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Creosote Registration Review Team 

Human Health & Environmental Effects 

Nathan Mottl 

Tim McMahon 

Siroos Mostaghimi 

Jim Breithaupt 

Bill Erickson 

Health Effects Division 

Kristin Rury 

Risk Management 

Sandra O’Neill 

Rose Kyprianou 

Tom Luminello 

Office of General Counsel 

Philip Ross 
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TERMS, ABBREVIATIONS AND SYMBOLS 

AD Antimicrobials Division 

A.I. or a.i. active ingredient 

aPAD acute population adjusted dose 

ASRI activated sludge respiration inhibition 

atm-m3

/mole atmospheric pressure-cubic meter per mole 

AWPA American Wood Protection Association 

BCF bioconcentration factor 

°C degrees Celsius 

CAS Chemical Abstracts Service 

CFR Code of Federal Regulations 

CHO Chinese hamster ovary 

CMA Chemical Manufacturers Association 

CO2 carbon dioxide 

COC concentration-of-concern 

cPAD chronic population adjusted dose 

DCI data call-in 

EC50 median (or 50 percent) effect concentration

EC05 5 percent effect concentration

ECOTOX ECOTOXicology 

EDI estimated daily intake 

EDSP Endocrine Disruptor Screening Program 

E-FAST Exposure and Fate Assessment Screening Tool 

EPI Suite Estimation Program Interface Suite 

EPA Environmental Protection Agency 

FDA Food and Drug Administration 

FFDCA Federal Food, Drug, and Cosmetic Act 

FIFRA Federal Insecticide, Fungicide, and Rodenticide Act 

FQPA Food Quality Protection Act 

FWP Final Work Plan 

g/mol grams per mole 

GLN guideline number 

HPV high production volume 

IDS Incident Data System 

Koc organic carbon normalized soil-water partition coefficient 

Kd soil-water partition coefficient 

Kow octanol-water partition coefficient 

LC50 median (or 50 percent) lethal concentration 

LD50 median (or 50 percent) lethal dose 

LOAEC lowest-observed-adverse-effect-concentration 

LOEC lowest-observed-effect-concentration 

LOAEL lowest-observed-adverse-effect-level 

Log Kow logarithm of the octanol-water partition coefficient

μg microgram 

ml/g milliliter per gram 

mg/kg milligram per kilogram 

mg/kg/day milligram per kilogram per day 

mg/L milligram per liter 

mm Hg millimeter of mercury 
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MOE margin of exposure 

MRID Master Record Identification Number 

MRL maximum residue limit 

N/A not applicable 

nm nanometers 

NOAEC no-observed-adverse-effect-concentration 

NOAEL no-observed-adverse-effect-level 

OCSPP Office of Chemical Safety and Pollution Prevention 

OECD Organization for Economic Co-operation and Development 

OPP Office of Pesticide Programs 

PAD population adjusted dose 

PAI pure active ingredient 

PDM Probabilistic Dilution Model 

% percent 

PC Code Pesticide Chemical Code 

PCF pounds per cubic foot 

pH power of hydrogen or power of the concentration of the hydrogen ion 

PHED Pesticide Handler’s Exposure Data 

PIS primary irritation score 

pKa power of the acid dissociation constant or negative base-10 logarithm of the acid 

dissociation constant of a solution 

ppb parts per billion 

ppm parts per million 

PWP Preliminary Work Plan 

QSAR quantitative structure-activity relationship 

RED Reregistration Eligibility Decision 

SAR structure activity relationship 

SF safety factor 

SSTS Section Seven Tracking System 

TEP typical end-use product 

TGAI technical grade active ingredient 

TMDL total maximum daily loads 

UF uncertainty factor 

UV/VIS ultraviolet/visible light absorption 

% w/w percent weight per weight. 

WP wettable powder 

WWTPs wastewater treatment plants 

 
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Table of Contents 

1 Introduction ............................................................................................................................. 7

1.1 Statutory and Regulatory Authority ................................................................................. 7

1.2 Case Overview ................................................................................................................. 8

1.3 Chemical Identification and Properties ............................................................................ 9

1.4 Use/Usage Description ................................................................................................... 10

1.4.1 Registrations ........................................................................................................... 10

1.4.2 Summary of Registered Uses .................................................................................. 11

1.4.3 Usage Information .................................................................................................. 11

1.5 Regulatory History ......................................................................................................... 11

1.5.1 Tolerance Information ............................................................................................ 11

1.6 Incidents ......................................................................................................................... 12

1.6.1 Human Health ......................................................................................................... 12

1.6.2 Ecological ............................................................................................................... 12

2 Anticipated Data Needs ........................................................................................................ 12

3 Human Health Risk Assessment ........................................................................................... 15

3.1 Existing Toxicological Endpoints .................................................................................. 15

3.2 Dietary Exposure ............................................................................................................ 16

3.2.1 Food ........................................................................................................................ 16

3.2.2 Drinking Water ....................................................................................................... 16

3.3 Occupational and Residential Exposures ....................................................................... 16

3.3.1 Occupational Handler Exposure ............................................................................. 16

3.3.2 Occupational Post-Application Exposure ............................................................... 17

3.3.3 Residential Handler Exposures ............................................................................... 17

3.3.4 Residential Post-Application Exposures ................................................................. 18

3.4 Aggregate and Cumulative Exposure ............................................................................. 18

3.4.1 Aggregate Exposures .............................................................................................. 18

3.4.2 Cumulative Exposures ............................................................................................ 18

4 Environmental Risk Assessment........................................................................................... 18

4.1 Environmental Fate Assessment .................................................................................... 19

4.1.1 Water Quality .......................................................................................................... 20

4.2 Environmental Exposure Pathways ................................................................................ 20

4.3 Ecological Effects Analysis ........................................................................................... 21

4.3.1 Available Ecotoxicity Endpoints ............................................................................ 21

4.3.2 Open literature ........................................................................................................ 22

4.4 Exposure Analysis Plan .................................................................................................. 22

4.4.1 Aquatic and Terrestrial Wildlife Exposure Estimates ............................................ 22

4.4.2 Screening Level Down-the-Drain Analysis ............................................................ 22

5 Endocrine Disruptor Screening Program (EDSP) ................................................................. 22

6 Optional Label Changes ........................................................................................................ 23

7 Guidance for Commenters .................................................................................................... 23

7.1 Preliminary Work Plan ................................................................................................... 23

7.1.1 Trade Irritants .......................................................................................................... 23

7.1.2 Water Quality .......................................................................................................... 24

7.1.3 Environmental Justice ............................................................................................. 24

7.1.4 Additional Information ........................................................................................... 24
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8 Next Steps ............................................................................................................................. 25

9 References ............................................................................................................................. 26

Appendix A Toxicology Profile ............................................................................................... 27

Appendix B Environmental Fate ............................................................................................. 43

Appendix C Ecotoxicology Profile .......................................................................................... 50

Appendix D Physical and Chemical Properties ....................................................................... 54

List of Tables 

Table 1 – Summary of Anticipated Risk Assessments and Data Needs for Registration Review: 

Creosote .......................................................................................................................................... 8

Table 2 – Anticipated Registration Review Schedule .................................................................... 9

Table 3 – Chemical Identification of Creosote ............................................................................... 9

Table 4 – Physical-Chemical Properties for Creosote .................................................................. 10

Table 5 – Summary of Creosote Registered Uses ........................................................................ 11

Table 6 – Studies Anticipated as Needed for the Registration Review of Creosote ..................... 13

Table 7 –Data Needs Required by the September 22, 2011 Data Call-In for the Creosote RED . 14

Table 8 – Existing Toxicological Endpoints ................................................................................. 15

Table 9 – Occupational Handler Exposure Scenarios for Creosote .............................................. 17

Table 10 – Available Creosote Ecological Effects Endpoints ...................................................... 21
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1 Introduction 

This document is the United States Environmental Protection Agency’s (USEPA, EPA or “the 

agency”) Preliminary Work Plan (PWP) for creosote. The PWP document explains what EPA's 

Office of Pesticide Programs (OPP) knows about coal tar creosote highlighting anticipated data 

and assessment needs, identifying the types of information that would be especially useful to the 

agency in conducting the review, and providing an anticipated timeline for completing creosote’s 

review. At the time of the 2008 Registration Eligibility Decision (RED), the creosote case 

included the following chemicals: coal tar creosote (PC Code 025004), creosote oil (PC Code 

025003), and coal tar (PC Code 022003). The last EPA registrations for both creosote oil and 

coal tar were cancelled in February of 2013.1

 As such, this registration review case will assess 

registrations only for coal tar creosote (PC Code 025004), herein referred to as creosote. 

The registration review process was designed to include a public participation component to 

solicit input from interested stakeholders. The agency intends, by sharing this information in the 

docket, to inform the public of what it knows about creosote and what types of new data or other 

information would be helpful for the agency to receive as it moves toward a decision on 

creosote. The agency encourages all interested stakeholders to review the PWP and to provide 

comments and additional information that will help the agency’s decision-making process for 

this chemical. 

1.1 Statutory and Regulatory Authority 

The Food Quality Protection Act (FQPA) of 1996 mandated a registration review program. All 

pesticides distributed or sold in the United States generally must be registered by the USEPA 

based on scientific data showing that they will not cause unreasonable risks to human health or 

the environment when used as directed on product labeling. The registration review program is 

intended to make sure that, as the ability to assess risk evolves and as policies and practices 

change, all registered pesticides continue to meet the statutory standard of no unreasonable 

adverse effects to human health or the environment. Changes in science, public policy, and 

pesticide use practices will occur over time. Through the registration review program, the agency 

periodically reevaluates pesticides to make sure that as change occurs, products in the 

marketplace can be used safely. Information on this program is provided at 

http://www2.epa.gov/pesticide-reevaluation/registration-review-process. 

The agency is implementing the registration review program pursuant to Section 3(g) of the 

Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) and will review each registered 

pesticide every 15 years to determine whether it continues to meet the FIFRA standard for 

registration. The regulations governing registration review begin at 40 CFR 155.40. The agency 

will consider benefits information and data as required by FIFRA. The public phase of 

registration review begins when the initial docket is opened for each case. The docket is the 

agency’s opportunity to state what it knows about the pesticide and what additional risk analyses 

and data or information it believes are needed to make a registration review decision. After 

reviewing and responding to comments and data received in the docket during this initial 

 

1

 “Product Cancellation Orders for Certain Pesticide Registrations”, 78 FR 8513-8522 (February 6, 2013). 
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comment period, the agency will develop and commit to a Final Work Plan (FWP) and 

anticipated schedule for the creosote case. 

1.2 Case Overview 

The docket for creosote (case 0139) has been established at http://www.regulations.gov in docket 

number EPA-HQ-OPP-2014-0823, documents associated with this registration review can be 

viewed at this docket. Tables 1-2 below summarize the issues relevant to this registration review 

case and the anticipated registration review schedule. 

Table 1 – Summary of Anticipated Risk Assessments and Data Needs for Registration 

Review: Creosote 

Risk Assessment 

Assessment 

Necessary to 

Support 

Registration 

Review 

Date of Most 

Recent 

Assessment 

(N/A = Not 

Applicable)

Type of 

Assessment 

Required 

(New/Updated) 

Data Anticipated as Needed 

(See Table 6 for details) 

Dietary (food) 

No (see 

Section 

3.2.1)

N/A None None 

Dietary (drinking water) 

No (see 

Section 

3.2.2)

N/A None None 

Occupational Handler Yes 9/5/2008 Updated Immunotoxicity 

Worker Exposure Study1

Occupational PostApplication 

No (see 

Section 

3.3.2) 

N/A None None (Post application job functions 

have been redefined as handlers) 

Residential Handler 

No (see 

Section 

3.3.3)

N/A None None 

Residential Post 

Application 

No (see 

Section 

3.3.4)

N/A None None 

Aggregate 

No (see 

Section 

3.4.1)

N/A None None 

Cumulative 

No (see 

Section 

3.4.2)

N/A None None 

Tolerance Review 

No (see 

Section 

1.5.1)

N/A None None 

Ecological Yes (see 

Section 4) 3/27/2008 Updated Ecotoxicity - see Table 6 

* Table 1 is a summary of the anticipated risk assessments and data needs for Registration Review. For data called in through the postReregistration Eligibility Decision (RED) Data Call-In (DCI), see Table 7. 

