user.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 40

3.1.5. EXPOSURE SCENARIOS AND MODEL INPUTS

Exposure Scenarios. Seven exposure scenarios were developed for the assessment, as 

summarized in Table 3-5. The following factors were considered in developing the scenarios:

• The type of application (i.e., brush-on or spray-on), weight fraction of applied 

product, application rate, surface area of object to be stripped, and emission rate of 

the chemical concern, which can affect the amount of DCM that ultimately is 

released to the indoor environment;

• The location where the product is applied, which relates to exposure factors such as 

the room volume and its air exchange rate with outdoors;

• The house volume and air exchange rate, for reasons similar to those for the 

product use location; and,

• Precautionary behaviors such as opening windows in the application room and the 

user leaving the application room during the effect period, and related changes to 

the air exchange rates and the proximity of the user to the source of DCM 

emissions.

Table 3-5. Consumer Exposure Scenarios for the DCM Inhalation Exposure Assessment.

Scenario ID

Scenario Description

Type of Application Location of Product 

Use

Concentration 

Characterizationa

1 Brush-on Workshop Central tendency

2 Brush-on Workshop User upper-end

3 Brush-on Workshop Non-user upper-end

4 Spray-on Workshop Central tendency

5 Spray-on Workshop User upper-end

6 Spray-on Workshop Non-user upper-end

7 Brush-on Bathroom Non-user upper-end

a

Conditions obtained by varying the most sensitive parameters: DCM mass emitted; user location during the effect 

or wait period; and the rest of the house (ROH) air exchange rate with outdoors.

The primary distinctions among the seven scenarios (guided by the sensitivity analysis) were: 

type of application (i.e., brush vs. spray); location of product application (i.e., workshop for 

most scenarios, bathroom for one scenario); and values used for other inputs including the 

DCM mass emitted, the user’s location during the effect or wait period, and the air exchange 

rate of the rest of the house (ROH) with outdoors. Of the scenarios listed in Table 3-5, two are 

considered central tendency1 for both the user and the non-user, two were developed to 

 1 As noted in Section 2.3.1 (Individual Risk) of the US EPA (1992a) exposure assessment guidelines, “Individual risk 

descriptors will generally require the assessor to make estimates of high-end exposure, and sometimes additional 

estimates (e.g., estimates of central tendency such as average or median exposure).” For this assessment, 

scenarios with central parameter values refer to a set of inputs that are expected to result in a central (i.e., near 

the median) estimate of individual exposure.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 41

estimate upper-end concentrations for the user, and two were developed to estimate upperend2 concentrations primarily for the non-user. Central-tendency values are exposure values 

expected to be near the average or median for the range of exposure values; upper–end values 

are plausible exposure values from the upper half of the range of expected exposure amounts. 

These descriptive exposure estimates are generally required for risk assessments.

The seventh scenario EPA used was a simulation of actual reported conditions from a Centers 

for Disease Control and Prevention (CDC)/NIOSH occupational exposure case for a DCM paint 

stripper used on a bathtub (CDC, 2012a, b). This scenario represents high product use in a 

confined (i.e., closed, poorly ventilated) space. The selected parameter values for this scenario

(e.g., large surface area, small room size, minimal ventilation, upper-end weight fraction, and 

low ROH ventilation) would increase concentrations and exposures so that the combinations of 

parameter values would be expected to result in upper-end to bounding4 concentrations for 

the user and non-user. The purpose of including this latter scenario in this assessment was to 

estimate the DCM concentrations to residential occupants outside the use zone. 

Further details of the exposure scenario inputs are discussed in Appendix F, F-3 in the section 

on Inhalation Exposure Scenario Inputs.

Summary of Exposure Scenarios and Model Inputs. The exposure scenario inputs included: 

amount of DCM release, stripping method, room of use volume and ventilation characteristics, 

house volume and ventilation characteristics, the user location during the wait period, and nonuser location. The inputs for all seven scenarios are summarized in Table 3-6, from which the 

major and subtle differences among the seven scenarios are shown. For example, Scenarios 2 

and 3, and their spray-application counterparts, Scenarios 5 and 6, are targeted toward 

estimation of upper-end exposures for the user and non-user, respectively, by changing the 

application amount, the location of the user, and the airflows. 

 2 As also noted in Section 2.3.1 of the above-cited guidelines, “a high end exposure estimate is a plausible estimate 

of the individual exposure for those persons at the upper end of an exposure distribution. The intent of this 

designation is to convey an estimate of exposures in the upper range of the distribution, but to avoid estimates 

that are beyond the true distribution. Conceptually, the high end of the distribution means above the 90th

percentile of the population distribution, but not higher than the individual in the population who has the highest 

exposure.” For this assessment, scenarios labeled “upper-end” were modeled by selecting low- and high-end 

values for sensitive parameters. An “upper-end” exposure estimate is above central tendency and may include the 

high end of the exposure distribution.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 42

Table 3-6. Summary of DCM Consumer Paint Stripping Scenario Descriptions and Parameters.

Scen

ario 

ID

Characteriz

ation

DCM Released

Stripping Method

Room of Use House User Location 

During Wait 

Periodb

Non-User 

Weight Location

Fraction

Surface Area 

Treateda, ft2

Application 

Rate, g/ft2

Release 

Fraction

Volume, 

m3

Ventilation/

ACH, 1/hr

Volume, 

m3

ROH ACH, 

hr-1

Brush-on Exposure Scenarios in Workshop

1 Central 0.53

(central)

10

coffee table

(central)

90 0.33 • Four segments for coffee table 

(i.e., two 5-ft2 segments with 

repeat application) and eight 

segments for chest of drawers 

(i.e., four 6.25-ft2 segments 

with repeat application)

• 2-minute application, 

15-minute wait, and 4-minute 

scrape per segment

• No overlapping activities

• Scrapings removed from house 

after last scraping

54

(central)

Open 

windows/ 

1.26

(professional 

judgment, 

90th 

percentile)

492 

(central)

0.45

(central)

ROH ROH 

(entire 

time) 2 Upper-end 

for user

0.88

(upperend)

Workshop

3 Upper-end 

for nonuser

25

chest of 

drawers

(upper-end)

0.18

(low-end)

ROH

Spray-on Exposure Scenarios in Workshop

4 Central 0.80

(central)

10

coffee table

(central)

68 0.66 • Four segments for coffee table 

(i.e., two 5-ft2 segments with 

repeat application) and eight 

segments for chest of drawers 

(i.e., four 6.25-ft2 segments 

with repeat application)

• 1-minute application, 

15-minute wait, and 4-minute 

scrape per segment

• No overlapping activities

• Scrapings removed from house 

after last scraping

54

(central)

Open 

windows/ 

1.26

(professional 

judgment, 

90th 

percentile)

492 

(central)

0.45

(central)

ROH ROH 

(entire 

time) 5 Upper-end 

for user

0.87

(upperend)

Workshop

6 Upper-end 

for nonuser

25

chest of 

drawers

(upper-end)

0.18

(low-end)

ROH
DOCUMENT-DO NOT CITE OR QUOTE 

Page 43

Table 3-6. Summary of DCM Consumer Paint Stripping Scenario Descriptions and Parameters.

Scen

ario 

ID

Characteriz

ation

DCM Released

Stripping Method

Room of Use House User Location 

During Wait 

Periodb

Non-User 

Weight Location

Fraction

Surface Area 

Treateda, ft2

Application 

Rate, g/ft2

Release 

Fraction

Volume, 

m3

Ventilation/

ACH, 1/hr

Volume, 

m3

ROH ACH, 

hr-1

Brush-on Exposure Scenario in Bathroom

7 Simulation 

for nonuser 

exposure

0.88

(upperend)

36

bathtub

(upper-end)

13.25 0.33 • Eight segments (i.e., four 9 ft2

segments with repeat 

application)

• 3-minute application, 

15-minute wait, and 6-minute 

scrape per segment

• No overlapping activities

• Scrapings removed from house 

after last scraping

9

(lowend)c

Window 

closed, no 

exhaust fan/ 

0.18d

(low-end)

492 

(central)

0.18

(low-end)

ROH ROH 

(entire 

time)

a

The surface area values were selected so that the calculated amount of product applied (g) corresponds approximately to the Abt (1992) survey results for amount of paint 

stripper used (50th percentile value of 32 ounces or 1,000 g for the central surface area of 10 ft2 and ~80th percentile value of 80 ounces or 2,500 g for the upper-end surface 

area of 25 ft2

). b

For all scenarios, the user is in the treatment room during the application and scraping times and in ROH after the last scraping. c

1 m3 for the vicinity of the tub (source cloud) and 8 m3 for the rest of the bathroom. d

Because the user is working in close proximity to the target (bathtub) for an extended period, a third zone (“source cloud”) was created within the bathroom to represent the 

DCM concentrations in the vicinity of the tub; this is a virtual zone, with no physical boundaries. The airflow rate between the cloud and the rest of the bathroom was based on 

work by Matthews et al. (1989) (for more information, see discussion in Appendix F, F-3. Inhalation Exposure Scenario Inputs (Airflow Rates and Volumes).
DOCUMENT-DO NOT CITE OR QUOTE 

Page 44

3.1.6. SUMMARY OF MODEL OUTPUTS AND EXPOSURE CALCULATIONS.

To account for an individual’s location at specific times, MCCEM outputs a detailed time series 

of zone-specific (e.g., house, workshop, and bathroom) and personal concentrations. This 

output is in the form of instantaneous values at the end of consecutive one-minute time 

intervals for the entire duration of the model run (i.e., 24 hrs in this case). A more detailed, 

mathematical description of the calculations is provided in Appendix F, F-3. Inhalation Model 

Outputs and Exposure Calculations.

Table 3-7 provides a summary of DCM exposure concentrations for the consumer user and nonuser of DCM-containing paint strippers. These concentrations were calculated by computing 

running averages and selecting the maximum of these averages. For example, for the one-hr

averaging period, the one-hr average concentration was calculated for each one-minute start 

time during the 24-hr period (e.g., zero to 60, one to 61, and etc.), for which the maximum of 

these averages is reported in Table 3-7. As the averaging time increases, the user to non-user 

exposure ratio decreases. For Scenario 1, for example, the ratio of user to non-user maximum 

one-minute concentration is ~5:1, as compared to a ratio of ~1.5:1 for the 24-hr user and nonuser TWA values. 

Appendix F, F-5. MCCEM Inhalation Modeling Scenario Summaries provides scenario summaries 

for each of the modeled scenarios, including both model inputs and results.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 45

Table 3-7. Summary of Modeled DCM Concentrations to Which Consumer Users and Non-Users are Exposed, by Scenario.

Scenario Individuala Maximum Values for Averaging Period, mg/m3 (ppm)

1 Minute 10 Minutes 30 Minutes 1 Hour 4 Hours 8 Hours 24 Hours

1. Brush application in workshop, 

central parameter values

User 630 (180) 380 (110) 270 (78) 220 (64) 120 (35) 69 (20) 23 (6.7)

Non-user 130 (38) 130 (38) 130 (37) 120 (36) 82 (24) 49 (14) 17 (4.8)

2. Brush application in workshop, 

upper-end values

User 1,300 (370) 1,300 (360) 1,100 (330) 1,100 (300) 420 (120) 220 (64) 75 (22)

Non-user 220 (63) 220 (63) 220 (62) 210 (59) 140 (39) 82 (24) 28 (8.0)

3. Brush application in workshop, 

upper-end values

User 1,800 (520) 1,200 (340) 900 (260) 760 (220) 560 (160) 400 (120) 160 (45)

Non-user 470 (140) 470 (140) 470 (140) 460 (130) 380 (110) 290 (83) 120 (34)

4. Spray application in workshop, 

central parameter values

User 1,500 (430) 780 (220) 600 (170) 490 (140) 270 (77) 150 (44) 52 (15)

Non-user 300 (87) 300 (87) 300 (86) 280 (82) 190 (54) 110 (32) 38 (11)

5. Spray application in workshop, 

upper-end values

User 2,000 (570) 1,900 (550) 1,800 (510) 1,600 (460) 620 (180) 330 (96) 110 (32)

Non-user 330 (95) 330 (95) 320 (93) 310 (89) 200 (59) 120 (35) 42 (12)

6. Spray application in workshop, 

upper-end values

User 2,800 (810) 1,600 (470) 1,300 (360) 1,100 (320) 810 (230) 580 (170) 230 (66)

Non-user 710 (210) 710 (210) 710 (200) 700 (200) 580 (170) 430 (120) 180 (51)

7. Brush application in bathroom, 

simulation

User 2,700 (770) 1,500 (440) 940 (270) 840 (240) 560 (160) 350 (100) 140 (40)

Non-user 220 (64) 220 (64) 220 (64) 220 (63) 190 (54) 150 (43) 70 (20)

a

Non-user assumed to be in ROH.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 46

3.2. HUMAN HEALTH ASSESSMENT: HAZARD IDENTIFICATION AND DOSE-RESPONSE 

The hazard summary information used in this assessment was based on the EPA’s Toxicological

Review of Methylene Chloride [i.e., Integrated Risk Information System (IRIS) assessment; (US 

EPA, 2011b)], the Acute Exposure Guideline Levels (AEGL) technical support document (US EPA,

2008), the Agency for Toxic Substances and Disease Registry’s (ATSDR’s) Toxicological Profile for 

Methylene Chloride (ATSDR, 2000, 2010), and the Technical Support Document Supporting the 

California’s Acute Reference Exposure Level (REL) for DCM (OEHHA, 2008). Additional 

information is provided in Appendix G.

3.2.1. TOXICOKINETICS AND BIOMONITORING

DCM is rapidly absorbed through inhalation exposure. The pulmonary uptake of DCM ranges 

roughly from 40 to 60 percent (Gamberale et al., 1975; Stewart et al., 1976; Andersen et al., 

1991; as cited in US EPA, 2008), but may be up to 70 percent during the first minutes of 

exposure (Riley et al., 1966; as cited in US EPA, 2008). The uptake decreases with exposure 

duration and concentration (Stewart et al., 1976; Peterson, 1978; as cited in US EPA, 2008), and 

a steady-state absorption rate is generally achieved within two hrs of exposures up to 200 ppm 

(DiVincenzo and Kaplan, 1981; DiVincenzo et al., 1972; as cited in US EPA, 2008). 

Results from studies of animals show that following absorption, DCM is rapidly distributed 

throughout the body, primarily reaching the liver, brain, and subcutaneous adipose tissue 

(Carlsson and Hultengren, 1975; US EPA, 2011b; as cited in ATSDR, 2000). DCM’s plasma halflife is estimated to be 40 minutes after inhalation exposure (DiVincenzo et al., 1972; as cited in 

ATSDR, 2000). Metabolism occurs predominantly in the liver, although additional 

transformation occurs in the lungs and kidneys (ATSDR, 2000).

In the liver, metabolism of DCM involves two primary pathways. The first pathway produces 

carbon monoxide (CO) and carbon dioxide (CO2), and saturation occurs at very low 

concentrations of a few hundred ppms. The second pathway yields formaldehyde and formic 

acid, and saturation occurs at very high concentrations (>10,000 ppm).

Acute toxic effects (i.e., central nervous system [CNS] depression) may persist for hrs after 

cessation of exposure because of continued metabolism of DCM released from tissue storage 

(ATSDR, 1990; as cited in ATSDR, 2000). Carboxyhemoglobin (COHb) levels can continue to 

increase reaching peak levels as much as five to six hrs after exposure (ATSDR, 2000). 

Elimination of DCM is predominantly through the lungs. Unchanged DCM also is found in small 

amounts in the urine and feces (ATSDR, 2000). At low doses, a large percentage of DCM is 

transformed into COHb and eliminated as CO, while at higher doses, more of the unchanged 

parent compound is exhaled (ATSDR, 1990; as cited in ATSDR, 2000). 

DCM has been detected in human breast milk (Pellizzari et al., 1982; US EPA, 1980 as cited in 

ATSDR, 2000), so it is possible that infants could be exposed to DCM through maternal 

exposures. However, physiologically based pharmacokinetic (PBPK) modeling suggests that 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 47

lactating females who breast feed their infants will not deliver DCM in quantities significant

enough to be harmful (Fisher et al., 1997; as cited in ATSDR, 2000). Blood concentrations of 

DCM were below the level of detection in 1,165 individuals who participated in the recent 

National Health and Nutrition Examination Survey (NHANES) 2003 to 2004 subsample of the US 

population (CDC, 2009). DCM was present in the urine of workers employed at a 

pharmaceutical factory. Urine levels appear to be nearly eliminated during the overnight 

period after exposure has occurred (HSDB, 2012). Human health effects associated with 

exposure to low environmental levels of DCM or low levels detected in biomonitoring studies 

are unknown (CDC, 2009).

3.2.2. ACUTE HAZARD

Acute inhalation exposure of humans to DCM has been associated with decreased oxygen 

availability from COHb formation and with neurological impairment from the interaction of 

DCM with membranes in the nervous system (Bos et al., 2006; ACGIH, 2001; ATSDR, 2000; 

Cherry et al., 1983; Putz et al., 1979; Gamberale et al., 1975; Winneke, 1974; as cited in US EPA, 

2011b). Acute lethality in humans following inhalation exposure is related to Central Nervous 

System (CNS) depressant effects. These effects include loss of consciousness and respiratory 

depression, resulting in irreversible coma, hypoxia, and eventual death (US EPA, 2008). The 

organ most often affected in exposures to high levels of DCM is the brain, followed by the lungs 

and heart. Especially at exposure to high concentrations in which death occurs within a 

relatively short time, it is unlikely that the formation of CO will have resulted in life-threatening 

levels of COHb (US EPA, 2008). Only one fatal case was reported to be related to a myocardial 

infarction (i.e., heart attack) without any signs of reported CNS depression (US EPA, 2008). Also 

in nonfatal cases, the adverse effects most frequently described are CNS-related only; in a few 

cases, cardiotoxic effects (i.e., evidenced by electrocardiogram [ECG] changes) were reported. 

Effects on lung, liver, or kidney have been reported as primary signs of DCM toxicity (US EPA, 

2008). It is noted that in some cases, high COHb levels (i.e., up to 40 percent) are measured 

without serious complaints. The reported COHb levels could not be linked to effects in a doserelated way in any of these cases (US EPA, 2008).

Acute exposure to humans results in acute neurobehavioral deficits measured in psychomotor 

tasks including: tests of hand-eye coordination, visual evoked response changes, and auditory 

vigilance, which may occur at concentrations >200 ppm with 4–8 hrs of exposure (Bos et al., 

2006; ACGIH, 2001; ATSDR, 2000; Cherry et al., 1983; Putz et al., 1979; Gamberale et al., 1975; 

Winneke, 1974, as cited in US EPA, 2011b). 

Neurological evaluations in animals during and after acute inhalation exposure to DCM (i.e., 

>200 to 1000 ppm for 1to 8 hrs) have resulted in CNS depressant effects with decreased motor 

activity, impaired memory, and changes in responses to sensory stimuli. Neurobehavioral, 

neurophysiological, and neurochemical/neuropathological studies have been used to 

characterize the effects of DCM on the CNS (US EPA, 2011b).
DOCUMENT-DO NOT CITE OR QUOTE 

Page 48

There are multiple lines of evidence demonstrating that DCM exposure (i.e., orally or via

inhalation) in adult animals results in measured changes in excitatory and inhibitory 

neurotransmitters, such as glutamate and acetylcholine and the inhibitory neurotransmitter, 

GABA. Additionally, dopamine and serotonin levels, which are associated with addiction and 

mood, were measured. Other parameters that were measured included DNA/protein content 

and changes in the cerebellum and hippocampus. Measurement of neurochemical changes 

provides mechanistic information, and neurobehavioral and neurophysiological effects can be 

correlated to these results. 

Though few developmental effects were observed at high exposures to DCM (Bornschein et al., 

1980; Schwetz et al., 1975), there are no studies that have adequately evaluated 

neurobehavioral and neurochemical changes resulting from gestational DCM exposure. The 

available data identify changes in behavior habituation at 4,500 ppm (Bornschein et al., 1980) 

and increases in COHb at 1,250 ppm (Schwetz et al., 1975). The behavioral changes observed at 

4,500 ppm indicate developmental neurotoxic effects; this is the only dose group used in the 

Bornschein et al. (1980) study. No other neurological endpoints have been evaluated in the 

available developmental studies of DCM. The significance of this data gap also is supported by 

evidence from adult neurotoxicity testing indicating that acute/short term exposures can affect 

neurotransmission and neurotransmitters levels. These effects on neurotransmitters levels,

while transient, may have qualitatively different outcomes if they occur during development of 

the nervous system when neurotransmitters serve a critical role in patterning the nervous

system (for review Barone et al., 2000). The potential for developmental neurotoxicity 

occurring at lower exposures to DCM represents a very important data gap.

3.2.3. CHRONIC HAZARD

Relatively little is known about the long-term neurological effects of chronic low level DCM 

exposures in humans, although there are studies that provide some evidence of an increased 

prevalence of neurological symptoms among workers with average exposures of 75 to 100 ppm 

(Cherry et al., 1981; as cited in US EPA, 2011b). Long-term effects on some neurological 

measures (i.e., possible detriments in attention and reaction time in complex tasks) have been 

observed in retired workers whose past chronic exposures were in the 100 to 200 ppm range 

(Lash et al., 1991; as cited in US EPA, 2011b). These studies are limited by the relatively small 

sample sizes and their low power for detection of statistically significant results.

Following repeated inhalation exposure to DCM, the liver is the most sensitive target for noncancer toxicity in rats and mice. Lifetime exposure was associated with hepatocyte vacuolation 

and necrosis in F344 rats exposed to 1,000 ppm for six hrs/day (Mennear et al., 1988; NTP, 

1986; as cited in US EPA, 2011b), hepatocyte vacuolation in Sprague-Dawley rats exposed to 

500 ppm for six hrs/day (Nitschke et al., 1988a; Burek et al., 1984 as cited in US EPA, 2011b), 

and hepatocyte degeneration in B6C3F1 mice exposed to 2,000 ppm for six hrs/day (i.e., lower 

concentrations were not tested in mice) (Mennear et al., 1988; NTP, 1986; as cited in US EPA, 

2011b). Other effects observed include renal tubular degeneration in F344 rats and B6C3F1
DOCUMENT-DO NOT CITE OR QUOTE 

Page 49

mice at 2,000 ppm, testicular atrophy in B6C3F1 mice at 4,000 ppm, and ovarian atrophy in 

B6C3F1 mice at 2,000 ppm.

DCM was determined as “likely to be carcinogenic in humans” under the Guidelines for 

Carcinogen Risk Assessment (US EPA, 2005; as cited in US EPA, 2011b). Results from two-year

bioassays provide adequate evidence of the carcinogenicity of DCM and data to describe doseresponse relationships in mice and rats exposed by inhalation. Oral exposure to DCM produced 

statistically significant increases in hepatocellular adenomas and carcinomas in male B6C3F1 

mice (Serota et al., 1986; Hazleton Laboratories, 1983; as cited in US EPA, 2011b). Inhalation 

exposure to concentrations of 2,000 or 4,000 ppm DCM produced increased incidences of lung 

and liver tumors in male and female B6C3F1 mice (Maronpot et al., 1995; Foley et al., 1993; 

Kari et al., 1993; Mennear et al., 1988; NTP, 1986; as cited in US EPA, 2011b). Significantly 

increased incidences of benign mammary tumors (adenomas or fibroadenomas) were observed 

in male and female F344/N rats exposed by inhalation to 2,000 or 4,000 ppm (NTP, 1986; 

Mennear et al., 1988; as cited in US EPA, 2011b).

The information on the Mode of Action (MOA) for one of the most sensitive adverse effects for 

acute exposure to DCM indicates both time dependent changes in some neurological endpoints 

that track more closely with the blood levels of parent compound versus generation of carbon 

monoxide or as measured by COHb (Putz et al., 1979; Winneke, 1981). The CNS depressant 

effects versus hypoxic response track with these two proximate toxicants (Winneke, 1981) and 

are relevant to both acute adult and developmental neurotoxicity. In the case of the MOA for 

chronic exposure, it is less clear what mediates the non-cancer effects with the exception of 

some cancers which have mutagenic mode of action (for review see US EPA, 2011b).

3.3. HUMAN HEALTH ASSESSMENT: DOSE-RESPONSE 

Non-cancer and cancer dose-response assessments have been conducted by various agencies

(For details, see Appendix H). For the non-cancer assessments, these values represent 

exposure levels that are either not expected to result in an appreciable adverse effect (e.g., 

CalEPA REL or EPA’s reference concentration [RfC]) or may represent a threshold where 

exposures above the value are expected to result in specific effects (e.g., EPA’s AEGL-2 for 

disability) or provide guidance on chemical exposures that may occur during normal operations 

(i.e., of spacecraft) as well as under some emergency situations (e.g., NASA Spacecraft 

Maximum Allowable Concentrations (SMACs; See Table 3-8)) (NRC, 1996). NAS developed the 

one-hr SMAC as the concentration of DCM that will not compromise the performance of 

specific tasks by healthy astronauts during emergency conditions or cause serious or 

permanent toxic effects. 

For the cancer assessments, the estimated values represent published upper-bound3 excess 

cancer risk from continuous exposure to a chemical at a concentration of 1 μg/m3. For 

 3 A plausible upper limit to the true value of a quantity, usually not a true statistical confidence limit.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 50

example, if a unit risk was 2 × 10-6 per μg/m3, then two excess cancer cases (upper bound 

estimate) would be expected to develop per 1,000,000 people if exposed daily for a lifetime to 

1 μg/m3 of the chemical. 

The assessments conducted by the US EPA, California’s Office of Environmental Health Hazard 

Assessment (OEHHA) derived a reference exposure limit (REL), NAS developed the one-hr

SMAC, and the National Advisory Committee on AEGLs (i.e.., Acute Exposure Guideline Levels 

for emergency response – Appendix F) were used to derive points of departure (PODs) for 

inhalation exposures of DCM associated with its use as a paint stripper in this assessment. 

These PODs represent the concentration levels from the principal studies where uncertainty 

factors (UFs) were applied to derive specific levels of exposure (e.g., CalEPA’s REL = POD ÷ UFs). 

For the non-cancer portion of this assessment, the composite UFs were used as the benchmark

margin of exposure (MOE). 

EPA developed a list of the human health toxicity values and the dose-response assessment 

information that were considered relevant for this analysis of acute and chronic exposure 

scenarios (Table 3-8). More extensive summaries of the hazard and dose-response information 

used in this assessment are provided in Appendices E and F, respectively. These data were used 

in conjunction with the occupational exposure and consumer monitoring data discussed in the 

following sections to characterize the potential risks to workers and residential users of DCMcontaining products.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 51

Table 3-8. Worker Inhalation Health Effect Reference Values Used in the Risk Assessment.

a

Non-Cancer Acute Effects

Reference 

Value Duration Reference Valueb

Health Effect

(Key Study) POD UFsc Additional Information Reference

AEGL-3 Acute, 8 hrs 7,400 mg/m3 Absence of central 

nervous system (CNS)-

related mortality in rats 

(Haskell Laboratory, 

1982), carboxyhemoglobin (COHb)

formation in humans 

(NRC, 2010)

DCM concentration 

in rat brain of 

3.01 mM and 

maximum of 

15 percent COHb 

formation in 

humans

Total UF 

= 3

UFA = 1

UFH = 3

Time scaling based on 

maximum DCM concentration 

(10, 30, and 60 minutes and 

4 hrs) or on COHb formation 

(8-hr exposure)

US EPA 

Acute, 4 hrs 17,000 mg/m (2008) 3

Acute, 1 hr 24,000 mg/m3

Acute, 30 

minutes

30,000 mg/m3

Acute, 10 

minutes

42,000 mg/m3

AEGL-2d Acute, 8 hrs 210 mg/m3 Absence of CNS effects in 

humans (Winneke, 

1974), COHb formation 

in humans (NRC, 2010)

DCM concentration 

in human brain of 

0.137 mM and 

maximum of 

4 percent COHb 

formation

Total UF 

= 1

UFH = 1

Time scaling based on 

maximum DCM concentration 

in human brain (10 and 30

minutes) or on COHb 

formation (1-, 4-, and 8-hr

exposure)

US EPA 

Acute, 4 hrs 350 mg/m (2008) 3

Acute, 1 hr 2,000 mg/m3

Acute, 30 

minutes

4,200 mg/m3

Acute, 10 

minutes

6,000 mg/m3

AEGL-1 Acute, 

4 and 8 hrs

Not recommended Not recommended because 

the calculated values were at 

or above the corresponding 

AEGL-2 values

US EPA 

(2008)

Acute, 1 hr 710 mg/m3 Absence of slight CNS 

effects (Stewart et al., 

1972)

DCM concentration 

in human brain of 

0.063 mM 

corresponding to 

514 ppm at 1-hr

exposure

Total UF 

= 3

UFH = 3

Time scaling based on 

maximum DCM concentration 

in human brain using a

physiologically based 

pharmacokinetic (PBPK) model

Acute, 30 

minutes 800 mg/m3

Acute, 10 

minutes

1,000 mg/m3

a

These interim AEGLs have been reviewed by the National Advisory Committee on AEGLs, but have not been finalized by the National Academies. b

Conversion factor: 1 mg/m3 = 0.28 ppm. c

UFL = LOAEL-to-NOAEL UF; UFA = interspecies UF; UFH = intraspecies UF; UFD = UF reflecting database deficiencies. d

AEGL-2 values are thresholds for disability and are generally considered action levels for risk in emergency response situations. They are used for consumer 

and worker exposure to better characterize the risk picture.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 52

Table 3-8. Worker Inhalation Health Effect Reference Values Used in the Risk Assessment.

Non-Cancer Acute Effects

Reference 

Value Duration

Reference 

Valuea

Health Effect

(Key Study) POD UFb Additional Information Reference

California 

REL

Acute,

1 hr

14 mg/m3 Impaired performance 

on dual-task and 

auditory vigilance tests in 

humans (Putz et al., 

1979)

LOAEL = 688 mg/m3

at 90 minutes or 

842 mg/m3 when 

time adjusted to a 

60-minute exposure

Total UF 

= 60

UFL = 6

UFH = 10

ten Berge equation (Cnxt = k, n

= 2) was used for time 

adjustment from 90 to 

60 minutes

OEHHA 

(2008)

SMAC Acute,

1 hr

350 mg/m3 CNS depression based on 

human observations 

(Putz et al., 1979; 

DiVincenzo and Kaplan, 

1981; Stewart et al., 

1972; Peterson, 1978; 

Andersen et al., 1991; 

Astrand et al., 1975; 

Ratney et al., 1974; as 

cited in NRC, 1996)

NOAEL = 350 mg/m3

for 1-hr exposure to 

DCM

UFs were 

not 

applied 

to 1-hr

SMAC 

value

NOAELs for CNS depression 

have not been reported for 

DCM exposures. A linear 

regression analysis estimated 

the DCM concentration (350 

mg/m3

) that produces ~3

percent COHb concentration in 

blood (NOAEL for CNS effects 

related to COHb formation)

NRC 

(1996, 

2008)

Non-Cancer 

Chronic Effects

RfC Chronic 0.6 mg/m3 Hepatic effects (hepatic 

vacuolation) in rats 

observed in 2-year 

inhalation bioassay 

(Nitschke et al., 1988a; 

as cited in US EPA, 

2011b)

1st percentile HEC: 

17.2 mg/m3

Total UF 

= 30

UFA = 3

UFH = 3

UFD = 3

PBPK modeling was used in the 

RfC derivation

US EPA 

(2011b)
DOCUMENT-DO NOT CITE OR QUOTE 

Page 53

Table 3-8. Worker Inhalation Health Effect Reference Values Used in the Risk Assessment.

a

onReference 

Value Duration Reference Valueb

Health Effect

(Key Study) POD UFsc Additional Information Reference

Cancer Chronic 

Effects

IUR Chronic 1 × 10-5 per 

mg/m3

Liver and lung cancer in 

male B6C3F1 mice

(Mennear et al., 1988; 

NTP, 1986; as cited in US 

EPA, 2011b)

Mouse BMDL10

combined with 

tissue-specific GSTinternal dose metric 

with allometric 

scaling

Not 

applicabl

e

Mutagenic mode of action; 

PBPK modeling and a 

multistage model with linear 

extrapolation from the POD

(BMDL10)

US EPA 

(2011b)

a

Conversion factor: 1 mg/m3 = 0.28 ppm. b

UFL = LOAEL UF; UFA = interspecies UF; UFH = intraspecies UF; UFD = database deficiency UF.

BMDL10 = lower 95 percent confidence limit of the 10 percent benchmark dose; GST = glutathione-S-transferase; HEC = human equivalent concentration; 

IUR = inhalation unit risk; LOAEL = lowest-observed-adverse-effect level; NOAEL = no-observed-adverse-effect level; SMAC = spacecraft maximum allowable 

concentration
DOCUMENT-DO NOT CITE OR QUOTE 

Page 54

3.4. HUMAN HEALTH RISK CHARACTERIZATION

3.4.1. RISK ESTIMATION APPROACH FOR ACUTE AND REPEATED EXPOSURES

Non-cancer risks were addressed by comparing consumer and worker exposures to levels of 

exposure that cause effects, or are thresholds for effects, in animals or humans as appropriate. 