1

Data already required by the 2011 post-RED Creosote DCI. 
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Table 2 – Anticipated Registration Review Schedule 

Anticipated Activity Target Date* Completion Date

Phase 1: Opening the Docket 

Open Docket and 60-Day Comment Period for Preliminary Work Plan 2015-03 2015-03 

Close Public Comment Period 2015-05 

Phase 2: Case Development 

Issue Final Work Plan 2015-09 

Issue Data Call-In (DCI) 2016-09 

Receive Data to be Considered in Risk Assessment 2018-09 

Open 30-Day Public Comment Period for Preliminary Risk Assessment(s) 2020-03 

Close Public Comment Period 2020-04 

Phase 3: Registration Review Decision and Implementation 

Open 60-Day Public Comment Period for Proposed Decision 2020-09 

Close Public Comment Period 2020-11 

Issue Final Decision 2121-03 

Begin Post-Decision Follow-up 2121 

Total (years) 6 

*The anticipated schedule will be revised as necessary (e.g., need arising under the Endocrine Disruptor Screening Program with 

respect to the active ingredient in this case).

1.3 Chemical Identification and Properties 

Table 3 presents the active ingredient to be assessed in case 0139: creosote (PC Code 025004). 

Table 3 – Chemical Identification of Creosote

Chemical Name Creosote 

Chemical 

Classification 

Polycyclic aromatic 

hydrocarbons (PAHs) 

PC Code 025004 

CAS Number 8001-58-9 

Molecular Formula Not applicable (Mix of 

compounds 

Molecular Weight (grams/mole) Not applicable (Mix of 

compounds 

Molecular Structure Not applicable (Mix of 

compounds 

Creosote consists primarily of liquid, solid PAHs, other hetero nuclear aromatic substances, and 

some tar acids and bases. 
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USEPA’s document, “Guidance for Reregistration of Pesticide Products Containing Coal Tar 

Creosote” recognizes that “hundreds of individual chemicals have been identified in coal tar 

creosote.” There are two major types of creosote, P1/P13 fraction which is used in the treatment 

of utility poles and pilings and P2 fraction which is used in the treatment of railroad ties/crossties 

and is more viscous than the P1/P13 blend (EPA 2008). These two fractions of creosote are 

derived by carbonizing coal through high temperature distillation and collecting the coal tar 

fractions that are comprised of light oil, middle oil, and heavy (oil) anthracene. 

The creosote product chemistry information relevant to risk assessment is summarized in Table 

4, and the details of the product chemistry information are discussed in Appendix D . 

Table 4 – Physical-Chemical Properties for Creosote 

Guideline No. Parameter Creosote Reference/Comments 

830.7050 UV/Visible Absorption Not available 

for mixture 

PAHs absorb UV light but no 

spectrum available for 

mixture 

830.7200 Melting point (oC) Not applicable MRID 48480902 

Product is liquid 

830.7220 Boiling point (oC) >180 MRID 48490902 

830.7370 Dissociation constant (pKa) Not applicable

MRID 48480902 

No acid or base functional 

groups 

830.7550 Octanol-water partition coefficient 

at 25 o

C (Log Kow) 3.25 MRID 48480902 

830.7840 Solubility in water (mg/L) 313 MRID 48480902 

830.7950 Vapor pressure (mmHg) 11.1 MRID 48480902 

24.4 o

C 

 None Henry's law constant at 25 o

C 

(atm-m3

/mol) Not calculated 

Product is a mixture with 

various chemical and physical 

properties 

atm-m3/mol = atmosphere cubic meter per mole; oC = degrees Celsius; mg/L = milligrams per liter; mmHg = 

millimeters of mercury. 

1.4 Use/Usage Description 

1.4.1 Registrations 

There are six creosote registrants holding a total of seventeen industrial wood preservative product 

registrations for wood protection as well as treating wood in marine environments. 

Currently there are 16 end-use products (EUP) registered for pressure treatment of wood, as well as 

in fresh water and marine environments, and one manufacturing use product (MUP) containing 

directions for further formulation into wood preservatives. Wood treated with these preservatives is 

specified for commercial and industrial uses at outdoor sites. 

Creosote formulations intended for use as a wood treatment are classified as restricted use 

pesticides (RUPs) for sale and use by certified applicators only. Indoor applications of creosote 

are prohibited as well as application to wood intended for use in interiors (with certain 

exceptions) or for use in contact with food, feed, or drinking water. These restrictions were 
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imposed on creosote registrations as part of the Agency’s Special Review process as indicated in 

the U.S.EPA Position Document 4 for Wood Preservative Pesticides: Creosote, 

Pentachlorophenol and Inorganic Arsenicals (1984, amended 1986). 

1.4.2 Summary of Registered Uses 

Table 5 presents a summary of the registered uses of creosote that will be assessed in this 

registration review. Creosote is applied by pressure treatment. 

Table 5 – Summary of Creosote Registered Uses 

Use Application Method Application Rate

Wood or Wood Structure Protection Treatments 

Pressure Treatment to Forest Products Pressure Treatment 6-12 lb/cu ft

1.4.3 Usage Information 

According to the Kline Biocides Report for 2004/2005, creosote is one of the leading wood 

preservatives for railroad ties. In 2004, U.S. consumption of creosote was estimated at 785 

million pounds, and was forecasted to grow at an average volume rate of 0.2% over the 

subsequent five years (Kline, 2005). 

1.5 Regulatory History 

Creosote has been registered as a heavy duty wood preservative since 1948. Since creosote is 

derived from the distillation of coal tar, consists of hundreds of compounds, and has a variable 

composition, the American Wood Protection Association (AWPA) established standards to 

differentiate between the different blends of creosote. The industry refers to these different blends 

of creosote as P1/P13 and P2. 

The agency completed a RED for creosote in 2008. EPA determined that creosote products 

contributed benefits to society and were eligible for reregistration provided the mitigation 

measures and associated label changes identified in the 2008 RED were implemented and 

required data were submitted. As mentioned in Section 1.4.1, restrictions were imposed on 

creosote registrations as part of the Agency’s Special Review process. 

A post-RED Generic-Data Call-In (GDCI) and Product-Specific-Data-Call-In (PDCI) were 

issued on September 22, 2011. For the status of these data, see Table 7. 

1.5.1 Tolerance Information 

For the active ingredient creosote, EPA has not established tolerances in raw agricultural 

commodities or processed food and feed products for creosote under the Federal Food, Drug and 
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Cosmetic Act (FFDCA) Section 408. There are also no tolerance exemptions for creosote under 

FFDCA Section 408. Creosote has not been cleared as a food additive by the US Food and Drug 

Administration (US FDA) under FFDCA Section 409. 

1.6 Incidents 

1.6.1 Human Health 

EPA conducted an epidemiology and incidents report on March 9, 2008 for the RED (EPA 

2008d). For registration review, EPA conducted a search for creosote in the Incident Data 

System (IDS) on January 7, 2015 covering the period from January, 1997 to January, 7, 2015. 

Over 28 incident reports exist in the Aggregate Incident Summary report. The last reported 

incident was in August 2011. The associated human health effects include irritation effects to 

eyes, respiratory (chemical pneumonia), and skin (blisters, erythema, and irritation). Other 

human health effects include muscle stiffness, dizziness, headache, fever and malaise. Whether 

these deleterious health effects result from exposure to creosote specifically, or to one or more 

other chemicals typically found as contaminants, is not clear. EPA will be conducting a more 

comprehensive incident report in registration review. 

1.6.2 Ecological 

As of December 22, 2014, the EPA/OPP Incident Data System (IDS) contains one aggregate 

incident summary from a creosote treatment facility in Pittsburgh, PA. Employees found a dead 

pigeon and a dead sparrow in 1999 and 3 dead pigeons between November 2002 and January 

2003. The dead birds were found in a building housing machinery used to pressure-treat 

creosote. The report states that the company does not feel that these bird mortalities were related 

to creosote. 

2 Anticipated Data Needs 

Several studies were required by the DCI following the assessment of creosote in the 2008 RED. 

In addition to the already-required RED DCI data, the following studies as listed in Table 6 are 

expected to be needed for the registration review of creosote. Table 7 outlines the data 

requirements required by the post-RED DCI issued on September 22, 2011. The agency 

anticipates reviewing any data received in response to the post-RED DCI as well as data 

requested for this registration review prior to conducting the registration review risk assessments 

for creosote. The ecological toxicity studies anticipated to be required for registration review 

could be conducted using the leachate from the leaching study required by the post–RED DCI in 

order to provide information for a robust assessment. Alternatively, information on effects on 

various taxa from monitoring studies conducted near aquatic sites could be submitted to allow 

the agency to determine risks from in situ use of creosote. This information would need to 

address acute and chronic effects in the water column as well as in sediments. 
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Table 6 – Studies Anticipated as Needed for the Registration Review of Creosote

GLN Study Name Test Substance

Time Frame 

(Measured in 

months from 

DCI Receipt)

Risk Assessment(s) 

Data Will Support

U

850.21001 Avian acute oral TGAI 12 

Ecological 

850.3020 Honey bee, acute oral toxicity 12 850.1010 Freshwater invertebrate, acute 

TEP: Leachate from creosote pilings or railroad ties 

24 

850.1025 

or 

850.1055 

Estuarine/marine bivalve, acute 12 

850.1035 Estuarine/marine invertebrate, acute 12 850.1075 Estuarine/marine fish, acute 18 850.1075 Freshwater fish, acute 18 850.1300 Freshwater invertebrate, life cycle 12 850.1350 Estuarine/marine invertebrate, life cycle 12 850.14002 Freshwater fish, early life-stage 12 850.14002 Estuarine/marine fish, early life-stage 12 850.42253 Seedling emergence, semi-aquatic plants 12 850.4400 Aquatic plants, vascular 12 850.45004 Algal toxicity (3 spp.) 12 850.45504 Cyanobacteria toxicity 12 870.7800 Immunotoxicity P1/P13 and P2 blends 12 Occupational worker None5,6,7 Whole sediment, chronic, freshwater (2 spp.) TEP: Leachate from creosote 

pilings or railroad ties 

24 Ecological 

None 

6, 7,8 Whole sediment, chronic, estuarine/marine 24 

1 The anticipated DCI will provide that OECD TG 233 using the "LD50- slope test" or "limit dose test" can be used instead of OCSPP 850.2100 for certa(e.g., causes no delayed effects, causes no regurgitation). Details on the species and conditions under which TG 233 would not fulfill the anticipated datat http://www.epa.gov/pesticides/science/efed/policy_guidance/team_authors/terrestrial_biology_tech_team/review_avian_acute_oral_oecd_tg223.htm 2 The anticipated DCI will provide that testing must be conducted with the most sensitive organism (either freshwater or estuarine/marine vertebrates, or estuarine/marine invertebrates), as determined from the results of the acute toxicity tests (acute EC50 freshwater invertebrates; acute LC50/EC50 estuarine freshwater fish LC50).3 Test guidelines 850.4100 and 850.4225 were merged and harmonized into OCSPP 850.4100 in a Federal Register Notice dated June 27, 2012 (FRL-934 On June 27, 2012, EPA announced certain revisions in harmonized guideline series 850 – Ecological Effects Tests – including renumbering and other some guideline studies. See “Final Test Guidelines; OCSPP 850 Series; Notice of Availability” 77 FR 38282, June 27, 2012. http://www.regulations.govHQ-OPPT-2009-0154-00285 The anticipated DCI will provide that the two species to be used to conduct this test are Hyallela azteca and Chironomus dilutes. The anticipated DCI wazteca, conduct study according to ORD Study Method EPA 600/R-099-064 but with 12 replicates per treatment (4 for 28-d survival and growth and 8 fwith 10 neonates per replicate, and for Chironomus dilutus, conduct study according to ORD Study Method: EPA 600/R-099-020 but with 10 replicates neonates per replicate. 6 The preferred sediment is formulated, guidance for the formulated sediment can be found in OECD 218 Sediment-Water Chironomid Toxicity Test usi
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7 The anticipated DCI will require that a protocol must be approved by the agency prior to the initiation of the study. 8 The anticipated DCI will provide that the species to be used to conduct this test is Leptocheirus plumulosus and to conduct the study according to ORD 

099-020 but with 10 replicates per treatment with 20 neonates per replicate. 

Table 7 –Data Needs Required by the September 22, 2011 Data Call-In for the Creosote RED 

GLN Study Name Status of DCI 

875.1100 Dermal exposure (outdoor) In place of these studies, the registrant submitted a draft protocol study for Exposure of Work

Pressure Treatment of Lumber for review. The agency is reviewing the protocol for this obseprotocol and results from the ensuing study are approved, this study would satisfy the exposuthe creosote case (GLNs 875.1100, 875.1200, 875.1300, 875.1400, and 875.1600). 

875.1200 Dermal exposure (indoor) 875.1300 Inhalation exposure (outdoor) 875.1400 Inhalation exposure (indoor) 875.1600 Applicator exposure monitoring data reporting 875.1700 Product use information No data have been submitted; this study is outstanding. Special Study – Leaching 

Leaching study for release of creosote components from creosote impregnated wood 

No data have been submitted; this study is outstanding. 

Special Study – Sediment 

Sediment concentration, Aquatic Structures No data have been submitted; this study is outstanding. 
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3 Human Health Risk Assessment 

The agency anticipates the need to conduct a new human health risk assessment for creosote 

based upon the updated exposure study data required by the 2011 post-RED DCI. Additionally, 

immunotoxicity data are anticipated to be required to conduct this risk assessment for 

registration review. Because creosote is currently registered for use in occupational settings, 

occupational handlers have the potential to be exposed through the pressure treatment process. 

EPA plans to estimate cancer and non-cancer risks to occupational handlers as a result of 

inhalation and dermal exposure to creosote during the pressure treatment process. 

3.1 Existing Toxicological Endpoints 

Table 8 presents the endpoints used in the agency’s most recent human health risk assessment for 

creosote in support of the 2008 RED. An immunotoxicity study is identified as an anticipated 

data need for the registration review for creosote. All available information including existing 

toxicology studies, valid scientific literature, and the studies that are expected to be required for 

registration review will be considered in establishing the endpoints to be used in the registration 

review risk assessment. A detailed description of the existing database of toxicity studies is 

provided in Appendix A .

Table 8 – Existing Toxicological Endpoints 

Exposure Scenario

Dose Used in 

Risk Assessment 

(mg/kg/day)

Target Margin of 

Exposure (MOE), 

Uncertainty Factor 

(UF), FQPA Safety 

Factor (SF)

Study and Toxicological Effects

Dermal (short-term) 

Oral NOAEL=50 

MOE = 100 

Developmental Toxicity study in the rat (MRID 

43584201); decreased body weight and food 

consumptions in maternal rats at 175 mg/kg/day 

Dermal 

(Intermediate-term) 

Dermal NOAEL 

= 40 mg/kg/day MOE = 100 

90-day dermal toxicity study in the rat (MRID 

43616201); increased incidence of dermal 

inflammation and decreased body weight gain at 

400 mg/kg/day 

Dermal (long-term) Oral LOAEL = 

25 mg/kg/day MOE = 300 

2-generation reproduction toxicity study in the rat 

(MRID 42893201 ); decreased pre-mating body 

weight at 25 mg/kg/day 

Inhalation –creosote 

(short-, 

intermediate-, and 

long-term) 

NOAEL = 

0.0047mg/m3

MOE = 100 

90-day inhalation toxicity study with P2 creosote 

(MRID 43600901); decreased body weight and 

weight gain, altered hematology and clinical 

chemistry, increased absolute and relative weight of 

the liver and thyroid, and increased incidence of 

lesions of the nasal cavity at 0.048 mg/m3 

Inhalation –

naphthalene (short-, 

intermediate-, and 

long-term) 

LOAEL = 52 

mg/m3 MOE = 300 

Two year inhalation toxicity study in the mouse; 

National Toxicology Program (1992a), as cited in 

USEPA: IRIS Toxicological Review of naphthalene 

(1998), based on nasal lesions in the respiratory and 

olfactory epithelium at 52 mg/m3
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Exposure Scenario

Dose Used in 

Risk Assessment 

(mg/kg/day)

Target Margin of 

Exposure (MOE), 

Uncertainty Factor 

(UF), FQPA Safety 

Factor (SF)

Study and Toxicological Effects

Dermal absorption Absorption value of 5%, determined from the results of in vivo / in vitro testing in rats and in 

vitro testing using human skin (MRIDs 47179501 and 47179502). 

3.2 Dietary Exposure 

A dietary (food and drinking water) exposure assessment is not required for creosote at this time. 

The only Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA)-registered uses of 

creosote are as wood preservatives. These uses are not expected to result in direct or indirect 

dietary (food) exposure. The use of creosote as a wood preservative is not expected to result in 

exposures to creosote in drinking waters; therefore, a drinking water assessment is not required 

at this time. 

3.2.1 Food 

No dietary exposure is expected from the registered uses of creosote. Therefore, the agency does 

not anticipate the need to conduct a dietary exposure assessment for creosote. 

3.2.2 Drinking Water 

EPA does not anticipate the need to conduct a drinking water assessment because dietary 

exposure from drinking water is not expected to occur from the registered uses of creosote. 

PAHs in raw water will tend to adsorb to any particulate matter and be removed by filtration 

before reaching the tap. PAHs in tap water will mainly be due to the presence of PAHcontaining materials in water storage and distribution systems (EPA, Technical Factsheet on: 

Polycyclic Aromatic Hydrocarbons). 

3.3 Occupational and Residential Exposures 

The agency anticipates the need to revise the occupational assessment conducted in support of 

the 2008 RED. This is needed to account for new exposure monitoring studies required by the 

2011 post-RED DCI. As a restricted use pesticide, creosote is neither permitted to be purchased 

nor expected to be applied by potential residential users. Since no residential handler uses are 

expected from the use of creosote, a residential risk assessment is not required. Additionally, 

EPA will not be assessing residential post-application exposures. 

3.3.1 Occupational Handler Exposure 

The agency conducted an occupational assessment for the RED for creosote on September 5, 

2008 (EPA 2008c). The occupational assessment was based on doses for occupational wood 

pressure treatment workers using chemical-specific dermal and inhalation monitoring data 

submitted by the Creosote Council III (MRID 45323401). 
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As a result of the risks of concern identified in the RED, the agency identified label changes 

intended to reduce exposure to creosote workers in wood treatment facilities. In an effort to 

determine if those mitigation measures are effective in reducing exposure, the agency issued a 

post-RED DCI requiring that new exposure monitoring studies be conducted at wood treatment 

facilities using personal protective equipment (PPE) and engineering controls identified in the 

2008 RED. 

The agency recently received an observational protocol from the Creosote Council III for a wood 

pressure treatment dermal and inhalation study. The agency expects to receive the completed 

study during registration review that will help the agency to determine new exposures based on 

the new engineering control measures specified in the RED. The scenario outlined in Table 9 

include the typical worker exposure scenarios for a variety of job functions within a wood 

treatment facility. 

For example, for pressure treatment facilities, workers operate and monitor application system 

valves and controls, open and close cylinder doors, and supervise the insertion and removal of 

charges (loads of dried or debarked poles) of timber from the treatment cylinders. Workers 

operate forklifts used to load untreated wood onto charge trams; move charges into and out of 

treatment cylinders; remove charge leads and bands from treated wood; distribute treated wood 

to load-out area, and load treated wood for shipment. Workers also perform various labor and 

cleanup duties in treatment and drip pad area including: sweeping and pressure-washing drip pad 

and tracks; removing and shredding all bands from treated stacks of lumber; picking up and 

disposing treated wood waste; cleaning cylinders; and, handling hazardous waste (EPA 2008c). 

Table 9 – Occupational Handler Exposure Scenarios for Creosote

Scenario Exposure Route(s) Duration

Occupational Exposures 

Pressure Treatment Workers Dermal and Inhalation Short, Intermediate, and Long Term 

3.3.2 Occupational Post-Application Exposure 

There is potential exposure to linemen and other workers installing or repairing creosote treated 

utility poles. Railroad workers may also be exposed during the installation of railroad ties. 

Because mechanical installation (e.g. railroad ties) and/or the use of appropriate PPE are 

recommended to reduce exposure/contact with creosote treated wood (EPA 2008c), the agency 

does not anticipate the need to conduct an occupational post-application exposure assessment. 

3.3.3 Residential Handler Exposures 

Creosote, which is a restricted use pesticide, is neither permitted to be purchased nor expected to 

be applied by potential residential users. Therefore, residential exposure is not expected from the 

wood preservative uses of creosote and a residential risk assessment is not anticipated to be 

needed for this registration review. 
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3.3.4 Residential Post-Application Exposures 

There are no approved pesticide uses of creosote to treat wood for residential use. The agency 

recognizes that materials such as utility poles or railroad ties may be sold for reuse after their 

original intended use has ended. Railroad ties are used for fuel for co-generation plants and there 

would be no residential exposure for that particular use. However, railroad ties may resold for 

use in residential settings (e.g. landscaping). Such reuse of creosote-treated wood is not subject 

to regulation by EPA under FIFRA; however, landscape retaining walls are not expected to be 

areas of frequent contact, and any contact with landscaping timbers is expected to be episodic in 

nature. Additionally, old railroad ties would likely have significantly less transferable creosote 

than freshly treated wood (EPA. 2008c). As a result, the agency does not anticipate significant 

exposure to occur and will not conduct a residential post-application risk assessment. 

3.4 Aggregate and Cumulative Exposure 

3.4.1 Aggregate Exposures 

Creosote is not registered for any food use, and it was also determined that creosote is not likely 

to impact the diet or drinking water. Additionally, residential exposures are not expected. 

Therefore, an aggregate exposure and risk assessment is not anticipated to be needed for 

creosote.

3.4.2 Cumulative Exposures 

A cumulative exposure and risk assessment for creosote was not performed for the 2008 RED. 

EPA has not made a common mechanism of toxicity finding for creosote. Creosote is a complex 

mixture of chemical substances that may act by various mechanisms to produce toxicity. For the 

purposes of this registration review, therefore, EPA has not assumed that creosote has a common 

mechanism of toxicity with other substances. For information regarding EPA’s efforts to 

determine which chemicals have a common mechanism of toxicity and to evaluate the 

cumulative effects of such chemicals, see http://www.epa.gov/pesticides/cumulative/. 