The ratio of this comparison is an indicator of the concern level for these effects. All consumer 

and worker exposure scenarios resulted in exposures that were very close to, or exceeded, the 

threshold or effect levels for DCM. Cancer risks were calculated only for worker exposure. 

Cancer incidence risks were calculated by multiplying the exposure estimates by the EPAdetermined cancer risk value. Cancer risks varied between levels of a few in a million to a few 

in a thousand. In 5 of the 7 worker exposure scenarios, the cancer risk was estimated to be 

more than one in a thousand.

To estimate non-cancer acute and chronic risks, EPA calculates a margin of exposure (MOE), 

which is the ratio of the one of the following, no-observed-adverse-effect level [NOAEL], 

NOAELHEC, or lowest-observed-adverse-effect level [LOAEL] or BMDL to the estimated 

exposure. This approach allows the reader to better understand the toxicological basis for the 

risks and the importance of the identified uncertainties and how they potentially affect EPA’s

determination of risk. This MOE is compared to a level of concern, which is the same value as 

the total UF relevant to a particular toxicity study (Table 3-9). EPA’s level of concern for noncancer effects depends on the specific scenarios assessed. MOEs that are lower than the level 

of concern are interpreted as potential human health risks, but do not necessarily mean that 

these health effects will occur. MOEs exceeding the level of concern (i.e., total UF (UFTotal)) are 

interpreted as a negligible concern for adverse human health effects. Typically, the larger the 

MOE, the more unlikely it is that a non-cancer adverse effect would occur. 

3.4.2. RISK ESTIMATION APPROACH FOR ACUTE EXPOSURES

EPA chose to use the CalEPA’s REL for DCM as the basis for its acute POD to address noncancer 

consumer exposures. This REL was derived by applying a composite UF of 60 to a POD, based 

on impaired cognitive performance in acutely exposed humans (Putz et al., 1979). EPA used this 

POD which was a LOAEL in a human study point of departure. This POD (688 mg/m3) was for 90 

minutes and was time adjusted to a 60-minute using a ten Berge equation (Cn

xt = k, n = 2) 

resulting in POD of 842 mg/m3

. The benchmark MOE for the acute inhalation is ≥60 where no 

adverse effects would be expected. This MOE of 60 is made up of a factor of 6 accounting for a

LOAEL to NOAEL extrapolation and factor of 10 accounting for human variability.

In addition, EPA assessed acute risks by calculating hazard quotients (HQacute). Air 

concentrations of DCM may reach dangerous levels in enclosed environments when individuals 

are using DCM-based paint strippers for a single daily use. Thus, air concentration thresholds 

for disability (i.e., typically notes for an AEGL-2) are compared with the estimated inhalation 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 55

exposures for residential users4 and other non-user residential occupants (e.g., children). This 

risk assessment presents the AEGL derivations with their POD and UFs as a point of comparison 

to other hazard estimates used in the MOE approaches.

AEGLs represent threshold exposure limits for the general public, including infants and children 

as well as other individuals who may be sensitive or susceptible. They are applicable for oncein-a-lifetime acute exposures (i.e., ≤24 hrs) to airborne concentrations of highly toxic chemicals 

typically occurring during emergency response situations. AEGL values are developed for three 

different health effect end point tiers (i.e., discomfort = AEGL-1 threshold; disability = AEGL-2 

threshold; and death = AEGL-3 threshold) at different durations of exposure (i.e., 10 minutes; 

30 minutes; one hr; four hrs; and eight hrs).

For this assessment, the one-hr AEGL-2 value provides a useful comparison between the 

threshold concentration for disability (i.e., AEGL-2) and air concentrations (i.e., measured or 

modeled) of DCM exposures to residential users and residential non-users or bystanders

(Appendix F). Exposure levels that are estimated to be less than the one-hr AEGL-2 (i.e., HQ <1) 

are not likely to be associated with DCM-induced incapacitating effects. However, EPA expects 

that exposure to levels greater than the one-hr AEGL-2 (i.e., HQ >1) are dangerous for human 

health.

MOE and HQ values give some indication of the degree of risk but alone cannot give an 

understanding of the exposure paradigm and how it relates to the endpoints used in the risk 

characterization. A more complete characterization is presented in Figures 3-5 to 3-8. Figures 

3-5 and 3-6 present exposures to the user for brush and spray applications respectively and 

their relation to the endpoints used in the risk characterization. In Figure 3-5 the “spikes” of 

exposure returning to a baseline in Scenarios 1, 3 and 7 represent the user applying DCM by 

brush in the workshop and leaving the workshop area to move to the rest of the house (ROH) 

while the DCM is working. The next spike is when the user returns to the workshop, removes

the paint and applies another coat of DCM. Scenario 2 lacks the pointed spikes of exposure 

because it reflects the user staying in the workshop during the entire paint stripping process. 

Figure 3-6 tells a similar story for user exposure during spray application.

The concentrations of DCM in the workshop and the ROH are presented in Figures 3-7 and 3-8 

for brush and spray applications respectively and their relation to the endpoints used in the risk 

characterization. The concentration of DCM in the ROH is also the exposure the non-user or 

bystander experiences.

 4 A user is defined as an individual(s) applying the product such as a DIY homeowner or a professional contractor. 

Other residential occupants are defined as other individual(s) present in the house who are not involved in the 

paint-stripping activity and are located in a house zone other than the one in which the paint-stripping activity is 

taking place (see Exposure section).
DOCUMENT-DO NOT CITE OR QUOTE 

Page 56

3.4.3. RISK ESTIMATION APPROACH FOR REPEATED EXPOSURES

EPA chose to use the chronic POD from EPA’s DCM RfC as the basis for its non-cancer 

occupational exposures. EPA’s chronic RfC for DCM was derived by applying a composite UF of 

30 to a POD; this is based on hepatic effects seen in a two-year rat inhalation study (US EPA 

2011b). The benchmark MOE for the acute inhalation is ≥30 where no adverse effects would be 

expected. This MOE of 10 is made up of a factor of 3 accounting for interspecies extrapolation 

for pharmacodynamics and, a factor of 3 accounting for human variability (see uncertainty 

section).

Liver and lung cancer in male B6C3F1 mice (Mennear et al., 1988; NTP, 1986 as cited in US EPA, 

2011b) were identified as the basis for estimating chronic cancer risk for occupational 

scenarios. To estimate excess cancer risk from chronic worker exposures to DCM included in 

this assessment (i.e., professional contractors, automotive and furniture refinishing, art 

restoration/conservation, aircraft paint stripping, and unspecified workplace setting involving 

immersion stripping of wood, and wood and metal paint stripping), a cancer risk estimate was 

calculated. This value is a unitless incremental probability of an individual developing cancer 

over a lifetime as a result of exposure to the potential carcinogen (i.e., incremental or excess 

individual lifetime cancer risk) (US EPA, 1989).

A summary of the toxicological endpoints and risk approaches used in EPA’s assessment of the 

hazard potential for DCM for paint stripping applications is provided in Table 3-9.

Table 3-9. Toxicological Endpoints and Approaches for Assessing Risks to DCM-Based Paint Strippers.

Exposure

Scenario

Concentration(s) and Time 

Duration(s) Used in 

Risk Assessment

Level of 

concern

Toxicological

Effect

Risk Estimation 

Approach

Non-Cancer Acute Inhalation Risks

Residential usersa

and non-usersb

LOAEL = 842 mg/m3 at 1 hrc

from California’s acute REL doseresponse assessment (OEHHA, 

2008)

UFL = 6

UFH = 10

Total UF = 60

CNS effects MOEd

NOAEL = 350 mg/m3 at 1 hr

from SMAC’s dose-response 

assessment (NRC, 1996, 2008)

UFH = 10

Total UF = 10

CNS effects MOE

1-hr AEGL-2 = 2,000 mg/m3

4-hr AEGL-2 = 350 mg/m3

8-hr AEGL-2 = 210 mg/m3

from AEGL's dose-response 

assessment (US EPA, 2008)

Hazard 

Quotient 

(HQ)

e > 1

CNS effects HQ

Non-Cancer Chronic Inhalation Risks

Small-shop 

workers

1st percentile HEC= 17.2 mg/m3

(equivalent to a NOAEL)

UFA = 3

UFH = 3

Liver toxicity MOE
DOCUMENT-DO NOT CITE OR QUOTE 

Page 57

from EPA RfC’s dose-response 

assessment (US EPA, 2011b)

Total UF=10

Cancer Chronic Inhalation Risks

Chronic inhalation, 

small-shop 

workers

1 × 10-5 per mg/m3

EPA’s inhalation unit risk (US EPA, 

2011b)

1 × 10-6 Liver and 

lung cancer

Excess cancer riskf

a

Users are assumed to be exposed to a 1-hr single daily use. The peak-TWA concentration for 1-hr exposures are 

used in the risk analysis.

b

These individuals are not involved in the paint-stripping activity and are located in a house zone other than the 

one in which the paint-stripping activity is taking place. These individuals may be healthy adults, infants, children, 

pregnant women, or the elderly. c

Details about the health effects, PODs, UFs, and key studies are described in Appendix F. d

MOE = NOAEL, NOAELHEC, LOAEL or BMDL (mg/m3) ÷ Human Exposure Estimate (mg/m3). e

HQ = Human Exposure Estimate (mg/m3) ÷ 1-hr AEGL-2 (mg/m3). f

Excess cancer risk = Human Exposure Estimate (mg/m3) × IUR (1 × 10-5 per mg/m3).

 

3.4.4. RISK ESTIMATES FOR NON-CANCER ACUTE INHALATION EXPOSURES IN A RESIDENTIAL SETTING

The potential risks of concern from acute DCM exposures indicate exceedances for both the 

MOE and HQ approaches. As presented in Table 3-10, the acute MOEs ranged from 0.2 to 7, 

whereas the HQacute values for one, four, and eight hrs ranged from 0.1 to 0.8, 0.3 to 2.3, and 

0.2 to 2.7, respectively (Table 3-11). All of these MOEs are significantly lower than the 

benchmark level of concern and are interpreted as potential human health risks of concern and 

in many cases represent exposures exceeding the PODs. Further, the HQ approach indicated 

the potential for incapacitating effects in some users (i.e., Scenarios 2, 3, 5, 6, and 7) and for 

non-users (i.e., Scenarios 3 and 6) exposed to DCM for four or eight hrs, but not for one-hr

exposures, (i.e., which is indicated by HQ>1 in bold). These results are presented graphically in 

Figures 3-5 to 3-8.

Table 3-10. MOEs for CNS Effects following Acute Exposure Scenarios for Consumer/Residential Users 

and Non-Users of DCM-Based Paint Strippers.

Exposure Scenario Individual

Maximum or Peak 

TWA Concentration 

for 1-hr Exposurea

,

mg/m3

MOEs

LOAEL=842 mg/m3

Level of Concern 

MOE <60

NOAEL=350 mg/m3

Level of Concern 

MOE <10

Scenario #1

Brush application in 

workshop, 

central parameter values

User 220 4 2

Non-user 120 7 3

Scenario #2

Brush application in 

workshop, 

upper-end values for user

User 1,100 0.8 0.3

Non-user 210 4 2

Scenario #3 User 760 1 0.5
DOCUMENT-DO NOT CITE OR QUOTE 

Page 58

Brush application in 

workshop, upper-end values 

for user and non-user

Non-user 460 2 0.8

Scenario #4

Spray application in 

workshop, central 

parameter values

User 490 2 0.7

Non-user 280 3 1

Scenario #5

Spray application in 

workshop, upper-end values 

for user

User 1,600 0.5 0.2

Non-user 310 3 1

Scenario #6

Spray application in 

workshop, upper-end values 

for user and non-user

User 1,100 0.8 0.3

Non-user 700 1 0.5

Scenario #7

Brush application in 

bathroom, simulation

User 840 1 0.4

Non-user 220 4 2

All of the MOE and some of the HQacute risk estimates indicate a potential risk of concern to 

human health in residential environments where DCM vapors are released during brush-on or 

spray-on applications of DCM-based paint strippers.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 59

Table 3-11. Acute HQs for Residential Users and Non-Users of DCM-based Paint Strippers.

Exposure Scenario Individual

Maximum or 

Peak TWA 

Concentration 

for 1-hr

Exposuresa

,

mg/m3

Maximum or 

Peak TWA 

Concentration 

for 4-hr

Exposuresa

,

mg/m3

Maximum or Peak 

TWA Concentration 

for 8-hr Exposuresa,

mg/m3

Acute HQ

1-Hr AEGL-2 =

2,000 mg/m3

Level of Concern 

HQ >1

4-Hr AEGL-2 =

350 mg/m3

Level of Concern 

HQ >1

8-Hr AEGL-2 =

210 mg/m3

Level of Concern 

HQ >1

Scenario #1

Brush application in 

workshop, 

central parameter values

User 220 120 69 0.11 0.34 0.33

Non-user 120 82 49 0.060 0.23 0.23

Scenario #2

Brush application in 

workshop, 

upper-end values for user

User 1,100 420 220 0.55 1.2 1.0

Non-user 210 140 82 0.11 0.40 0.39

Scenario #3

Brush application in 

workshop, upper-end values 

for user and non-user

User 760 560 400 0.38 1.6 1.9

Non-user 460 380 290 0.23 1.1 1.4

Scenario #4

Spray application in 

workshop, central parameter 

values

User 490 270 150 0.25 0.77 0.71

Non-user 280 190 110 0.14 0.54 0.52

Scenario #5

Spray application in 

workshop, upper-end values 

for user

User 1,600 620 330 0.80 1.8 1.6

Non-user 310 200 120 0.16 0.57 0.57

Scenario #6

Spray application in 

workshop, upper-end values 

for user and non-user

User 1,100 810 580 0.55 2.3 2.8

Non-user 700 580 430 0.35 1.7 2.0

Scenario #7

Brush application in 

bathroom, simulation

User 840 560 350 0.42 1.6 1.7

Non-user 220 190 150 0.11 0.54 0.71

a

These are the user’s personal-concentration results reported in the Exposure assessment and reflect temporary relocation of the user to Zone 2 rest of house (i.e., 

ROH) during wait times between applying and scrapping the DCM-based paint stripper.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 60

Figure 3-5. Comparison of Acute Toxicity Values and User Exposures during Brush Application in a Residential Workshop.

0.01

0.1

1

10

100

1000

10000

100000

0 1 2 3 4 5 6 7 8

DCM Concentration (mg/m3)

Time (Hours)

Scenario #2: Exposure Concentrations for User during 

Brush Application in Workshop, 

Upper-End Values for User

User Personal 

Concentration

California acute REL

Adjusted SMAC

AEGL-1 (Detectability)

AEGL-2 (Disability)

AEGL-3 (Lethality)

0.01

0.1

1

10

100

1000

10000

100000

0 1 2 3 4 5 6 7 8

DCM Concentration (mg/m3)

Time (Hours)

Scenario #7: Exposure Concentrations for User during 

Brush Application in Bathroom, 

Simulation

User Personal 

Concentration

California acute REL

Adjusted SMAC

AEGL-1 (Detectability)

AEGL-2 (Disability)

AEGL-3 (Lethality)

0.01

0.1

1

10

100

1000

10000

100000

0 1 2 3 4 5 6 7 8

DCM Concentration (mg/m3)

Time (Hours)

Scenario #1: Exposure Concentrations for User during 

Brush Application in Workshop, 

Central Parameter Values

User Personal 

Concentration

California acute REL

Adjusted SMAC

AEGL-1 (Detectability)

AEGL-2 (Disability)

AEGL-3 (Lethality)

0.01

0.1

1

10

100

1000

10000

100000

0 1 2 3 4 5 6 7 8

DCM Concentration (mg/m3)

Time (Hours)

Scenario #3: Exposure Concentrations for User during 

Brush Application in Workshop, 

Upper-End Values for User and Non-User

User Personal 

Concentration

California acute REL

Adjusted SMAC

AEGL-1 (Detectability)

AEGL-2 (Disability)

AEGL-3 (Lethality)
DOCUMENT-DO NOT CITE OR QUOTE 

Page 61

0.01

0.1

1

10

100

1000

10000

100000

0 1 2 3 4 5 6 7 8

DCM Concentration (mg/m3)

Time (Hours)

Scenario #5: Exposure Concentrations for User during 

Spray Application in Workshop, 

Upper-End Values for User

User Personal 

Concentration

California acute REL

Adjusted SMAC

AEGL-1 (Detectability)

AEGL-2 (Disability)

AEGL-3 (Lethality)

0.01

0.1

1

10

100

1000

10000

100000

0 1 2 3 4 5 6 7 8

DCM Concentration (mg/m3)

Time (Hours)

Scenario #6: Exposure Concentrations for User during 

Spray Application in Workshop, 

Upper-End Values for User and Non-User

User Personal 

Concentration

California acute REL

Adjusted SMAC

AEGL-1 (Detectability)

AEGL-2 (Disability)

AEGL-3 (Lethality)

0.01

0.1

1

10

100

1000

10000

100000

0 1 2 3 4 5 6 7 8

DCM Concentration (mg/m3)

Time (Hours)

Scenario #4: Exposure Concentrations for User during 

Spray Application in Workshop, 

Central Parameter Values

User Personal 

Concentration

California acute REL

Adjusted SMAC

AEGL-1 (Detectability)

AEGL-2 (Disability)

AEGL-3 (Lethality)
DOCUMENT-DO NOT CITE OR QUOTE 

Page 62

Figure 3-6. Comparison of Acute Toxicity Values and User Exposures during Spray Application in a Residential Workshop.

Figure 3-7. Comparison of Acute Toxicity Values and Zone-Specific DCM Concentrations for Brush Application in Residential Workshop or 

Bathroom.

0.01

0.1

1

10

100

1000

10000

100000

0 1 2 3 4 5 6 7 8

DCM Concentration (mg/m3)

Time (Hours)

Scenario #2: Zone-Specific Concentrations during 

Brush Application in Workshop, 

Upper-End Values for User

Zone 1 (Workshop)

Zone 2 (ROH)

California acute REL

Adjusted SMAC

AEGL-1 (Detectability)

AEGL-2 (Disability)

AEGL-3 (Lethality)

0.01

0.1

1

10

100

1000

10000

100000

0 1 2 3 4 5 6 7 8

DCM Concentration (mg/m3)

Time (Hours)

Scenario #7: Zone-Specific Concentrations during 

Brush Application in Bathroom, 

Simulation

Zone 1 (Source Cloud)

Zone 2 (Bathroom)

Zone 3 (ROH)

California acute REL

Adjusted SMAC

AEGL-1 (Detectability)

AEGL-2 (Disability)

AEGL-3 (Lethality)

0.01

0.1

1

10

100

1000

10000

100000

0 1 2 3 4 5 6 7 8

DCM Concentration (mg/m3)

Time (Hours)

Scenario #1: Zone-Specific Concentrations during 

Brush Application in Workshop, 

Central Parameter Values

Zone 1 (Workshop)

Zone 2 (ROH)

California acute REL

Adjusted SMAC

AEGL-1 (Detectability)

AEGL-2 (Disability)

AEGL-3 (Lethality)

0.01

0.1

1

10

100

1000

10000

100000

0 1 2 3 4 5 6 7 8

DCM Concentration (mg/m3)

Time (Hours)

Scenario #3: Zone-Specific Concentrations during 

Brush Application in Workshop, 

Upper-End Values for User and Non-User

Zone 1 (Workshop)

Zone 2 (ROH)

California acute REL

Adjusted SMAC

AEGL-1 (Detectability)

AEGL-2 (Disability)

AEGL-3 (Lethality)
DOCUMENT-DO NOT CITE OR QUOTE 

Page 63

Figure 3-8. Comparison of Acute Toxicity Values and Zone-Specific DCM Concentrations for Spray Application in Residential Workshop. 

0.01

0.1

1

10

100

1000

10000

100000

0 1 2 3 4 5 6 7 8

DCM Concentration (mg/m3)

Time (Hours)

Scenario #5: Zone-Specific Concentrations during 

Spray Application in Workshop, 

Upper-End Values for User

Zone 1 (Workshop)

Zone 2 (ROH)

California acute REL

Adjusted SMAC

AEGL-1 (Detectability)

AEGL-2 (Disability)

AEGL-3 (Lethality)

0.01

0.1

1

10

100

1000

10000

100000

0 1 2 3 4 5 6 7 8

DCM Concentration (mg/m3)

Time (Hours)

Scenario #6: Zone-Specific Concentrations during 

Spray Application in Workshop, 

Upper-End Values for User and Non-User

Zone 1 (Workshop)

Zone 2 (ROH)

California acute REL

Adjusted SMAC

AEGL-1 (Detectability)

AEGL-2 (Disability)

AEGL-3 (Lethality)

0.01

0.1

1

10

100

1000

10000

100000

0 1 2 3 4 5 6 7 8

DCM Concentration (mg/m3)

Time (Hours)

Scenario #4: Zone-Specific Concentrations during 

Spray Application in Workshop, 

Central Parameter Values

Zone 1 (Workshop)

Zone 2 (ROH)

California acute REL

Adjusted SMAC

AEGL-1 (Detectability)

AEGL-2 (Disability)

AEGL-3 (Lethality)
DOCUMENT-DO NOT CITE OR QUOTE 

Page 64

3.4.5. OCCUPATIONAL RISK ESTIMATES FOR CHRONIC INHALATION

For occupational chronic inhalation concerns, the MOEs calculated for small-shop workers 

handling DCM-based paint strippers are shown in Table 3-12. For the risk calculations, EPA

assumed that the worker is exposed for eight hrs/day, 250 days/year, for a working lifetime of 

40 years. The ranges of MOEs for the different industries indicate potential risks of concern 

(i.e., the industry based MOE were below the benchmark MOE 10) with two exceptions, the 

lower end exposures for furniture refinishing and the art restoration industry had a low concern 

for non-cancer risks based on an MOE of 31 and 38, respectively. 

Table 3-12. Occupational Risks for Repeated Exposures to DCM from Paint Stripping Activities.

Industry

Range of

8-hr TWA 

Exposures 

(mg/m3

)

a

ADC 

(mg/m3

)

b

LADC 

(mg/m3)

b

Range of Chronic 

MOEsc

NOAEL = 17.2 mg/m3

Level of Concern 

MOE <10

Range of

Inhalation Cancer 

Risks

Professional 

contractors

60-2,980 14-680 7.8-390 1-0.03e 8 × 10-5-4 × 10-3

Automotive 

refinishing

90-416 21-95 12-54 0.8-0.18 1 × 10-4-5 × 10-4

Furniture 

refinishing

2.4-1,270 0.55-290 0.32-170 31-0.059 3 × 10-6f-2 × 10-3

Art restoration 

and conservationd

2 0.46 0.26 37 3 × 10-6 f

Aircraft paint 

stripping

86-3,802 20-870 11-500 0.86-0.020 1 × 10-4-5 × 10-3

Unspecified 

workplace setting: 

immersion 

stripping of wood

35-7,000 8.0-1,600 4.6-910 2.2-0.011 5 × 10-5-9 × 10-3

Unspecified 

workplace setting: 

wood and metal 

paint stripping

633-1,017 150-230 83-130 0.12-0.074 8 × 10-4-1 × 10-3

a

These exposures include 8-hr TWA exposures that were either directly measured or calculated from shorter time 

frame exposures by the study authors.

b

ADCs and LADCs are calculated from 8-hr TWA exposures reported in the exposure assessment (Section 3, 

Table 3-3). Conservative exposure assumptions are used in the ADC and LADC calculations: 8 hrs/day, 

250 days/year for 40 years. c

MOEs are calculated by dividing the POD for chronic liver toxicity (US EPA, 2011b) (17.2 mg/m3 or HEC) by the 

ADCs. There is a risk concern when MOE < UFTotal = 30. d

The data point provided for this industry was obtained from OSHA IMIS. No other literature data were obtained.

e

Bolded values indicate that the MOE or excess cancer risks were exceeded. f

Italicized values indicate a marginal concern for excess cancer risk.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 65

3.5. DISCUSSION OF KEY SOURCES OF UNCERTAINTY AND DATA LIMITATIONS

This section contains discussion of key uncertainties and data limitations for three main topics 

of the assessment:

• Occupational Exposure Estimates,

• Consumer Exposure Estimates, and

• Toxicity and Risk Assessment.

3.5.1. KEY UNCERTAINTIES AND DATA LIMITATIONS FOR OCCUPATIONAL EXPOSURE ESTIMATES 

The principal limitation of the worker exposure data is the uncertainty in the 

representativeness of the data. EPA reviewed a number of published exposure studies with

inherent data limitations including: number of facilities, job sites, or residences; most often,

limited number of sites investigated. This reduced information sampling pool introduces 

uncertainty and precludes EPA from ascertaining whether the observed data are fairly 

representative of the broad array of possible sites at all geographic locations across the US and 

for all workers within the particular end-use application. The level of exposure to DCM during 

stripping processes depends highly on the use of adequate engineering controls (i.e., general 

and local exhaust ventilation systems) and work practices as seen by the range of exposure data 

(TNO, 1999). Therefore, these differences can limit the representativeness of any one site with 

regards to all sites within the specific end-use application. As a result of these uncertainties,

the actual exposure distributions are unknown; the assumed central tendency and high-end 

exposures may, or may not, fall within the range of exposures estimated for this assessment.

An additional data limitation for occupation exposure estimation is the age of the identified 

exposure studies. Most of the exposure studies were conducted in the 1990s, with some predating the 1990s; some studies were more recent. Some references have discussed a trend to 

reduce the use of DCM in paint stripping products (i.e., OSHA promulgated new exposure limits 

for DCM in 1997). These factors can limit the representativeness of 1990 and older data with 

regards to present day workplace conditions and exposures. As a result of these uncertainties, 

it is not known, but it is possible, that actual exposure distributions could be declining during 

the monitoring period considered in this assessment.

The OSHA IMIS data have the same data limitations as discussed above for the published 

occupational exposure studies. IMIS data also have additional data limitations to consider. 

Whereas most exposure studies provide information on the investigated site, engineering 

controls, and working activities, this is not the case for IMIS data. The IMIS data include only a 

brief description of the monitored worker activity, but do not provide information on whether 

the activity involved chemical paint stripping (i.e., particularly using DCM). Therefore, the 

relevance of IMIS data to exposures that occur from DCM-based paint stripping is uncertain;

EPA cannot draw conclusions about worker exposures within the art restoration and 

conservation uses based upon the IMIS data. As a result, central tendency and high-end 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 66

exposures may be above or below the estimated exposures for these industries in this 

assessment.

Lack of certainty in the identity of activities that are sources of exposures of DCM can make risk 

determinations more difficult. DCM can be used in both paint strippers and paints and 

coatings. This leads to a recognized uncertainty when evaluating data for certain industries. 

When evaluating OSHA IMIS data or other release and exposure information, unless the worker 

activity or release source specifically cites paint stripping activities, it is not known whether 

reported data are representative of paint stripping activities or might also include other 

activities such as surface coating. The same uncertainty holds for data for painting and wall 

covering contracting (NAICS 238320), flooring contracting (NAICS 238330), automotive body, 

paint, and interior repair and maintenance (NAICS 811121), and reupholstery and furniture 

repair (NAICS 811420) industries. These industries are expected to conduct both paint stripping 

and surface coating activities; the extent of use for DCM-containing paints and coatings in these 

industries is unknown. It also should be noted that exposures also may be overestimated if 

DCM sources other than paint stripping products were present (i.e., and not accounted for)

during air monitoring.

Assumed values for several parameters used in the equation to estimate ADCs and LADCs 

introduce additional uncertainties. Exposure frequencies are assumed to be 250 days/year 

(every work day) and the number of working years per lifetime is assumed as 40 years, which 

seems likely to be a high-end estimate. As a result of these uncertainties, some exposures in 

this assessment will be overestimated for workers who are not exposed each work day or for 

their full working career.

3.5.2. KEY UNCERTAINTIES AND DATA LIMITATIONS FOR CONSUMER EXPOSURE ESTIMATES

The inhalation exposure assessment is composed of modeled exposure scenarios for which the 

inputs are based on experimental data, survey information, and a number of assumptions with 

varying degrees of uncertainty. The results are characterized as either plausible estimates of 

individual exposure, i.e., central tendency, or possibly greater than the distribution of actual 

exposures, i.e., bounding.

The extent of the uncertainties identified below is not known, so the impact for the parameters 

that are discussed could result in either larger or smaller exposure estimates.

There is a high degree of confidence in the weight fraction and product density data for the 

paint stripper products. These values are based on currently available consumer products, as 

identified in Brown (2012). However, these values were not weighted by percent market share. 

Similarly, there is a high degree of confidence in the values chosen to represent the house 

volume and air exchange rate, as they are based on scientifically defensible data cited in the 

EPA’s Exposure Factors Handbook (EFH) (US EPA, 2011c). The confidence level is similarly high 

for the amount of product applied and application rates, with data ties to surveys cited in the 

EFH as well as experiments conducted by US EPA (1994b). For the stripping sequence, the wait 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 67

time per segment has a high level of confidence because the time is based on what is shown on 

current product labels. The application and scraping times have a slightly lower confidence 

level because they are based on the US EPA (1994b) study, which only included a limited 

number of experiments. 

High-quality US EPA (1994b) data were available as a quantitative basis for development of the 

estimates for the fraction of applied chemical mass that is released to the indoor air (see 

Appendix F, F-1. Estimation of Emission Profiles for Paint Removers/Strippers), but there were 

only a few cases on which the estimates were based.

Given the potential variability across paint stripping scenarios for estimating consumer 

exposure, not only for airflow rates but also for factors such as amount of product used, 

application rates and locations in the house, there is some unknown degree of uncertainty in 

the percentiles of the exposure distribution that are represented by the modeled scenarios. 

Therefore, in this case, the general term “upper-end”—instead of more definitive descriptors, 

e.g., high-end—was used to characterize plausible exposure values greater than central 

tendency; the more definitive descriptors would imply an inappropriate level of accuracy.

The bathtub stripping scenario is an occupational exposure for the user that was modeled to 

estimate potential exposures for residential non-users occupying the rest of the house (ROH)

during bathtub refinishing in the home. Given the model’s sensitivity of concentrations in the 

ROH to room-of-use ACH and interzonal air flow, there is uncertainty about the likelihood that a 

non-user would be exposed to this scenario’s ROH concentrations; thus, EPA characterized the 

non-user exposures as upper-end to bounding.

3.5.3. UNCERTAINTIES IN THE HAZARD AND RISK ASSESSMENT

The human health risk assessment is based on toxicity values that considered human and 

animal data in their derivations.

Single occupational exposure scenario risks were assessed by comparing the exposures to the 

California REL, National Research Council (NRC) Spacecraft Maximum Allowable Concentration

(SMAC), and AEGL-2 levels. The California REL was the most conservative acute point of 

departure estimate for non-cancer effects because it assessed a level that would not cause 

effects in the general population as opposed to the SMACs that assess risk to healthy adults

working in a very specific occupational context of operating a spacecraft. 

The absence of data on susceptible populations and the NOAEL, EPA used default or modified 

default values to calculate acceptable MOE values. Neurotoxicity in adults was the endpoint 

used to derive the POD; it is possible that younger ages may respond differently (in terms of 

dose, magnitude or response, or different response). Thus, the MOEs presented for acute 

consumer exposure scenarios in Table 3-10 may under-estimate risk to younger age groups for 

this endpoint.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 68

The chronic non-cancer risk for exposure scenarios were assessed using the POD from the US 

EPA (2011b) IRIS derivation of an inhalation RfC value. An acceptable MOE was informed by the 

uncertainty analysis developed for the IRIS assessment.

The inhalation database for DCM includes several well-conducted chronic inhalation studies. In 

these chronic exposure studies, the liver was identified as the most sensitive noncancer target 

organ in rats (Nitschke et al., 1988a; NTP, 1986; Burek et al., 1984). The critical effect of 

hepatocyte vacuolation was corroborated in the principal study (Nitschke et al., 1988a) and in a 

supporting study (Burek et al., 1984), both of which identified 500 ppm as the lowest inhalation 

LOAEL for noncancer liver lesions. 

Uncertainty in extrapolating from laboratory animals to humans (UFA) was reduced because 

EPA used PBPK modeling to extrapolate internal doses from rats to humans; thus, reducing

toxicokinetic uncertainty in extrapolation from the rat liver lesion data. However, this use of 

PBPK modeling does not account for the possibility that humans may be more sensitive than 

rats to DCM due to toxicodynamic differences. An UF of 3 to account for this toxicodynamic 

uncertainty was employed in the MOE. 

Uncertainty about variability in the average humans to more sensitive humans (UFH) is 

accounted for partially in the probabilistic human PBPK model used in this assessment because 

it incorporates the best available information about variability in toxicokinetic disposition of 

dichloromethane in humans, but does not account for humans who may be sensitive due to 

toxicodynamic factors. Thus, an UF of 3 was employed in the MOE to account for possible such 

differences in sensitive humans. 

Uncertainty in extrapolating from LOAELs to NOAELs (UFL) was not employed in the MOE

because BMD modeling was used to determine the POD, and this factor was addressed as one 

of the considerations in selecting the bench mark response (BMR). The BMR was selected based 

on the assumption that it represents a minimum biologically significant change. 