4 Environmental Risk Assessment 

The ecological risk assessment planned during registration review will allow the agency to 

determine potential acute and chronic risks to aquatic organisms exposed to creosote and its’ 

degradates and impurities transported from antimicrobial use sites into the terrestrial and aquatic 

environments. The agency has not yet conducted a risk assessment that supports a complete 

endangered species determination for the antimicrobial uses of creosote. The registration review 

risk assessment will allow the agency to determine whether each use has 'no effect' or 'may 

affect' federally listed threatened or endangered species (listed species) or their designated 

critical habitats. When an assessment concludes that a pesticide’s use 'may affect' a listed species 

or its designated critical habitat, the agency will consult with the U.S. Fish and Wildlife Service 

and/or National Marine Fisheries Services (the Services), as appropriate. 

The agency conducted a preliminary environmental risk assessment for the 2008 RED (EPA 

2008 a,b). The uses assessed were railroad ties and aquatic structures. Because no guideline 
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ecotoxicity studies have been submitted, the assessment was based on the limited ecotoxicity 

data information available in the open literature. 

The 2008 risk assessment concluded that, although there are many PAHs in creosote, many occur 

only in minor amounts. The agency identified eight PAHs of potential concern in the aquatic 

environment from leaching of creosote-treated wood based on several factors including total 

amount of PAH, toxicity to aquatic organisms and detection in available monitoring data. 

Although the literature is not comprehensive for any of the eight PAHs for acute and chronic 

toxicity to freshwater and estuarine/marine fish, pelagic and benthic invertebrates, and aquatic 

plants, the agency concluded that there are potential risks to fish and invertebrates from the use 

of creosote-treated wood in aquatic and railroad structures. 

Further, based on findings from a field study in the Sooke Basin (Vancouver Bay, Canada), PAH 

accumulation in sediments may be sufficiently high to pose a risk to benthic organisms in the 

immediate vicinity of creosote-treated pilings for at least a year. Although survival and 

spawning were not affected, short-term adverse effects on growth of mussels were reported 

immediately around pilings at the Sooke Basin field site. One year after pilings were installed in 

Sooke Basin, an assemblage of invertebrate organisms inhabited the creosote-treated pilings, 

suggesting minimal long-term impacts to some non-listed species. 

Laboratory and field investigation found a major detrimental impact on hatching and 

development of fish (herring) eggs attached to aquatic pilings, even from pilings that were 40 

years old, suggesting that some sensitive species may be adversely affected by creosote-treated 

pilings. 

Impacts of creosote-treated aquatic pilings are likely to vary locally, depending on abiotic and 

biotic factors such as current speed, amount of structure per unit area, air and water temperature, 

salinity, and the aquatic species occurring in the immediate area of the structures. 

Creosote treated railroad structures are likely to have less direct impact than the treated aquatic 

structures, but there is the potential for movement of PAHs into the aquatic environment. 

4.1 Environmental Fate Assessment 

Creosote or the P1/P13 and P2 fractions of creosote are obtained from the carbonization of 

bituminous coal and are mixtures of organic molecules (about 200-250 identifiable substances) 

consisting of simple PAHs, multi-aromatic fused rings, cyclic nitrogen-containing heteronuclear 

compounds, and phenolic substances. It is estimated that about 85 percent of the creosote 

mixture consists of PAHs and the remainder consists of cyclic heteronuclear nitrogen and 

oxygen-containing molecules. Since the PAHs constitute the majority of the percent mass of 

creosote, they are the focus of this environmental fate assessment. 

Most of the PAHs are non-volatile; therefore, creosote normally does not contaminate the air. 

The major route of exposure is from PAHs leaching from treated wood into surrounding soil or 

water columns. 
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Degradation of the PAH components can occur by both abiotic and biotic mechanisms. PAHs do 

not undergo abiotic hydrolysis based on the chemical structure and the lack of hydrolyzable 

functional groups. However, PAHs can readily photodegrade in water because these compounds 

absorb UV light. Photooxidized products of PAHs can be stable and persist in air/water and soils 

and may become an environmental concern as these photooxidized products are also 

bioaccumulative (Kirso, 1991). 

Biotic degradation occurs more readily under aerobic conditions, therefore degradation will be 

slower in anaerobic sediments. Degradation also occurs more readily for the PAHs that have 

fewer rings (2- and 3- ring compounds) versus the 4- or 5-ring compounds (Karthikeyan and 

Bhandari, 2001, Bouwer et al., 1996, Chapman et al., 1995). 

The mobility of PAHs is dependent on the size of the individual compound. PAHs that have 

lower molecular weight are more mobile than those of higher molecular weight. However, even 

the lower molecular weight compounds have limited movement in soil (Villholth, 1999). PAH 

residues around treated wood (railroad ties, utility poles) are expected to be higher than those 

further from treated wood. In water, PAHs with more rings (e.g. acenaphthene) are more likely 

to sorb to sediment and bioconcentrate in aquatic organisms than those with fewer rings, 

including naphthalene, 1-methyl naphthalene, and 2-methyl naphthalene (Godsy et al., 1992). 

Leaching from treated wood tends to occur in the first 7 days and is higher under flooded 

conditions (Bestari et al., 1998a). For more information on the environmental fate of creosote, 

see Appendix B 

4.1.1 Water Quality 

The only PAH in creosote that is identified as a cause of water body impairment is naphthalene. 

Naphthalene is identified as a cause of impairment for two streams in New Hampshire, one 

stream in Washington State, and one stream in Virginia under section 303(d) of the Clean Water 

Act.2 However, no Total Maximum Daily Loads (TMDL) have been developed for creosote as a 

mixture.3

 More information on impaired water bodies and TMDLs can be found at EPA’s 

website.4 

4.2 Environmental Exposure Pathways 

PAHs leaching from treated wood are the primary source of environmental exposure to nontarget 

organisms. PAHs may leach into the soil surrounding treated railroad ties and other treated 

wood and might be transported into the aquatic environment via various environmental 

pathways, including runoff and leaching. Creosote-treated wood used directly in the aquatic 

environment will leach PAHs directly into surface waters and sediments. Heavier PAHs 

reaching the aquatic environments are expected to bind to organic matter and sediments and 

 

2 http://iaspub.epa.gov/tmdl_waters10/attains_nation_cy.cause_detail_303d?p_cause_group_id=885

3

http://iaspub.epa.gov/tmdl_waters10/attains_nation.tmdl_pollutant_detail?p_pollutant_group_id=885&p_pollutant_

group_name=PESTICIDES

4 http://www.epa.gov/owow/tmdl/
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potentially expose benthic invertebrates. Lighter PAHs will mostly occur in the water column 

and may potentially expose fish, aquatic invertebrates, and aquatic plants to those PAHs. 

Based on antimicrobial use patterns, the agency developed conceptual models (CMDs) depicting 

potential routes of environmental exposure to terrestrial and aquatic receptor groups. The 

“Conceptual Models for Environmental Exposure Pathways of Antimicrobial Pesticides” are 

located in the docket at www.regulations.gov (EPA-HQ-OPP-2014-0638-0002). For “In‐Use 

Service of Wood Treated Wood Products” see page 29 in that document. 

4.3 Ecological Effects Analysis 

4.3.1 Available Ecotoxicity Endpoints 

Ecotoxicity studies conducted in accordance with the 850 OCSPP Harmonized Test Guidelines 

to address the data requirements for pesticide registration are not currently available for creosote. 

Some supplemental data are available in the OPP Ecotoxicity Database for creosote. The 

anticipated ecotoxicity data requirements for creosote are specified in more detail in Appendix C 

. Available endpoints, and data gaps for each receptor group, are listed below. For a complete 

list of the ecotoxicity data anticipated to be required in registration review, see Table 6. 

Table 10 – Available Creosote Ecological Effects Endpoints

Receptor 

Group 

Test 

Material

Risk 

Scenario Toxicity Endpoint Reference 

Freshwater fish TGAI Acute LC50 = 570 μg ai/L TN 24011

Chronic Data gap -- 

Freshwater invertebrates TGAI Acute EC50 = 76 μg ai/L TN 23921

Chronic Data gap -- 

Freshwater benthic 

invertebrates TGAI Chronic Data gap -- 

Estuarine/marine fish TGAI Acute LC50 = 720 μg ai/L 402284011

Chronic Data gap -- 

Estuarine/marine 

invertebrates TGAI Acute EC50 = 18 μg ai/L 402284011

Chronic Data gap -- 

Estuarine/marine benthic 

invertebrates TGAI Chronic Data gap -- 

Algae TGAI 

EC50

NOAEC Data gap -- 

Aquatic vascular plants TGAI EC50

NOAEC Data gap -- 

Semi-aquatic plants TGAI EC50

NOAEC Data gap -- 

Birds TGAI Acute Data gap -- 

Dietary Data gap -- 
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Nontarget insects TGAI Acute Data gap -- 

1

These studies are considered supplemental. Data are anticipated to be required.

4.3.2 Open literature 

Open literature studies also will be identified through EPA’s ECOTOXicology (ECOTOX) 

database. The ECOTOX database will be searched when the risk assessment is prepared. Any 

acute or chronic endpoints more sensitive than what is currently available will be used in the risk 

assessment and risk characterization. Information on the agency’s use of open literature is found 

on the agency’s website: 

http://www.epa.gov/pesticides/science/efed/policy_guidance/team_authors/endangered_species_

reregistration_workgroup/esa_evaluation_open_literature.htm. 

4.4 Exposure Analysis Plan 

4.4.1 Aquatic and Terrestrial Wildlife Exposure Estimates 

Available models will be used to determine the estimated environmental concentration (EECs) in 

the aquatic environment. Resulting exposure estimates will be compared to the toxicity endpoints 

to determine if levels of concern are exceeded for each receptor group. 

4.4.2 Screening Level Down-the-Drain Analysis 

The agency does not anticipate the need for a Down-the-Drain (DtD) assessment because the 

creosote treated wood at the site of the treatment is dried with a drain pad underneath and any 

leaked chemical is recycled for use. Remaining chemical in the pad (if any) must be treated as a 

hazardous waste and disposal (if any) must be conducted according to a state pesticide or 

environmental control agency, or by guidance from a hazardous waste representative. 

5 Endocrine Disruptor Screening Program (EDSP) 

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

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

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

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

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

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

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

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

taxonomic groups. As part of the 2008 RED for creosote, EPA reviewed these data and selected 

the most sensitive endpoints for relevant risk assessment scenarios from the existing hazard 

database. However, as required by FFDCA section 408(p), creosote is subject to the endocrine 

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

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

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

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

may designate.” The EDSP employs a two-tiered approach to making the statutorily required 
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determinations. Tier 1 consists of a battery of 11 screening assays to identify the potential of a 

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

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

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

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

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

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

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

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

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

identified for EDSP screening was published on June 14, 20135

 and includes some pesticides 

scheduled for registration review and chemicals found in water. Neither of these lists should be 

construed as a list of known or likely endocrine disruptors. 

For further information on the status of the EDSP, the policies and procedures, the lists of 

chemicals, future lists, the test guidelines and the Tier 1 screening battery, please visit our 

website.6

6 Optional Label Changes 

The agency invites comment on any label amendments that could be considered to eliminate the 

anticipated need for EPA to require certain data, reduce the possibility that EPA’s planned risk 

assessments overestimate risk due to reliance on conservative assumptions, and/or improve label 

clarity. 

7 Guidance for Commenters 

7.1 Preliminary Work Plan 

The public is invited to comment on EPA’s Preliminary Work Plan and rationale. The agency 

will carefully consider all comments as well as any additional information or data provided in a 

timely manner prior to issuing a final work plan for the creosote registration review case. 

7.1.1 Trade Irritants 

Through the registration review process, the agency intends to solicit information on trade 

irritants and, to the extent feasible, take steps toward facilitating irritant resolution. The agency 

will work to harmonize tolerances and international maximum residue limits (MRLs) and may 

modify tolerance levels to do so, when possible. Stakeholders are asked to comment on any 

trade irritant issues resulting from lack of MRLs or disparities between U.S. tolerances and 

 

5

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

chemicals. 6

 http://www.epa.gov/endo/ 
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MRLs in key export markets, providing as much specificity as possible regarding the nature of 

the concern. 