There is an additional potential concern for immunological effects as suggested by a single 

acute inhalation study, specifically immunosuppressive effects that may be relevant for 

infectious diseases spread through inhalation. 

The POD is based on results from a chronic-duration inhalation toxicity study such that no UF is 

necessary. The uncertainties associated with this derivation of the choice of this POD for 

chronic noncancer outcomes and the cancer assessment are discussed more extensively in the 

US EPA (2011b) document. It is interesting to note that the calculated MOE values are often 

one to two orders of magnitude below the acceptable benchmark MOE.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 69

3.5.4. CONCLUSIONS OF UNCERTAINTIES AND LIMITATIONS

EPA reviewed a number of published exposure studies with inherent data limitations including: 

number of facilities, job sites, or residences; most often, only a single site was investigated. 

This limited sampling pool introduces uncertainty and precludes EPA from ascertaining whether 

the observed data are fairly representative of the broad array of possible sites at all geographic 

locations across the US and all workers within the particular end-use application. The level of 

exposure to DCM during stripping processes depends highly on the use of adequate 

engineering controls (i.e., general and local exhaust ventilation systems) and work practices as 

seen by the range of exposure data (TNO, 1999). Therefore, these differences can limit the 

representativeness of any one site with regards to all sites within the specific end-use 

application. The result of these uncertainties is that actual exposure distributions are unknown; 

central tendency and high-end exposures may, or may not, fall within the range of exposures 

estimated for this assessment. It also should be noted that exposures may be overestimated if 

DCM sources other than paint stripping products were present (i.e., and not accounted for) 

during air monitoring.

There is general confidence in the characterization of the hazard database for acute and chronic 

effects used for the points of departure. However, there is residual uncertainty in domains of 

the hazard characterization for some outcomes. These uncertainties are drawn from concern 

for potential developmental neurotoxicity and immunological effects as suggested by the 

modes of action affecting the nervous system both CNS depression and COHb and indications 

from acute inhalation study, specifically immunosuppressive effects that may be relevant for 

infectious diseases spread through inhalation. 

3.6. RISK CHARACTERIZATION CONCLUSIONS 

In this assessment, EPA focused on DCM use as a paint stripper in the home and in small

commercial shops. Exposures of concern were by the inhalation route.

Non-cancer risks were addressed by comparing consumer and worker exposures to levels of 

exposure that are known to cause effects, or are identified as thresholds for effects, in animals 

or humans. The ratio of this comparison serves as an indicator of EPA’s level concern for these 

effects. All consumer and worker exposure scenarios resulted in exposures that were very 

close to, or exceeded, the threshold of effect levels for DCM. Cancer risks were calculated only 

for worker exposure. Cancer incidence risks were calculated by multiplying the exposure 

estimates by the EPA cancer risk value. Cancer risks varied between levels of a few in a million 

to a few in a thousand. In 5 of the 7 worker exposure scenarios the cancer risk was estimated 

to be a few in a thousand.

The assessment of consumer inhalation exposures found a potential risk of concern for human 

health in residential environments where DCM vapors are released during brush-on or spray-on 

applications of DCM-based paint strippers. The POD for the acute hazard scenarios is based 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 70

upon impaired cognitive performance in humans (Putz et al., 1979). All of the MOE and some of 

the HQacute risk estimates (i.e., acute non-cancer inhalation exposures) indicate a potential risk 

of concern to human health in residential environments, for both users and non-users, where 

DCM vapors are released during brush-on or spray-on applications of DCM-based paint 

strippers. This conclusion is based on workplace air monitoring data and a modeling-based 

approach employed to estimate acute inhalation exposures to residential users and non-users.

Chronic worker inhalation exposure estimates were developed from published monitoring 

studies and modeled exposure estimates. The non-cancer risks of concern of these exposures 

was determined by comparing them to the POD which was based on a HEC developed from 

histopathological changes in the liver of rodents resulting from chronic inhalation (US EPA, 

2011b). The MOE calculations for specific use scenarios were compared to MOE for chronic 

and acute benchmarks. 

EPA’s assessment found potential non-cancer and cancer risks of potential concern for workers 

and non-cancer risks for residential users and non-users (e.g., children) who use DCM-based 

paint strippers. MOEs indicate that there are potential risks of potential concern for 

occupational non-cancer risks associated with exposures to DCM-based paint strippers in the 

following industries: professional contractors, aircraft paint stripping, workplace settings doing 

immersion stripping of wood, and wood and metal paint stripping. 

For occupational chronic inhalation concerns, the MOEs for small-shop workers handling DCMbased paint strippers were calculated. The ranges of MOEs for the different industries were 

below the level of concern (i.e., 10) with the following exceptions; some furniture refinishing 

and art restoration industry scenarios which had a low concern for non-cancer risks based on 

MOE’s ranging from 31-38 derived from lower exposure scenarios. 

EPA determined that the probability of developing cancer (i.e., chronic cancer risks) in all 

occupational scenarios was above 1 × 10-6

, with the exception of the estimates for the art 

restoration industry and some furniture refinishing scenarios with lower exposures, which 

indicated a marginal concern at 3 × 10-6 (Table 3-12).
DOCUMENT-DO NOT CITE OR QUOTE 

Page 71

References

Abt (1992). Methylene chloride consumer products use survey findings. Prepared by Abt Associates, Inc., 

for the U.S. Consumer Product Safety Commission, Bethesda, MD. 

ACGIH (2001). Dichloromethane. Documentation of the threshold limit values and biological exposure 

indices. American Conference of Governmental Industrial Hygienists, Cincinnati, OH. (as cited in US EPA, 

2011b).

Aerias (2012). Methylene chloride. Aerias. Air quality Sciences. 

http://www.aerias.org/DesktopDefault.aspx?tabindex=0&tabid=75. Accessed August 9, 2012. 

Alexander, H. C., McCarty, W. M., and Bartlett, E. A. (1978). Toxicity of perchloroethylene, 

trichloroethylene, 1,1,1-trichloroethane, and methylene chloride to fathead minnows. Bull. Environ. 

Contam. Toxicol. 20(3), 344-352. 

Alexeeff, G. V., and Kilgore, W. W. (1983). Learning impairment in mice following acute exposure to 

dichloromethane and carbon tetrachloride. J. Toxicol. Environ. Health 11(4-6), 569-581. (as cited in US 

EPA, 2011b).

Allen, J., Kligerman, A., Campbell, J., Westbrook-Collins, B., Erexson, G., Kari, F., and Zeiger, E. (1990). 

Cytogenetic analyses of mice exposed to dichloromethane. Environ. Mol. Mutagen. 15(4), 221-228. (as 

cited in US EPA, 2011b).

Allred, E. N., Bleecker, E. R., Chaitman, B. R., Dahms, T. E., Gottlieb, S. O., Hackney, J. D., Hayes, D., 

Pagano, M., Selvester, R. H., Walden, S. M., and Warren, J. (1989a). Acute effects of carbon monoxide 

exposure on individuals with coronary artery disease. Research Report No. 25. Health Effects Institute, 

Cambridge, MA. (as cited in NRC, 2010).

Allred, E. N., Bleecker, E. R., Chaitman, B. R., Dahms, T. E., Gottlieb, S. O., Hackney, J. D., Pagano, M., 

Selvester, R. H., Walden, S. M., and Warren, J. (1989b). Short-term effects of carbon monoxide exposure 

on the exercise performance of subjects with coronary artery disease. N. Engl. J. Med. 321(21), 1426-

1432. (as cited in NRC, 2010).

Allred, E. N., Bleecker, E. R., Chaitman, B. R., Dahms, T. E., Gottlieb, S. O., Hackney, J. D., Pagano, M., 

Selvester, R. H., Walden, S. M., and Warren, J. (1991). Effects of carbon monoxide on myocardial 

ischemia. Environ. Health. Perspect. 91, 89-132. (as cited in NRC, 2010).

Andersen, M. E., Clewell, H. J., 3rd, Gargas, M. L., MacNaughton, M. G., Reitz, R. H., Nolan, R. J., and 

McKenna, M. J. (1991). Physiologically based pharmacokinetic modeling with dichloromethane, its 

metabolite, carbon monoxide, and blood carboxyhemoglobin in rats and humans. Toxicol. Appl. 

Pharmacol. 108(1), 14-27. (as cited in US EPA, 2008).

Anderson, E. W., Andelman, R. J., Strauch, J. M., Fortuin, N. J., and Knelson, J. H. (1973). Effect of lowlevel carbon monoxide exposure on onset and duration of angina pectoris. A study in ten patients with 

ischemic heart disease. Ann. Intern. Med. 79(1), 46-50. (as cited in NRC, 2010).
DOCUMENT-DO NOT CITE OR QUOTE 

Page 72

Aranyi, C., O'Shea, W. J., Graham, J. A., and Miller, F. J. (1986). The effects of inhalation of organic 

chemical air contaminants on murine lung host defenses. Fundam. Appl. Toxicol. 6(4), 713-720. 

Aronow, W. S., Harris, C. N., Isbell, M. W., Rokaw, S. N., and Imparato, B. (1972). Effect of freeway travel 

on angina pectoris. Ann. Intern. Med. 77(5), 669-676. (as cited in NRC, 2010).

Ash (2009). Methylene chloride. In Specialty Chemicals Source Book. p. 1361.

Astrand, I., Ovrum, P., and Carlsson, A. (1975). Exposure to methylene chloride. I Its concentration in 

alveolar air and blood during rest and exercise and its metabolism. Scand. J. Work Environ. Health 1(2), 

78-94. (as cited in NRC, 1996). 

ATSDR (1990). Methylene chloride toxicity. Case studies in environmental medicine. Agency for Toxic 

Substances and Disease Registry, U.S. Department of Health and Human Services, Atlanta, GA. PB 85-

241529. (as cited in ATSDR, 2000).

ATSDR (2000). Toxicological profile for methylene chloride. Agency for Toxic Substances and Disease 

Registry, Atlanta, GA. http://www.atsdr.cdc.gov/toxprofiles/tp14.pdf. Accessed August 8, 2012. 

ATSDR (2010). Addendum to the toxicological profile for methylene chloride. Agency for Toxic 

Substances and Disease Registry, U.S. Department of Health and Human Services, Atlanta, GA. 

http://www.atsdr.cdc.gov/toxprofiles/methylene_chloride_addendum.pdf. Accessed August 16. 2012. 

Barone, S., Jr., Das, K.P., Lassiter, T.L., and White, L.D. (2000) Vulnerable processes of nervous system 

development: A review of markers and methods. NeuroToxicology 21(1-2), 15-36.

Barry, K. H., Zhang, Y., Lan, Q., Zahm, S. H., Holford, T. R., Leaderer, B., Boyle, P., Hosgood, H. D., 3rd, 

Chanock, S., Yeager, M., Rothman, N., and Zheng, T. (2011). Genetic variation in metabolic genes, 

occupational solvent exposure, and risk of non-Hodgkin lymphoma. Am. J. Epidemiol. 173(4), 404-413. 

(as cited in US EPA, 2011b).

Bornschein, R. L., Hastings, L., and Manson, J. M. (1980). Behavioral toxicity in the offspring of rats 

following maternal exposure to dichloromethane. Toxicol. Appl. Pharmacol. 52(1), 29-37. (as cited in US 

EPA, 2011b).

Bos, P. M., Zeilmaker, M. J., and van Eijkeren, J. C. (2006). Application of physiologically based 

pharmacokinetic modeling in setting acute exposure guideline levels for methylene chloride. Toxicol. Sci.

91(2), 576-585. (as cited in US EPA, 2011b).

Brown (2012). Formulations spreadsheet file provided in personal communication from Judith Brown 

EPA/OPPT to Conrad Flessner.

Buccafusco, R. J., Ells, S. J., and LeBlanc, G. A. (1981). Acute toxicology of priority pollutants to bluegill 

(Lepomis macrochirus). Bull. Environ. Contam. Toxicol. 26(4), 446-452. 

Burek, J. D., Nitschke, K. D., Bell, T. J., Wackerle, D. L., Childs, R. C., Beyer, J. E., Dittenber, D. A., Rampy, 

L. W., and McKenna, M. J. (1984). Methylene chloride: A two-year inhalation toxicity and oncogenicity 

study in rats and hamsters. Fundam. Appl. Toxicol. 4(1), 30-47. (as cited in US EPA, 2011b).
DOCUMENT-DO NOT CITE OR QUOTE 

Page 73

Cal EPA (2000). Public health goals for chemicals in drinking water. Dichloromethane (methylene 

chloride, DCM). California Environmental Protection Agency. 

http://oehha.ca.gov/water/phg/pdf/dcm.pdf. Accessed August 7, 2012. 

Cal EPA (2006). Methylene chloride consumer product paint strippers: Low-VOC, low toxicity 

alternatives. California Environmental Protection Agency. www.irta.us/PaintStrippers06.pdf. Accessed 

August 7, 2012. 

Carlsson, A., and Hultengren, M. (1975). Exposure to methylene chloride. III. Metabolism of 14C-labelled 

methylene chloride in rat. Scand. J. Work Environ. Health 1(2), 104-108. (as cited in ATSDR, 2000).

Carpenter, S. P., Lasker, J. M., and Raucy, J. L. (1996). Expression, induction, and catalytic activity of the 

ethanol-inducible cytochrome P450 (CYP2E1) in human fetal liver and hepatocytes. Mol. Pharmacol.

49(2), 260-268 (as cited in ATSDR, 2000). 

Casanova, M., Conolly, R. B., and Heck, H. d. A. (1996). DNA-protein cross-links (DPX) and cell 

proliferation in B6C3F1 mice but not Syrian golden hamsters exposed to dichloromethane: 

pharmacokinetics and risk assessment with DPX as dosimeter. Fundam. Appl. Toxicol. 31(1), 103-116. (as 

cited in US EPA, 2011b).

Casanova, M., Deyo, D. F., and Heck, H. (1992). Dichloromethane (methylene chloride): Metabolism to

formaldehyde and formation of DNA-protein cross-links in B6C3F1 mice and Syrian golden hamsters. 

Toxicol. Appl. Pharmacol. 114(1), 162-165. (as cited in US EPA, 2011b).

CDC (2009). Fourth national report on human exposure to environmental chemicals. Centers for Disease 

Control and Prevention, Atlanta, GA. http://www.cdc.gov/exposurereport/pdf/FourthReport.pdf. 

Accessed August 16, 2012. 

CDC (2012a). Tub refinisher died due to methylene chloride overexposure while stripping a bathtub. 

Michigan case report: 10M1013. Centers for Disease Control and Prevention. 

http://www.cdc.gov/niosh/face/stateface/mi/10MI013.html. Accessed August 1, 2012. 

CDC (2012b). Fatal exposure to methylene chloride among bathtub refinishers-United States, 2000-

2011. Centers for Disease Control and Prevention. Morbidity and Mortality Weekly Report 61, 119-122. 

http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6107a2.htm. Accessed August 7, 2012. 

Cherry, N., Venables, H., and Waldron, H. A. (1983). The acute behavioural effects of solvent exposure. J. 

Soc. Occup. Med. 33(1), 13-18. (as cited in US EPA, 2011b).

Cherry, N., Venables, H., Waldron, H. A., and Wells, G. G. (1981). Some observations on workers exposed 

to methylene chloride. Br. J. Ind. Med 38(4), 351-355. (as cited in US EPA, 2011b).

d'Errico, A., Malats, N., and Vineis, P. (1999). Review of studies of selected metabolic polymorphisms 

and cancer. International Agency for Research on Cancer. IARC Sci. Publ. (148), 323-393. (as cited in 

ATSDR, 2000).
DOCUMENT-DO NOT CITE OR QUOTE 

Page 74

Dill, D. C., Murphy, P. G., and Mayes, M. A. (1987). Toxicity of methylene chloride to life stages of the 

fathead minnow, Pimephales promelas Rafinesque. Bull. Environ. Contam. Toxicol. 39(5), 869-876. 

DiVincenzo, G. D., and Kaplan, C. J. (1981). Uptake, metabolism, and elimination of methylene chloride 

vapor by humans. Toxicol. Appl. Pharmacol. 59(1), 130-140. (as cited in US EPA, 2008).

DiVincenzo, G. D., Yanno, F. J., and Astill, B. D. (1972). Human and canine exposures to methylene 

chloride vapor. Am. Ind. Hyg. Assoc. J. 33(3), 125-135. (as cited in ATSDR, 2000 and US EPA, 2008).

Dow (1999). Alternatives to chlorinated solvents. Newsletter 3(4).

EC (2000). IUCLID dataset. Dichloromethane. European Commission. European Union. 

EC (2004). Effectiveness of vapour retardants in reducing risks to human health from paint strippers 

containing dichloromethane. European Commission. European Union, Brussels. 

ECHA (2011). Proposal for identification of a substance as a category 1A or 1B CMR, PBT, vPvB or a 

substance of an equivalent level of concern: Annex XV Dossier: Identification of 1-methyl-2-pyrrolidone 

as SVHC. European Chemicals Agency. 

Enander, R. T., Cohen, H. J., Gute, D. M., Brown, L. C., Desmaris, A. M., and Missaghian, R. (2004). Lead 

and methylene chloride exposures among automotive repair technicians. J. Occup. Environ. Hyg. 1(2), 

119-125. 

EU (2007a). Impact assessment of potential restrictions on the marketing and use of dichloromethane in 

paint strippers. Revised final report-Annexes. European Commission. 

http://ec.europa.eu/enterprise/sectors/chemicals/files/markrestr/j549_dcm_annex_en.pdf. Accessed 

August 6, 2012. 

EU (2007b). Impact assessment of potential restrictions on the marketing and use of dichloromethane in 

paint strippers. Final report. European Commission. 

http://ec.europa.eu/enterprise/sectors/chemicals/files/markrestr/j549_dcm_final_report_en.pdf. 

Accessed August 6, 2012. 

FDA (1989). Use of methylene chloride as an ingredient of cosmetic products. Food and Drug 

Administration. CFR 21 CFR 700.25

Felter, S. P., Conolly, R. B., Bercu, J. P., Bolger, P. M., Boobis, A. R., Bos, P. M., Carthew, P., Doerrer, N. G., 

Goodman, J. I., Harrouk, W. A., Kirkland, D. J., Lau, S. S., Llewellyn, G. C., Preston, R. J., Schoeny, R., 

Schnatter, A. R., Tritscher, A., van Velsen, F., and Williams, G. M. (2011). A proposed framework for 

assessing risk from less-than-lifetime exposures to carcinogens. Crit. Rev. Toxicol. 41(6), 507-544. 

Fisher, J., Mahle, D., Bankston, L., Greene, R., and Gearhart, J. (1997). Lactational transfer of volatile 

chemicals in breast milk. Am. Ind. Hyg. Assoc. J. 58(6), 425-431. (as cited in ATSDR, 2000).

Foley, J. F., Tuck, P. D., Ton, T. V., Frost, M., Kari, F., Anderson, M. W., and Maronpot, R. R. (1993). 

Inhalation exposure to a hepatocarcinogenic concentration of methylene chloride does not induce 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 75

sustained replicative DNA synthesis in hepatocytes of female B6C3F1 mice. Carcinogenesis 14(5), 811-

817. (as cited in US EPA, 2011b).

Frey, H. C., and Patil, S. R. (2002). Identification and review of sensitivity analysis methods. Risk Anal.

22(3), 553-578. 

Gamberale, F., Annwall, G., and Hultengren, M. (1975). Exposure to methylene chloride. II. Psychological 

functions. Scand. J. Work Environ. Health 1(2), 95-103. (as cited in US EPA, 2011b and US EPA, 2008).

Garte, S., and Crosti, F. (1999). A nomenclature system for metabolic gene polymorphisms. International 

Agency for Research on Cancer. IARC Sci. Publ. (148), 5-12. (as cited in ATSDR, 2000).

Geiger, D. L., Poirier, S. H., Brooke, L. T., and Call, D. J. (1986). Acute toxicities of organic chemicals to 

fathead minnows (Pimephales promelas). Center for Lake Superior Environmental Studies, University of 

Wisconsin, Superior, WI

Gold, L. S., Stewart, P. A., Milliken, K., Purdue, M., Severson, R., Seixas, N., Blair, A., Hartge, P., Davis, S., 

and De Roos, A. J. (2011). The relationship between multiple myeloma and occupational exposure to six 

chlorinated solvents. Occup. Environ. Med. 68(6), 391-399. (as cited in US EPA, 2011b).

Graves, R. J., Coutts, C., and Green, T. (1995). Methylene chloride-induced DNA damage: An interspecies 

comparison. Carcinogenesis 16(8), 1919-1926. (as cited in US EPA, 2011b).

Grevenkamp, A. (2007). Overexposure and control of methylene chloride in a furniture stripping 

operation. J. Occup. Environ. Hyg. 4(5), D39-D41. 

Hardin, B. D., and Manson, J. M. (1980). Absence of dichloromethane teratogenicity with inhalation 

exposure in rats. Toxicol. Appl. Pharmacol. 52(1), 22-28. (as cited in US EPA, 2011b).

Haskell Laboratory (1982). Inhalation approximate lethal concentration of methylene chloride with 

cover letter dated 081092. Submitted under TSCA Section 8E. Doc #88-920009163. OTS0546445. (as 

cited in US EPA, 2008).

Hazleton Laboratories (1983). 24-month oncogenicity study of methylene chloride in mice: Final report. 

(45-8303005). National Coffee Association, New York, NY. (as cited in US EPA, 2011b).

Hearne, F. T., and Pifer, J. W. (1999). Mortality study of two overlapping cohorts of photographic film 

base manufacturing employees exposed to methylene chloride. J. Occup. Environ. Med. 41(12), 1154-

1169. (as cited in US EPA, 2011b).

Heineman, E. F., Cocco, P., Gomez, M. R., Dosemeci, M., Stewart, P. A., Hayes, R. B., Zahm, S. H., 

Thomas, T. L., and Blair, A. (1994). Occupational exposure to chlorinated aliphatic hydrocarbons and risk 

of astrocytic brain cancer. Am. J. Ind. Med. 26(2), 155-169. (as cited in US EPA, 2011b).

Heitmuller, P. T., Hollister, T. A., and Parrish, P. R. (1981). Acute toxicity of 54 industrial chemicals to 

sheepshead minnows (Cyprinodon variegatus). Bull. Environ. Contam. Toxicol. 27(5), 596-604. 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 76

Heppel, L. A., and Neal, P. A. (1944). Toxicology of dichloromethane (methylene chloride): II: Its effect 

upon running activity in the male rat. J. Ind. Hyg. Toxicol. 26, 17-21. (as cited in US EPA, 2011b).

Heppel, L. A., Neal, P. A., Perrin, T. L., Orr, M. L., and Porterfield, V. T. (1944). Toxicology of 

dichloromethane (methylene chloride): I: Studies on effects of daily inhalation. J. Ind. Hyg. Toxicol. 26, 8-

16. (as cited in US EPA, 2011b).

HSDB (2012). Dichloromethane; Hazardous Substances Data Bank Number: 66. National Library of 

Medicine. http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~tDtTex:1. Accessed August 15, 2012. 

HSE (2001). Health risks during furniture stripping using dichloromethane (DCM). Health and Safety 

Executive. www.hse.gov.uk/pubns/wis19.pdf. Accessed August 6, 2012. 

HSIA (2008). White paper on methylene chloride. Halogenated Solvents Industry Alliance, Inc. 

HSIA (2010). Dichloromethane (methylene chloride). Halogenated Solvents Industry Alliance, Inc. 

IARC (1999). Dichloromethane. International Agency for Research on Cancer. IARC Monogr. Eval. 

Carcinog. Risks Hum. 71, 251-315. http://monographs.iarc.fr/ENG/Monographs/vol71/mono71-10.pdf. 

Accessed August 6, 2012. 

IARC (2010). Occupational exposure as a painter. International Agency for Research on Cancer. IARC 

Monogr. Eval. Carcinog. Risks Hum. 98-394. 

http://monographs.iarc.fr/ENG/Monographs/vol98/mono98-6.pdf. Accessed August 6, 2012. 

ICIS (2007). Chemical profile. Methylene chloride. ICIS Chemical Business Americas (April 2-8, 2007), 34. 

http://www.icis.com/publications. Accessed August 15, 2012. 

IPCC Fourth Assessment Report (2007). Dichloromethane, Section 2.10.2. Table 2.14. OECD HPV 

Chemicals Programme. http://webnet.oecd.org/hpv/ui/SponsoredChemicals.aspx. Accessed August 15, 

2012. 

IRTA (2006). Assessment, development and demonstration of alternatives for five emerging solvents.

Institute for Research and Technical Assistance. 

www.cdph.ca.gov/programs/hesis/Documents/emergingsolvents.pdf. Accessed August 6, 2012. 

Kari, F. W., Foley, J. F., Seilkop, S. K., Maronpot, R. R., and Anderson, M. W. (1993). Effect of varying 

exposure regimens on methylene chloride-induced lung and liver tumors in female B6C3F1 mice. 

Carcinogenesis 14(5), 819-826. (as cited in US EPA, 2011b).

Kjellstrand, P., Holmquist, B., Jonsson, I., Romare, S., and Mansson, L. (1985). Effects of organic solvents 

on motor activity in mice. Toxicology 35(1), 35-46. (as cited in US EPA, 2011b).

Kleinman, M. T., Davidson, D. M., Vandagriff, R. B., Caiozzo, V. J., and Whittenberger, J. L. (1989). Effects 

of short-term exposure to carbon monoxide in subjects with coronary artery disease. Arch. Environ. 

Health 44(6), 361-369. (as cited in NRC, 2010).
DOCUMENT-DO NOT CITE OR QUOTE 

Page 77

Kleinman, M. T., Leaf, D. A., Kelly, E., Caiozzo, V., Osann, K., and O'Niell, T. (1998). Urban angina in the 

mountains: Effects of carbon monoxide and mild hypoxemia on subjects with chronic stable angina. 

Arch. Environ. Health 53(6), 388-397. (as cited in NRC, 2010).

Kühn, R., Pattard, M., Pernak, K.-D., and Winter, A. (1989). Results of the harmful effects of selected 

water pollutants (anilines, phenols, aliphatic compounds) to Daphnia magna. Water Res. 23(4), 495-499. 

http://www.sciencedirect.com/science/article/pii/0043135489901413

Lanes, S. F., Cohen, A., Rothman, K. J., Dreyer, N. A., and Soden, K. J. (1990). Mortality of cellulose fiber 

production workers. Scand. J. Work Environ. Health 16(4), 247-251. (as cited in US EPA, 2011b).

Lanes, S. F., Rothman, K. J., Dreyer, N. A., and Soden, K. J. (1993). Mortality update of cellulose fiber 

production workers. Scand. J. Work Environ. Health 19(6), 426-428. (as cited in US EPA, 2011b).

Lang, M., and Pelkonen, O. (1999). Metabolism of xenobiotics and chemical carcinogenesis. Metabolic 

polymorphisms and susceptibility to cancer. International Agency for Research on Cancer, 13-22, Lyon, 

France. (as cited in ATSDR, 2000).

Lash, A. A., Becker, C. E., So, Y., and Shore, M. (1991). Neurotoxic effects of methylene chloride: are they 

long lasting in humans? Br. J. Ind. Med 48(6), 418-426. (as cited in US EPA, 2011b).

LeBlanc, G. A. (1980). Acute toxicity of priority pollutants to water flea (Daphnia magna). Bull. Environ. 

Contam. Toxicol. 24(5), 684-691. 

Lide, D. (2001). Physical constants of organic compounds. In CRC Handbook of Chemistry and Physics, 

82nd edition. p. 3-206. CRC Press Inc., Boca Raton, FL.

Lofgren, D. J., Reeb-Whitaker, C. K., and Adams, D. (2010). Surveillance of Washington OSHA exposure 

data to identify uncharacterized or emerging occupational health hazards. J. Occup. Environ. Hyg. 7(7), 

375-388. 

Mannsville (1999). Chemical products synopsis. Methylene chloride. Mannsville Chemical Products Corp. 

http://mannsvillechemical.com/synopsis/. Accessed August 10, 2012. 

Maronpot, R. R., Devereux, T. R., Hegi, M., Foley, J. F., Kanno, J., Wiseman, R., and Anderson, M. W. 

(1995). Hepatic and pulmonary carcinogenicity of methylene chloride in mice: a search for mechanisms. 

Toxicology 102(1-2), 73-81. (as cited in US EPA, 2011b).

Matthews, T. G., Thompson, C. V., Wilson, D. L., Hawthorne, A. R., and Mage, D. T. (1989). Air velocities 

inside domestic environments: An important parameter in the study of indoor air quality and climate. 

Environ. Int. 15(1–6), 545-550. http://www.sciencedirect.com/science/article/pii/0160412089900743

McCammon, C. S., Glaser, R. A., Wells, V. E., Phipps, F. C., and Halperin, W. E. (1991). Exposure of 

workers engaged in furniture stripping to methylene chloride as determined by environmental and 

biological monitoring. Appl. Occup. Environ. Hyg. 6(5), 371-379. 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 78

Mennear, J. H., McConnell, E. E., Huff, J. E., Renne, R. A., and Giddens, E. (1988). Inhalation toxicity and 

carcinogenesis studies of methylene chloride (dichloromethane) in F344/N rats and B6C3F1 mice. Ann. 

N. Y. Acad. Sci. 534, 343-351. (as cited in US EPA, 2011b).

Merlin, G., Thiebaud, H., Blake, G., Sembiring, S., and Alary, J. (1992). Mesocosms' and microcosms' 

utilization for ecotoxicity evaluation of dichloromethane, a chlorinated solvent. Chemosphere 24(1), 37-

50. 

Miligi, L., Costantini, A. S., Benvenuti, A., Kriebel, D., Bolejack, V., Tumino, R., Ramazzotti, V., Rodella, S., 

Stagnaro, E., Crosignani, P., Amadori, D., Mirabelli, D., Sommani, L., Belletti, I., Troschel, L., Romeo, L., 

Miceli, G., Tozzi, G. A., Mendico, I., and Vineis, P. (2006). Occupational exposure to solvents and the risk 

of lymphomas. Epidemiology 17(5), 552-561. (as cited in US EPA, 2011b).

MSU/MIFACE (2011). Tub refinisher died due to methylene chloride overexposure while stripping a 

bathtub. Michigan State University (MSU) Michigan Fatality Assessment and Control Evaluation 

(MIFACE) Occupational and Environmental Medicine, East Lansing, MI. 

http://www.oem.msu.edu/MiFace/10MI013Report.pdf MIFACE investigation report #10MI013.

National Institute of Technology and Evaluation (2002). Biodegradation and bioaccumulation of the 

existing chemical substances under the Chemical Substances Control Law.

http://www.safe.nite.go.jp/english/kizon/KIZON_start_hazkizon.html. Accessed March 19, 2012. 

NIH (2005). Substance profiles, dichloromethane. National Institutes of Health. 

http://ntpsearch.niehs.nih.gov/query.html?qt=Dichloromethane&col=001main. Accessed August 15, 

2012. 

NIH (2012). Household products database, methylene chloride. May 2012. National Institutes of Health. 

www.householdproducts.nlm.nih.gov. Accessed August 15, 2012. 

NIOSH (1977). Health hazard evaluation determination report 75-195-396. United Airlines maintenance 

base San Francisco International Airport Burlingame, California. National Institute for Occupational 

Safety and Health, Cincinnati, OH. www.ntis.gov/search/product.aspx?ABBR=PB273779. Accessed 

August 6, 2012. 

NIOSH (1990). Walk-though survey report: Control of methylene chloride in furniture stripping at 

Colonial Furniture Stripping. ECTB number: 170-14a. National Institute for Occupational Safety and 

Health, Cincinnati, OH. www.cdc.gov/niosh/surveyreports/pdfs/170-14a.pdf. Accessed August 6, 2012. 

NIOSH (1991). In-depth survey report. The control of methylene chloride in furniture stripping at 

Association for Retarded Citizens. ECTB number: 170-18a. National Institute for Occupational Safety and 

Health, Cincinnati, OH. http://www.cdc.gov/niosh/surveyreports/pdfs/170-18a.pdf. Accessed August 6, 

2012. 

NIOSH (1992). Health hazard evaluation. Ackerman and Sons, Littleton, Colorado. HETA 92-0360-2372.

National Institute for Occupational Safety and Health. www.cdc.gov/niosh/hhe/reports/pdfs/1992-0360-

2372.pdf. Accessed August 7, 2012. 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 79

NIOSH (1993). Health hazard evaluation. Rosebud Company. HETA 93-0844-2411. National Institute for 

Occupational Safety and Health. http://www.cdc.gov/niosh/hhe/reports/pdfs/1993-0844-2411.pdf. 

Accessed August 7, 2012. 

NIOSH (2011a). NIOSH pocket guide to chemical hazards. Methylene chloride. National Institute for 

Occupational Safety and Health. http://www.cdc.gov/niosh/npg/npgd0414.html. Accessed July 20, 

2012. 

NIOSH (2011b). NIOSH pocket guide to chemical hazards. Introduction. National Institute for 

Occupational Safety and Health. http://www.cdc.gov/niosh/npg/pgintrod.html. Accessed July 20, 2012. 

Nitschke, K. D., Burek, J. D., Bell, T. J., Kociba, R. J., Rampy, L. W., and McKenna, M. J. (1988a). Methylene 

chloride: A 2-year inhalation toxicity and oncogenicity study in rats. Fundam. Appl. Toxicol. 11(1), 48-59. 