7.1.2 Water Quality 

The agency invites submission of water quality data for this pesticide. To the extent possible, 

data should conform to the quality standards in Appendix A of the OPP Standard Operating 

Procedure: Inclusion of Impaired Water Body and Other Water Quality Data in OPP’s 

Registration Review Risk Assessment and Management Process7 in order to ensure they can be 

used quantitatively or qualitatively in pesticide risk assessments. 

7.1.3 Environmental Justice 

EPA seeks to achieve environmental justice, the fair treatment and meaningful involvement of all 

people, regardless of race, color, national origin, or income, in the development, implementation, 

and enforcement of environmental laws, regulations, and policies. To help address potential 

environmental justice issues, the agency seeks information on any groups or segments of the 

population who, as a result of their location, cultural practices, or other factors, may have 

atypical, unusually high exposure to creosote compared to the general population. Please 

comment if you are aware of any sub-populations that may have atypical, unusually high 

exposure compared to the general population.

7.1.4 Additional Information 

Stakeholders are also specifically asked to provide available information and data that will assist 

the agency in refining its risk assessments, including any species-specific ecological effects 

determinations. 

As mentioned in Section 1.5, the agency determined in the 2008 RED that creosote products 

contribute benefits to society and were eligible for reregistration. In registration review, EPA 

plans to update the benefits and alternatives assessments for creosote. Stakeholders are 

encouraged to provide updated information on benefits and alternatives during the PWP 

comment period. 

The agency is interested in receiving the following information: 

1. Confirmation on the following label information: 

A. Sites of application 

B. Geographic limitations on use 

2. Use or potential use distribution 

3. State or local use restrictions 

4. Ecological incidents (non-target plant damage and avian, fish, reptilian, amphibian and 

mammalian mortalities) not already reported to the agency 

5. Monitoring data 

 

7 http://www.epa.gov/oppsrrd1/registration_review/water_quality_sop.htm
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8 Next Steps 

After the 60-day comment period closes in May 2015, the agency will review and respond to any 

comments received in a timely manner, and then issue a Final Work Plan for the creosote case. 

 
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9 References 

Bestari, K.T. Jim et al. 1998a. Distribution and composition of polycyclic aromatic 

hydrocarbons within experimental microcosms treated with liquid creosote. Environ. 

Toxicol. Chem. 17(12):2359-2368. 

Bouwer, E.J. et al. 1996. Annals of New York Academy of Sciences. pp. 103-115. 

Chapman, P.J. et al. 1995. Fossil Fuel Biodegradation: Laboratory Studies. Environ. Health 

Perspec. 103, Supplemental 5:80-83. 

EPA 2002. ECOTOX User Guide: ECOTOXicology Database System. Version 3.0. Available: 

http://www.epa.gov/ecotox/ 

EPA. 2008a. Updated Ecological Risk Assessment for Creosote. W. Erickson, AD/RASSB, 

March 27, 2008. 

EPA. 2008b. Reregistration Eligibility Decision for Creosote (Case 0139). EPA 739-R-08-007. 

EPA. 2008c. Creosote Occupational/Residential Exposure Assessment. PC Codes 022003, 025003, 

and 025004, Case 0139, Antimicrobials Division, 9/5/2008, Timothy Leighton, Ph.D. 

EPA. 2008d. Epidemiology and Incidents Reports Associated with Creosote. Cases 0139, 

Antimicrobials Division, 3/9/08. 

EPA. Technical Factsheet on: Polycyclic Aromatic Hydrocarbons (PAHs). 

http://www.epa.gov/ogwdw/pdfs/factsheets/soc/tech/pahs.pdf 

Godsy, E.M. et al. 1992. Ground Water. 30(2):232-242. 

Karthikeyan, R. and A. Bhandari. 2001. Anaerobic biotransformation of aromatic and 

polycyclic aromatic hydrocarbons in soil microcosms: a review. Journal of Hazardous 

Substance Research. 3:3-19. 

Kirso, U. et al. 1991. Photochemical oxidation of PAH and heteroaromatic analogues in 

different model conditions. Polycyclic Aromatic Hydrocarbons: Proceedings of the 

Thirteenth International Symposium on Polynuclear Aromatic Hydrocarbons. 

Kline, 2005. Specialty Biocides North America 2004-2005, Volume II: United States, Kline and 

Company, Inc. 

Villholth, K.G. 1999. Colloid characterization and colloidal phase partitioning of polycyclic 

aromatic hydrocarbons in two creosote-contaminated aquifers in Denmark. Environ. Sci. 

Technol. 33:691-699. 
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Appendix A Toxicology Profile 

The agency anticipates the need to require immunotoxicology data for creosote. 

Acute Toxicity for Product Labeling 

Acute toxicity studies available for labeling purposes have been summarized in Tables A1 and 

A2 for the two creosote blends: P1/P13 and P2. 

Table A1 – Acute Toxicity Studies for Creosote P1/P13 blend 

Guideline No./ Study 

Type MRID No. Results Toxicity Category

870.1100/ 

Acute oral toxicity 43032101 LD50 male= 2451 mg/kg; female = 1893 mg/kg III

870.1200/ 

Acute dermal toxicity 43032102 LD50 male and female: > 2000 mg/kg III

870.1300/ 

Acute inhalation toxicity 43032103 LC50 > 5 mg/L IV 

870.2400/ 

Acute eye irritation 43032104 Irritation clearing in 8-21 days II 

870.2500/ 

Acute dermal irritation 43032105 Erythema to day 14 III 

870.2600/ 

Skin sensitization 43032106 Study unacceptable* Y 

*Even though dermal sensitization studies were unacceptable, it is assumed that both blends are dermal sensitizers. 

Table A2 – Acute Toxicity Studies for Creosote P2 blend

Guideline No./ Study 

Type MRID No. Results Toxicity Category

870.1100/ 

Acute oral toxicity 43032301 LD50 male= 2524 mg/kg; female = 1993 mg/kg III

870.1200/ 

Acute dermal toxicity 43032302 LD50 male and female: > 2000 mg/kg III

870.1300/ 

Acute inhalation toxicity 43032303 LC50 > 5.3 mg/L IV 

870.2400/ 

Acute eye irritation 43032304 Irritation clearing within 7 days III 

870.2500/ 

Acute dermal irritation 43032305 No irritation after 7 days III 

870.2600/ 

Skin sensitization 43032306 Study unacceptable* Y 

*Even though dermal sensitization studies were unacceptable, it is assumed that both blends are dermal sensitizers.
Page 28 of 54

Subchronic Toxicity 

There are dermal subchronic (90-day) toxicity studies for the P1/P13 (MRID 43616101) and P2 

(MRID 43616201) blends of creosote. These studies are summarized below. 

90-Day Dermal Toxicity Studies 

Executive Summary (P1/P13 blend): In a 90-day dermal toxicity study (MRID # 43616101), 10 

Charles River Crl:CD BR rats (10/sex/dose) were given dermal applications of P1/P13 creosote 

in corn oil mixture at dosage levels of 0, 4, 40 or 400 mg/kg bw/day. There were no treatmentrelated effects from dermal application of P1/P13 creosote on body weight, food consumption, 

ophthalmology, hematology, clinical chemistry, or organ weights at any dose level tested. 

Mortality (death of one male rat at 400 mg/kg/day) was observed on day 79 of the study. No testarticle related microscpoic lesions were noted at the application site on the skin at any dose level. 

Based on the results of this study, the systemic LOAEL was determined to be 400 mg/kg bw/day 

for both male and female rats, based on mortality. The systemic NOAEL was determined to be 

40 mg/kg/day. 

This study is classified as acceptable and satisfies the guideline requirement (OCSPP 870.3250) 

for a subchronic dermal toxicity study in rats for P1/P13 creosote. No additional data are 

anticipated to be required. 

Executive Summary (P2 blend): In a 90-day dermal toxicity study (MRID # 43616201), Charles 

River rats ( 10/sex/dose) were given dermal applications of P2 creosote in corn oil at dosage 

levels of 0, 4, 40 or 400 mg/kg bw/day. There was no mortality observed in this study at any 

dose level. Body weight in high dose males was decreased 7-8% during weeks 9-12 of the study, 

and bodyweight gain decreased 15% in high dose males for the treatment period. Food 

consumption in high dose males was decreased during weeks 2-4 and week 6 by 4-10% vs 

control. Only slight dermal irritation was observed in high dose males. No effects were observed 

on hematology or clinical chemistry. Treated skin in the 400 mg/kg/day dose groups (male and 

female) was observed with increased incidence of dermal inflammation. Based on the results of 

this study, the systemic LOAEL is 400 mg/kg/day, based on decreased body weight gain in male 

rats. The systemic NOAEL is 40 mg/kg/day. For females, the NOAEL is set at 400 mg/kg 

bw/day since no systemic toxic effects were noted in any of the treated groups. 

This study is classified as acceptable and satisfies the guideline requirement (OCSPP 870.3250) 

for a subchronic dermal toxicity study in rats for P2 creosote. No additional data are anticipated 

to be required. 

90-Day Inhalation Toxicity Studies 

There are 90-day inhalation toxicity studies available for the P1/P13 blend (MRID 43601001) 

and P2 blend (MRID 43600901). These studies are summarized below. 

Executive Summary (P1/P13 blend): In a subchronic inhalation toxicity study with P1/P13 

creosote (MRID # 43601001), 20 Sprague-Dawley rats/sex/group were treated for thirteen 

weeks, five days a week, six hours per day with P1/P13 Creosote CTM via whole body exposure 
Page 29 of 54

at doses of 0, 5.4, 49 and 106 mg/m3

 (0.005, 0.049 and 0.106 mg/L in air, respectively) measured 

gravimetrically. The aerosol MMAD was between 2.2 and 3.0 microns with a geometric 

standard deviation between 1.91 and 1.99. Subsequent to the exposure period 10 

animals/sex/group were allowed to recover for 6 weeks. During the study one male rat of the 

mid dose group (49 mg/m3) died from myocardial degeneration that resulted in heart failure. 

One male and one female rat in the highest dose group had similar lesions observed at terminal 

necropsy. Cardiac pathology (ie: hemorrhage, lymphocytic infiltration and cardiomyopathy) was 

noted in all animals of all groups (including controls) and this condition may have been 

exacerbated by treatment with creosote in the mid and high dose animals. Significant treatmentrelated findings in the mid and high dose animals after the exposure period included decreased 

body weight gains of both sexes (resolved by the end of recovery period), altered hematological 

parameters (decreased hemoglobin, hematocrit, numbers of erythrocytes, increased numbers of 

reticulocytes, polychromasia, poikilocytosis, anisocytosis -both sexes) and biochemical 

parameters (increased serum cholesterol levels - both sexes, phosphorous levels - males only). 

Macroscopic discolouration of the lungs, which persisted throughout the recovery period, was 

correlated with the presence of black pigment granules within alveolar macrophages of animals 

of all treatment groups. An increase in liver/brain weights (statistically significant only in the 

females), increased lung/trachea/body weight ratios and the presence of small cystic spaces 

containing basophilic mucoid material in the nasal cavity epithelium was still evident after the 

recovery period in both sexes. 

Male and female rats of the low dose group were observed to have mild poikilocytosis and 

anisocytosis while the females only showed the occasional cyst of the epithelium in the nasal 

cavity. All hematological findings in low dose animals showed recovery. 

Based on the results of this study, the systemic LOAEL is 49 mg/m 3

 for both sexes, based on 

cardiac pathology, decreased body weight gain, altered hematology and clinical chemistry, and 

gross pathological findings in the lungs. The systemic NOAEL is 5.4 mg/m3 (0.005 mg/L) for 

P1/P13. 

This study is classified as acceptable (guideline) and satisfies the guideline requirement (OCSPP 

870.3465) for a subchronic inhalation toxicity study in rats. No additional data are anticipated to 

be required. 

Executive Summary (P2 blend): In a 13-week inhalation toxicity study (MRID # 43600901), 20 

Sprague-Dawley rats/sex/group were treated for 5 days/week, 6 hours/day with P2 Creosote 

CTM via whole body exposure at doses of 0, 4.7, 48 or 102 mg/m3

 (0, 0.005, 0.048 or 0.102 

mg/L ) in air measured gravimetrically. The aerosol size MMAD was between 2.4 and 2.9 

microns with a geometric standard deviation between 1.85 and 1.91. Subsequent to the exposure 

period 10 rats/sex/group were allowed to recover from treatment for 6 weeks. 

During the exposure period, two animals (low dose female; mid dose male) were sacrificed in 

extremis and the cause of morbidity was not related to treatment. Significant treatment-related 

findings in mid and high dose animals included decreased terminal body weight and body weight 

gain (m/f), altered hematological parameters (decreased hemoglobin content, hematocrit, 

erythrocyte and platelet counts; increased reticulocyte counts and mild poikilocytosis, m/f) and 

biochemical parameters (increased serum cholesterol levels, m/f). In both sexes macroscopic 
Page 30 of 54

discolouration of the lungs persisted through the recovery period and correlated with the 

presence of black pigment granules within alveolar macrophages. Both sexes showed increased 

absolute and relative liver and thyroid weights and increased lung/trachea/body weight ratios. 

Absolute and relative thyroid weights of high dose animals actually increased after the recovery 

period. An increased incidence of lesions of the nasal cavity epithelium (chronic inflammation) 

was noted following treatment (all treatment groups, m/f) but appeared to lessen in incidence and 

severity during the recovery period (mainly the high dose group, m/f). During exposure an 

increased incidence of thyroid follicular epithelial cell hypertrophy occurred in all male groups 

including control and in the high dose female group. At recovery the male incidence remained 

similar to that observed at exposure while the incidence in females of the high dose group had 

declined. The incidence of thyroid follicular cell hypertrophy was slightly increased in low and 

mid dose females after the recovery period. Slightly increased incidence of mild poikilocytosis 

was observed in all treatment groups (m/f) including the low dose group and control, which 

persisted through the recovery period. Low dose animals exhibited lesions of the nasal cavity 

epithelium which had resolved after the recovery period. Based on the results of this study, the 

systemic LOAEL is 48 mg/m3

, based on decreased body weight and weight gain, altered 

hematology and clinical chemistry, increased absolute and relative weight of the liver and 

thyroid, and increased incidence of lesions of the nasal cavity. The systemic NOAEL is set at 

4.7 mg/m3 (0.0047mg/L ) for P2 Creosote CTM in rats. 

This study is classified as acceptable (guideline) and satisfies the guideline requirement (OCSPP 

870.3465) for a subchronic inhalation toxicity study in rats for P2 creosote. No additional data 

are anticipated to be required. 

Developmental Toxicity 

There are developmental toxicity studies available for the P1/P13 blend (MRID 43584201 and 

MRID 44839802) and the P2 blend (MRID 43584202). These studies are summarized below. 

Executive Summary (P1/P13 blend): In a developmental toxicity study using P1/P13 creosote 

(MRID # 43584201), pregnant female Sprague-Dawley rats (30/dose) were administered P1/P13 

creosote at dose levels of 0, 25, 50, and 175 mg/kg/day on gestation days 6 through 15 inclusive. 

Decreased body weight and food consumption were observed in dams at the 175 mg/kg/day dose 

level. Decreased uterine weight was observed in dams at the high dose, which is reflected partly 

by the decreased live fetuses per litter at the high dose (although mean fetal weight was not 

affected). Cesarean section observations showed significantly increased resorptions and postimplantation loss as well as decreased number of live fetuses per litter at the 175 mg/kg/day 

dose. Based on the results of this study, the maternal NOAEL is 50 mg/kg/day, and the maternal 

LOAEL is 175 mg/kg/day, based on decreased body weight gain and food consumption during 

the study. 

No treatment-related malformations (external, visceral or skeletal) were observed in any of the 

fetuses at 25 mg/kg bw/day. At 50 mg/kg bw/day, the overall incidence of malformations on a 

fetal and litter basis were statistically elevated compared to controls. However, these individual 

malformations were not seen at higher dose levels and/or fell within the range of historical 

control data. At 175 mg/kg/day there was (i) an overall significant increased incidence of 

developmental malformations, (ii) increased incidence of cardiovascular, vertebral and digital 
Page 31 of 54

malformations, compared to lower dose levels, concurrent controls or historical controls (2429 

and 2898 fetuses examined viscerally and skeletally respectively) and (iii) an increased incidence 

of malformations at this dose level in spite of increased fetal loss (resorptions) (Beck and Lloyd, 

1963) thus resulting in fewer fetuses available for teratogenic examination. Although the 

incidence of fetal malformations observed at 175 mg/kg/day dose level in rats was low and could 

be related to maternal stress (decreased body weight gain and food consumption), the teratogenic 

potential of P1/P13 Creosote cannot be ruled out. Based on these data, the developmental 

toxicity NOAEL is 50 mg/kg/day, and the developmental toxicity LOAEL is 175 mg/kg/day, 

based on increased post-implantation loss, increased mean resorptions, decreased live fetuses per 

litter, and increased developmental malformations. 

In a developmental toxicity study in rabbits (MRID 44839802), artificially inseminated New 

Zealand White Rabbits (20/dose) were administered creosote P1/P13 in corn oil by gavage on 

gestation days 6 through 18. Doses were 0, 1, 9, and 75 mg/kg/day. At the 75 mg/kg/day dose 

level, increased abortions (3 rabbits vs. 0 control), reduced live fetuses (28 vs. 50 in control), and 

decreased implantation sites were noted in maternal rabbits. There was no significant effect of 

creosote P1/P13 treatment on offspring in this study. The Maternal NOAEL in this study is 

determined to be 9 mg/kg/day based on effects noted at 75 mg/kg/day. The Developmental 

NOAEL is determined to be 75 mg/kg/day, and the LOAEL > 75 mg/kg/day.

This study is classified as acceptable and satisfies the guideline requirement (83-3) for a 

developmental toxicity study in rats with P1/P13 creosote. No additional data are anticipated to 

be required.

Executive Summary (P2 blend): In a developmental toxicity study (MRID # 43584202), 

pregnant female Sprague-Dawley rats (30/dose) were administered P2 creosote by gavage on 

gestation days 6 through 15 inclusive at dose levels of 0, 25, 75, and 225 mg/kg/day. Although 

decreases in body weight and food consumption were observed at all dose levels, food efficiency 

appeared affected only at the high dose of 225 mg/kg/day. Thus, the cesarean section effects 

observed at this dose (decreased implantations/dam, increased pre- and post-implantation loss, 

increased resorptions, decreased uterine weight) could be secondary to the decreased food 

efficiency observed at this dose. This distinction is a fine one, however, based on results with 

P1/P13 creosote in which no decrease in food efficiency was observed at a dose of 175 mg/kg, 

but increased resorptions, increased post-implantation loss, and decreased live fetuses per litter 

were observed at 175 mg/kg. The Maternal NOAEL in this study is determined to be 75 

mg/kg/day, and the LOAEL 225 mg/kg/day, based on decreased food efficiency observed in 

maternal rats at 225 mg/kg/day. 

With regards to assessing the teratogenic potential of P2 Creosote in rats, no treatment-related 

malformations (external, visceral or skeletal) were observed at the 25 mg/kg bw/day dose level. 

The single incidences of malformations [craniorachischisis, hydrocephaly and malpositioned eye 

(same pup)] observed at the 75 mg/kg bw/day dose level, and hydrocephaly at the 225 mg/kg 

bw/day dose level compared to none observed in lower dose levels, concurrent controls or 

historical controls (2429 and 2898 fetuses examined viscerally and skeletally respectively) were 

considered treatment-related. It should be noted that at 225 mg/kg bw/day one whole litter was 

resorbed and the number of fetuses examined at this level for visceral and skeletal malformations 

was approximately 50% of those examined at the mid-dose level. The developmental toxicity 
Page 32 of 54

NOAEL is determined to be 25 mg/kg/day in this study, based on the incidences of 

malformations observed at 75 mg/kg/day which exceeded both concurrent and historical control 

incidence. 

This study is classified as acceptable and satisfies the guideline requirement (83-3) for a 

developmental toxicity study in rats with P2 creosote. No additional data are anticipated to be 

required. 

Reproductive Toxicity 

There is one study available for reproductive toxicity of the P1/P13 creosote blend (MRID 

42893201). This study is summarized below. Based on the available data showing similarity in 

toxicity between the P1/P13 and P2 blends, a reproductive study with P2 creosote is not 

anticipated to be needed. 

Executive Summary (P1/P13 blend): In a two-generation reproduction toxicity study (MRID 

42893201), Charles River Crl:CD rats, 26/sex/group, were dosed by gavage with P1/P13 

creosote in corn oil at doses of 0, 25, 75, and 150 mg/kg/day. Pre-mating treatment phase lasted 

approximately 17 weeks, which may have contributed to the decreased fertility observed in this 

study. Systemic effects observed in this study for parental animals included a dose-related 

decrease in body weight during the pre-mating period at all dose levels. Salivation was observed 

at 75 mg/kg/day and above in the F1 generation. Effects in offspring included a dose-related 

decrease in growth of the F0 generation starting at 25 mg/kg/day (as shown by decreased pup 

weight). For the F0 pups, mean number of live pups per litter was decreased at 75 and 150 

mg/kg/day, and percent live pups at 175 mg/kg/day was also decreased. In the F1 pups, the 

percent live pups was decreased at 75 and 150 mg/kg/day, but pup growth was affected only at 

150 mg/kg/day as shown by decreased mean pup weight. Decreased fertility and pregnancy 

indices were observed in the F1 female parental rats at all dose levels, but this was not 

interpreted as a treatment-related effect, as it was more likely related to the fact that the critical 

weight for fertility was exceeded by the 17-week pre-mating interval. Based on the results of 

this study, the Parental Systemic NOAEL is < 25 mg/kg/day, and the parental systemic LOAEL 

is 25 mg/kg/day, based on decreased pre-mating body weight. The developmental NOAEL in 

this study is < 25 mg/kg/day, and the developmental LOAEL is 25 mg/kg/day, based on a doserelated decrease in pup body weight for the F0 pups from days 14-21. The reproductive NOAEL 

is < 25 mg/kg/day, and the reproductive LOAEL is 25 mg/kg/day, based on reduced pregnancy 

and fertility indices in F1 female parental rats. 

This study is classified as acceptable and satisfies the guideline requirement (870.3800) for a 

developmental toxicity study in rats with P1/P13 creosote. No additional data are anticipated to 

be required. 