(as cited in US EPA 2011b).

Nitschke, K. D., Eisenbrandt, D. L., Lomax, L. G., and Rao, K. S. (1988b). Methylene chloride: Twogeneration inhalation reproductive study in rats. Fundam. Appl. Toxicol. 11(1), 60-67. (as cited in US EPA 

2011b).

NRC (1996). Spacecraft maximum allowable concentration for selected airborne contaminants: 

Methylene chloride (Volume 2). National Academy Press. National Research Council, Washington, DC. 

http://www.nap.edu/catalog.php?record_id=5170. Accessed August 16, 2012. 

NRC (2001). Standing operating procedures for developing acute exposure guideline levels for hazardous 

chemicals. National Academy Press. National Research Council, Washington DC. 

http://www.epa.gov/oppt/aegl/pubs/sop.pdf. Accessed August 16, 2012. 

NRC (2008). Spacecraft maximum allowable concentration for selected airborne contaminants: 

Methylene chloride (Volume 5). National Academy Press. National Research Council, Washington, DC. 

http://www.nap.edu/catalog.php?record_id=12529. Accessed August 16, 2012. 

NRC (2010). Acute exposure guideline levels for carbon monoxide (final). National Academy Press. 

National Research Council, Washington, DC. http://www.nap.edu/catalog.php?record_id=12770. 

Accessed August 16, 2012. 

NTP (1986). NTP toxicology and carcinogenesis studies of dichloromethane (methylene chloride) (CAS 

No. 75-09-2) in F344/N rats and B6C3F1 mice (inhalation studies). National Toxicolgy Program. (as cited 

in US EPA, 2011b).

O'Neil, M. J., Smith, A., Heckelman, P. E., and Obenchain, J. R. (2001). Methylene chloride. In The Merck 

index, 13th edition. p. 1082.

OECD (2010). OECD Environmental health and safety publications. Series on emission scenario 

documents. Emission scenario document on coating and application via spray painting in the automotive 

refinishing industry. Number 11. Organization for Economic Co-operation and Development. 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 80

OEHHA (1999). Air toxics hot spots program risk assessment guidelines, Part I: The determination of 

acute reference exposure levels for airborne toxicants. Office of Environmental Health Hazard 

Assessment, Sacramento, CA. http://oehha.ca.gov/air/pdf/acuterel.pdf. Accessed August 16, 2012. 

OEHHA (2001). Methylene chloride: Prioritization of toxic air contamination-children’s environmental 

health protection act. Office of Environmental Health Hazard Assessment, Sacramento, CA. 

http://oehha.ca.gov/air/toxic_contaminants/pdf_zip/methylene%20chloride_final.pdf. Accessed August 

16, 2012. 

OEHHA (2008). Acute reference exposure level (REL) and toxicity summary for methylene chloride.

Office of Environmental Health Hazard Assessment, Sacramento, CA. 

http://oehha.ca.gov/air/hot_spots/2008/AppendixD2_final.pdf#page=187. Accessed August 16, 2012. 

OSHA (1997a). Intro to 29 CFR parts 1010, 1915 and 1926, occupational exposure to methylene chloride. 

Occupational Safety & Health Administration. CFR 29 CFR 1910, 1915, 1926. 

http://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=PREAMBLES&p_id=998. 

Accessed July 20, 2012. 

OSHA (1997b). Substance safety data sheet and technical guidance for methylene chloride. Occupational 

Safety & Health Administration. CFR 29 CFR 1910.1052 App A. 

http://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=STANDARDS&p_id=10095. 

Accessed July 20, 2012. 

OSHA (2010a). Methylene chloride – Safety and health topics. Occupational Safety and Health 

Administration. http://www.osha.gov/SLTC/methylenechloride/. Accessed August 15, 2012. 

OSHA (2010b). Regulatory review of 29 CFR 1910.1052: Methylene chloride. Occupational Safety & 

Health Administration. Accessed August 2, 2012. 

OSHA (2012). Integrated Management Information System (IMIS), methylene chloride (CASRN 75-09-2).

Occupational Safety and Health Administration. 

Pelkonen, O., Raunio, H., and Rautio, A. (1999). Xenobiotic-metabolizing enzymes and cancer risk: 

correspondence between genotype and phenotype. In Metabolic polymorphisms and susceptibility to 

cancer. International Agency for Research on Cancer, 77-78, Lyon, France. (as cited in ATSDR, 2000).

Pellizzari, E. D., Hartwell, T. D., Harris, B. S., 3rd, Waddell, R. D., Whitaker, D. A., and Erickson, M. D. 

(1982). Purgeable organic compounds in mother's milk. Bull. Environ. Contam. Toxicol. 28(3), 322-328. 

(as cited in ATSDR, 2000).

Peterson, J. E. (1978). Modeling the uptake, metabolism and excretion of dichloromethane by man. Am. 

Ind. Hyg. Assoc. J. 39(1), 41-47. (as cited in US EPA, 2008).

Pollack-Nelson, C. (1995). Analysis of methylene chloride product labelling. Ergonomics 38(11), 2176-

2187. 

Putz, V. R., Johnson, B. L., and Setzer, J. V. (1979). A comparative study of the effects of carbon 

monoxide and methylene chloride on human performance. J. Environ. Pathol. Toxicol. 2(5), 97-112. 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 81

Raje, R., Basso, M., Tolen, T., and Greening, M. (1988). Evaluation of in vivo mutagenicity of low-dose 

methylene chloride in mice. Int. J. Toxicol. 7, 699-703. (as cited in US EPA, 2011b).

Ratney, R. S., Wegman, D. H., and Elkins, H. B. (1974). In vivo conversion of methylene chloride to carbon 

monoxide. Arch. Environ. Health 28(4), 223-226. (as cited in NRC, 1996). 

Rebert, C. S., Matteucci, M. J., and Pryor, G. T. (1989). Acute effects of inhaled dichloromethane on the 

EEG and sensory-evoked potentials of Fischer-344 rats. Pharmacol. Biochem. Behav. 34(3), 619-629. (as 

cited in US EPA, 2011b).

RIDEM (2011). Environmental/occupational health complicance certification program. Certification 

workbook for auto body repair facilities. Rhode Island Department of Environmental Management. 

www.dem.ri.gov/programs/benviron/assist/abdycert/cheklist.pdf. Accessed August 7, 2012. 

Riley, D. M., Fischhoff, B., Small, M. J., and Fischbeck, P. (2001). Evaluating the effectiveness of riskreduction strategies for consumer chemical products. Risk Anal. 21(2), 357-369. 

Riley, D. M., Small, M. J., and Fischhoff, B. (2000). Modeling methylene chloride exposure-reduction 

options for home paint-stripper users. J. Expo. Anal. Environ. Epidemiol. 10(3), 240-250. 

Riley, E. C., Fassett, D. W., and Sutton, W. L. (1966). Methylene chloride vapor in expired air of human 

subjects. Am. Ind. Hyg. Assoc. J. 27(4), 341-348. (as cited in US EPA, 2008).

Roderer, G. (1990). Testung Wassergefahrdender Stoffe als Grundlage fur Wasserqualitats standards.

Testbericht: Wassergefahrdende Stoffe Fraunhofer-Institut fur Umweltchemie und Okotoxikologie, 

Schmallenberg

Schwetz, B. A., Leong, K. J., and Gehring, P. J. (1975). The effect of maternally inhaled trichloroethylene, 

perchloroethylene, methyl chloroform, and methylene chloride on embryonal and fetal development in 

mice and rats. Toxicol. Appl. Pharmacol. 32(1), 84-96. (as cited in US EPA, 2011b).

Seidler, A., Mohner, M., Berger, J., Mester, B., Deeg, E., Elsner, G., Nieters, A., and Becker, N. (2007). 

Solvent exposure and malignant lymphoma: a population-based case-control study in Germany. J. 

Occup. Med. Toxicol. 2, 2. (as cited in US EPA, 2011b).

Serota, D. G., Thakur, A. K., Ulland, B. M., Kirschman, J. C., Brown, N. M., Coots, R. H., and Morgareidge, 

K. (1986). A two-year drinking-water study of dichloromethane in rodents. II. Mice. Food Chem. Toxicol.

24(9), 959-963. (as cited in US EPA, 2011b).

Sheps, D. S., Adams, K. F., Jr., Bromberg, P. A., Goldstein, G. M., O'Neil, J. J., Horstman, D., and Koch, G. 

(1987). Lack of effect of low levels of carboxyhemoglobin on cardiovascular function in patients with 

ischemic heart disease. Arch. Environ. Health 42(2), 108-116. (as cited in NRC, 2010).

Sills, R. C., Hailey, J. R., Neal, J., Boorman, G. A., Haseman, J. K., and Melnick, R. L. (1999). Examination of 

low-incidence brain tumor responses in F344 rats following chemical exposures in National Toxicology 

Program carcinogenicity studies. Toxicol. Pathol. 27(5), 589-599. (as cited in US EPA, 2011b).
DOCUMENT-DO NOT CITE OR QUOTE 

Page 82

Smithsonian (2012a). Does my painting need to be cleaned? Smithsonian Museum Conservation 

Institute. http://si.edu/mci/english/learn_more/taking_care/painting_clean.html. Accessed July 20, 

2012. 

Smithsonian (2012b). What does it mean to have a painting restored and how do I pick a conservator? 

Smithsonian Museum Conservation Institute. 

http://si.edu/mci/english/learn_more/taking_care/conservation_meaning.html. Accessed July 20, 2012. 

SRRP (1992). Source reduction and recycling of halogenated solvents in the adhesives industry. Source 

Reduction Research Partnership. Jacobs Engineering Group. Metropolitan Water District of Southern 

California. Environmental Defense Fund, Pasadena, CA. 

Stewart, R. D., Fisher, T. N., Hosko, M. J., Peterson, J. E., Baretta, E. D., and Dodd, H. C. (1972). 

Experimental human exposure to methylene chloride. Arch. Environ. Health 25(5), 342-348. (as cited in 

US EPA, 2008).

Stewart, R. D., Hake, C. L., and Wu, A. (1976). Use of breath analysis to monitor methylene chloride 

exposure. Scand. J. Work Environ. Health 2(2), 57-70. (as cited in US EPA, 2008).

Strange, R. C., and Fryer, A. A. (1999). The glutathione S-transferases: influence of polymorphism on 

cancer susceptibility. International Agency for Research on Cancer. IARC Sci. Publ. (148), 231-249. (as 

cited in ATSDR, 2000).

Stubbins, M. J., and Wolf, C. R. (1999). Additional polymorphisms and cancer. International Agency for 

Research on Cancer IARC Sci. Publ. (148), 271-301. (as cited in ATSDR, 2000).

Syracuse Res. Corp. (1978). Results of continuous exposure of fathead minnow embryo to 21 priority 

pollutants. Syracuse Research Corporation. Submitted under TSCA Section 4. OTS0511060. EPA Doc. 

#40-7848049.

Thomas, P. E., Bandiera, S., Maines, S. L., Ryan, D. E., and Levin, W. (1987). Regulation of cytochrome P450j, a high-affinity N-nitrosodimethylamine demethylase, in rat hepatic microsomes. Biochemistry

26(8), 2280-2289. (as cited in ATSDR, 2000).

TNO (1999). Methylene chloride: Advantages and drawbacks of possible market restrictions in the EU. 

STB-99-53 Final. European Commision. TNO-STB, Brussels, Belgium. 

Tomenson, J. A. (2011). Update of a cohort mortality study of workers exposed to methylene chloride 

employed at a plant producing cellulose triacetate film base. Int. Arch. Occup. Environ. Health 84(8), 

889-897. (as cited in US EPA, 2011b).

US Census (2007a). 2007 NAICS index file. North American Industry Classification System. U.S. Census 

Bureau. http://www.census.gov/cgi-bin/sssd/naics/naicsrch?chart=2007. Accessed August 9, 2012. 

US Census (2007b). American FactFinder: 2007 Economic Census.

US EPA (1978). In-depth studies on health and environmental impacts of selected water pollutants. US 

Environmental Protection Agency, Duluth, MN. 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 83

US EPA (1980). Acquisition and chemical analysis of mother’s milk for selected toxic substances. US 

Environmental Protection Agency, Research Triangle Park, NC. EPA 560/13-80-029. PB 81-231029. (as 

cited in ATSDR, 2000).

US EPA (1989). Risk assessment guidance for superfund, volume I: Human health evaluation manual 

(Part A). Chapter 8-risk characterization. Office of Solid Waste and Emergency Response, US 

Environmental Protection Agency, Washington, DC. 

http://www.epa.gov/oswer/riskassessment/ragsa/pdf/rags_ch8.pdf. EPA/540/1-89/002.

US EPA (1991). Integrated Risk Information System (IRIS) Dichloromethane. U.S. Enviornmental 

Protection Agency. 

http://cfpub.epa.gov/ncea/iris/index.cfm?fuseaction=iris.showQuickView&substance_nmbr=0070. 

Accessed August 15, 2012. 

US EPA (1992a). Guidelines for exposure assessment. US Environmental Protection Agency. 

http://ofmpub.epa.gov/eims/eimscomm.getfile?p_download_id=429103. Accessed August 7, 2012. 

EPA/600/Z-92-001.

US EPA (1992b). Classification criteria for environmental toxicity and fate of industrial chemical. US 

Environmental Protection Agency. 

US EPA (1993). Locating and estimating air emissions from sources of methylene chloride. Office of Air 

Quality Planning and Standards, US Environmental Protection Agency, Research Triangle Park, NC. EPA454/R-93-006.

US EPA (1994a). OPPT chemical fact sheet. Chemicals in the environment: Methylene chloride 

(dichloromethane) (CAS No. 75-09-2). U.S. Enviornmental Protection Agency. 

www.epa.gov/chemfact/f_dcm.txt. Accessed August 7, 2012. EPA 749-F-94-018.

US EPA (1994b). Consumer exposure to paint stripper solvents. US Environmental Protection Agency, 

Washington, DC. 

US EPA (1995a). Estimation of distributions for residential air exchange rates. US Environmental 

Protection Agency. National Center for Environmental Assessment. EPA600R95180.

US EPA (1995b). Estimation of distributions for residential air exchange rates. EPA Contract No. 68-D9-

0166. US Environmental Protection Agency, Office of Pollution Prevention and Toxics, Washington, DC. 

http://nepis.epa.gov/Exe/ZyPURL.cgi?Dockey=910063GS.txt. Accessed August 15, 2012. 

US EPA (1996). Consumer/small shop paint stripping use cluster. AR-161. Risk management report. 

Public comment draft. US Environmental Protection Agency. 

US EPA (1997). Use of Small-Chamber Data to Estimate and Model Chemical Emissions from Latex and 

Alkyd Paints. Prepared by GEOMET Technologies, Inc. under EPA Contract No. 68-D3-0013 for the Office 

of Pollution Prevention and Toxics, February 4, 1997.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 84

US EPA (1999). Category for persistent, bioacculative, and toxic new chemical substances. US 

Environmental Protection Agency. Fed. Regist. 64(213), 60194-60204. 

US EPA (2000). Methylene chloride (dichloromethane) hazard summary. Technology Transfer Network. 

U.S. Enviornmental Protection Agency. http://www.epa.gov/ttn/atw/hlthef/methylen.html. Accessed 

August 7, 2012. 

US EPA (2005). Guidelines for carcinogen risk assessment. U.S. Enviornmental Protection Agency, 

Washington, DC. http://www.epa.gov/cancerguidelines/. Accessed August 17, 2012. EPA/630/P03/001F. (as cited in USEPA, 2011b).

US EPA (2006a). 2006 Inventory update reporting. Methylene chloride (CASRN 75-09-2). US 

Environmental Protection Agency. 

http://cfpub.epa.gov/iursearch/2006_iur_companyinfo.cfm?chemid=4942&outchem=both. Accessed 

August 15, 2012. 

US EPA (2006b). Proposed test rule for certain chemicals on the ATSDR/EPA CERCLA priority list of 

hazardous substances. U.S. Enviornmental Protection Agency. Fed. Regist. 71(203), 61926-61944. 

http://www.gpo.gov/fdsys/pkg/FR-2006-12-18/pdf/E6-21494.pdf. Accessed August 7, 2012. 

US EPA (2008). Interim acute exposure guideline levels (AEGL) for methylene chloride. National Advisory 

Committee. U.S. Environmental Protection. 

http://www.epa.gov/oppt/aegl/pubs/methylene_chloride_interim_dec_2008_v1.pdf. Accessed August 

16, 2012. 

US EPA (2009). Risk assessment guidance for superfund. Volume I: Human health evaluation manual 

(part F, supplemental guidance for inhalation risk assessment). US Environmental Protection Agency. 

www.epa.gov/oswer/riskassessment/ragsf/pdf/partf_200901_final.pdf. Accessed August 7, 2012. EPA540-R-070-002.

US EPA (2010a). Multi-chamber concentration and exposure model (MCCEM) version 1.2. US 

Environmental Protection Agency. http://www.epa.gov/oppt/exposure/pubs/mccem.htm. Accessed 

October 31, 2012. 

US EPA (2010b). Methylene chloride (dichloromethane; CASRN 75-09-2). DD course setting meeting. US 

Environmental Protection Agency. 

US EPA (2011a). Conduct efficient TRI analyses and integrate with mapping, TRI.NET. US Environmental 

Protection Agency, Office of Environmental Information. http://www.epa.gov/tri/tridotnet/index.html. 

Accessed August 15, 2012. 

US EPA (2011b). Toxicological review of dichloromethane (methylene chloride; CAS No. 75-09-2). US 

Environmental Protection Agency, Washington, DC. http://www.epa.gov/iris/toxreviews/0070tr.pdf. 

Accessed August 17, 2012. EPA/635/R-10/003F.

US EPA (2011c). Exposure factors handbook: 2011 Edition. US Environmental Protection Agency. 

National Center for Environmental Assessment. http://www.epa.gov/ncea/efh/pdfs/efh-complete.pdf. 

Accessed August 7, 2012. 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 85

US EPA (2012a). Estimation Programs Interface SuiteTM for Microsoft® Windows, v4.10. US 

Environmental Protection Agency, Washington, DC. 

http://www.epa.gov/opptintr/exposure/pubs/episuitedl.htm. Accessed August 15, 2012. 

US EPA (2012b). TSCA work plan chemicals: Methods document. US Environmental Protection Agency. 

www.epa.gov/oppt/existingchemicals/pubs/wpmethods.pdf. Accessed August 9, 2012. 

van Veen, M. P., Fortezza, F., Spaans, E., and Mensinga, T. T. (2002). Non-professional paint stripping, 

model prediction and experimental validation of indoor dichloromethane levels. Indoor Air 12(2), 92-97. 

Vincent, R., Poirot, P., Subra, I., Rieger, B., and Cicolella, A. (1994). Occupational exposure to organic 

solvents during paint stripping and painting operations in the aeronautical industry. Int. Arch. Occup. 

Environ. Health 65(6), 377-380. 

von Bringmann, G., and Meinck, F. (1964). Wassertoxikologische beurteilung von industrieabwassern. 

Gesund. Ing. 85, 229-260. 

Wang, R., Zhang, Y., Lan, Q., Holford, T. R., Leaderer, B., Zahm, S. H., Boyle, P., Dosemeci, M., Rothman, 

N., Zhu, Y., Qin, Q., and Zheng, T. (2009). Occupational exposure to solvents and risk of non-Hodgkin 

lymphoma in Connecticut women. Am. J. Epidemiol. 169(2), 176-185. (as cited in US EPA, 2011b).

Weinstein, R. S., Boyd, D. D., and Back, K. C. (1972). Effects of continuous inhalation of dichloromethane 

in the mouse: morphologic and functional observations. Toxicol. Appl. Pharmacol. 23(4), 660-679. (as 

cited in US EPA, 2011b).

Westat Inc. (1987). A national usage survey of household solvent products (Weststat, Rockville, MD). US 

Environmental Protection Agency, Washington, DC. PB88-132881.

Winneke, G. (1974). Behavioral effects of methylene chloride and carbon monoxide as assessed by 

sensory and psychomotor performance. In Behavioral toxicology: Early detection of occupational 

hazards. p. 130-144 U.S. Department of Health, Education and Welfare Washington, DC. (as cited in US 

EPA, 2011b and US EPA, 2008).

Winneke, G. (1981). The neurotoxicity of dichloromethane. Neurobehav. Toxicol. Teratol.3(4), 391-395.

WM Barr (2008). Material Safety Data Sheet. Klean-Strip Color Change Stripper. Product code: 

GKCC00326. W.M. Barr and Company. http://www.wmbarr.com/ProductFiles/GKCC00326.pdf. Accessed 

August 6, 2012. 

WM Barr (2009a). Material Safety Data Sheet. Klean Strip Aircraft Remover. Product code: A3900.2.

W.M. Barr and Company. 

WM Barr (2009b). Material Safety Data Sheet. Klean Strip Klean Kutter. Product code: 130. W.M. Barr 

and Company. http://www.wmbarr.com/ProductFiles/130%20(Klean%20Kutter).pdf. Accessed August 6, 

2012. 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 86

WM Barr (2009c). Material Safety Data Sheet. Klean Strip Aircraft Remover. Product code: 3404.11.

W.M. Barr and Company. http://www.wmbarr.com/ProductFiles/3404.11.pdf. Accessed August 6, 2012. 

WM Barr (2010a). Material Safety Data Sheet. Klean-Strip Naked Gun Spray Gun Paint Remover. Product 

code: 35M.6. W.M. Barr and Company. 

WM Barr (2010b). Material Safety Data Sheet. Klean-Strip Peeler. Product code: A223.2. W.M. Barr and 

Company. http://www.wmbarr.com/ProductFiles/KS%20Peeler%20(A223.2)%207-23-10.pdf. Accessed 

August 6, 2012. 

WM Barr (2011a). Material Safety Data Sheet. Klean Strip Adhesive Remover/Klean Strip Premium 

Stripper. Product code: 4015.26. W.M. Barr and Company. 

http://www.wmbarr.com/ProductFiles/KS%20Adhesive%20Remover%20(4015-26)%205-17-11.pdf. 

Accessed August 6, 2012. 

WM Barr (2011b). Material Safety Data Sheet. Klean-Strip Strip X Stripper. Product code: 105.25. W.M. 

Barr and Company. 

WM Barr (2011c). Material Safety Data Sheet. Klean-Strip Premium Sprayable Stripper. Product code: 

31051.6. W.M. Barr and Company. http://www.wmbarr.com/ProductFiles/MSWRPTM.pdf. Accessed 

August 6, 2012. 

WM Barr (2012). Material Safety Data Sheet. Premium Stripper. Product code: 4100.2. W.M. Barr and 

Company. http://www.wmbarr.com/ProductFiles/KS%20Premium%20Stripper%203%2028%202012.pdf. 

Accessed August 6, 2012. 

Wollbrinck, T. (1993). The composition of proprietary paint strippers. Journal of the Amercian Institute 

for Conservation 32(1), Article 5 (pp. 43-57). http://cool.conservation-us.org/jaic/articles/jaic32-01-

005_indx.html. Accessed August 6, 2012. 

Wong, K. L. (1990). Carbon monoxide. In Spacecraft maximum allowable concentrations for selected 

airborne contaminants. Vol. Vol 1, p. 61-90. National Academy Press, Washington, D.C. (as cited in NRC 

1996).
DOCUMENT-DO NOT CITE OR QUOTE 

Page 87

Appendices
DOCUMENT-DO NOT CITE OR QUOTE 

Page 88

Appendix A: Summary of Environmental Effects-Aquatic Toxicity

Acute Toxicity to Fish

Fathead minnows (Pimephales promelas) were exposed to unspecified measured 

concentrations of DCM under flow-through conditions for 96 hours. A 96-hour LC50 of 99 mg/L 

was reported (Alexander et al., 1978).

Fathead minnows (P. promelas) were exposed to unspecified measured concentrations of DCM 

under flow-through conditions for 96 hours. A 96-hour LC50 of 193 mg/L was reported 

(Alexander et al., 1978).

Fathead minnows (P. promelas) were exposed to unspecified nominal concentrations of DCM 

under static conditions for 96 hours. A 96-hour LC50 of 310 mg/L was reported (Alexander et 

al., 1978).

Fathead minnows (P. promelas) were exposed to unspecified measured concentrations of DCM 

under flow-through conditions for 96 hours. A 96-hour LC50 of 193 mg/L was reported (Geiger

et al., 1986).

Fathead minnows (P. promelas; 10/replicate) were exposed to measured concentrations of 79, 

135, 207, 357, 527, and 855 DCM under flow-through conditions for 96 hours. A 96-hour LC50

of 502 mg/L was reported (Dill et al., 1987).

Sheepshead minnows (Cyprinodon variegates) were exposed to unspecified nominal 

concentrations of DCM under static conditions for 96 hours. A 96-hour LC50 of 330 mg/L was 

reported (Heitmuller et al., 1981).

Zebrafish (Danio reio) were exposed to unspecified concentrations of DCM under unspecified 

conditions for 96 hours. The 96-hour LC50 of 254 mg/L was reported (Roderer, 1990).

Bluegill sunfish (Lepomis macrochirus) were exposed to unspecified nominal concentrations of 

DCM under static conditions for 96 hrs. A 96-hr LC50 of 220 mg/L was reported (Buccafusco et 

al., 1981).

Chronic Toxicity to Fish

Fathead minnows (P. promelas) were exposed to measured concentrations 29, 55, 82, 142, 209, 

and 321 of DCM under flow-through conditions for 28 days. The 28-day lowest-observed-effect 

concentration (LOEC) ranged between 82.5 and 142 mg/L and a maximum acceptable toxicant 

concentration (MATC) of 108 mg/L was reported (Dill et al., 1987).

Acute Toxicity to Aquatic Invertebrates

Water fleas (Daphnia magna) were exposed to unspecified nominal concentrations of DCM 

under static conditions for 48 hrs. A 48-hr EC50 of 1,682 mg/L was reported (Kühn et al., 1989).
DOCUMENT-DO NOT CITE OR QUOTE 

Page 89

Water fleas (D. magna) were exposed to unspecified nominal concentrations of DCM under 

static conditions for 48 hrs. A 48-hr EC50 of 1,250 mg/L was reported (von Bringmann and 

Meinck, 1964).

Water fleas (D. magna) were exposed to unspecified nominal concentrations of DCM under 

static conditions for 48 hrs. A 48-hr EC50 of 220 mg/L was reported (LeBlanc, 1980).

Opossum shrimp (Americamysis bahia) were exposed to unspecified nominal concentrations of 

DCM under static conditions for 96 hrs. A 96 hr EC50 of 256 mg/L was reported (Syracuse Res. 

Corp., 1978).

Toxicity to Aquatic Plants

Green algae (Pseudokirchneriella subcapitata) were exposed to unspecified nominal 

concentrations of DCM under static conditions for 96 hrs. A 96-hr EC50 of 500 mg/L was 

reported (US EPA, 1978). 

Diatoms (Skeletomema costatum) were exposed to unspecified nominal concentrations of DCM 

under static conditions for 96 hrs. A 96-hr EC50 of 662 mg/L was reported (Syracuse Res. Corp., 

1978). 

Green algae (Scenedesmus subspicatus) were exposed to unspecified nominal concentrations of 

DCM under static conditions for 96 hrs. A 96-hr EC50 of 1,000 mg/L was reported (Merlin et al., 

1992). 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 90

Appendix B: Inventory Update Reporting Rule Data for DCM

The following information comes from EPA’s Inventory Update Reporting Rule public database 

for the 2006 reporting cycle (US EPA, 2006a).

Table B-1. Manufacturing and Importing Company and Site Information for DCM.

Company Site City State Zip Code Manufacture Import

Basic Chemicals 

Company, LLC

Basic Chemicals 

Co - Geismar

Geismar LA 70734 Yes No

Basic Chemicals

Company, LLC

Basic Chemicals 

Co - Wichita 

Plant

Wichita KS 67215 Yes No

Chemcentral 

Corporation

Chemcentral 

International

Pompano Beach FL 33069 No Yes

E. I. du Pont de 

Nemours and 

Company

Dupont -

Headquarters 

(imported 

centrally 

through broker)

Wilmington DE 19898 No Yes

Ineos Chlor 

Americas, Inc.

Ineos Chlor 

Americas, Inc

Wilmington DE 19810 No Yes

Petrochem 

Americas LLC

Petrochem 

Americas LLC

Plano TX 75093 No Yes

TR 

International, 

Inc.

TR International 

Inc - Seattle

Seattle WA 98101 No Yes

The Dow 

Chemical 

Company

Dow Chemical -

Freeport, TX

Freeport TX 77541 Yes No

The Dow 

Chemical 

Company

Dow Chemical -

Pittsburg, CA

Pittsburg CA 94565 Yes No

The Dow 

Chemical 

Company

Dow Chemical -

Headquarters

Midland MI 48674 No Yes

The Dow 

Chemical 

Company

Dow Chemical -

Plaquemine

Plaquemine LA 70764 Yes No

Vulcan 

Materials 

Company

Vulcan Materials 

Co - Wichita 

Plant

Wichita KS 67215 Yes No

Vulcan 

Materials 

Company

Vulcan Materials 

Co - Geismar 

Plant

Geismar LA 70734 Yes No
DOCUMENT-DO NOT CITE OR QUOTE 

Page 91

Appendix C: Household Products Data for DCM

The following information comes from NIH’s Household Products Database. 

Table C-1. Household Products Containing DCM from NIH’s Household Products Database.

Brand Category Form Percent DCM

Jasco Brushable Semi-Paste Premium Paint & 

Epoxy Remover

Arts and crafts Liquid 60-100

Savogran Liquid Kutzit-08/31/2007 Arts and crafts Liquid 20-25

Carb Medic Carburetor Choke and Valve Cleaner08/01/2002-old productAuto products Liquid 60-70

Sprayway Industrial Gasket Remover No. 719 Auto products Aerosol 70-80

Gunk Carb Medic Carburetor and Choke Cleaner04/07/2010Auto products Aerosol 15-40

Carb Medic Carb/Choke/Valve Cleaner-old 

product

Auto products Aerosol 40-50

Gumout Professional Non Flammable Brake Parts 

Cleaner

Auto products Aerosol 5-30

Espree Tire Shine Auto products Aerosol 50

Lectra Motive Auto Care-old product Auto products Aerosol 1-20

Anti-Seize Lubricant-old product Auto products Aerosol 60-65

Carb Medic Carburetor Choke and Valve Cleanerold productAuto products Liquid 40-50

Champion Sprayon Degreasing Solvent Auto products Aerosol 70-75

ProsALL Prosolv Auto products Aerosol 70-75

Zinsser Brush & Roller Wash Home maintenance Liquid

Crown Handi-Strip All Purpose Liquid Stripper Home maintenance Liquid 40-60

Crown Tuff-Strip Heavy Duty Semi-Paste Stripper Home maintenance Liquid 80-90

UGL ZAR Paint and Varnish Remover Home maintenance Liquid 90

Savogran Prepaint Deglosser Home maintenance Liquid 35-40

Savogran Water Rinsing Kwikeeze Home maintenance Liquid 5-10

Savogran Sprayable Strypeeze-08/22/2001 Home maintenance Aerosol 85-90

Klean-Strip Klean Kutter Home maintenance Liquid 25-30

Klean-Strip Metal & Masonry Paint Remover Home maintenance Liquid 75-85

Klean-Strip Premium Stripper, Aerosol Home maintenance Aerosol 70-95

Klean-Strip Deep Down Stain Stripper-old product Home maintenance Aerosol <60

Zinc It Electric Grade Lubricant Home maintenance Aerosol 32
DOCUMENT-DO NOT CITE OR QUOTE 

Page 92

Table C-1. Household Products Containing DCM from NIH’s Household Products Database.

Brand Category Form Percent DCM

Savogran Kutzit Paint & Varnish Remover-old 

product

Home maintenance Liquid >24

Champion Sprayon Paint Off Home maintenance Aerosol 80 – 85

Sprayway Vandalism Mark and Stain Remover 

No. 870

Home maintenance Aerosol 43

Zinsser Adhesive Remover Home maintenance Liquid 71

Crown Solu-Strip Semi-Paste Adhesive Remover Home maintenance Liquid 80-90

Crown Handi-Strip All Purpose Sprayable 

Stripper, Aerosol

Home maintenance Aerosol 45-60

Savogran Adhesive Remover Home maintenance Liquid 85-90

Savogran Paint Stripper, Aerosol Home maintenance Aerosol 25-30

Savogran Heavy Duty SuperStrip Home maintenance Liquid 85-90

Klean-Strip Brush Cleaner Home maintenance Liquid 1-3

Klean-Strip KS-3 Premium Stripper Home maintenance Liquid 60-100

Klean-Strip Premium Sprayable Stripper Home maintenance Liquid 70-85

Klean-Strip Strip-X Stripper Home maintenance Liquid 30-50

Jasco Semi-Paste Varnish & Stain Remover Home maintenance Liquid 25-40

Klean-Strip Graffiti Remover-old product Home maintenance Aerosol 75-80

Savogran Strypeeze Paint/Varnish Remover-old 

product

Home maintenance Liquid >10

Parks Pro Liquid Paint Stripper-discontinued Home maintenance Liquid 40-90

Paint & Varnish Remover No. 2600, Aerosol Home maintenance Aerosol

Klean-Strip Adhesive Remover Inside the home Liquid 60-100

Aqua Mix Sealer and Adhesive Remover-old 

product

Inside the home Liquid

Parks Adhesive Remover-discontinued Inside the home Liquid 40-90

Radio Shack Rosin Flux Stripper Inside the home Liquid 39.83

Parks Adhesive Remover-09/04/1998-

discontinued

Inside the home Liquid 65-70

Monsanto Amplify Herbicide (agricultural) Pesticides Granules <16
DOCUMENT-DO NOT CITE OR QUOTE 

Page 93

Appendix D: Paint Stripping Processes and Associated Worker Activities, and Facility and

Population Data and Information

This appendix presents background information related to the analysis of worker exposures.