Chronic Toxicity/Carcinogenicity 

The chronic toxicity/carcinogenicity data base submitted to the agency for creosote consists of a 

six-month initiation/promotion study of creosote conducted in mice (MRID 44844401), and a 

published study by Culp et al. (1998). The six month initiation/promotion study was not 

designed for purposes of deriving a quantitative risk estimate of carcinogenic potency. The 
Page 33 of 54

study of Culp et al. (1998) did examine tumors induced by coal tar mixtures and was ued for 

quantitative cancer assessment 

Executive Summary (P1/P13 blend): In a submitted dermal carcinogenicity study (MRID 

44844401), North American P1/P13 creosote composite (100.0%, lot no. P1/13-009-A) was 

administered to groups of 30 male Crl:CD-1® mice by applying 50 μL aliquots of 1%, 50% or 

100% corresponding to 10 μg/μL, 500 μg/μL, or undiluted creosote to the shaved backs of the 

mice. Acetone was utilized as a solvent throughout the study and was used as the solvent 

control. 9,10-Dimethyl-1,2-benzanthracene (DMBA) was utilized as a tumor initiator, and 12-0-

tetradecanoylphorbol-13-acetate (TPA) was used as a tumor promoter in the study. Creosote was 

tested as a tumor initiator with TPA as promotor, as a promotor with DMBA as initiator, and as 

both initiator and promotor (complete carcinogen). A positive control group with DMBA and 

TPA, and acetone controls groups with DMBA and TPA were included. The initiation phase 

consisted of 5 applications/week for 2 weeks followed by a two week rest period, and then 

promotion (2 applications/week for 26 weeks). 

Creosote treatment at 50% and 100% especially during the promotion phase caused skin irritation and clinical signs including severe erythema, slight edema, eschar, and exfoliation. 

Increased incidences of thickened skin (7-11/30, p < 0.01), scabbing (16-20/30, p < 0.01), acute 

inflammation (12-18/30, p < 0.01), ulceration (6-10/30, p < 0.05-0.01), and epithelial hyperplasia 

(13-23/30, p < 0.01) were seen at the application site during necropsy compared to the 

DMBA/acetone controls (0/30). Dermal treatment with creosote did not result in a significant 

decrease in survival, although 6 mice died during treatment in the DMBA/100% creosote group 

compared to none in the acetone control groups. Group mean body weights of males treated 

with 100% creosote during the initiation phase were decreased by 6-8% by the end of the 2-week 

treatment regimen; however, they gained weight rapidly over the next week and no further 

decreases in weight or weight gain were seen with creosote treatment compared to the acetone 

controls. Food consumption in the experimental groups was generally greater than in the solvent 

control groups. 

Increased incidences of enlarged lymph nodes were seen with 50% (6/30, p < 0.05), and 100% 

creosote (5-9/30, p < 0.05-0.01) during the promotion phase with DMBA as initiator and with 

100% creosote as both initiator and promotor (6-9/30, p < 0.05-0.01) compared to 0/30 in the 

solvent controls. Incidences of enlarged spleen were also increased (15-19/30, p < 0.01) with 

50% and 100% creosote in the promotion phase compared to the controls (1/30). 

The LOAEL is 50 μL of 50% or 25,000 μg/day twice/week applied to the skin for 26 weeks, 

based on skin toxicity, enlarged lymph nodes and enlarged spleen. The NOAEL was 50 μL of 

1% or 500 μg/day applied to the skin twice/week for 26 weeks. 

Topical treatment of male Crl:CD-1® mice for 2 weeks in the initiation phase of the study with 

all concentrations of creosote followed by treatment with TPA resulted in increased incidences 

of neoplasms, chiefly skin papillomas (acetone/TPA control, 0%; creosote/TPA treated, 80-90%, 

p < 0.01). Treatment twice a week for 26 weeks during the promotion phase with 50 μL of 

500μg/μL or undiluted creosote following the DMBA initiation phase resulted in tumor 

incidences of 100% compared to 3% in the DMBA/acetone control. Topical treatment with 

undiluted creosote in both the initiation and promotion phases resulted in a 100% tumor 
Page 34 of 54

incidence compared to 0% in the acetone control group. Creosote acted as an initiator, promoter, 

and complete carcinogen under the conditions of this study. 

This carcinogenicity study in the mouse is acceptable/nonguideline. The study had numerous 

deficiencies that limited the information obtainable on possible systemic toxic effects, but the 

data demonstrated unequivocally the oncogenic nature of creosote when applied to the skin of 

Crl CD-1® mice. The deficiencies did not affect this outcome of the study, which was designed 

to assess the skin tumor initiating, promoting, and complete carcinogenicity of creosote. 

Executive Summary (two coal tar mixtures and pure benzo[a]pyrene (BaP)): In an oral 

carcinogenicity study conducted by Culp et al. (1998), the carcinogenicity of two coal tar 

mixtures and pure benzo[a]pyrene (BaP) was studied. Coal tar mixture 1 (CTM-1) was a 

composite of coal tar samples from seven coal gasification plant waste sites and was dosed at 

0.0, 0.01, 0.03, 0.1, 0.3, 0.6, and 1.0% of diet. Coal tar mixture 2 (CTM-2) was a composite of 

coal tars from three waste sites with high BaP content and was dosed at 0.0, 0.01, 0.03, 0.1, 0.3% 

of diet. An additional group was dosed with pure BaP at 0, 0.0005, 0.0025, and 0.01 % in diet. 

A control group received solvent control in diet. Each group consisted of 48 mice. 

In mice exposed to coal tar, coal tar acted as a systemic carcinogen and induced a dose-related 

increase in hepatocellular adenomas and carcinomas, alveolar/bronchiolar adenomas and 

carcinomas, forestomach squamous epithelial papillomas and carcinomas, small intestine 

adenocarcinomas, histiocytic sarcomas, hemangiosarcomas in multiple organs, and sarcomas in 

several tissues. 

The incidence of forestomach tumors increased sharply between the 0.1 and 0.3% doses. 

However, there was not a proportional increase in forestomach tumors above 0.3% because these 

mice died from adenocarcinomas of the small intestine. Tumors of the esophagus, observed in 

BaP treated mice, were not observed in the CTM1 or CTM-2 treated groups. Lung and 

hepatocellular tumors observed in the CTM1 and CTM2 groups were not observed in BaP 

treated animals. 

Multiple neoplasms were noted in liver, lung, forestomach, and the small intestines of exposed 

mice. Liver neoplasms occurred in 1, 0, and 4 mice fed 0.03, 0.1 and 0.3% CTM-1, respectively. 

Lung neoplasms occurred in 21, 11 and 13 mice fed 0.3%, 0.6%, 1.0% CTM-1, respectively. 

Eight mice in the 0.3% CTM-2 group had multiple lung neoplasms. Forestomach carcinomas 

were found in 2 and 1 mice fed 0.6% or 1.0% CTM-1, respectively. Adenocarcinomas were 

found in the small intestines (jejunum) of 2 and 12 mice fed 0.6% and 1.0% CTM-1, 

respectively. Groups dosed with 0.3% CTM-1 or CTM-2 had significantly reduced survival. 

In those mice exposed to benzo(a)pyrene, BaP appeared to act as a point-of-contact carcinogen, 

causing an increased incidence of papillomas and/or carcinomas of the forestomach, esophagus 

and tongue. The incidence of forestomach tumors increased steeply between 5 and 25 ppm, 

equivalent to 20.5 and 104 μg BaP/day. Tumors of the esophagus were not observed in the 

CTM1 or CTM-2 treated groups. Lung and hepatocellular tumors, observed in CTM treated 

mice, were not observed in mice fed BaP. 

Multiple neoplasms of the forestomach occurred in 8 and 21 mice fed 25 and 100 ppm BaP, 

respectively. Multiple neoplasms of the esophagus and tongue were noted in 6 and 3 mice, 
Page 35 of 54

respectively, fed 100 ppm BaP. It should be noted that all animals in 100 ppm group died before 

termination of the study. 

This carcinogenicity study in the mouse is acceptable/nonguideline. The study contained 

information useful for deriving a quantitative estimate of cancer potency for creosote. 

Mutagenicity 

In consideration of the available evidence that creosote is a positive mutagen, the agency waived 

the requirement for the standard mutagenicity battery, and instead required dominant lethal 

testing of both the P1/P13 and P2 blends, which is designed to assess heritable mutations. The 

executive summaries of these studies are shown below. 

Executive Summary (P1/P13 blend): In a rat dominant lethal assay (MRID not available), male 

HSD:Sprague-Dawley CD rats were treated orally once per day for five consecutive days with 

Cresosote P1/P13 at target doses of 725, 362.5 or 181.25 mg/kg body weight/day in a volume of 

2.5 mL/kg. Actual doses determined by chemical analysis were 857.5, 330.5 and 230.8 

mg/kg/day. Twenty-one rats were dosed at the two lower doses and 26 rats at the highest dose. 

The vehicle was corn oil. Seven days after the initial dosing, each male was mated with two 

untreated females per week for 10 weeks. Females were sacrificed 13 days after the midweek of 

the presumptive mating day and the following data collected: total implantations per female, 

corpora lutea per female, preimplantation losses per female, live implantations per female, dead 

implantations per female, proportion of females with one or more dead implantations, proportion 

of females with two or more dead implantations and dead implantations/total implantations 

(expressed as a percentage). The fertility index, computed as the number of fertile females (with 

corpora lutea present) per number of mated females, was also determined. 

Creosote P1/P13 was tested to toxic doses. In the dominant lethal study, all rats in the top two 

treatment groups but none in the low dose group showed decreased activity following dosing and 

all rats in the high dose group had dyspnea. Two animals in the low dose group and two in the 

high dose group had material around the nose and mouth. Other pharmacotoxic signs were 

limited to a few animals in the high dose group and included lacrimation, deposition of the test 

material around the eyes, increased salivation and anogenital staining. One high dose rat died 

following the fourth dose. A dose-related decrease in body weight in the low-, mid-, and highdose animals, compared to the solvent controls, was seen during the dosing period, and this 

initial weight loss was not recovered in mid- and high-dose rats during the ten week mating 

period. Statistically significant differences from control values were seen in a number of 

endpoints throughout the study; however, with the exception of results from mating group nine, 

none were endpoints indicative of a dominant lethal effect. In mating group nine, statistically 

significant increases were seen in dead implantations per female, the percentage of females with 

 one implantation, the percentage of females with  two implantations and the percent dead 

implantations per total implantations. These increases were seen at the low and mid doses but 

not at the high dose. Also, the vehicle control values in mating group nine were unusually low 

compared to those in the other weekly mating groups (there were fewer preimplantation losses 

(0.85 per female) and fewer dead implantations (0.41 per female) than seen for the vehicle 

controls in the other mating groups (1.53 ± 0.37 and 0.85 ± 0.20 per female, respectively) and 
Page 36 of 54

values for percentage of females with  one and two dead implantations and the percent dead 

implantations per total implantations were depressed). The results, although statistically 

significant, are thus not considered biologically significant. Positive and solvent control values 

were appropriate except where noted for the vehicle controls in mating group nine. Based on the 

results of this study, there was no evidence that Creosote P1/P13 induced dominant lethals in any 

germ cell stage in male rats as tested in this study. No additional data are anticipated to be 

required. 

Executive Summary (P2 blend): In a rat dominant lethal assay (MRID not available), male 

HSD:Sprague-Dawley CD rats were treated orally once per day for five consecutive days with 

Creosote P2 at target doses of 775, 387.5 or 193.75 mg/kg body weight/day in a volume of 2.5 

mL/kg. Actual doses by chemical analysis were 866.3, 431, or 199.3 mg/kg body weight/day. 

Twenty-one rats were dosed at the two lower doses and 26 rats at the highest dose. The vehicle 

was corn oil. Seven days after the initial dosing, each male was mated with two untreated 

females per week for 10 weeks. Females were sacrificed 13 days after the midweek of the 

presumptive mating day and the following data collected: total implantations per female, 

corpora lutea per female, preimplantation losses per female, live implantations per female, dead 

implantations per female, proportion of females with one or more dead implantations, proportion 

of females with two or more dead implantations and dead implantations/total implantations 

(expressed as a percentage). The fertility index, computed as the number of fertile females (with 

corpora lutea present) per number of mated females, was also determined. 