Descriptions of Processes and Activities

Techniques for paint stripping typically include manual coating, tank dipping, and spray 

application (TNO, 1999). Pouring, wiping, and rolling are also possible application techniques, 

and application can be manual or automated (ECHA, 2011). An individual’s exposure to paint 

stripping chemicals greatly depends on control measures taken and work practices adopted 

(TNO, 1999). The following sections summarize processes and activities for the industries found 

to employ paint stripping.

Paint Stripping By Professional Contractors

Paint strippers can be used by professional contractors to strip paint and varnish from walls, 

wood flooring, and kitchen and wood cabinets. Professional contractors are expected to 

purchase strippers in commercially available container sizes that commonly range from one 

liter up to five gallons, although they may also purchase consumer paint stripper products from 

hardware stores. Stripper is typically applied to wall or floor surfaces using a hand-held brush. 

Strippers used in these applications often have a high viscosity since they can be applied to 

vertical surfaces. After application, the stripper is allowed to set and soften the old coating. 

Once the stripper has finished setting, the old coating is removed from the surface by scraping 

and brushing. During wood floor stripping, old coating and stripper may also be removed using 

an electric floor buffer. After the old coating is removed, the surface is wiped clean before 

moving to the next stages of the job. The stripping process is often completed on an 

incremental basis with treatment for one section of wall or flooring being completed before 

moving to the next section (EU, 2007b; IRTA, 2006; NIOSH, 1993; TNO, 1999).

Professional contractors may also be employed to refinish or reglaze bathtubs. Various health 

case studies have noted the use of DCM-based strippers during bathtub refinishing or reglazing 

(CDC, 2012b, a; MSU/MIFACE, 2011). Case studies have identified professional bathtub 

refinishers that repaired and resurfaced countertops, tubs, and sinks in both apartment 

buildings and private homes (CDC, 2012a; MSU/MIFACE, 2011). The OSHA IMIS data identified 

a single OSHA inspection in 2007 of two bathtub reglazers. The bathtub reglazers’ company 

was identified under NAICS code 811420 – Reupholstery and Furniture Repair (OSHA, 2012). 

However, this assessment discusses bathtub reglazing in the context of professional 

contractors, as professional contractors and professional bathtub refinishers or reglazers are 

both expected to perform their work at customer sites (for example, in the cited case studies of 

bathtub refinishers/reglazers, apartment buildings, and private homes). This professional 

contractor-type work differs from furniture refinishing, which typically entails the refinishing of 

customer furniture at fixed furniture refinishing facilities.

A case study has indicated that bathtub refinishing or reglazing can involve a worker pouring 

and brushing stripper onto a bathtub using a paintbrush. The worker then scrapes the finish 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 94

from the bathtub after leaving the stripper in contact with the bathtub for 20 to 30 minutes 

(CDC, 2012a; MSU/MIFACE, 2011). This case study has noted a stripper DCM concentration of 

60 to 100 percent (CDC, 2012a; MSU/MIFACE, 2011); however, multiple health case studies 

have noted the use of aircraft and marine coating remover in bathtub refinishing/reglazing 

(CDC, 2012b).

Paint Stripping at Automotive Body Repair and Maintenance Shops

Automotive refinishing shops apply coatings to motor vehicles subsequent to the original 

manufacturing process. The overall refinishing process typically involves the following steps:

• Structural repair;

• Surface preparation (cleaning and sanding);

• Primer coat mixing;

• Spray application of primer coat;

• Curing;

• Sanding;

• Solvent wipe-down;

• Topcoat (basecoat color and clearcoat) mixing;

• Spray application of topcoat; and

• Curing.

The surface preparation step of the refinishing process involves:

“removing residual wax, grease, or other contaminants from the surface to be 

painted, to ensure adhesion of the new coating. The new coating may be 

applied over an existing coating if it is free of chips or cracks after it has been 

roughened through sanding. Alternatively, the previous coating may be 

removed using a mechanical method (e.g., sanding) or a paint-removing solvent. 

After the coating is roughened or removed, the surface is typically wiped down 

with a solvent- or water-based surface preparation product” (OECD, 2010). 

Wood Furniture Stripping

During furniture stripping, paint stripper may be applied to the furniture by either dipping the 

furniture in an open tank containing the stripper, brushing or spraying the stripper onto the 

furniture surface, or manually applying the stripper. Larger facilities may pump the stripper 

through a brush. The application method depends on the size and structure of the furniture as 

well as the capabilities of the facility. The application area typically has a sloped surface to 

allow for collection and recycling of unused stripper. Larger facilities use a flow tray to apply 

the stripper to parts. The flow tray is a sloped, shallow tank with a drain at the lower end. 

After application, the stripper is left to soak on the furniture surface to soften the surface 

coating. Once soaking is complete, the unwanted coating is scraped and brushed from the 

furniture surface. The furniture is then transferred to a washing area where residuals are 

washed from the furniture. Washing can be performed using low-pressure washing operations 

or high-pressure water jets or high-pressure wands. Wash water may contain oxalic acid to 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 95

brighten the wood surface. Wash water is collected and either recycled or disposed of as 

waste. After washing, the furniture is transferred to a drying area where it is allowed to dry 

before being transferred to other refinishing processes (e.g., sanding, painting, reupholstery) 

(HSE, 2001; IRTA, 2006; NIOSH, 1990, 1992).

Larger facilities likely purchase stripper in drum quantities from suppliers. Smaller facilities that 

use hand stripping instead of stripping equipment likely purchase their stripper from hardware 

and home improvement stores. Stripper applied using application equipment has low viscosity, 

so it can be pumped through the pumps in the flow tray. Strippers applied using hand stripping 

are typically more viscous, so they will remain on the part long enough to strip the coating 

(IRTA, 2006).

Figure D-1 shows a typical flow tray used by larger furniture strippers to apply stripper to 

furniture parts, obtained from Cal EPA (2006). Figure D-2 shows a typical water wash booth 

used to wash stripper and coating residue from stripped furniture, obtained from IRTA (2006). 

Figure D-3 shows an example diagram of a dipping tank for furniture stripping complete with 

local exhaust ventilation, obtained from HSE (2001).

Source: IRTA (2006).

Figure D-1. Typical Flow Tray for Applying Stripper to Furniture. 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 96

Source: IRTA (2006).

Figure D-1. Typical Water Wash Booth Used to Wash Stripper and Coating Residue from Furniture. 

Source: HSE (2001).

Figure D-2. Example Diagram of a Dipping Tank for Furniture Stripping.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 97

Art Restoration and Conservation

Art restoration and conservation can include the care and maintenance of paintings to reverse 

negative effects of aging and dirt accumulation. It can also include repairing paintings that have 

suffered paint loss, weakened canvas, tears, water damage, fire damage, and insect damage 

(Smithsonian, 2012b). Art restoration and conservation can include paint cleaning, which can 

entail removing dirt and other obscuring material, removing varnish, or removing overpaint 

while maintaining the original layer of paint (Smithsonian, 2012a). These activities can involve 

the use of paint strippers. Although paint strippers used in this field can contain DCM, the use 

of DCM is not always favored, as DCM can penetrate through the overpaint layer that is being

removed and into the original paint layer that is being conserved. N-Methylpyrrolidone (NMP) 

may serve as a suitable substitute for DCM in strippers used in this field (Wollbrinck, 1993). 

More detailed information on the use of paint strippers in art restoration and conservation was 

not identified. It is anticipated that paint strippers are applied manually in this field.

Aircraft Paint Stripping

During aircraft paint stripping, paint stripper is pumped from bulk storage containers and 

applied to the body of the aircraft using hoses. Once the paint stripper has been applied, it is 

allowed to set for a certain period of time (usually about 30 minutes) to allow the paint to 

soften. Once setting is complete, the stripper and loose paint are scraped down into a 

collection area. Any remaining stripper and paint residue are then brushed away with water 

and brushes. Once the surface of the aircraft has dried, a new layer of primer, paint, and top 

coat are applied (NIOSH, 1977).

Ship Paint Stripping

Process description information for paint stripping of ships has not been identified. It is 

anticipated that paint stripping of ships may involve similar processes as the paint stripping of 

aircraft.

Respiratory Protection

If respiratory protection is required, OSHA requires supplied-air respirators, as air-purifying 

respirators do not provide adequate respiratory protection against DCM (OSHA, 1997b). Of the 

13 MSDSs for paint strippers obtained through the literature search, 10 of the MSDSs were for 

DCM-containing paint strippers. Eight of the 10 MSDSs recommended a NIOSH-approved, selfcontained breathing apparatus or air-supplied respirator if respiratory protection is required. 

One MSDS recommends NIOSH-approved respiratory protection for organic solvent vapors, 

which may include the use of supplied air. The remaining MSDS only recommends a NIOSHapproved respirator for organic solvent vapors without further specification of the respirator 

type (WM Barr, 2008, 2009a, b, c, 2010a, b, 2011a, c, b, 2012).

Facility and Worker Population Data

This section summarizes data on the number of establishments, number of paid employees and 

workers, and production hrs and work day estimates (for manufacturing industries). Some of 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 98

these data are useful for determining the average number of workers per establishment, which 

can indicate relative sizes of the businesses.

Paint Stripping By Professional Contractors

Table D-1 summarizes the number of establishments and average number of construction 

workers for painting and wall covering contractors and flooring contractors according to the 

2007 US Economic Census (US Census, 2007b). The Census data do not include hrs worked for 

construction industry sectors. Note that these Census data do not include bathtub 

refinishers/reglazers. Census data that include bathtub refinishers/reglazers were not 

identified.

Table D-1. 2007 US Economic Census Data for Painting and Wall Covering and Flooring Contractors.

2007 NAICS 2007 NAICS Title 2007 Number of 

Establishments

2007 Average Number of 

Construction Workers

238320 Painting and wall 

covering contractors

35,619 174,276

238330 Flooring contractors 14,575 49,085

Source: US Census (2007b).

The number of painting and wall covering contractors and flooring contractors who use 

DCM-based paint strippers, or the number of jobs per year a contractor uses DCM-based paint 

strippers, and the number of construction workers within a job site exposed to DCM-based 

paint strippers is unknown. The number of establishments and construction workers from the 

US Census provide some context for potential numbers of establishments and construction 

workers potentially exposed to DCM during paint stripping; while some fraction of these 

workers may be exposed to DCM, the Census data do not include self-employed, single person 

businesses, and some of these workers may also be exposed to DCM.

Paint Stripping at Automotive Body Repair and Maintenance Shops

Table D-2 summarizes the number of establishments and average number of paid employees 

for automotive body, paint, and interior repair and maintenance according to the 2007 US 

Economic Census (US Census, 2007b). The Census data do not include hrs worked for this 

industry sector.

Table D-2. 2007 US Economic Census Data for Automotive Body, Paint, and Interior Repair and 

Maintenance.

2007 NAICS 2007 NAICS Title 2007 Number of 

Establishments

2007 Number of Paid 

Employees

811121 Automotive body, paint, 

and interior repair and 

maintenance

35,581 223,942

Source: US Census (2007b).
DOCUMENT-DO NOT CITE OR QUOTE 

Page 99

In 1998, the Rhode Island Department of Environmental Management (DEM) surveyed over 

350 body shops and found that 20 percent of the shops still used DCM as a paint stripper at 

that time. It is unknown if this fraction of body shops in Rhode Island in 1998 (that used DCM) 

is representative of body shops within the entire US Rhode Island DEM recommends 

eliminating the use of DCM-based paint strippers as a pollution prevention measure (RIDEM, 

2011). Therefore, it is uncertain if the 20 percent of shops that used DCM in 1998 is 

representative of the fraction of shops that use DCM in the present day.

The present day number of automotive body repair and maintenance shops within the US that 

use DCM-based paint strippers, and the number of employees within an establishment exposed 

to DCM-based paint strippers are unknown. Therefore, the number of establishments and 

employees from the US Census are possibly overestimates of the number of establishments and 

employees potentially exposed to DCM during paint stripping.

A 2003 Rhode Island study that monitored exposures to DCM in a vehicle repainting shop noted 

a use rate of DCM of one to two gallons per week for that particular facility (Enander et al., 

2004).

Wood Furniture Stripping

Table D-3 summarizes the number of establishments and average number of paid employees 

for reupholstery and furniture repair according to the 2007 US Economic Census (US Census, 

2007b). The Census data do not include hrs worked for this industry sector.

Table D-3. 2007 US Economic Census Data for Reupholstery and Furniture Repair.

2007 NAICS 2007 NAICS Title 2007 Number of 

Establishments

2007 Number of Paid 

Employees

811420 Reupholstery and furniture 

repair

4,693 16,142

Source: US Census (2007b).

OSHA conducted a Regulatory Impact Analysis (RIA) in 1996 of the 1997 OSHA Methylene 

Chloride Standard. In the RIA, OSHA estimated 6,152 establishments engaged in furniture paint 

stripping using DCM and estimated 7,872 workers exposed during this activity. The 2010 OSHA 

Regulatory Review of the Methylene Chloride Standard estimates that the number of 

reupholstery and furniture repair facilities decreased to fewer than 6,000 by 2003. The 2007 US 

Economic Census reports a further decline in the total number of establishments. However, it 

is unknown if these data are representative of the number of establishments and workers that 

use DCM in the present day (OSHA, 2010b).

The present day number of reupholstery and furniture repair establishments that use DCMbased paint strippers and the number of employees within an establishment exposed to DCMbased paint strippers are unknown. Therefore, the number of establishments and employees 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 100

from the US Census are possibly overestimates of the number of establishments and employees 

potentially exposed to DCM during paint stripping.

The Institute for Research and Technical Assistance (IRTA) surveyed the furniture stripping 

industry in the South Coast Basin in Southern California to determine the usage of DCM based 

strippers (Table D-4). IRTA then used these data to estimate the number of firms in the state of 

California that use DCM-based strippers (IRTA, 2006). The source did not identify the year in 

which these data were obtained. These data are presented in Table D-4. It is unknown if the 

distribution of facility annual use rate of stripper is representative of firms across the entire US.

Table D-4. Estimated Annual DCM Based Stripper Usage in California.

Annual Stripper Usage (Gallons per Year) Number of Firms in California

1,200-2,000 6

700-1,200 30

200-700 40

5-200 172

<5 248

Total 496a

a

IRTA (2006) notes a total of 596 firms in California. However, an actual summation of the firms gives a total of 

496.

Source: IRTA (2006).

IRTA (2006) identifies the facilities that use >200 gallons/year of stripper as larger facilities that 

purchase stripper in drum quantities from suppliers. The firms that use <200 gallons/year of 

stripper likely use hand stripping and purchase their stripper from hardware and home 

improvement stores (IRTA, 2006).

Art Restoration and Conservation

Table D-5 summarizes the number of establishments and average number of paid employees 

for independent artists, writers, and performers and museums according to the 2007 US 

Economic Census (US Census, 2007b). The Census data do not include hrs worked for these 

industry sectors.

Table D-5. 2007 US Economic Census Data for Industry Sectors that May Engage in Art Restoration 

and Conservation Activities.

2007 NAICS 2007 NAICS Title 2007 Number of 

Establishments

2007 Number of Paid 

Employees

711510 Independent Artists, 

Writers, and Performers

20,612 48,321

712110 Museums 4,664 83,899

Source: US Census (2007b).
DOCUMENT-DO NOT CITE OR QUOTE 

Page 101

NAICS code 711510 includes a wide variety of professions, including independent art restorers 

and independent conservators. The majority of the professions listed within this NAICS code 

according to the US Census Bureau are not expected to engage in paint stripping. Furthermore, 

the extent that art restorers and conservators engage in paint stripping, particularly using 

DCM-based paint strippers is unknown. Similarly, the number of museums within NAICS code 

712110 that engage in paint stripping, and use DCM-based paint strippers, is unknown. 

Therefore, the number of establishments and employees from the US Census are likely 

overestimates of the number of establishments and employees potentially exposed to DCM 

during paint stripping.

Aircraft Paint Stripping

Table D-6 summarizes the number of establishments, average number of production workers, 

and production workers hrs for aircraft manufacturing according to the 2007 US Economic 

Census (US Census, 2007b). The table also estimates the average worker days per year and 

average worker hrs per day. These parameters are estimated from the production workers hrs 

and the average number of production workers. The average worker days per year are 

estimated assuming eight worker hrs per day, and the average worker hrs per day are 

estimated assuming 250 worker days per year. The estimates of worker days per year and 

worker hrs per day are within 10 percent of the EPA New Chemicals Program default values of 

250 days/year and eight hrs/day, respectively.

Table D-6. 2007 US Economic Census Data for Aircraft Manufacturing.

2007 Economic Census Data

Parameters Calculated from 

the Corresponding 2007 

Economic Census Data

2007 

NAICS 

Code

2007 NAICS 

Title

Number of 

Establishments

Average 

Number of 

Production 

Workers

Production 

Workers Hrs 

(1,000 Hrs)

Average 

Worker Days 

per Year 

(Assuming 

8 Hrs/Day)

Average 

Worker Hrs per 

Day (Assuming 

250 Days/Year)

336411 Aircraft 

manufacturing

254 81,456 157,589 242 7.74

Source: US Census (2007b).

In the RIA, OSHA estimated 300 establishments engaged in paint stripping of aircraft using DCM 

and estimated 2,470 workers potentially exposed during this activity. However, it is unknown if 

these data are representative of the number of establishments and workers that use DCM in 

the present day (OSHA, 2010b). The 1996 RIA number of DCM-using establishments estimate is 

similar to the 2007 US Economic Census number of establishments. However, the 2007 US 

Economic Census presents a much greater number of workers than the RIA estimate of number 

of workers exposed to DCM.

The present day number of aircraft manufacturing establishments that use DCM-based paint 

strippers and the number of employees within an establishment exposed to DCM-based paint 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 102

strippers are unknown. Therefore, the number of establishments and employees from the US 

Census are possibly overestimates of the number of establishments and employees potentially 

exposed to DCM during paint stripping.

Ship Paint Stripping

Table D-7 summarizes the number of establishments, average number of production workers, 

and production workers hrs for ship building and repairing according to the 2007 US Economic 

Census (US Census, 2007b). The table also estimates the average worker days per year and 

average worker hrs per day. These parameters are estimated from the production workers hrs 

and the average number of production workers. The average worker days per year are 

estimated assuming eight worker hrs per day, and the average worker hrs per day are 

estimated assuming 250 worker days per year. The estimates of worker days per year and 

worker hrs per day are within 10 percent of the EPA New Chemicals Program default values of 

250 days/year and eight hrs/day, respectively.

Table D-7. 2007 US Economic Census Data for Ship Building and Repairing.

2007 Economic Census Data

Parameters Calculated from 

the Corresponding 2007 

Economic Census Data

2007 

NAICS 

Code

2007 NAICS 

Title

Number of 

Establishments

Average 

Number of 

Production 

Workers

Production 

Workers Hrs 

(1,000 Hrs)

Average 

Worker Days 

per Year 

(Assuming 

8 Hrs/Day)

Average 

Worker Hrs per 

Day (Assuming 

250 Days/Year)

336611 Ship building 

and repairing

656 65,737 136,929 260 8.33

Source: US Census (2007b).

The number of ship building and repair establishments that use DCM-based paint strippers and 

the number of employees within an establishment exposed to DCM-based paint strippers are 

unknown. Therefore, the number of establishments and employees from the US Census are 

possibly overestimates of the number of establishments and employees potentially exposed to 

DCM during paint stripping.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 103

Appendix E: Occupational Exposure Literature Data

This assessment uses existing inhalation exposure data to estimate occupational exposures to 

DCM. Multiple exposure studies were identified through a literature search. Additionally, 

inhalation exposure data from OSHA and state health inspections were obtained from the 

OSHA IMIS database. A summary of relevant data from the literature search follows.

Professional Contractors

Bathtub Refinishing Exposures and Fatalities

In 2012, the US Centers for Disease Control and Prevention (CDC) reported on bathtub 

refinisher fatalities associated with DCM stripping agents. Key excerpts from the CDC Morbidity 

and Mortality Weekly Report (MMWR) follow.

In addition to three deaths identified by the Michigan Fatality Assessment and Control 

Evaluation (FACE) program, OSHA identified 10 other bathtub refinisher fatalities associated 

with DCM stripping agents that had been investigated in nine states during 2000 to 2011. Each 

death occurred in a residential bathroom with inadequate ventilation. Protective equipment, 

including a respirator, either was not used or was inadequate to protect against DCM vapor, 

which has been recognized as potentially fatal to furniture strippers and factory workers, but 

has not been reported previously as a cause of death among bathtub refinishers (CDC, 2012b).

A review of the IMIS, a database for federal and state OSHA investigations, identified 12 

DCM-related deaths associated with professional bathtub refinishing operations during 2000 to 

2011. One of the three deaths identified by the Michigan program was not in IMIS because the 

decedent was self-employed and was therefore outside OSHA’s enforcement jurisdiction. The 

ages of the 13 decedents ranged from 23 to 57 years (median: 39 years). Twelve were male. 

Ten different products were associated with the 13 deaths. Six of the products were marketed 

for use in the aircraft industry, the rest for use on wood, metal, glass, and masonry. None of 

the product labels mentioned bathtub refinishing. The percentage of DCM in the products 

ranged from 60 to 100 percent (CDC, 2012b).

Toxicology tests from specimens collected at autopsy indicated DCM blood levels ranging from 

18 to 223 mg/L in the six decedents for whom values were recorded; a level of <2 mg/L is 

expected in a person working within the OSHA allowable air standard for exposure to DCM 

fumes. Among the five decedents whose COHb levels were tested, levels ranged from absent 

to mildly elevated (range: zero to five percent), indicating that CO was unlikely to have been the 

primary cause of death (although the durations of exposure to DCM and receipt of oxygen 

during resuscitation efforts, two factors that can affect COHb levels, were not known). Analysis 

of IMIS data regarding deaths from DCM showed an increase in cases involving bathtub 

refinishing since 2000. During 1976 to 1999, only two (eight percent) of all DCM deaths 

investigated by OSHA were linked to bathtub refinishing. Since 2000, 13 (75 percent) of the 

DCM deaths investigated by OSHA occurred during bathtub refinishing (CDC, 2012b).
DOCUMENT-DO NOT CITE OR QUOTE 

Page 104

A report of a May 2010 fatality investigated by the Michigan FACE program contained 

estimated exposure concentrations. Based on the size of the bathroom, size of the tub, and an 

estimate that six fluid ounces (177 mL) of DCM-based stripper was used during a typical job, 

and the aircraft paint stripper product used contained 60 to 100 percent DCM, exposure levels 

were estimated for both the tub and bathroom environments. The concentration of DCM 

vapor was estimated at 92,949 to 154,916 ppm in the bathtub and 5,099 to 8,499 ppm in the 

bathroom. These concentrations exceed the NIOSH Immediately Dangerous to Life and Health 

(IDLH) level of 2,300 ppm (CDC, 2012b). Further details are available in the MMWR (CDC, 

2012b), the NIOSH FACE Program Michigan Case Report 10MI013 (CDC, 2012a), and the 

Michigan State University (MSU)/FACE Report (MSU/MIFACE, 2011).

The MSU/Michigan FACE report noted that Washington State’s Department of Labor and 

Industries Division of Occupational Safety and Health (DOSH) inspection data include a case of a 

high DCM exposure while stripping a bathtub. A bathtub refinishing employee was monitored 

while stripping a residential bathtub with Kleen Strip Aircraft Remover. The MSDS indicated the 

product contained <85 percent DCM. Information sheets with the product recommended the 

use of supplied air. The employee had purchased ventilation equipment, which was in use at 

the time of monitoring. The employee wore a half-face air purifying respirator. Two personal 

samples were taken in the breathing zone of the employee for 15 minutes during the stripping 

task. These personal samples were 2,180 and 2,000 ppm DCM. Two area samples were also 

taken and were 545 and 314 ppm DCM. All of the samples significantly exceeded the OSHA 

15-minute TWA STEL of 125 ppm, and the two breathing zone samples were close to the NIOSH 

IDLH value of 2,300 ppm (MSU/MIFACE, 2011). Although the exact date of the Washington 

DOSH inspection was not cited, the inspection occurred in the time period between April 2003 

and August 2008 (Lofgren et al., 2010).

Paint Stripping by Professional Contractors

DCM exposure data for paint stripping conducted by professional contractors were not 

identified in the literature search. However, some DCM exposure data were identified for 

consumer use of DCM-based paint strippers in a European Union (EU) report. The EU report 

states that there is “probably...no fundamental difference between the application of paint 

removers by professional painters and consumers” and goes on to further state that, in regard 

to the cited consumer exposure studies, “the test situations and data described...are assumed 

valid for occupational exposure during professional use as well” (TNO, 1999). However, 

professional contractors are expected to have a higher frequency of exposure as compared to 

consumers. It is also not clear whether overall activity patterns and practices of contractors 

match those of consumers or whether the overall distributions of exposures of contractors and 

consumers have any semblance to one another. Despite these uncertainties, some of the 

literature data for consumers may be considered.

The EU report identified the following consumer exposures to DCM during paint stripping from 

a literature review. A 1990 EPA investigation estimated consumer exposure levels ranging from 

35 mg/m3 (10 ppm) to a few short-term exposures of over 14,100 mg/m3 (4,063 ppm). The 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 105

majority of the exposures were below 1,770 mg/m3 (510 ppm). A separate study conducted by 

a solvent manufacturer measured exposures during tests conducted in a small room. One test 

conducted with ventilation (although the ventilation rate or air change rate were not specified) 

measured a two-hr TWA exposure of 289 mg/m3 (83.3 ppm). The peak exposure during 

application was 460 mg/m3 (133 ppm). The peak exposure during scrape-off ranged from 

710 to 1,410 mg/m3 (205 to 406 ppm), with a maximum of 3,530 mg/m3 (1,017 ppm). When no 

ventilation was used, the worst-case exposure exceeded 14,000 mg/m3 (4,035 ppm). Based on 

the solvent manufacturer, eight-hr TWA exposures under supplier-recommended ventilation 

would be 187 to 226 mg/m3 (54 to 65 ppm) (TNO, 1999).

The same EU report also cites a literature review conducted by the United Kingdom (UK) in 

1998, which identified reports of one-hr TWA exposures of 840 to 2,765 mg/m3 (240 to 

790 ppm) in an unventilated room, and 129.5 to 948 mg/m3 (37 to 270 ppm) with the door 

open. An older study from 1981 found eight-hr TWA exposures of 460 to 2,980 mg/m3 (133 to 

859 ppm) in unventilated rooms and 60 to 400 mg/m3 (17 to 115 ppm) in ventilated rooms 

(TNO, 1999).

Midwest Research Institute (MRI) prepared a report for EPA in 1994 that resulted from an 

experimental investigation of consumer exposures to solvents contained in paint stripping 

products with eliminated or reduced DCM content. MRI investigated five paint strippers, two 

of which contained DCM (along with other solvents, but the concentrations were not specified). 

The paint stripping was conducted in a laboratory-based, environment-controlled, room-sized 

test chamber. The paint strippers were used on a plywood panel coated with a primer coat and 

two finish coats. The air exchange rate for the experiments ranged from 0.54 to 0.76 air 

changes per hr (ACH), with an average of 0.58 ACH. The air exchange rate of approximately 0.5 

ACH was intended to replicate the ventilation rate of an enclosed room in a typical residence as 

a worst-case scenario. During each experiment, the following samples were taken: a personal 

breathing zone sample of the test subject using the paint stripper; two stationary air samples 

for the duration of the paint stripping task; and one stationary air sample beginning at the start 

of the paint stripping and lasting for eight hrs (US EPA, 1994b).

In the MRI investigation, the first DCM-based paint stripper was spray applied. The breathing 

zone concentrations of DCM were 3,000 and 3,400 mg/m3 (865 and 980 ppm). The stationary 

length-of-task concentrations ranged from 2,900 to 3,600 mg/m3 (836 to 1,037 ppm). The 

eight-hr TWA concentration ranged from 1,700 to 2,000 mg/m3 (490 to 576 ppm). The second 

DCM-based paint stripper was brush applied. The breathing zone and stationary length-of-task 

concentrations ranged from 380 to 490 mg/m3 (110 to 141 ppm). The eight-hr TWA 

concentration ranged from 230 to 270 mg/m3 (66 to 78 ppm) (US EPA, 1994b).

DCM exposure data were identified in the OSHA IMIS data set. Table E-1 provides a summary 

by job category of the OSHA inspection data. For both wall and flooring contractors, the 

inspection exposures ranged from zero to 28.3 mg/m3 (zero to 8.2 ppm) and include both 

eight-hr TWA and STEL/ceiling exposures. These exposures include a wide variety of job 

activities, although two monitored worker activities appear to have involved stripping but 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 106

without specification of the application method (OSHA, 2012). The relevance of these 

exposures to DCM-based paint stripping is uncertain.

Table E-1. Summary by Industry and Job Category of OSHA IMIS Data for DCM from 1992 to 2012.

NAICS/SIC Code Job Category Sample 

Type

Exposure 

Type Data Type Concentration 

(mg/m3

)

a

Number of 

Data 

Points

336411

(Aircraft Manufacturing)

Painter Personal TWA Minimum 0 3

Average 12.7

Maximum 20.8

8999

(Aircraft Refinishing)b

Finisher Personal TWA Minimum 7.3 4

Average 16.9

Maximum 33.7

336611

(Ship Building and 

Repairing)

Assembler Personal TWA Minimum 6.1 3

Average 19.5

Maximum 33.7

Foamer Personal TWA Minimum 3.5 3

Average 13.9

Maximum 27.8

General 

laborer

Personal TWA Single data 

point

3.5 1

Gluer Personal TWA Minimum 0 2

Average 5.2

Maximum 10.4

Mechanic/ 

electrician

Personal STEL Single data 

point

0 1

Refrigeration Personal TWA Two data 

points

0 2

Upholsterer Personal TWA Minimum 1.11 2

Average 1.20

Maximum 1.29

238320

(Painting and Wall 

Covering Contractors)

Manager Personal Ceiling Single data 

point

3.5 1

Painter Personal TWA Minimum 0 2

Average 6.9

Maximum 13.9

Stripper Personal Ceiling Minimum 0 4

Average 0
DOCUMENT-DO NOT CITE OR QUOTE 

Page 107

Table E-1. Summary by Industry and Job Category of OSHA IMIS Data for DCM from 1992 to 2012.

NAICS/SIC Code Job Category Sample 

Type

Exposure 

Type Data Type Concentration (mg/m3

)

a

Number of 

Data 

Points

Maximum 0

TWA Minimum 6.3 2

Average 11.0

Maximum 15.8

238330

(Flooring Contractors)

Carpet 

installer

Personal STEL Single data 

point

27.8 1

General 

laborer

Personal TWA Single data 

point

28.3 1

H&S Officer Personal STEL Single data 

point

4.5 1

711510

(Independent Artists, 

Writers, and 

Performers)

Manager Personal TWA Single data 

point

2.0 1

811121

(Automotive Body, 

Paint, and Interior 

Repair and 

Maintenance)

Adhesive 

application

Personal STEL Single data 

point

6.9 1

TWA Minimum 13.9 2

Average 19.1

Maximum 24.3

Autobody 

repairman

Personal Ceiling Single data 

point

27.8 1

STEL Single data 

point

13.9 1

TWA Minimum 0.0 2

Average 15.6

Maximum 31.3

Bed liner Personal Ceiling Single data 

point

0 1

General 

laborer

Personal TWA Single data 

point

1.3 1

Gluer Personal TWA Minimum 6.9 2

Average 13.4

Maximum 19.8

Owner Personal STEL Single data 

point

27.8 1
DOCUMENT-DO NOT CITE OR QUOTE 

Page 108

Table E-1. Summary by Industry and Job Category of OSHA IMIS Data for DCM from 1992 to 2012.

NAICS/SIC Code Job Category Sample 

Type

Exposure 

Type Data Type Concentration (mg/m3

)

a

Number of 

Data 

Points

Painter Personal STEL Minimum 3.5 2

Average 14.1

Maximum 24.8

TWA Minimum 0.5 5

Average 3.8

Maximum 12.3

Sander Personal STEL Single data 

point

3.1 1

Spray painter Personal TWA Single data 

point

2.4 1

Stripper Personal STEL Minimum 6.2 2

Average 10.7

Maximum 15.3

TWA Single data 

point

28.6 1

Surface 

preparation

Personal STEL Minimum 6.9 2

Average 20.6

Maximum 34.3

TWA Single Data 

Point

8.9 1

Upholsterer Personal STEL Single Data 

Point

10.4 1

811420

(Reupholstery and 

Furniture Repair)

Area sample Area TWA Minimum 0.0 3

Average 13.9

Maximum 31.3

Bathtub 

reglazer

Personal STEL Single data 

point

0 1

Caser Personal TWA Single data 

point

24.3 1

Degreaser Personal TWA Single data 

point

3.5 1

Finisher Personal STEL Single data 

point

1.3 1

TWA Minimum 3.8 6

Average 8.1
DOCUMENT-DO NOT CITE OR QUOTE 

Page 109

Table E-1. Summary by Industry and Job Category of OSHA IMIS Data for DCM from 1992 to 2012.

NAICS/SIC Code Job Category Sample 

Type

Exposure 

Type Data Type Concentration (mg/m3

)

a

Number of 

Data 

Points

Maximum 17.0

General 

laborer

Personal Ceiling Single data 

point

0 1

STEL Minimum 0 5

Average 9.9

Maximum 20.8

TWA Minimum 0 2

Average 8.7

Maximum 17.4

Gluer Personal TWA Minimum 6.9 3

Average 12.0

Maximum 17.4

H&S officer Personal Ceiling Single data 

point

16.3 1

TWA Minimum 1.7 6

Average 11.6

Maximum 30.1

Industrial 

hygienist

Personal Ceiling Single data 

point

0 1

Owner Personal Ceiling Single data 

point

0 1

STEL Minimum 0 3

Average 11.7

Maximum 21.2

TWA Minimum 6.9 5

Average 19.8

Maximum 25.7

Refinisher Area STEL Single data 

point

0 1

Personal Ceiling Minimum 10.4 2

Average 12.2

Maximum 13.9

STEL Minimum 0 11

Average 10.1
DOCUMENT-DO NOT CITE OR QUOTE 

Page 110

Table E-1. Summary by Industry and Job Category of OSHA IMIS Data for DCM from 1992 to 2012.

NAICS/SIC Code Job Category Sample 

Type

Exposure 

Type Data Type Concentration (mg/m3

)

a

Number of 

Data 

Points

Maximum 20.8

TWA Minimum 0.8 11

Average 13.3

Maximum 30.7

Repairman Personal Ceiling Single data 

point

31.3 1

STEL Minimum 31.3 2

Average 32.7

Maximum 34.0

TWA Single data 

point

0.74 1

Restorer Area Ceiling Single data 

point

0 1

Personal Ceiling Single data 

point

0 1

STEL Minimum 17.4 2

Average 24.3

Maximum 31.3

TWA Minimum 3.5 4

Average 11.2

Maximum 19.1

Sander Personal TWA Minimum 9.0 2

Average 19.3

Maximum 29.5

Seamstress Personal TWA Minimum 13.9 3

Average 18.1

Maximum 25.9

Secretary Personal TWA Single data 

point

19.1 1

Spray painter Personal TWA Single data 

point

12.5 1

Spray room 

with vent

Personal STEL Single data 

point

11.1 1

Stripper Area TWA Minimum 6.9 2
DOCUMENT-DO NOT CITE OR QUOTE 

Page 111

Table E-1. Summary by Industry and Job Category of OSHA IMIS Data for DCM from 1992 to 2012.

NAICS/SIC Code Job Category Sample 

Type

Exposure 

Type Data Type Concentration (mg/m3

)

a

Number of 

Data 

Points

Average 13.9

Maximum 20.8

Personal Ceiling Minimum 6.9 3

Average 18.5

Maximum 27.8

STEL Minimum 0 31

Average 14.9

Maximum 31.3

TWA Minimum 0 35

Average 15.7

Maximum 33.9

Unknown Personal TWA Single data 

point

3.5 1

Upholsterer Area TWA Single data 

point

20.8 1

Personal Ceiling Single data 

point

3.5 1

TWA Minimum 3.5 5

Average 9.2

Maximum 24.3

STEL Minimum 10.4 2

Average 10.4

Maximum 10.4

Utility worker Personal TWA Single data 

point

33.4 1

Wood worker Personal STEL Single data 

point

0 1

TWA Single data 

point

17.0 1

a

Original concentrations were given in ppm. These values were converted to mg/m3 using the conversion of 

1 ppm = 3.47 mg/m3 (NIOSH, 2011a). This conversion assumes standard temperature and pressure of 1 atm and 

25 °C.

b

Standard Industry Classification (SIC) code 8999 is for Services, Not Elsewhere Classified. This particular 

inspection data point was for a facility called Aircraft Refinishing Technology, Inc., and was assumed to be 

applicable for aircraft refinishing.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 112

Paint Stripping at Automotive Body Repair and Maintenance Shops

A 2004 publication describes a study in Rhode Island that conducted personal air sampling of 

workers in two complete vehicle repainting facilities (shops that specialize in repainting the 

entire surface of cars and small trucks) and one vocational technical school. The DCM 

monitoring was conducted on a single worker in a vehicle repainting shop for one day in the 

spring and one day in the fall. This worker engaged in paint stripping one to two times per 

week and three to four hrs per day. The spring TWA exposure was 26 ppm and the fall TWA 

exposure was 120 ppm. These exposures exceeded OSHA’s eight-hr TWA action level 

(12.5 ppm) and PEL (25 ppm), respectively. Additionally, three task-based samples were taken 

in the spring (with sampling times ranging from nine to 18 minutes). These exposures were 72, 

93, and 120 ppm, which were all below the OSHA STEL (125 ppm) (Enander et al., 2004).

DCM exposure data were identified in the OSHA IMIS data set. Table E-1 provides a summary 

by job category of the OSHA inspection data. For automotive body repair and maintenance, the 

inspection exposures ranged from zero to 34.3 mg/m3 (zero to 9.9 ppm) and include both eighthr TWA and STEL/ceiling exposures. These exposures include a wide variety of job activities, 

although three separate monitored worker activities appear to include stripping (note that 

stripping could include sanding, which is a mechanical paint stripping method as opposed to the 

chemical paint stripping method, such as the use of DCM) (OSHA, 2012). The relevance of 

these exposures to DCM-based paint stripping is uncertain.

Wood Furniture Stripping

In 1992, the NIOSH surveyed a furniture refinishing shop located in Littleton, Colorado. NIOSH 

was invited to conduct the survey by the facility owner. The facility stripped furniture in a 

separate room using a pump and brush technique to apply paint stripper and remove the paint. 

The stripper is pumped from a 55-gallon drum to the brush, collected from the table, and 

recycled. The facility employed five refinishers. The stripping time of each worker averaged at 

a few hrs per week, but reached as high as three to four hrs in a day. While stripping, the 

workers wore rubber aprons, full-length rubber gauntlets, a face shield, and plastic upper arm 

covers, and they also may have worn the safety goggles they wore in the wood shop area 

(NIOSH, 1992).

NIOSH conducted three surveys: an initial survey on October 10, 1992; a second survey on 

November 20, 1992 after an exhaust ventilation system was installed on the furniture stripping 

booth; and a third survey on February 10, 1993 after an exhaust ventilation system was 

installed on the wash booth (NIOSH, 1992). Tables E-2, E-3, and E-4 present the measurements 

that NIOSH made during these three surveys. The results indicate that the addition of 

engineering controls reduced exposure concentrations in both the personal and area samples.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 113

Table E-2. Summary of Personal and Area Concentrations in a Furniture Refinishing Shop that Uses a 

Pump and Brush Stripping Technique Measured Before Engineering Controls were Added.

Initial Survey (Before Controls Added)

Personal Samples Area Samples

Activity Concentration 

(ppm)

Sampling Time 

(Minutes) Location Concentration (ppm)

Sampling Time 

(Minutes)

Stripping large 

chest

414 78 Door at room 

entrance

166 102

Stripping 

headboard

523 101 Door at room 

entrance

167 78

Stripping wicker 

chairs

398 23 Edge of stripping 

booth above 

recycle can

246 59

Stripping large 

dresser and 

drawers

445 58 Above water 

reservoir between 

wash booth and 

outside wall

52 62

Stripping large 

dresser and 

drawers

393 30 Workbench south 

of wash booth

37 182

Hand strip table 

with Palco gel 

stripper

83 14 Above drum of 

bulk stripper

120 60

Hand strip table 

with gel

174 16 Above drum of 

bulk stripper

86 102

Source: NIOSH (1992).
DOCUMENT-DO NOT CITE OR QUOTE 

Page 114

Table E-3. Summary of Personal and Area Concentrations in a Furniture Refinishing Shop that Uses a 

Pump and Brush Stripping Technique Measured After Engineering Controls were Added to the 

Stripping Booth.

Second Survey (After Controls Added to Stripping Booth)

Personal Samples Area Samples

Activity Concentration 

(ppm)

Sampling 

Time 

(Minutes)

Location Concentration 

(ppm)

Sampling 

Time 

(Minutes)

Stripping six 

chairs

10 35 Center of room (before 

ventilation system turned 

on)

32 18

Stripping crib 95 33 Above newly stripped chairs 85 82

Strip large 

desk

110 103 South central part of room 

near newly stripped crib

25 42

Near newly stripped desk 

drawers

32 59

Edge of wash booth (near 

worker breathing zone)

120 33

Edge of wash booth (near 

worker breathing zone)

58 34

Edge of wash booth (near 

worker breathing zone)

59 101

On work bench behind wash 

booth

4.5 102

Above DCM waste buckets 15 215

Above wash sludge tank 6.3 57

Source: NIOSH (1992).
DOCUMENT-DO NOT CITE OR QUOTE 

Page 115

Table E-4. Summary of Personal and Area Concentrations in a Furniture Refinishing Shop that Uses a 

Pump and Brush Stripping Technique Measured After Engineering Controls were Added to the 

Stripping Booth and Wash Booth.

Third Survey (After Controls Added to Stripping Booth and Wash Booth)

Personal Samples Area Samples

Activity Concentration 

(ppm)

Sampling 

Time 

(Minutes)

Location Concentration 

(ppm)

Sampling 

Time 

(Minutes)

Stripping rocking 

chair

19 24 Center of room 2.1 30

Stripping seven 

chairs

90 52 Near entrance to 

room

5.4 102

Stripping chairs 36 97 Above door to 

entrance of room

4 84

Stripping large 

dresser

70 113 Above door to 

entrance of room

8.4 178

Stripping dresser 

drawers

110 61 Above stripping drum <4 25

Above stripping drum 2.6 75

Above stripping drum 5 87

Above stripping drum ND 182

Above wash sludge 

tank

5 92

Near drying chairs 11 113

Above dresser while 

drying

18 107

ND – not detected at a limit of 0.01 mg per sample

Source: NIOSH (1992).

The initial survey indicated that personal exposure concentrations associated with stripping 

activities ranged from 83 to 523 ppm (over a range of sampling times) with an average of 

347 ppm. After the addition of the stripping booth exhaust ventilation system, the second 

survey indicated that personal exposure concentrations associated with stripping activities 

dropped to a range of 10 to 110 ppm (over a range of sampling times) with an average of 

72 ppm. This range and average concentration are generally consistent with the personal 

exposure concentrations associated with stripping activities observed on the third survey (after 

controls were added to the wash booth). Personal samples were not taken during washing 

activities, and area samples were not taken at consistent, wash-booth area locations during all 

surveys. However, the area samples altogether do indicate a reduction in concentrations after 

installation of the ventilation systems. The eight-hr TWA exposures (eight-hr averages of the 

individual samples and not the samples themselves) were below the pre-1997 OSHA PEL of 500 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 116

ppm but above the ACGIH Threshold Limit Value (TLV) of 50 ppm. NIOSH noted that after the 

ventilation systems were installed, the eight-hr TWA exposures were all below 50 ppm (NIOSH, 

1992).

A 2007 publication describes follow-up activities by OSHA in the inspection of a small business 

that repaired and restored custom-made furniture. The facility employed 18 workers, but only 

a single worker worked three to four days per week using DCM to remove paint and varnish 

from furniture in one section of the facility. The worker used a compressed-air system to spray 

DCM onto the furniture on a shallow tray. Excess stripper drained through the tray and was 

recirculated into a 208-L drum for reuse. OSHA conducted personal monitoring of the worker 

and measured an eight-hr TWA exposure of 108 ppm, which was above the OSHA PEL of 

25 ppm. OSHA also measured seven STEL sampling results, which ranged from 153 to 662 ppm, 

with an average of 404 ppm. These measurements were all above the OSHA STEL of 125 ppm. 

The worker was observed wearing a full-face elastomeric respirator with organic vapor 

cartridges and impervious gloves and an apron. The facility was cited for the overexposure and 

required to implement controls, including work practice and engineering controls and the use 

of a NIOSH-approved supplied-air respirator (Grevenkamp, 2007).

A 1991 publication describes a NIOSH industrial hygiene survey of 14 furniture stripping 

workers exposed to DCM across five furniture stripping shops. NIOSH measured personal TWA 

exposures of the workers to DCM ranging from 15 to 366 ppm. The highest average exposures 

to DCM by job category were: 191 ppm (strippers); 145 ppm (washers); and 31 ppm 

(refinishers) (IARC, 1999; McCammon et al., 1991). These TWA exposures were below the pre1997 OSHA PEL of 500 ppm.

In 1990, NIOSH conducted a survey of a furniture stripping workshop in Meadow Lands, 

Pennsylvania. This workshop used a flow-over tank with a solution recycling system to strip 

furniture. The furniture is placed in tank, covered with stripping solution, and then scrubbed by 

a worker. During scrubbing, the worker alternates between brushing the furniture and covering

it with more stripping solution. After stripping, the furniture is rinsed and brushed, dried, 

sanded, and refinished. The facility used a stripping solution that contained 60 volume percent 

DCM. The workshop installed a ventilation system in response to the results of an OSHA 

inspection. The NIOSH survey was conducted after installation of the ventilation system to 

determine its adequacy. NIOSH found the ventilation system to be inadequate as exposure 

levels exceeded the pre-1997 OSHA PEL of 500 ppm. Measurements conducted by NIOSH 

found TWA exposure levels ranging from 613 to 1,152 ppm during stripping (averaged over 

stripping times of 177 to 260 minutes). NIOSH made recommendations for improving the 

ventilation system. After modifications to the ventilation system were made, NIOSH measured 

personal exposures during stripping on three different days and found DCM concentrations 

during stripping ranging from 22 to 35 ppm over stripping times of 4.5 to 6.25 hrs. The 

corresponding eight-hr TWA exposures ranged from 13 to 27 ppm. Additional personal samples 

measured for various ventilation system configurations resulted in DCM concentrations ranging 

from seven to 59 ppm (averaged over time periods of 49 to 147 minutes). NIOSH also 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 117

measured task-specific exposures for various ventilation system configurations and found the 

following ranges of DCM area concentrations for each task (NIOSH, 1991):

• Stripping area: 8 to 31 ppm;

• Rinsing area: 5 to 94 ppm;

• Stripping solution 55-gallon drum area: 0 to 293 ppm; and

• Other areas: 5 to 89 ppm.

The percentages of a worker’s entire exposure due to each task area were as follows (NIOSH, 

1991):

• Stripping area: 14 to 73 percent;

• Rinsing area: 12 to 51 percent;

• Stripping solution 55-gallon drum area: 0 to 22 percent; and

• Other areas: 2 to 51 percent.

In 1990, NIOSH conducted a survey of a furniture stripping facility in Cincinnati, Ohio. This 

facility was operated solely by the owner. The facility conducted dip-tank paint stripping using 

a DCM-based paint stripper (72 weight percent DCM) and hand stripping using a paint stripper 

that did not contain DCM. NIOSH measured one-hr TWA concentrations of breathing zone and 

area samples. NIOSH observed breathing zone concentrations of 100 and 77 ppm of the facility 

owner and the NIOSH employee, respectively. NIOSH observed three area concentrations of 

20, 63, and 90 ppm. The highest area concentration was observed near the dip tank, the 

middle concentration was observed near the rinse area, and the lowest concentration was 

observed near the doorway to the stripping area. These measurements were below the pre1997 OSHA PEL of 500 ppm. NIOSH noted local exhaust near the dip tank with very low intake 

velocity and generally inadequate air movement in the stripping area. NIOSH also noted that 

the facility owner wore neoprene gloves and boots while stripping, rinsing, and handling the 

solution-soaked furniture, but no other personal protective equipment was worn (NIOSH, 

1990).

A 1990 EPA source cites exposure levels in furniture paint stripping with inadequate control 

measures as ranging from 258 to 3,812 mg/m3 (74 to 1,099 ppm) (TNO, 1999).

DCM exposure data were identified in the OSHA IMIS data set. Table E-1 provides a summary 

by job category of the OSHA inspection data. For furniture refinishing, the inspection exposures 

ranged from zero to 34.0 mg/m3 (zero to 9.8 ppm) and included both eight-hr TWA and 

STEL/ceiling exposures. These exposures include a wide variety of job activities, although of the 

170 data points, 71 data points appear to have involved stripping, 26 data points appear to 

have involved refinishing, and one data point was for a bathtub reglazer. Only one of the 

71 stripping data points, which was a STEL measurement, indicated the job activity as “spraying 

MC” (presumably MC stands for methylene chloride). None of the other job activities indicated 

the application method (OSHA, 2012). The relevance of these exposures to DCM-based paint 

stripping is uncertain.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 118

Art Restoration and Conservation

Exposure data associated with art restoration and conservation were not identified in the 

literature search. A single exposure data point was identified in the OSHA IMIS data set 

(Table E-1) with an eight-hr TWA exposure of two mg/m3 (0.58 ppm). This exposure was for a 

manager (OSHA, 2012). The relevance of this exposure to DCM-based paint stripping is 

uncertain.

Aircraft Paint Stripping

DCM exposure data of the breathing zone of workers engaged in paint stripping of aircraft in 

the US in 1977 were identified. A set of 23 breathing zone samples of paint stripping of wide 

body aircraft (over a range of sampling times of 56 to 126 minutes) had a range of exposures of 

79 to 950 mg/m3 (23 to 274 ppm) with a mean of 393 mg/m3 (113 ppm). A set of 20 breathing 

zone samples of paint stripping of narrow body aircraft (over a range of sampling times of 16 to 

33 minutes) had a range of exposures of 38 to 2,820 mg/m3 (11 to 813 ppm) with a mean of 

795 mg/m3 (229 ppm) (IARC, 2010).

A UK study observed aircraft paint stripping using a spray process and found DCM eight-hr TWA 

exposures of 29 to 95 ppm, with a mean of 62 ppm (210 mg/m3

). Peak levels were as high as 

1,600 ppm (5,400 mg/m3) (EU, 2007a; TNO, 1999).

A French study in 1994 observed the paint stripping of a Boeing 747 in an aeronautical 

workshop. During paint stripping operations, DCM concentrations ranged from 299.2 mg/m3

(83.1 ppm) to 1,888.9 mg/m3 (524.7 ppm). The eight-hr TWA exposures to DCM ranged from 

86 mg/m3 (23.9 ppm) to 1,239.5 mg/m3 (344.3 ppm) (EU, 2007a; IARC, 1999; Vincent et al., 

1994).

Norwegian studies from 2001 and 2002 found eight-hr TWA exposures to DCM associated with 

paint removal of aircraft of 1,444 and 3,802 mg/m3 (416 and 1,096 ppm) from personal samples 

(EU, 2007a).

DCM exposure data were identified in the OSHA IMIS data set. Table E-1 provides a summary 

by job category of the OSHA inspection data. For aircraft manufacturing and refinishing, the 

inspection exposures ranged from zero to 33.7 mg/m3 (zero to 9.7 ppm) all as eight-hr TWA 

exposures. These exposures include both painting and finishing activities (OSHA, 2012). The 

relevance of these exposures to DCM-based paint stripping is uncertain.

Ship Paint Stripping

Limited data were identified for paint stripping of ships. A 1980 UK study observed eight 

painters over two days in a dockyard. The study results include a mean concentration of DCM 

associated with one painter conducting paint stripping of 214.7 mg/m3 (61.9 ppm) (IARC, 2010).

DCM exposure data were identified in the OSHA IMIS data set. Table E-1 provides a summary 

by job category of the OSHA inspection data. For ship building and repairing, the inspection 

exposures ranged from zero to 33.7 mg/m3 (zero to 9.7 ppm) and included both eight-hr TWA 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 119

and STEL exposures. These exposures did not appear to explicitly include monitored paint 

stripping activities (OSHA, 2012). The relevance of these exposures to DCM-based paint 

stripping is uncertain.

Paint Stripping in Non-specific Workplace Settings

Some EU exposure data were identified that were characterized for “general industrial use.” 

However, more specific information on the industries (such as applicable NAICS or Standard 

Industrial Classification [SIC] codes, primary industrial functions or products, or number of sites 

or workers) was not provided in the identified reference.

A 1998 report by the UK identified exposures during immersion stripping of wood. They 

reported eight-hr TWA exposures ranging from 38.5 to 7,000 mg/m3 (11 to 2,017 ppm) with a 

mean of 700 mg/m3 (202 ppm) for the period of 1980 to 1994. The eight-hr TWA exposures 

were lower during the period of 1990 and 1994, with a range of 35 to 2,100 mg/m3 (10 to 605 

ppm) and a mean of 350 to 420 mg/m3 (101 to 121 ppm) (TNO, 1999).

A 1980 US study observed the breathing zone of three workers engaged in paint stripping from 

wood and metal and obtained seven samples ranging in DCM TWA concentration from 633 to 

1,017 mg/m3 (182 to 293 ppm) (TNO, 1999).

Summary of OSHA IMIS Data

As noted previously, OSHA IMIS data were among the data collected during the literature 

search for occupational exposure data. The sources of DCM exposure in IMIS are generally not 

provided and may or may not include DCM-containing paint stripping products. IMIS data may 

be examined to provide insights in some occupational categories where no other data are 

found to be directly attributable to the use of DCM-containing paint stripping products.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 120

APPENDIX F: RESIDENTIAL/CONSUMER EXPOSURE ASSESSMENT

F-1. Estimation of Emission Profiles for Paint Removers/Strippers

In 1993, MRI conducted a series of chamber studies for EPA on paint stripping products (US 

EPA, 1994b). For each study, continuous air concentrations were measured using a Fourier 

transform infrared (FTIR) spectrometer. In addition, three stationary samplers and a personal 

sampler were used to collect an integrated sample on activated charcoal. These data were 

analyzed and a process was undertaken to fit the data to exponential equations to represent 

the time-varying emission profile that led to the air concentrations. The US EPA (1994b) study 

tested five products, three of which contained either DCM or NMP, as described in Table F-1.

Table F-1. US EPA (1994b) Study: Products Emissions Fit to Exponential Profile.

Product Application Type Chemical

BIX Spray-On Stripper Spray DCM

Strypeeze Brush DCM

Wood Finisher’s Pride Brush NMP

In evaluating the experimental data, an exponential emission was chosen because of the 

general shape of the concentration profile and similarity to other emission behavior (e.g., 

chemicals from paint). The emission equation has the following form:

(F-1)

where:

E0 = initial emission rate (the emission rate at t = 0), mg/hr

k = first-order rate constant, hr-1

t = time since application, hr

Integrating Equation E-1 to time of infinity gives the mass released represented by the 

exponential, as follows:

Mass Released (F-2)

Or:

(F-3)
DOCUMENT-DO NOT CITE OR QUOTE 

Page 121

Integration of the single compartment, mass-balance equation for the air concentration 

equation for a single and double exponential representation of the emissions is given in 

Equations F-4 and F-5 (US EPA, 1997), respectively.

(F-4)

where:

V = chamber volume, m3

Q = air flow rate in and out of the chamber, m3/hr

(F-5)

where:

E01 = initial emission rate for the first exponential, mg/hr

E02 = initial emission rate for the second exponential, mg/hr

k1 = first-order rate constant for the first exponential, hr-1

k2 = first-order rate constant for the second exponential, hr-1

The two DCM products were applied in eight, approximately one-minute applications, with 

each one-minute application followed by an approximately 10-minute wait time prior to the 

start of the subsequent application, resulting in about 11 minutes between applications. In 

each case, the emissions from each application are represented by a single or double 

exponential, with each exponential identical to the other seven, but with a different start time 

set at the midpoint of the application period. Based on this approach, the start times of the 

eight DCM exponentials are 0.5, 11.5, 22.5, 33.5, 44.5, 55.5, 66.5, and 77.5 minutes from the 

start of the stripping activity.

For the two DCM products, a single exponential was found to provide a good fit to the data. 

The fitting process involves:

(1) Extracting measured concentration values from the US EPA (1994b) data and co-plot the 

points with Equation F-4. The concentration values were extracted for runs 4, 5, and 6 

for BIX Spray-On and runs 7, 8, and 9 at each 0.5-hr time point as well as peaks and 

significant changes in slope. This resulted in eight or nine data points per run.

(2) Calculating the mass of DCM applied during the test and assigning 1/8th of the applied 

mass to each of the eight exponentials.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 122

(3) Iterating to obtain the best fit to the experimental data by varying the “Fraction 

Released” and the first-order rate constant (k) using Equation F-4 and the following 

relationship:

(F-6)

This analysis was conducted using Excel to solve the equations and plot the results. The best fit 

was arrived at by visual comparison of the results of Equation F-4 with the extracted US EPA 

(1994b) data, attempting to fit the Equation F-4 curve midway between the maximum and 

minimum values of the data. In general, the height of the concentration curve is related 

primarily to the DCM mass released, and the length and shape of the decay portion of the curve 

is closely related to the first-order rate constant, k. The resulting fit for the BIX Spray-On 

Stripper product is shown in Figure F-1, and the fit for the Strypeeze product (brush application) 

is shown in Figure F-2. In each figure, the underlying eight exponentials are shown in the lower 

part of the figure, with the sum shown as the fitted, dashed line. The parameters for these two 

DCM cases are shown in Table F-2.

Figure F-1. Model Fit to MRI (US EPA, 1994b) Data for BIX Spray-On (Spray Application).

Published data/EPA report
DOCUMENT-DO NOT CITE OR QUOTE 

Page 123

From Published data/EPA report 

Figure F-2. Model Fit to MRI (US EPA, 1994b) Data for Strypeeze (Brush Application).

Table F-2. Fitted Parameters to the US EPA (1994b) Study Results for the Two DCM-Containing Paint 

Strippers.

Product Mass of Product

Applied, g

DCM Mass 

Applied, g

DCM Fraction 

Released

First-Order Rate 

Constant, Hr-1

BIX Spray-On Stripper 540 495 0.66 10

Strypeeze 722 121 0.33 10

A numerical integration of the fitted “sum of 8 exponentials” shown in Figures F-1 and F-2 was 

performed by using the average concentration for each one-minute interval and conducting a 

mass-balance calculation for the test chamber, accounting for the mass in the chamber and the 

mass that has been removed through ventilation. The resulting mass released from the product

as a function of time is shown in Figures F-3 and F-4 for BIX Spray-On and Strypeeze stripper, 

respectively. 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 124

Figure F-3. Theoretical Cumulative Mass of DCM Released for BIX Spray-On Stripper.

Figure F-4. Theoretical Cumulative Mass of DCM Released for Strypeeze Stripper.

111 

111 minutes
DOCUMENT-DO NOT CITE OR QUOTE 

Page 125

Discussion and Conclusions

From the exponential fits to the US EPA (1994b) data, we estimate that 66 percent of the 

applied DCM in the spray product (Figure F-1) was released to air, versus 33 percent of the 

applied DCM in the brush product (Figure F-2). We estimate that virtually all of the 66 and 

33 percent of the DCM mass will be released by two hrs after application for the spray and 

brush product, respectively, very shortly after the last scraping is finished, due to the higher 

volatility. Thus, the concentration-decline part of Figures F-1 and F-2, after the peak, is due 

almost exclusively to ventilation rather than to declining emissions, and therefore, these 

exposures could be virtually eliminated through ventilation.

Factors that should be considered in applying these findings to a model-based approach using 

MCCEM include the effect of varying the product use behavior and the effect of the quantity of

the chemical applied. It appears that the off-gassing rate is a function of the mass applied and 

the duration of application; based on the limited data available, the emission rate does not 

exhibit significant inhibition of volatilization due to increased concentrations in the range of air 

concentrations observed in the US EPA (1994b) study. If this holds true, the results of this 

analysis can be applied to a variety of product use behavior by modifying MCCEM to represent 

this behavior. MCCEM’s capability of representing the application as an incremental 

exponential may further improve the representativeness of the predicted concentrations. 

F-2. Sensitivity Analysis for Inhalation Scenarios

For this analysis, each input that could be measured on a continuum (e.g., emission rate, 

airflow rate) was first halved and then doubled while holding all others at their base-case 

values. For an input to which the model output is directly and linearly proportional, and for 

which the exposure measure for the base case is denoted as X, the result for the halved case 

would be 1⁄2X and the result for the doubled case would be 2X. Computing and averaging the 

two differences from the base case gives the following result:

([X-1/2X] + [2X-X]) / 2) / X = 3⁄4 or 75 percent (F-7)

For an input that cannot be varied over a continuum, or that can be dealt with only discretely or 

perhaps dichotomously (e.g., in the use zone or not at certain key times), the above procedure 

can still be used, but the sensitivity measure reduces to:

|Y-X| / X (expressed as a percent) (F-8)

where Y is the output associated with the change in location pattern from the base case.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 126

F-3. Inhalation Exposure Scenario Inputs

Method of Application. A review of product labels and technical data sheets indicates that paint 

stripping products can be applied using either brush-on or spray-on (i.e., aerosol or triggerpump) application methods. Exposures were assessed for both brush-on and spray-on products 

due to differences in chemical release characteristics, DCM weight fraction of products, 

application rates, and time required for application, as discussed below.

Application Amount (Product Mass). The product application mass (grams of product) was 

determined for each of the cases examined using application rates, (g/ft2) calculated from the 

US EPA (1994b) chamber tests and the surface areas of objects to be stripped (ft2). Surface 

areas were selected so that the resulting product mass corresponded approximately to central 

(near the median) and upper-end (near the 90th percentile) estimates for the amount of paint 

stripper product used per event from the large nationwide survey by Abt (1992), as reported in 

EFH (US EPA 2011c) Table 17-20. The EFH reports a median value of 32 fluid ounces or 1⁄4 gallon. 

Conversion to metric units (3.75 liters per gallon) and consideration of the nominal product 

density (~1.1 g/cm3) (calculated from Brown, 2012) yields a product mass on the order of 1,000 

grams as a central estimate. An upper-end application amount (~80th percentile) from the 

same survey is 80 oz or 2,500 g. Similarly, the small Riley et al. (2001) survey reported 32 

ounces as the median amount of paint stripper product used. Specific product masses used in 

this assessment for the brush-on scenarios were 900 g for Scenarios 1 and 2 and 2,250 g for 

Scenario 3.

For Scenario 7, a lower mass (477 g, derived from largest application amount identified in the 

NIOSH report) was used, but the application occurred in a confined space (bathroom) and was 

assumed to be performed by a professional, as opposed to a DIY worker for the other scenarios. 

Product masses for the spray-on scenarios were 680 g for Scenarios 4 and 5 and 1,700 g for 

Scenario 6.

As previously mentioned, the application amounts assumed in this assessment for Scenarios 1 

through 6 are a product of application rates calculated from the US EPA (1994b) experiments 

and the surface area of objects to be treated. The calculated application rates were ~90 g/ft2 

for a brush-on application of a DCM-containing product (722 g of product applied to 8 ft2) and 

~68 g/ft2 for a spray-on application of a DCM-containing product (540 g of product applied to 8 

ft2). These application rates are similar to those recommended on the Savogran Company 

website for paint strippers in general—1 gallon per 50 to 100 ft2 (~42 to 83 g/ft2 based on a 

nominal density of 1.1 g/cm3)

5

. The applied surface areas selected for central and upper-end 

values were 10 and 25 ft2. The upper-end surface area is 2.5 times higher than the central 

surface area and provides sufficient distinction from the central case. Application targets with 

surface areas close to the two specified surface areas (10 and 25 ft2) were used in the exposure 

scenarios to reflect real-world situations. A coffee table with nominal dimensions of 4 ft × 2.5 ft 

 5 See the following URL: http://www.savogran.com/Information/removerfaq.html.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 127

for the top surface was selected for the central case (10 ft2)

6 and a chest of drawers with 

nominal dimensions of 4 ft high by 2.5 ft wide by 1.5 ft deep7 was selected for the upper-end 

case (4 × 2.5 ft2 for front + 2.5 × 1.5 ft2 for top + 2 × 4.5 × 1.5 ft2 for sides ≈25 ft2). For the 

bathroom scenario, a bathtub surface area of 36 ft2 was calculated assuming nominal 

dimensions of 5 ft wide by 2.5 ft deep by 1.5 ft high.

Stripping Sequence. The stripping sequence chosen to characterize product application was 

based in part on product label instructions, which for some DCM-containing products (i.e., 

Klean Strip® products) indicate that no more than 9 ft2 should be stripped at a time. 

Accordingly, the 10-ft2 surface for the coffee table was divided into two application segments of 

5 ft2 each. The 25-ft2 surface for the chest was divided into four application segments of 6.25 ft2

each and the 36-ft2 surface for the bathtub was divided into four application segments of 9 ft2 

each. The segments were assumed to be treated in sequence with a repeat application of the 

sequence. Thus, in effect, there were four segments for the coffee table and eight segments 

each for the chest and bathtub. Repeating the stripping sequence corresponds to instructions 

on the majority of product labels indicating that the stripping procedures should be repeated to 

remove multiple coats of paint or stubborn paint. All residuals from the scraping were assumed 

to be removed from the house on completion of the last segment/application.

The entire stripping sequence for each segment consisted of applying the product to the target 

surface followed by a wait or effect period and then scraping the treated surface. For both the 

coffee table and the chest scenarios, a two-minute applying time per segment was used for 

brush applications and a one-minute applying time per segment was used for spray 

applications. Application was followed by a 15-minute wait period and then a four-minute 

scraping period per segment. For the bathtub scenario (brush-on only) with a larger surface 

area, the applying time was increased to three minutes per segment and the scraping time was 

increased to six minutes per segment; the wait time remained the same at 15 minutes per 

segment. The wait time of 15 minutes was selected based on wait times on the product labels, 

which varied from five minutes to two hrs, with the majority of labels indicating a wait time of 

15 minutes.

Back-to-back stripping sequences with no overlapping activities were modeled because it is 

likely that the user will take breaks during the wait time. In the Riley survey (Riley et al., 2001), 

65 percent of the participants reported taking breaks outside the work area and 20 percent of 

the participants reported taking breaks inside the work area, with break times ranging from five 

to 30 minutes. The number of breaks was not reported. Additionally, conducting overlapping 

stripping activities for multiple segments (i.e., applying or scraping one segment during the wait 

period of another segment) would be unrealistic for most consumer users. 

 6 See the following URL: http://furniture.about.com/od/furnishingdesignresources/a/measurements.htm. 7 See the following URL for an illustrative chest of drawers with nearly the same dimensions:

http://www.furnitureunfinished.com/product_info.php?cPath=116_135&products_id=1093.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 128

As an example, the timing of the entire sequence for a brush-on application to the chest surface 

is shown in Table F-3. For this scenario, the table indicates a total duration of 21 minutes per 

segment or 168 minutes for the entire episode of product use. For the coffee table with half 

the number of segments, the duration of the episode was 84 minutes. For the bathtub 

scenario, the total durations increased to 24 minutes per segment or 192 minutes for the entire 

episode. For the spray-on application (applicable to the coffee table and chest but not the tub), 

the application time was cut in half (i.e., from two minutes to one) while retaining the waiting 

time of 15 minutes and the scraping time of four minutes, resulting in slightly lower total 

durations than the brush-on scenarios.

Table F-3. Time Schedule for Brush-on Application to Chest Surface: Four Segments with Repeat 

Application.

Segment/Application Elapsed Time from Time Zero, Minutes 

Apply Wait Scrape

First 1/4, 1st time 0-2 2-17 17-21

Second 1/4, 1st time 21-23 23-38 38-42

Third 1/4, 1st time 42-44 44-59 59-63

Fourth 1/4, 1st time 63-65 65-80 80-84

First 1/4, 2nd time 84-86 86-101 101-105

Second 1/4, 2nd time 105-107 107-122 122-126

Third 1/4, 2nd time 126-128 128-143 143-147

Fourth 1/4, 2nd time 147-149 149-164 164-168

Amount of Chemical Released. The amount of chemical released during and after the stripping 

event is the product of three parameters: amount applied (discussed above), weight fraction of 

chemical in the applied product, and fraction of the chemical that is released to indoor air. 

From the product list developed by Brown (2012), the median DCM weight fraction was 

determined to be 0.53 for the brush-on application (range of 0.20 to 0.93) and 0.8 for the 

spray-on application (range of 0.45 to 0.88). The corresponding 90th percentile weight fractions 

were 0.88 for brush-on and 0.87 for spray-on. A weight fraction of 1.0 (maximum exposure 

estimate derived from product label) was assumed for the bathtub application. The weight 

fractions were determined from the Brown (2012) spreadsheet by using only products intended 

for consumer use (i.e., adhesive removers, paint brush cleaners, deglossers, and industrial/

commercial use products were removed). The application method (brush- or spray-on) for a 

product was determined by examining the product labels/technical data sheets and product 

names, and through Internet research. If an application method could not be determined 

through the above methods, then the product was assigned to the brush category, as most 

paint stripping products are applied by the brush method and formulations such as semi-paste 

would be difficult to apply using a sprayer. If a weight-fraction range was provided in the 

product list, then the average of the minimum and maximum weight fractions was used in 

calculations. The weight fractions were not weighted to reflect the market share of products.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 129

Analysis of the US EPA (1994b) data indicated DCM release fractions of 0.33 for brush-on and 

0.66 for spray-on. The resultant mass released for the different application targets and 

methods is summarized in Table F-4.

Table F-4. DCM Mass Released, by Application Target and Method.

Target (Surface Area)

and Method

Application

Rate, g/ft2a

Weight 

Fractionb

Release 

Fraction

DCM Mass 

Released, g

Coffee table (10 ft2)

 Brush-on

 Spray-on

90

68

0.53 | 0.88

0.80 | 0.87

0.33

0.66

157.4 | 261.4

359.0 | 390.5

Chest of drawers (25 ft2)

 Brush-on

 Spray-on

90

68

0.88

0.87

0.33

0.66

653.4

976.1

Bathroom tub (36 ft2)

 Brush-on 13.25 1.0 0.33 157.4

a

Reflects repeat application for each segment.

b

For the coffee-table case, two weight fractions are given; one for central and one for near-high-end.

Airflow Rates and Volumes. The model run requires conceptualization of a residence in terms 

of the number of zones and their respective volumes. The airflow rates needed to model the 

central and upper-end scenarios described above are: (1) rates between indoors and outdoors 

for each zone; and (2) rates between the zones. The occupational scenario simulation (tub 

stripping in bathroom), which is somewhat more complex to conceptualize, is described below, 

after the central and upper-end scenarios.

For the central and upper-end scenarios, the house in which the modeled stripper application 

occurs is conceptualized as having two zones: (1) the workshop where application occurs; and 

(2) the ROH. The house volume chosen for the model runs (492 m3

) was the central value listed 

in the EFH. The volume assigned to the in-house workshop area was 54 m3

, corresponding to a 

12 ft × 20 ft with 8-ft ceiling (20 × 12 × 8 = 1,920 ft3 or ~54 m3

). This room volume is similar to 

the value reported in Riley et al. (2001) for the mean volume of the room used for paint 

stripping (51 m3

). The volume for the ROH (438 m3) is determined by subtraction (492 m3 – 54 

m3

). For the bathtub scenario, the bathroom volume was set at 9 m3 for consistency with that 

reported in CDC, 2012. 

The indoor-outdoor airflow for any zone of the house is governed by the choice of air exchange 

rate, in ACH. The central and low-end values for the air exchange rate, 0.45/hr and 0.18/hr, 

used in assigning the indoor-outdoor airflow rate for the ROH are the mean and 10th percentile 

values, respectively, from the EFH. (Note that a low-end ACH would be expected to contribute 

to upper-end concentration estimates.) For the workshop, it was assumed that multiple 

windows were opened. The indoor-outdoor airflow rate assigned to this zone (68 m3/hr) was 

obtained by multiplying the room volume of 54 m3 by the 90th percentile (1.26/hr) of the air-
DOCUMENT-DO NOT CITE OR QUOTE 

Page 130

exchange-rate distribution from the EFH, thought to be a reasonable representation of the openwindow case.

The use of open windows in the room of use is supported by both label instructions and survey 

data. The majority of the labels indicate that adequate ventilation must be used and that, to 

prevent build-up of vapors, windows and doors should be opened to achieve cross ventilation. 

Additionally, Pollack-Nelson (1995) reported that an average of 70.7 percent of paint stripper 

users (all products) kept a window or door open during use based on data from the Westat Inc. 

(1987) survey and that 88.8 percent of paint stripper users (all products) kept a window or door 

open during use based on data from the Abt (1992) survey. The increase was significant 

between the survey years (before and after CPSC labeling requirements took effect). The more 

recent small Riley et al. (2001) survey also indicates that the majority of paint-stripper users 

(55 percent) opened a window. Both Pollack-Nelson (1995) and Riley et al. (2001) also reported 

that some users used an exhaust fan during the stripping process, which would affect the air 

exchange rate. The percentage of fan users was not reported in Pollack-Nelson (1995). The 

Riley et al. (2001) data suggest that only ~27 percent of the users who worked indoors used an 

open window and fan. Due to the small percentage of respondents who reported using a fan, 

coupled with the fact that some of labels indicate that the product should be kept away from 

heat, sparks, flame, and all other sources of ignition, none of the scenarios were assumed to 

involve use of a fan in the room of product application.

The interzonal airflow rate was estimated using the following algorithm, developed by 

US EPA (1995a):

Q = (0.078 + 0.31*ACH) * house volume

where Q is the interzonal airflow rate, in m3/hr, and ACH is the air exchange rate, in 1/hr. 

Substitution of the central air exchange rate of 0.45/hr and the house volume of 492 m3 yields 

an estimated interzonal airflow rate of 107 m3

/hr. The corresponding number for the upper-end 

scenario, with an air exchange rate of 0.18/hr, was 65.8 m3

/hr. Figure F-5 depicts the volumes 

and airflows that were used for the workshop scenarios.

Figure F-5. Zone Volumes and Airflow Rates for Workshop Scenarios.

As previously mentioned, the bathroom scenario (Figure F-6) is more complex. Because the 

user is working in close proximity to the target (bathtub) for an extended period, a third zone 

Room of 

Use

(54 m3)

68

m3

/hr

107

m3

/hr

Rest of 

House

(438 m3)

197

m3

/hr

Central Values

Room of 

Use

(54 m3)

68

m3

/hr

65.8

m3

/hr

Rest of 

House

(438 m3)

78.8

m3

/hr

Values for Upper-end 

Concentration Scenarios

denotes air flow
DOCUMENT-DO NOT CITE OR QUOTE 

Page 131

(“source cloud”) was created within the bathroom to represent the DCM concentrations in the 

vicinity of the tub; this is a virtual zone, with no physical boundaries. The airflow rate between 

the cloud and the rest of the bathroom was based on the study by Matthews et al. (1989), who 

determined experimentally that such an airflow could be estimated as the product of the room 

air velocity (in m/hr) and the entry/exit surface area (in m2). Using their suggested value of 65 

m/hr for air velocity together with an assumed entry/exit surface area of 5 ft by 2 ft (10 ft2 or 

0.93 m2) yields an estimated airflow rate of 60 m3/hr between the source cloud and the rest of 

the bathroom. Based on professional judgment, the interzonal airflow rate between the 

bathroom and rest of the house was assumed to be ~2/3 lower than that for the workshop 

central scenarios, given the small bathroom volume. The indoor-outdoor airflows were based 

on an assumed air exchange rate of 0.18 ACH.

Figure F-6. Zone Volumes and Airflow Rates for Bathroom Scenario.

Locations of Exposed Individuals. Two location patterns were specified, one for a product user 

and one for a non-user. The user was assumed to be in the work area for stripper application 

and scraping for all scenarios. For the waiting phase of the stripping process, the user was 

assumed to be in the ROH as a central-tendency assumption for the user (Scenarios 1 and 4), in 

the workshop as an upper-end assumption for the user (Scenarios 2 and 5), and in the ROH for 

Scenarios 3, 6, and 7, which were developed to model upper-end concentrations primarily for 

the non-user. The user was placed in the remainder of the house during the waiting phase for 

Scenarios 1, 3, 4, 6, and 7 because the user is assumed to be aware of inhalation health 

concerns from the label warnings (“Vapor Harmful”) and because some labels such as the Klean 

Strip® products specifically state that the user should leave the room during the wait period. As 

previously mentioned, the Riley et al. (2001) survey also reported that 65 percent of users 

reported taking breaks outside the work area. Breaks typically involved a specific break activity 

and location, such as going to the kitchen and making a sandwich or going outside to do yard 

work. For the upper-end Scenarios 2 and 5, it was assumed that the user would stay in the 

workshop, based on the fact that some people do not read/skim labels (~28 percent in 1990) 

denotes air flow

1.6

m3/hr

Rest of 

Bathroom

(8 m3)

35

m3/hr

Rest of 

House

(483 m3

)

“Source Cloud”

(1 m3)

86.9

m3/hr

60

m3/hr
DOCUMENT-DO NOT CITE OR QUOTE 

Page 132

(Pollack-Nelson, 1995) and may therefore not be aware of health concerns or precautionary 

techniques. Many labels do not specifically state to leave room during the wait period, and the 

Riley et al. (2001) survey indicated that 20 percent of participants reported taking breaks inside 

the work area. For all scenarios, the user was assumed to leave the workroom immediately 

after the stripping process, based on the Westat Inc. (1987) and Abt (1992) surveys with a 

median value of zero minutes spent in the room after using the product (US EPA, 2011b).

The non-user was assumed to be in the ROH throughout the model run, as was the user for the 

portion of the run after all applying/scraping was completed. For the bathroom scenario, the 

user was assumed to be in the ROH during the wait times.

It was further assumed that the scrapings were removed from the house as soon as scraping 

was completed for the last segment. The implication for modeling purposes is that any 

remaining DCM emissions would be truncated at that time. However, the modeled DCM 

emissions were not truncated as an expedience; given the high volatility of DCM (vapor 

pressure = 352.5 Torr), its emission rate would essentially drop to zero in a very short time, on 

the order of 10 minutes. 

F.4. Inhalation Model Outputs and Exposure Calculations

Personal Concentrations

Peak TWA concentrations for different averaging periods, described below, were calculated 

from the one-minute averages for both the user and non-user based on their respective 

personal concentration time series. The calculations took into account the possibility that the 

user can change zones within a one-minute interval (e.g., at an elapsed time of 6.25 minutes). 

The personal concentration was calculated for each one-minute interval in the modeling period 

(24 hrs or 1,440 one-minute intervals) as follows:

For each time interval, i to i +1, for i = 0 to 1,440:

(F-9)

Where: 

PCi,i+1 = the personal concentration over the time interval i to i +1

C1,i and C1,i+1 = the concentrations in the use zone at times i and i+1, respectively

CROH,i and CROH,i+1 = the concentrations in the ROH zone at times i and i+1, respectively

Fi,i+1 = the fraction of time spent in the use zone during the time interval i to i +1

These calculations, illustrated in Figure F-7, were implemented in an Excel spreadsheet for each 

of the seven scenarios.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 133

Figure F-7. Example of the Personal Concentration Calculation as Defined in Equation F-9.

TWA Concentrations

In addition to the maximum one-minute concentration and the 24-hr average concentration to 

which the user and non-user were exposed, a peak TWA personal concentration was calculated 

for each of the following averaging periods: 10 minutes, 30 minutes, one hr, four hrs, and eight 

hrs. The peak TWA concentration for any averaging period was defined as the highest value of 

the consecutive running averages for that averaging period. For any averaging period, there 

are (1,440 – length of the averaging period) TWA concentration values within the 24-hr (1,440-

minute) time series. For example, there are 1,430 10-minute averaging periods (1,440-10), the 

first of which is for time zero to 10 minutes, the second of which is for time one to 11 minutes, 

and so on, with the last for time 1,430 to 1,440 minutes. The running averages for each 

averaging period were computed in an Excel spreadsheet, from which the maximum value was 

determined.

Modeling Results

The zone-specific and personal concentrations predicted by MCCEM are presented in Figures F-8

though F-118

. Figure F-8 shows the zone-specific and the user’s personal-concentration results 

for Scenario 1 (brush application in the workshop with central parameter values, top two 

figures) and Scenario 4 (spray application) in the workshop using central parameter values. The 

dips in the user’s personal concentration during the application periods reflect temporary 

relocation to the ROH (Zone 2) during wait times between applying and scraping. The nonuser’s personal concentrations are the same as those in the ROH. As indicated in Figure F-8, the 

peak concentrations are higher for the spray-application scenario than those for the brushapplication scenario, even though the mass of product applied is higher for brush application 

(900 g stripper applied for brush as compared to 680 g for spray). This difference is explained 

primarily by two factors: (1) the weight fraction of DCM in the stripper product (0.8 for the 

spray product as compared to 0.53 for the brush product); and (2) the higher fraction of the 

 8 Figures F-8 through F-11 are provided at the end of this section.

Time Interval

= (D5 + D4) / 2

Fraction of Time Spent 

in Use Zone

= H5*J5 + I5*(1-J5)
DOCUMENT-DO NOT CITE OR QUOTE 

Page 134

applied mass emitted, double that for the spray application as compared to the brush 

application (i.e., 66 percent as compared to 33 percent) based on analysis of the US EPA 

(1994b) chamber data. As a result, the DCM mass emitted for the spray stripping is ~2.25 times 

as high as the mass released during the brush stripping (680 g × 0.8 × 0.66 = 359 g for the spray 

activity as compared to 900 g × 0.53 × 0.33 = 160 g for the brush activity).

Other than the mass of DCM emitted and some minor differences in application time, 

Scenarios 1 and 4 are identical, which leads to a similar ratio in air concentrations. For 

example, for Scenario 4, the peak concentration in Zone 1 is 1,800 mg/m3, whereas the peak for 

Scenario 1 is 780, a ratio of 2.30. The similar ratios for applied mass and resultant peak air 

concentration apply when other model inputs, such as room volumes and air exchange rates, 

are kept at the same or similar values. The shape of the user’s personal concentration profile 

reflects the location of the user at various times during the stripping, waiting, and scraping 

activities.

Figure F-9 shows the zone and user personal concentration results for Scenarios 2 and 5 (brush 

and spray application, respectively) for the workshop with parameter values selected to 

estimate upper-end concentrations for the user. In this comparison, the emitted DCM mass is 

390 g for the spray vs. 260 g for the brush application, a ratio of ~1.5. The peak concentrations 

(2,000 mg/m3 for spray-on vs. 1,300 mg/m3 for brush-on) again have a ratio (1.54) that is similar 

to that for the applied mass.

Figure F-10 shows the zone and user personal concentration results for Scenarios 3 and 6 

(brush and spray application, respectively) for the workshop with parameter values selected to 

estimate upper-end concentrations for the non-user as well as the user. In this comparison, the 

spray-to-brush ratio of ~1.5 for applied mass translates directly to the 24-hr TWA concentration 

to which the non-user is exposed (180 mg/m3 for spray application vs. 120 mg/m3 for brush 

application). The more pronounced crossover of the Zone 1 and 2 concentration time series for 

these scenarios, shortly after the user finishes the last scraping, can be explained by the indooroutdoor air exchange rates: 1.26/hr for the workshop vs. 0.18/hr for the ROH. Due to the 

higher dilution rate, the workshop concentrations fall more quickly after the stripping activity is 

completed than do the concentrations in the ROH.

Figure F-11 shows the air concentrations for the simulation scenario, namely the bathtub 

stripping activity with a modeled peak concentration of ~3,500 mg/m3

. The saw-tooth 

appearance of the concentration rise associated with the stripping activity—particularly 

pronounced in this scenario but evident in the other scenarios as well—is due to the eight 

application segments. Scenario 7 was intended, in part, to simulate the situation described in a 

CDC/NIOSH case fatality assessment (CDC, 2012a, b). The modeled peak concentration 

reported here for Scenario 7, on the order of 1,000 ppm, is substantially lower than that 

calculated (155,000 ppm) for the fatality assessment, but the value reported by CDC/NIOSH was 

a bounding estimate obtained by assuming that all DCM mass is released instantaneously. By 

comparison, monitoring of a bathtub application by Washington State Occupational Safety and 

Health staff, as described in the CDC/NIOSH report, indicated a 15-minute TWA personal 

concentration for the applicator on the order of 2,000 ppm.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 135

a) Scenario 1, Brush Applied

b) Scenario 4, Spray Applied

Figure F-8. Modeled DCM Concentrations for Scenarios 1 and 4, Stripper Application in Workshop using Central Parameter Values.

(Non-user assumed to be in ROH)
DOCUMENT-DO NOT CITE OR QUOTE 

Page 136

a) Scenario 2, Brush Applied

b) Scenario 5, Spray Applied

Figure F-9. Modeled DCM Concentrations for Scenarios 2 and 5, Stripper Application in Workshop using Parameter Values selected for Upperend User’s Exposure.

(Non-user assumed to be in ROH)

(Non-user assumed to be in ROH)
DOCUMENT-DO NOT CITE OR QUOTE 

Page 137

a) Scenario 3, Brush Applied

b) Scenario 6, Spray Applied

Figure F-10. Modeled DCM Concentrations for Scenarios 3 and 6, Stripper Application in Workshop using Parameter Values Selected for 

Upper-End-user’s and Non-user’s Exposure.

(Non-user assumed to be in ROH)

(Non-user assumed to be in ROH)
DOCUMENT-DO NOT CITE OR QUOTE 

Page 138

Figure F-11. Modeled DCM Concentrations for Scenario 7, Brush Application in Bathroom (Simulation).

(Non-user assumed to be in ROH)
DOCUMENT-DO NOT CITE OR QUOTE 

Page 139

F.5. MCCEM Inhalation Modeling Scenario Summaries

Formula: CH2Cl2

CAS Number: 75-09-2

Molecular Weight: 84.93 g/mol

Density: 1.33 g/cm2 (liquid)

Appearance colorless liquid

Melting Point: -96.7 deg C = -142 deg F = 176 K

Boiling Point: 39.6 deg C = 103 deg F = 313 K 

Solubility in Water: 13 g/L @ 20 deg C

Vapor Pressure: 47 kPa = 352.535 Torr = 0.4639 atm = 6.817 psi

Conversion units: 1 ppm = 3.4736 mg/m3

Saturation Concentration: 463,862 ppm = 1,611,281 mg/m3

DCM Scenario 1. Coffee Table, Brush-On, Workshop, User in ROH during wait time, 0.45 ACH, 

0.53 Weight Fraction 

MCCEM Input Summary

Application Method:

Brush-on

Volumes:

Workshop volume = 54 m3

ROH volume = 492 – 54 = 438 m3

Airflows:

Workshopoutdoors68 m3/h

ROH-outdoors 197.1 m3/h (0.45 ACH)

Workshop-ROH 107 m3/h

DCM Mass Released:

Coffee table = 10 sq ft surface area

Applied product mass = 90 g/sq ft = 900 g

DCM mass = 900 g × 0.53 (wt fraction) × 0.33 (release fraction) = 157.4 g

For each of the 4 application sections:

k = 10/hr

Mass = 157.4/4 = 39.35 g

Eo = Mass * k = 393.5 g/hr (NOTE: only k and Mass are needed as MCCEM inputs)

Application Times by Section:

Episode

Elapsed time from time zero, 

minutes 

Apply Wait

Scrap

e

first 1/2, 1st time 0-2 

min

2-17 

min

17-21 

min

second 1/2, 1st time 21-23 

min

23-38 

min

38-42 

min

first 1/2, 2nd time 42-44 

min

44-59 

min

59-63 

min
DOCUMENT-DO NOT CITE OR QUOTE 

Page 140

second 1/2, 2nd time 63-65 

min

65-80 

min

80-84 

min

Model Run Time:

0-24 hrs

User takes out scrapings after 84 minutes, emissions truncated

Activity Patterns:

User in workshop during application and scrape periods, in ROH during wait periods

User in ROH for the remainder of the run (22 hrs, 36 minutes)

MCCEM Results Summary

Personal Exposures (maximum values over first 24 hrs):

In mg/m3

Individ

ual 1 min 10 min

30 

min 1 hr 4 hr 8 hr 24 hr

User 632.4 376.1 269.4 224.0 120.5 68.6 23.3

Other 131.7 131.5 129.5 123.8 82.1 49.1 16.8

In ppm

Individ

ual 1 min

10 

min

30 

min 1 hr 4 hr 8 hr

24 

hr

User 182.1 108.3 77.6 64.5 34.7 19.7 6.7

Other 37.9 37.8 37.3 35.6 23.6 14.1 4.8

Plots:
DOCUMENT-DO NOT CITE OR QUOTE 

Page 141
DOCUMENT-DO NOT CITE OR QUOTE 

Page 142

DCM Scenario 2. Coffee Table, Brush-On, Workshop, User in Workshop during wait time, 0.45 

ACH, 0.88 Weight Fraction

MCCEM Input Summary

Application Method:

Brush-on

Volumes:

Workshop volume = 54 m3

ROH volume = 492 – 54 = 438 m3

Airflows:

Workshopoutdoors68 m3/h

ROH-outdoors 197.1 m3/h (0.45 ACH)

Workshop-ROH 107 m3/h

DCM Mass Released:

Coffee table = 10 sq ft surface area

Applied product mass = 90 g/sq ft = 900 g

DCM mass = 900 g × 0.88 (wt fraction) × 0.33 (release fraction) = 261.4 g

For each of the 4 application sections:

k = 10/hr

Mass = 261.4/4 = 65.35 g

Eo = Mass * k = 653.5 g/hr (NOTE: only k and Mass are needed as MCCEM inputs)

Application Times by Section:

Episode

Elapsed time from time zero, 

minutes 

Apply Wait Scrape

first 1/2, 1st time 0-2 

min

2-17 

min

17-21 

min

second 1/2, 1st time 21-23 

min

23-38 

min

38-42 

min

first 1/2, 2nd time 42-44 

min

44-59 

min

59-63 

min

second 1/2, 2nd time 63-65 

min

65-80 

min

80-84 

min

Model Run Time:

0-24 hrs

User takes out scrapings after 84 minutes, emissions truncated

Activity Patterns:

User in workshop during application, wait and scrape periods

User in ROH for the remainder of the run (22 hrs, 36 minutes)

MCCEM Results Summary

Personal Exposures (maximum values over first 24 hrs):

In mg/m3
DOCUMENT-DO NOT CITE OR QUOTE 

Page 143

Indivi

dual 1 min 10 min

30 

min 1 hr 4 hrs

8 

hrs

24 

hrs

User 1,292.4 1,251.7 1,136

.7

1,058

.0 416.7 223.8 75.3

Other 218.7 218.3 215.1 205.6 136.3 81.5 27.9

In ppm

Individ

ual 1 min

10 

min

30 

min 1 hr 4 hrs 8 hrs

24 

hrs

User 372.0 360.4 327.2 304.6 120.0 64.4 21.7

Other 63.0 62.9 61.9 59.2 39.2 23.5 8.0

Plots:
DOCUMENT-DO NOT CITE OR QUOTE 

Page 144
DOCUMENT-DO NOT CITE OR QUOTE 

Page 145

DCM Scenario 3. Chest, Brush-On, Workshop, User in ROH during wait time, 0.18 ACH, 0.88 

Weight Fraction

MCCEM Input Summary

Application Method:

Brush-on

Volumes:

Workshop volume = 54 m3

ROH volume = 492 – 54 = 438 m3

Airflows:

Workshopoutdoors68 m3/h

ROH-outdoors 78.8 m3/h (0.18 

ACH)

Workshop-ROH 65.8 m3/h

DCM Mass Released:

Chest = 25 sq ft surface area

Applied product mass = 90 g/sq ft = 2,250 g

DCM mass = 2,250 g × 0.88 (wt fraction) × 0.33 (release fraction) = 653.4 g

For each of the 4 application sections:

k = 10/hr

Mass = 653.4/8 = 81.675 g

Eo = Mass * k = 816.75 g/hr (NOTE: only k and Mass are needed as MCCEM inputs)

Application Times by Section:

Episode

Elapsed time from time zero, 

minutes 

Apply Wait Scrape

first 1/4, 1st time 0-2 min

2-17 

min

17-21 

min

second 1/4, 1st time

21-23 

min

23-38 

min

38-42 

min

third 1/4, 1st time

42-44 

min

44-59 

min

59-63 

min

fourth 1/4, 1st time

63-65 

min

65-80 

min

80-84 

min

first 1/4, 2nd time

84-86 

min

86-101 

min

101-

105 min

second 1/4, 2nd time

105-

107 min

107-

122 min

122-

126 min

third 1/4, 2nd time

126-

128 min

128-

143 min

143-

147 min

fourth 1/4, 2nd time

147-

149 min

149-

164 min

164-

168 min

Model Run Time:

0-24 hrs
DOCUMENT-DO NOT CITE OR QUOTE 

Page 146

User takes out scrapings after 168 minutes, emissions truncated

Activity Patterns:

User in workshop during application and scrape periods, in ROH during wait periods

User in ROH for the remainder of the run (21 hrs, 12 minutes)

MCCEM Results Summary

Personal Exposures (maximum values over first 24 hrs):

In mg/m3

Indivi

dual 1 min 10 min

30 

min 1 hr 4 hrs 8 hrs

24 

hrs

User 1,810.

4

1,178.1 898.3 762.4 562.8 400.1 157.1

Other 472.7 472.3 469.7 461.4 383.0 287.9 118.2

In ppm

Individ

ual 1 min

10 

min

30 

min 1 hr 4 hrs 8 hrs

24 

hrs

User 521.2 339.2 258.6 219.5 162.0 115.2 45.2

Other 136.1 136.0 135.2 132.8 110.2 82.9 34.0

Plots:
DOCUMENT-DO NOT CITE OR QUOTE 

Page 147
DOCUMENT-DO NOT CITE OR QUOTE 

Page 148

DCM Scenario 4. Coffee Table, Spray-On, Workshop, User in ROH during wait time, 0.45 ACH, 0.8 

Weight Fraction 

MCCEM Input Summary

Application Method:

Spray-on

Volumes:

Workshop volume = 54 m3

ROH volume = 492 – 54 = 438 m3

Airflows:

Workshop-outdoors 68 m3/h

ROH-outdoors 197.1 m3/h (0.45 ACH)

Workshop-ROH 107 m3/h

DCM Mass Released:

Coffee table = 10 sq ft surface area

Applied product mass = 68 g/sq ft = 680 g

DCM mass = 680 g × 0.8 (wt fraction) × 0.66 (release fraction) = 359 g

For each of the 4 application sections:

k = 10/hr

Mass = 359/4 = 89.75 g

Eo = Mass * k = 897.5 g/hr (NOTE: only k and Mass are needed as MCCEM inputs)

Application Times by Section:

Episode

Elapsed time from time zero, 

minutes 

Apply 1 WaitScrap

e1

first 1/2, 1st time 0-1 

min

1-16 

min

16-20 

min

second 1/2, 1st time 20-21 

min

21-36 

min

36-40 

min

first 1/2, 2nd time 40-41 

min

41-56 

min

56-60 

min

second 1/2, 2nd time 60-61 

min

61-76 

min

76-80 

min

Model Run Time:

0-24 hrs

User takes out scrapings after 80 minutes, emissions truncated

Activity Patterns:

User in workshop during application and scrape periods, in ROH during wait periods

User in ROH for the remainder of the run (22 hrs, 40 minutes)

MCCEM Results Summary

Personal Exposures (maximum values over first 24 hrs):

In mg/m3

Individ 1 min 10 30 1 hr 4 hrs 8 hrs 24 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 149

ual min min hrs

User 1,502.

0

781.0 598.2 491.7 266.9 152.

1

51.7

Other 303.1 302.5 298.0 284.8 187.8 112.

0

38.3

In ppm

Individ

ual 1 min

10 

min

30 

min 1 hr 4 hrs 8 hrs

24 

hrs

User 432.4 224.8 172.2 141.6 76.8 43.8 14.9

Other 87.2 87.1 85.8 82.0 54.1 32.3 11.0

Plots:
DOCUMENT-DO NOT CITE OR QUOTE 

Page 150
DOCUMENT-DO NOT CITE OR QUOTE 

Page 151

DCM Scenario 5. Coffee Table, Spray-On, Workshop, User in workshop during wait time, 0.45 

ACH, 0.87 Weight Fraction

MCCEM Input Summary

Application Method:

Spray-on

Volumes:

Workshop volume = 54 m3

ROH volume = 492 – 54 = 438 m3

Airflows:

Workshopoutdoors68 m3/h

ROH-outdoors 197.1 m3/h (0.45 ACH)

Workshop-ROH 107 m3/h

DCM Mass Released:

Coffee table = 10 sq ft surface area

Applied product mass = 68 g/sq ft = 680 g

DCM mass = 680 g × 0.87 (wt fraction) × 0.66 (release fraction) = 390.5 g

For each of the 4 application sections:

k = 10/hr

Mass = 390.5/4 = 97.625 g

Eo = Mass * k = 976.25 g/hr (NOTE: only k and Mass are needed as MCCEM inputs)

Application Times by Section:

Episode

Elapsed time from time zero, 

minutes 

Apply 1 WaitScrap

e1

first 1/2, 1st time 0-1 

min

1-16 

min

16-20 

min

second 1/2, 1st time 20-21 

min

21-36 

min

36-40 

min

first 1/2, 2nd time 40-41 

min

41-56 

min

56-60 

min

second 1/2, 2nd time 60-61 

min

61-76 

min

76-80 

min

Model Run Time:

0-24 hrs

User takes out scrapings after 80 minutes, emissions truncated

Activity Patterns:

User in workshop during application, wait and scrape periods

User in ROH for the remainder of the run (22 hrs, 40 minutes)
DOCUMENT-DO NOT CITE OR QUOTE 

Page 152

MCCEM Results Summary

Personal Exposures (maximum values over first 24 hrs):

In mg/m3

Indivi

dual

1 

min 10 min 30 min 1 hr 4 hrs 8 hrs

24 

hrs

User 1,99

1.0

1,926.

4

1,760.

8

1,609.

4

619.

4

332.

4

111.

9

Other 329.

6

329.0 324.1 309.8 204.

2

121.

9

41.7

In ppm

Individ

ual 1 min

10 

min

30 

min 1 hr 4 hrs 8 hrs

24 

hrs

User 573.2 554.6 506.9 463.3 178.3 95.7 32.2

Other 94.9 94.7 93.3 89.2 58.8 35.1 12.0

Plots:
DOCUMENT-DO NOT CITE OR QUOTE 

Page 153
DOCUMENT-DO NOT CITE OR QUOTE 

Page 154

DCM Scenario 6. Chest, Spray-On, Workshop, User in ROH during wait time, 0.18 ACH, 0.87 

Weight Fraction

MCCEM Input Summary

Application Method:

Spray-on

Volumes:

Workshop volume = 54 m3

ROH volume = 492 – 54 = 438 m3

Airflows:

Workshopoutdoors68 m3/h

ROH-outdoors 78.8 m3/h (0.18 ACH)

Workshop-ROH 65.8 m3/h

DCM Mass Released:

Chest = 25 sq ft surface area

Applied product mass = 68 g/sq ft = 1,700 g

DCM mass = 1,700 g × 0.87 (wt fraction) × 0.66 (release fraction) = 976.1 g

For each of the 8 application sections:

k = 10/hr

Mass = 976.1/8 = 122.0 g

Eo = Mass * k = 1,220 g/hr (NOTE: only k and Mass are needed as MCCEM inputs)

Application Times by Section:

Episode

Elapsed time from time zero, 

minutes 

Apply Wait Scrape

first 1/4, 1st time 0-1 min

1-16 

min

16-20 

min

second 1/4, 1st time

20-21 

min

21-36 

min

36-40 

min

third 1/4, 1st time

40-41 

min

41-56 

min

56-60 

min

fourth 1/4, 1st time

60-61 

min

61-76 

min

76-80 

min

first 1/4, 2nd time

80-81 

min

81-96 

min

96-100 

min

second 1/4, 2nd time

100-

101 min

101-

116 min

116-

120 min

third 1/4, 2nd time

120-

121 min

121-

136 min

136-

140 min

fourth 1/4, 2nd time

140-

141 min

141-

156 min

156-

160 min

Model Run Time:

0-24 hrs

User takes out scrapings after 160 minutes, emissions truncated
DOCUMENT-DO NOT CITE OR QUOTE 

Page 155

Activity Patterns:

User in workshop during application and scrape periods, in ROH during wait periods

User in ROH for the remainder of the run (21 hrs, 20 minutes)

MCCEM Results Summary

Personal Exposures (maximum values over first 24 hrs):

In mg/m3

Indivi

dual

1 

min 10 min 30 min 1 hr 4 hrs

8 

hrs

24 

hrs

User 2,82

1.3

1,632.

3

1,266.

5

1,108.

6

813.

6

580

.2

228.2

Other 713.

5

713.0 709.0 696.5 575.

9

431

.3

176.6

In ppm

Individ

ual 1 min

10 

min

30 

min 1 hr 4 hrs 8 hrs

24 

hrs

User 812.2 469.9 364.6 319.1 234.2 167.0 65.7

Other 205.4 205.3 204.1 200.5 165.8 124.2 50.8

Plots:
DOCUMENT-DO NOT CITE OR QUOTE 

Page 156
DOCUMENT-DO NOT CITE OR QUOTE 

Page 157

DCM Scenario 7. Bathtub, Brush-On, Bathroom + Source Cloud, User in ROH During Wait Time, 

0.18 ACH, 1.0 Weight Fraction

MCCEM Input Summary

Application Method:

Brush-on

Volumes:

Source Cloud = 1 m3

Rest of Bathroom volume = 9 - 1 = 8 m3

ROH volume = 492 – 9 = 483 m3

Airflows:

Source CloudBathroom60 m3/h (0 to 

outdoors/ROH)

Bathroom-outdoors 1.6 m3/h

ROH-outdoors 86.9 m3/h (0.18 ACH)

Bathroom-ROH 35 m3/h

DCM Mass Released:

Tub = 36 sq ft surface area

Applied product mass = 90 g/sq ft = 3,240 g

DCM mass = 477 g × 0.1.0 (wt fraction) × 0.33 (release fraction) = 157.4 g

For each of the 8 application sections:

k = 10/hr

Mass = 157.4/8 = 19.7 g

Eo = Mass * k = 197 g/hr (NOTE: only k and Mass are needed as MCCEM inputs)

Application Times by Section:

Episode

Elapsed time from time zero, 

minutes 

Apply Wait Scrape

first 1/4, 1st time 0-3 min

3-18 

min

18-24 

min

second 1/4, 1st time 24-27 

min

27-42 

min

42-48 

min

third 1/4, 1st time 48-51 

min

51-66 

min

66-72 

min

fourth 1/4, 1st time 72-75 

min

75-90 

min

90-96 

min

first 1/4, 2nd time 96-99 

min

99-114 

min

114-

120 min

second 1/4, 2nd time 120-

123 min

123-

138 min

138-

144 min

third 1/4, 2nd time 144-

147 min

147-

162 min

162-

168 min

fourth 1/4, 2nd time 168-

171 min

171-

186 min

186-

192 min

Model Run Time:
DOCUMENT-DO NOT CITE OR QUOTE 

Page 158

0-24 hrs

User takes out scrapings after 192 minutes, emissions truncated

Activity Patterns:

User in source cloud during application and scrape periods, in ROH during wait periods

User in ROH for the remainder of the run (20 hrs, 48 minutes)

MCCEM Results Summary

Personal Exposures (maximum values over first 24 hrs):

In mg/m3

Indivi

dual 1 min 10 min

30 

min 1 hr 4 hrs 8 hrs

24 

hrs

User 2,684.

7

1,545.7 938.2 843.7 563.9 354.0 140.2

Other 223.7 223.6 222.2 218.2 186.8 149.5 69.5

In ppm

Individ

ual 1 min

10 

min

30 

min 1 hr 4 hrs 8 hrs

24 

hrs

User 772.9 445.0 270.1 242.9 162.3 101.9 40.4

Other 64.4 64.4 64.0 62.8 53.8 43.0 20.0

Plots:
DOCUMENT-DO NOT CITE OR QUOTE 

Page 159
DOCUMENT-DO NOT CITE OR QUOTE 

Page 160

Appendix G: Human Health Toxicity Summary

The information presented in this section is not intended to be an exhaustive discussion of 

DCM’s toxicity, but rather a summary of its toxicity via the inhalation route of exposure. Thus, 

the reader is referred to the original documents for detailed toxicity data supporting the 

summary presented in this document.

A two-generation inhalation exposure to DCM revealed no significant effects on reproductive 

performance in rats (up to 1,500 ppm) (Nitschke et al., 1988b; as cited in US EPA, 2011b). 

Some evidence of a decrease in fertility index was seen in male mice exposed to 150 and 200 

ppm (Raje et al., 1988; as cited in US EPA, 2011b), and no adverse effects on fetal development 

of mice or rats exposed to up to 1,250 ppm were seen by Schwetz et al. (1975); (as cited in US 

EPA, 2011b). Decreases in fetal body weight and changes in behavioral habituation were 

observed in offspring of Long-Evans rats exposed to 4,500 ppm during the gestational period 

(Bornschein et al., 1980; Hardin and Manson, 1980; as cited in US EPA, 2011b). 

Exposure-related non-cancer effects on the lungs consisted of foreign-body pneumonia in rats 

exposed to 8,400 ppm, six hrs/day for 13 weeks (NTP, 1986; as cited in US EPA, 2011b). Several 

neurological mediated parameters, including decreased activity (Kjellstrand et al., 1985; 

Weinstein et al., 1972; Heppel and Neal, 1944; Heppel et al., 1944; as cited in US EPA, 2011b), 

impairment of learning and memory (Alexeeff and Kilgore, 1983; as cited in US EPA, 2011b), and 

changes in responses to sensory stimuli (Rebert et al., 1989; as cited in US EPA, 2011b), are 

reported from acute and short-term DCM exposure. Evidence of a localized 

immunosuppressive effect in the lung resulting from inhalation DCM exposure was seen in an 

acute exposure (three hrs, 100 ppm) study in CD-1 mice (Aranyi et al., 1986; as cited in US EPA, 

2011b).

DCM is “likely to be carcinogenic in humans” under the Guidelines for Carcinogen Risk 

Assessment (US EPA, 2005; as cited in US EPA, 2011b). Results from two-year bioassays provide 

adequate evidence of the carcinogenicity of DCM in mice and rats exposed by inhalation, as 

well as adequate data to describe dose-response relationships. Oral exposure to DCM 

produced statistically significant increases in hepatocellular adenomas and carcinomas in male 

B6C3F1 mice (Serota et al., 1986; Hazleton Laboratories, 1983; as cited in US EPA, 2011b). 

Inhalation exposure to concentrations of 2,000 or 4,000 ppm DCM produced increased 

incidences of lung and liver tumors in male and female B6C3F1 mice (Maronpot et al., 1995; 

Foley et al., 1993; Kari et al., 1993; Mennear et al., 1988; NTP, 1986; as cited in US EPA, 2011b). 

Significantly increased incidences of benign mammary tumors (adenomas or fibroadenomas) 

were observed in male and female F344/N rats exposed by inhalation to 2,000 or 4,000 ppm 

(NTP, 1986; Mennear et al., 1988; as cited in US EPA, 2011b).

While not statistically significant an increased incidence of CNS tumors was observed in a twoyear study using relatively low exposure levels (0, 50, 200, and 500 ppm) in Sprague-Dawley 

rats observed a total of six astrocytoma or glioma (mixed glial cell) tumors in the exposed 

groups (Nitschke et al., 1988a; as cited in US EPA, 2011b). These tumors are exceedingly rare in 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 161

rats, and there are few examples of statistically significant trends in animal bioassays (Sills et 

al., 1999; as cited in US EPA, 2011b). Studies in humans also provide evidence for an 

association between occupational exposure to DCM and increased risk for some specific 

cancers, including brain cancer (Hearne and Pifer, 1999; Heineman et al., 1994; Tomenson, 

2011; as cited in US EPA, 2011b), liver cancer (Lanes et al., 1993; Lanes et al., 1990; as cited in 

US EPA, 2011b), non-Hodgkin lymphoma (Barry et al., 2011; Wang et al., 2009; Seidler et al., 

2007; Miligi et al., 2006; as cited in US EPA, 2011b), and multiple myeloma (Gold et al., 2011; as 

cited in US EPA, 2011b).

The hypothesized mode of action for DCM-induced lung and liver tumors is through a 

mutagenic mode of carcinogenic action. Key events within this hypothesis are: (1) DCM 

metabolized via glutathione S-transferase (GST) metabolism, with increasing metabolism 

through this pathway with increasing exposure levels above the saturation of cytochrome P450 

enzyme (CYP2E1); (2) reaction of GST-pathway metabolites with deoxyribonucleic acid (DNA), 

leading to (3) mutations in critical genes that result in tumor initiation; and (4) tumor growth 

promoted by unidentified molecular or cellular events. In this proposed mode of action, 

metabolism by CYP2E1, which is more predominant at lower exposures (or tissues 

concentrations) than metabolism by GST, is considered a protective mechanism against the 

formation of putatively carcinogenic metabolites from the GST pathway (US EPA, 2011b).

The weight of evidence from a large collection of in vivo and in vitro studies support the 

proposed mutagenicity of DCM and the key role of GST metabolism and the formation of DNAreactive GST-pathway metabolites. The data pertaining to chromosomal damage provide 

greater weight to this collection of evidence than the indicator genotoxicity assays; among 

chromosomal damage studies, in vivo evidence provides greater weight than in vitro evidence 

(US EPA, 2011b). The database for DCM provides support along each of these lines: (1) in vivo

evidence of chromosomal mutations (chromosomal aberrations) in the mouse lung and 

peripheral red blood cells in the absence of evidence of cytoxicity (these observations were not 

seen in the mouse bone marrow, a site that would be expected to be much more limited in 

terms of degree of DCM metabolism); (2) in vitro chromosomal instability evidence in human 

cells, other mammalian cells (i.e., Chinese hamster ovary cell [CHO]), and bacterial systems; and 

(3) positive DNA damage assays in numerous in vivo and in vitro studies (US EPA, 2011b). As 

noted previously, unscheduled DNA synthesis is generally a relatively insensitive measure of 

genotoxicity, and is given little weight in this synthesis of the data. Available studies also 

demonstrate target tissue specificity, with DNA-protein cross-links, single-stranded DNAbinding proteins (DNA SSBs), and sister chromatid exchanges seen in liver and lung cells of 

B6C3F1 mice following acute inhalation exposure to concentrations producing liver and lung 

tumors with chronic exposure (Casanova et al., 1996; Casanova et al., 1992; Graves et al., 1995; 

Allen et al., 1990; as cited in US EPA, 2011b). Dose-response concordance and temporality have 

also been seen, with evidence of mutagenicity (as determined by the micronucleus test or 

presence of chromosome aberrations) and genotoxicity (as determined by the presence of 

DNA-protein cross links or DNA SSBs) at the exposure levels inducing liver tumors in B6C3F1 

mice (NTP, 1986; as cited in US EPA, 2011b). Similar results were seen in inhalation exposure 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 162

studies in liver and lung cells of B6C3F1 mice in studies using the dose range used in the NTP 

(1986) study (US EPA, 2011b).

Certain human subpopulations may be more susceptible to exposure to DCM than others. One 

basis for this concern is the potential effect of COHb, a metabolic byproduct of DCM exposure. 

The COHb generated from DCM is expected to be additive to COHb from other sources. Thus, 

DCM exposure at high concentrations may pose an additional human health burden. Of 

particular concern are smokers (who maintain significant constant levels of COHb) and persons 

with existing cardiovascular disease. In addition, higher-than-normal levels of CO may result 

when alcoholics are exposed to DCM, since ethanol increases the expression and activity of 

CYP2E1 (Carpenter et al., 1996; as cited in ATSDR, 2000). Similarly, enhanced expression of 

CYP2E1 occurs in the condition of diabetes, although insulin erases that effect (Thomas et al., 

1987; as cited in ATSDR, 2000).

Varying susceptibility to DCM may be correlated with polymorphism in its metabolizing 

enzymes. Genetic polymorphisms have been identified for both glutathione S-transferase 

theta-1 and CYP2E1 (Garte and Crosti, 1999; as cited in ATSDR, 2000), and the health 

consequences of these variants are being investigated (d'Errico et al., 1999; Lang and Pelkonen, 

1999; Pelkonen et al., 1999; Strange and Fryer, 1999; Stubbins and Wolf, 1999; as cited in 

ATSDR, 2000).

Hemoglobin in the fetus has a higher affinity for CO than does adult hemoglobin. Thus, the 

neurotoxic and cardiovascular effects may be exacerbated in fetuses and in infants with higher 

residual levels of fetal hemoglobin when exposed to high concentrations of DCM (OEHHA, 

2001). For repeated exposures, steady-state considerations tend to eliminate the difference 

between children and adults after a short time (ATSDR, 2000).
DOCUMENT-DO NOT CITE OR QUOTE 

Page 163

Appendix H: Human Health Dose-Response Assessment

The reader is referred to the IRIS assessment (US EPA, 2011b), the Acute Exposure Guideline 

Levels technical support document (US EPA, 2008), the Technical Support Document Supporting 

the California’s Acute Reference Exposure Level and the National Academies’ Spacecraft 

Maximum Allowable Concentrations for Selected Airborne Contaminants (Volumes 2 and 5; 

NRC, 1996, 2008) for detailed explanations of toxicological studies and derivation approaches 

for these values.

AEGLs 

Air concentrations of DCM may reach dangerous levels in enclosed environments when 

individuals are using DCM-based paint strippers on a single daily use. Thus, air concentration 

thresholds for disability (AEGL-2) are compared with the inhalation exposure estimates for 

residential users9 and other residential occupants (e.g., children). This risk assessment retained 

the same POD and UFs used in the AEGL derivations.

AEGLs represent threshold exposure limits for the general public, including infants and children 

as well as other individuals who may be sensitive or susceptible. They are applicable for oncein-a-lifetime acute exposures (i.e., ≤24 hrs) to airborne concentrations of highly toxic chemicals 

typically occurring during emergency response situations. AEGL values are developed for three 

different health effect end point tiers (discomfort = AEGL-1 threshold; disability = AEGL-2 

threshold; and death = AEGL-3 threshold) at different durations of exposure (10 minutes; 30 

minutes; one hr; four hrs; and eight hrs). Figure H-1 depicts the three AEGL tiers and the 

associated health effects.

Two toxic endpoints were of importance for setting the AEGL-values with PBPK modeling: CNS 

depression caused by the concentration of the parent compound in brain and the formation of 

COHb from the CO metabolite. A GST isozyme is responsible for the metabolic pathway yielding 

CO. It is estimated that 20 percent of the US population lack this enzyme resulting in higher 

COHb levels in enzyme-deficient individuals (US EPA, 2008). 

CNS effects are expected to occur soon after the onset of exposure, while peak levels of COHb 

can be reached hrs after cessation of exposure. Likewise, it was expected that the toxic 

endpoint of interest would change over an exposure range of 10 minutes to eight hrs. The 

AEGL-values for the shorter exposure durations would be triggered by the CNS effects, whereas

the formation of COHb would determine the AEGL values for longer exposure durations (US 

EPA, 2008). 

 9 A user is defined as an individual(s) applying the product such as a DIY homeowner or a professional contractor. 

Other residential occupants are defined as other individual(s) present in the house that are not involved in the 

paint-stripping activity and are located in a house zone other than the one in which the paint-stripping activity is 

taking place (see Exposure section).
DOCUMENT-DO NOT CITE OR QUOTE 

Page 164

Source: NRC (2001).

Figure H-1. Illustration of the Different AEGL Threshold10 Levels. 

The AEGL-1 values were based on the observation in humans that exposure concentrations of 

868 and 986 ppm (3,100 and 3,521 mg/m3) led to light-headedness and difficulties in 

enunciation (Stewart et al., 1972; as cited in US EPA, 2008). These effects were absent at a 

one-hr exposure to 514 or 515 ppm (1,836 or 1,839 mg/m3). The concentration of 514 ppm 

was used as the POD for the AEGL-1 derivations. These effects could be attributed to the DCM 

concentration in the brain rather than to CO (US EPA, 2008). A PBPK model estimated that 

0.063 mM was the human brain concentration of DCM following a one-hr exposure to 514 ppm. 

Since susceptibility for gross CNS-depressing effects do not vary by more than a factor of twoto three-fold in humans, an intraspecies UF of three was applied, resulting in a maximum target 

concentration of DCM in the human brain of 0.021 mM. The human PBPK model used this 

concentration to estimate the AEGL values for the different time durations (i.e., 10 minutes to 

eight hrs). Because the calculated AEGL-1 values at four and eight hrs (160 and 140 ppm, 

respectively) were at or above the corresponding AEGL-2 values, no AEGL-1 values for these 

time periods were recommended (US EPA, 2008).

 10 AEGLs are considered threshold levels that represent an estimated point of transition and reflect the best efforts 

to establish quantitatively a demarcation between one defined set of symptoms or adverse effects and another 

defined set of symptoms or adverse effects (NRC, 2001).
DOCUMENT-DO NOT CITE OR QUOTE 

Page 165

AEGL-2 derivations were estimated for CNS effects based on a human study reporting the 

absence of AEGL-2 related CNS effects11 during a DCM exposure to 751 ppm (2,682 mg/m3

) for 

230 minutes (Winneke, 1974; as cited in US EPA, 2008). A PBPK model estimated that 

0.137 mM was the human brain concentration of DCM. AEGL-2 values were also estimated for 

the formation of COHb formation, assuming a maximum COHb level of four percent in patients 

with coronary artery disease humans (NRC, 2010). PBPK modeling was used to calculate 

exposure concentrations for both types of effects (i.e., CNS effects and COHb formation). The 

lowest value selected as the AEGL-2 value for each time period. An intraspecies UF of one for 

the CNS effects was considered sufficient since the toxic effects studied were less severe than 

those defined for AEGL-2 and the application of a greater value would result in values that were 

inconsistent with the available human data. Similarly, an intraspecies UF of one was applied for 

the effects associated to COHb formation because the POD was based on experimental data on 

the most susceptible individuals (i.e., coronary artery disease patients), which is also protective 

for other human subpopulations (NRC, 2010).

AEGL-3 derivations were based on an animal study reporting no CNS-related mortality in rats 

exposed to 11,000 ppm (39,286 mg/m3

) DCM for four hrs (Haskell Laboratory, 1982; as cited in 

US EPA, 2008). A rat PBPK model estimated that 3.01 mM was the maximum target DCM 

concentration in rat brain. AEGL-2 values were also estimated for the formation of COHb 

formation, assuming a maximum COHb level of approximately 15 percent in humans (NRC, 

2010). PBPK modeling was used to calculate exposure concentrations for both types of effects. 

The lowest value selected as the AEGL-2 value for each time period. An interspecies UF of one 

for the CNS effects was considered to be sufficient since the differences in susceptibility 

regarding mortality between species appear to be very small and because a human PBPK model 

is used to calculate the external human exposure (US EPA, 2008). An intraspecies UF of three 

was applied since the susceptibility for CNS-depressing effects is not expected to vary by more 

than a factor of two- to three-fold in the human population (US EPA, 2008). Application of an 

overall UF of three results in a maximum target DCM concentration in human brain of 1.0 mM. 

Similarly, an intraspecies factor of three was applied for the effects associated to COHb 

formation because the POD was supported by information on effects, such as myocardial 

infarction and stillbirths, reported in more susceptible subpopulations (NRC, 2010).

AEGLs are designed for once-in-a-lifetime exposures to airborne chemicals. However, a single 

exposure may not be realistic for a user exposed to DCM-based strippers on an intermittent 

basis12. On this basis, it could be argued that they are not appropriate to evaluate the risks of 

DCM-based paint strippers. DCM’s short half-life and recent reports of human fatalities led us 

to focus the analysis on a single daily use of the paint stripping product. DCM’s plasma half-life 

is estimated to be 40 minutes after inhalation exposure (DiVincenzo et al., 1972; as cited in 

ATSDR, 2000). DCM-based paint stripping products have caused fatal acute exposures among 

 11 This is an effect level and should not be considered as a NOAEL. 12 Intermittent exposures could be short-term, subchronic, or chronic with the key characteristic that the exposure 

is discontinuous (Felter et al., 2011). The gap of time between exposures would be sufficiently long to prevent that 

the steady-state levels of the chemical would not be achieved or maintained (Felter et al., 2011). 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 166

bathtub refinishers (CDC, 2012b). Such real-life situations support our current approach of 

using the AEGLs to determine if levels would surpass the AEGL-2 threshold for disability. 

California’s Acute REL

Risks to acute intermittent exposures in users and other residential occupants (e.g., children) 

are evaluated with the one-hr acute REL developed by OEHHA. This risk assessment retained 

the same POD and UFs used in the acute REL derivations.

The acute REL is defined as the concentration level at or below which no adverse health effects 

are anticipated (i.e., one or eight hrs) in a human population, including sensitive subgroups, 

exposed on an intermittent basis (OEHHA, 1999). Since safety factors are incorporated to 

address data gaps and uncertainties, exceeding the REL does not automatically indicate an 

adverse health impact (OEHHA, 1999). 

OEHHA developed a one-hr acute REL based on Putz et al. (1979). The study reported 

significant performance decrements on dual-task and auditory vigilance tests in volunteers 

(n = 12) exposed to 195 ppm DCM (696 mg/m3

) for 1.5 hrs (Putz et al., 1979; as cited in OEHHA, 

2008). The blood COHb levels increased from 1.35 percent pre-exposure to 5.1 percent postexposure. The 1.5-hr exposure to 195 ppm was considered the LOAEL in the REL derivations. A 

UF of six was applied to the LOAEL13 to develop a NOAEL and an intraspecies UF of 10 was 

applied to account for variability in the human population. An equivalent one-hr exposure was 

estimated from the 1.5-hr exposure using the ten Berge equation (Cn * T = k, n = 2) resulting in a 

one-hr acute REL of four ppm (14 mg/m3). The rationale for the choice of n = 2 was not 

documented in the OEHHA document.

SMAC 

SMACs are developed by NAS to provide guidance on chemical exposures that may occur during 

normal operations of spacecraft as well as emergency situations (NRC, 1996). This analysis is 

using the SMAC’s dose-response assessment as the starting point for deriving protective air 

concentrations for residential users of DCM-based paint strippers as well as other residential 

occupants that may be indirectly exposed (e.g., children). However, this risk assessment is 

applying an intraspecies UF of 10 to the SMAC’s POD to make it relevant to our exposure 

scenarios.

The one-hr SMAC is the concentration of DCM that will not compromise the performance of 

specific tasks by healthy astronauts during emergency conditions or cause serious or 

permanent toxic effects. SMACs are designed for healthy individuals, and reversible effects 

might occur but they are not expected to impair the astronauts’ judgment or interfere with 

proper responses to emergencies. By definition, the SMACs are not safe levels and are not 

meant to protect the general population, including children and the elderly. 

 13 The acute REL documentation does not provide the justification for why a factor of six was selected over other 

possible value.
DOCUMENT-DO NOT CITE OR QUOTE 

Page 167

The following paragraphs were extracted from NRC (1996) and explain the dose-response 

evaluation leading to the selection of 100 ppm (350 mg/m3

) as the one-hr SMAC: 

“...one of the major acute effects of methylene chloride is CNS depression, which 

appears to be due to CO formed from methylene chloride's metabolism. A 4-hr 

exposure to methylene chloride at 200 ppm, which yields 5% COHb in blood, 

impairs the hand-eye coordination and auditory vigilance (Peterson, 1978), but 

there are no data on the no-observed-adverse-effect level (NOAEL) of methylene 

chloride. It makes sense to adopt the NOAEL of COHb used in setting the 1-h and

24-h SMACs of CO as a potential basis for setting the 1-h and 24-h SMACs of 

methylene chloride. Three percent COHb is the target COHb concentration used 

to set both the 1-h and 24-h SMACs for carbon monoxide (Wong, 1990). The task 

here is to determine the methylene chloride concentrations that produce about 

3% COHb in 1 and 24 hr. Assuming a baseline COHb concentration of 0.6% due 

to endogenous CO production, the task is to determine the methylene chloride 

concentrations that would increase the COHb concentration by 2.4%. 

To derive the 1-hr SMAC based on CO formation, a linear regression line was 

fitted through the data of percent COHb increase versus C x T by forcing the 

fitted line through the origin. All the data in the above table were used except 

the data points at 3750 and 1972 ppm-hr because their corresponding responses 

of 10% and 9.3% increases in COHb were too far away from the region of 

interest, 2.4%. The linear regression yielded a line with a slope of 0.0038, r2 of 

0.74, and a 95 % confidence limit of 100 ppm-hr at a 2.4% increase in COHb. 

Accordingly, 100 ppm is selected as the 1-hr SMAC based on CO formation (NRC, 

1996).” 

The value of 100 ppm (350 mg/m3

) is considered a NOAEL (NRC, 2008) for CNS effects 

associated to COHb formation and is used as the POD for acute inhalation risk estimates. The 

application of UFs was not included in the derivation of the one-hr SMAC value, which is 

consistent with the intended purpose of the SMAC values. An evaluation of the COHb data for 

different human subpopulations supports the approach of retaining the default intraspecies UF 

of 10 under the premise that a level of three percent COHb is considered protective of 

neurotoxic effects in most individuals (e.g., healthy individuals, children), but may not be 

protective enough for patients with coronary artery disease and the fetus (NRC, 2010). At 

COHb levels of two or four percent, patients with coronary artery disease may experience a 

reduced time until onset of angina (chest pain) during physical exertion (Allred et al., 1989a; 

Allred et al., 1989b, 1991; as cited in NRC, 2010). Other studies have also confirmed a reduced 

time to onset of exercise-induced chest pain at a COHb between 2.5 and 4.5 percent (Aronow

et al., 1972; Anderson et al., 1973; Sheps et al., 1987; Kleinman et al., 1989; Kleinman et al., 

1998; as cited in NRC, 2010). Fetuses are at higher risk for CO toxicity because of higher CO 

affinity and slower CO elimination (NRC, 2010). There are no studies reporting effects on the 

unborn after a single acute exposure resulting in lower COHb levels (US EPA, 2000; as cited in 

NRC, 2010). 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 168

EPA’s RfC

Non-cancer risks to chronic inhalation exposures in small-shop workers are evaluated with the 

EPA’s RfC. The RfC is defined as the 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 effects during a 

lifetime. 

Liver lesions characterized by hepatic vacuolation are commonly reported in rodents repeatedly 

exposed to DCM by inhalation. The chronic RfC was based on a NOAEL of 200 ppm for 

hepatocyte vacuolation in female rats exposed to DCM for six hrs/day, five days/week for two 

years (Nitschke et al., 1988a; as cited in US EPA, 2011b). A rat PBPK model was used to 

estimate rat internal doses from the Nitschke et al. (1988a) study. The rat internal doses and 

their corresponding incidence data for hepatic effects (hepatic vacuolation) were used to 

estimate the rat internal lower 95 percent confidence limit of the 10 percent benchmark dose 

(BMDL10) (US EPA, 2011b). Because the dose-metric is a rate of metabolism and the clearance 

of these metabolites may be slower per volume tissue in the human compared with the rat, the 

rodent internal dose-metric was adjusted by dividing by a pharmacokinetic allometric scaling 

factor of BW0.75 (operationalized as [BWhuman/BWrat]

0.25 ≈ 4.09) to obtain a human equivalent 

internal BMDL10 (US EPA, 2011b). The human equivalent internal BMDL10 was then converted 

to the human equivalent concentration (HEC) using a human PBPK model that provided a 

distribution of HECs. The 1st percentile of the distribution of HECs, 17.2 mg/m3

, was used as a 

POD for the RfC (US EPA, 2011b).

The POD was divided by a total UF of 30 to obtain a chronic RfC of 0.6 mg/m3. PBPK modeling 

supported the reduction of the default inter- and intraspecies UFs. A factor of three was used 

to account for the toxicodynamic uncertainty of the animal to human extrapolation. Similarly, a 

factor of three was applied to account for possible toxicodynamic differences in sensitive 

humans. Another factor of three was used to address deficiencies in the DCM toxicity database 

at chronic low exposures. 

EPA’s IUR

EPA has concluded that DCM is carcinogenic by a mutagenic mode of action (US EPA, 2011b). 

The EPA IUR (assuming a 70-year human lifetime) is used to estimate cancer risks for chronic 

inhalation exposures in small-shop workers. The IUR was derived from mouse liver and lung 

tumor incidence data (Mennear et al., 1988; NTP, 1986; as cited in US EPA, 2011b). A mouse 

PBPK model was used to calculate long-term daily average internal liver doses. The selected 

internal dose-metrics for liver tumors and lung tumors were long-term average daily mass of 

DCM metabolized via the GST pathway per unit volume of liver and lung, respectively. This 

approach was taken based on evidence that GST-pathway metabolites produced from DCM are 

primarily responsible for its carcinogenicity in mouse liver. The multistage dose-response 

model (Benchmark Dose Software [BMDS] version 2.0) was used to fit the mouse liver tumor 

incidence and PBPK model-derived internal dose data and to derive a mouse internal BMD and 
DOCUMENT-DO NOT CITE OR QUOTE 

Page 169

BMDL10 (US EPA, 2011b). Because the metric is a rate of metabolism rather than the 

concentration of putative toxic metabolites, and data pertaining to the reactivity or clearance 

rate of the relevant metabolite(s) are lacking, the human BMDL10 was derived by multiplying 

the mouse BMDL10 by a BW0.75 allometric scaling factor (operationalized as [BWhuman/BWmouse] 

0.25 ≈ 7) to account for the potential slower clearance per volume tissue in the human 

compared with the mouse. A linear extrapolation approach using the internal human BMDL10

for liver and lung tumors was used to calculate human tumor risk factors by dividing the 

benchmark response (BMR) of 0.1 by the human BMDL for each tumor type. Currently, there 

are no data from chronic inhalation cancer bioassays in mice or rats providing support for a 

nonlinear dose-response relationship (US EPA, 2011b).

A probabilistic human PBPK model was used to determine a distribution of human internal 

doses from a unit of concentration (one μg/m3) and corresponding IUR values expressed as 

external concentrations (μg/m3). The mean of the distribution of candidate values from the 

most sensitive (GST-T1+/+) genotype (i.e., the group that would be expected to be most sensitive 

to the carcinogenic effects of DCM) was chosen as the IUR for liver and lung tumors. A 

procedure for combining risks for liver and lung tumors was used to derive DCM’s IUR. The 

slope of the linear extrapolation from the lower 95 percent bound estimate BMDL10 is 

1 × 10-8 per μg/m3 or the inhalation risk, which represents an upper-bound estimate for 

continuous lifetime exposure (70 years) without consideration of increased early-life 

susceptibility due to DCM's mutagenic mode of action.