Creosote P2 was tested to an adequate dose. All rats in all treatment groups showed decreased 

activity following dosing. Other clinical signs, limited to a few animals in which there was a 

back-up of test material during dosing, were lacrimation, deposition of the test material around 

the eyes and increased salivation in one high-dose male, labored breathing in one low-dose male 

and two high-dose males, and material around nose and mouth in two low-dose, one mediumdose and four high-dose males. Reduced food consumption was seen in all high-dose rats. No 

dosing- or test material-related deaths occurred during the study. A dose-related decrease in 

body weight in the low-, mid-, and high-dose animals, compared to the solvent controls, was 

seen during the dosing period, and this initial weight loss was not recovered in mid- and highdose rats during the ten week mating period. Statistically significant differences from solvent 

control values (p  0.05) were seen for a number of endpoints during the first nine weekly 

mating intervals but, with one exception, not in endpoints considered indicative of dominant 

lethality. The one exception was a significant increase in the number of dead implants over the 

solvent control value in the sixth mating group at the lowest Creosote P2 dose. This increase 

was not considered biologically relevant because no significant increases were seen at higher 

doses or in other endpoints concerning dead implants. In the tenth mating group (exposure to the 

test material at the spermatogonial stem cell stage), an apparently dose-related increase was seen 

in the number of dead implantations per female, the percentage of females with  1 dead implant, 

the percentage of females with  2 dead implants and the percentage of dead implantations per 

total implantations. The increases reached statistical significance at the highest dose for the first 

two endpoints. Positive and solvent control values were appropriate. The data in this study, 

while indicating a positive effect at week 10 of treatment, are not considered to be treatmentrelated, based on the conclusion that while dead implantations per female was significantly 

increased at the highest dose tested at mating week 10, the number of live implants/female was 
Page 37 of 54

not significantly reduced (<5% lower than control). In addition, no dominant lethal effects were 

seen at weeks 8 or 9, which would also sample spermatogonial cells. Therefore, creosote P2 is 

considered to be negative for dominant lethal effects in rats. No additional data are anticipated 

to be required. 

Other Toxicological Effects 

Neurotoxicity 

There are no current agency guideline neurotoxicity studies available for creosote. Of the 

existing studies available, there is no evidence of neurotoxicity for either the P1/P13 or P2 blends 

of creosote, although there is valid concern for some of the components of creosote, which are 

known to be neurotoxic (i.e. naphthalene). Data from the ATSDR Toxicological profile for 

Creosote showed increased brain-to-body weight ratios after exposure of male and female rats to 

beechwood creosote (used therapeutically in the past as a disinfectant and expectorant, and 

composed mainly of phenol, cresols, guaicol, xylenol, and creosol) to 257 mg/kg/day in the diet 

for 3 months in male rats, or exposure of female rats for 52 weeks to 297 mg/kg/day in the diet, 

or exposure of male and female rats for 96 weeks in the diet to 143 and 394 mg/kg/day, 

respectively. Acute exposure of male and female rats to 600 and 313 mg/kg beechwood creosote 

resulted in convulsions. Although signs of neurologic involvement were evident, no treatmentrelated pathological findings of the central nervous system were noted at necropsy in these 

studies. No additional data are anticipated to be required. 

Dermal Absorption 

Dermal absorption of creosote was assessed through review of submitted studies on the P1/P13 

blend: An in vivo dermal absorption study in the rat (MRID 47179501), and an in vitro dermal 

absorption study using rat and human skin preparations (MRID 47179502). P1/P13 creosote was 

chosen as the test material for these studies by agreement between the agency and the registrant, 

as this blend is used for treatment of wood intended for terrestrial, fresh water, and marine use 

and has the greatest potential for dermal exposure. A protocol was submitted to the agency and 

approved prior to conduct of these studies.

Executive Summary (P1/P13 blend): In an in vivo dermal penetration study (MRID 47179501) 

AWPA P1-P13 Creosote (98.5% a.i.) spiked with eight radiolabeled target chemicals (approx. 

43% of the chemicals in creosote) was applied to the clipped dorso-lumbar skin (10.5 cm2

) of 

eight male Sprague-Dawley rats at a dose of 10.7 mg/cm2 skin (10 μL/cm2, total radioactivity 

16.7 μCi). The exposure duration was eight hours. At the end of 8 hours, animals were removed 

from the metabolism cages, and the application sites were washed with 2% Ivory soap solution 

followed by a water rinse and then a dry natural sponge. Four rats were then euthanized (0 hours 

post-exposure) while the other four rats were returned to the metabolism cages for further excreta 

collection. These four rats were sacrificed at 496 hours post-exposure. 

The mean percent recovery of the radioactivity in the applied dose was 95.009% (±2.569%) and 

96.609% (±3.628%) at 0 and 496 hours post-exposure, respectively. The majority of the 

administered dose was recovered from the skin wash sponges; the mean percent recovery was 

59.283% (±12.54%) for the 0-hr post-exposure group and 56.822% (±8.294%) for the 496-hr 
Page 38 of 54

post-exposure group. The mean percent absorbed dose was 6.342% (±0.808%) at 0 hours postexposure and 33.959% (±8.445%) at 496 hours post-exposure, with a mean percent of 1.553% 

(±0.299%) and 0.005% (±0.003%), respectively, present in the skin after removal of the stratum 

corneum. Most of the absorbed dose had been excreted by 496 hours post-exposure, with a mean 

of 18.97% (±4.97%) of the dose eliminated in the urine and 12.60% (±4.11%) eliminated in the 

feces. 

In a supplemental dermal penetration study intended to clarify the results for the 496 postexposure group in the initial main study, AWPA P1-P13 Creosote (98.5% a.i.) spiked with eight 

radiolabeled target chemicals was applied to the shaved dorsal skin (10.5 cm2) of four male 

Sprague-Dawley rats at a dose of 10.7 mg/cm2 skin (10 μL/cm2, total radioactivity 18.9 μCi). 

The exposure duration was 8 hours. Animals were sacrificed at 496 hrs post-exposure (504 hrs 

post-dosing). In the supplemental absorption study, the O-ring, which demarcated the application 

area, was applied without glue following the dose application, and was removed at the end of the 

8-hr exposure. In the main study, the O-ring had been glued to the skin one day prior to dose 

application and remained in place until study termination. 

In the supplemental study, the mean percent recovery of the radioactivity in the applied dose was 

92.775% (±2.70%) at 496 hours post-exposure. The majority of the administered dose was 

recovered from the body wrap (34.228±6.328%), skin wash (22.240±7.818%), and O-ring 

(27.452±3.680%). Although the mean percent absorbed dose was reported in this supplemental 

experiment as 8.853±1570%, with a mean percent of 0.005% present in the skin after removal of 

the stratum corneum, the presence of a significant amount of radioactivity in the body wrap after 

8 hours adds uncertainty as to the actual available dose. In addition, in the first experiment, 

dermal absorption was still evident after washing of the skin at 8 hours and monitoring of urinary 

and fecal excretion of radioactivity from 8 hours onward. Therefore, the data are not conclusive 

of a reduced dermal absorption based on the contention that the O-ring or the glue had an 

influence on dermal absorption. 

In a preliminary plasma kinetic (dermal bioavailability) study, neat creosote was applied to the 

clipped dorso-lumbar skin (10.5 cm2) of four male Sprague-Dawley rats (10 μL/cm2) for an 

exposure duration of 8 hours; animals were sacrificed 168 hours post-dosing (160 hours postexposure). None of the twelve target creosote chemicals analyzed in the plasma were detected 

above their detection limit. 

This study in the rat is acceptable-non-guideline. Although only one exposure duration and one 

exposure concentration were evaluated, this was part of an agreement in study design between 

the agency and the registrant. No additional data are anticipated to be required. 

In an in vitro dermal absorption study using rat and human skin preparations (MRID 47179502), 

AWPA P1-P13 Creosote (98.5% a.i.) spiked with eight radiolabeled target chemicals was 

applied to 6 rat and 6 human skin preparations mounted in individual static diffusion cells at a 

nominal dose of 10,700 μg creosote/cm2 (1 μCi/skin). Samples were collected from the receptor 

chambers at 0.5, 1, 2, 4, and 8 hours post-application. The skin was washed 8 hours postapplication and the study terminated. The amount of the applied dose absorbed was considered to 

be the amount of radioactivity measured in the receptor fluid. 
Page 39 of 54

The mean total recovery of the applied dose for the rat and human skin was 78.3% and 83.9%, 

respectively. The mean absorbed dose was 15.1% for the rat skin and 3.34% for the human skin. 

The mean rate of penetration was 85.3 μg equiv/cm2/hr for the rat skin and 19.7μg equiv/cm2/hr 

for the human skin. The mean rate of penetration and the mean total penetration for the rat skin 

were approximately 4.3 times and 4.4 times greater than that for the human skin, respectively. 

This in vitro dermal absorption study is classified as unacceptable, based on several deficiencies 

in the study, including: evaluation of only one exposure duration; evaluation of only one dose 

level; no data on solubility as a rate-limiting factor for creosote dermal absorption; and lack of a 

24 hour time point measurement. 

The agency reached the following conclusion on dermal absorption of creosote, using available 

in vivo dermal absorption data: based on (1) the lack of data demonstrating that the concentration 

of the creosote solution did not exceed solubility limits and therefore did not have an artefactual 

influence on the magnitude of absorption in the in vitro test system, and (2) the continued 

absorption observed after eight hours in the in vivo study [the O-ring influence could not be 

conclusively demonstrated to be acting as a depot for radioactivity]), the agency’s conclusion 

was to use the value of 34% from the in vivo absorption study and recognize the 8-fold 

difference in absorption between human and rat skin from the in vitro study. Therefore, a value 

of 5% for dermal absorption was used (34% divided by 8 and rounded upward). 

Immunotoxicity 

An immunotoxicity study is a data requirement for all uses of antimicrobial pesticide chemicals 

under 40 CFR Part 158W, Data Requirements for Antimicrobial Pesticide Data Requirements 

(78 FR, no. 89, 26978, May 8, 2013). It is an anticipated data requirement for registration 

review. The expected data call-in notice will provide that the registrant can address this data 

requirement by submitting a study according to the OCSPP 870.7800 guideline, citing 

information from the scientific literature that adequately addresses immunotoxicity of creosote, 

or submitting a request for waiver of this study using the agency’s published guidance, available 

at: http://www.epa.gov/pesticides/regulating/part158-tox-data-requirement.pdf.

 
Page 40 of 54

Toxicology References for Appendix A 

MRID 43032101: North American P1/P13 Creosote: Acute Oral Toxicity Study in Rats. Study 

conducted by IRDC, Mattawan, MI for the Creosote Council II. Unpublished. HED document 

no. 011033. 

MRID 43032102: North American P1/P13 Creosote: Acute Dermal Toxicity Study in Rats. 

Study conducted by IRDC, Mattawan, MI for the Creosote Council II. 

Unpublished. HED document no. 011033. 

MRID 43032103: North American P1/P13 Creosote: Acute Inhalation Toxicity Study in Rats. 

Study conducted by IRDC, Mattawan, MI for the Creosote Council II. 

Unpublished. HED document no. 011033. 

MRID 43032104: North American P1/P13 Creosote: Eye Irritation Study in Rabbits. Study 

conducted by IRDC, Mattawan, MI for the Creosote Council II. Unpublished. HED document 

no. 011033. 

MRID 43032105: North American P1/P13 Creosote: Primary Dermal Irritation Test in Rabbits. 

Study conducted by IRDC, Mattawan, MI for the Creosote Council II. 

Unpublished. HED document no. 011033. 

MRID 43032106: North American P1/P13 Creosote: Dermal Sensitization Study (Buehler) in the 

Albino Guinea Pig. Study conducted by IRDC, Mattawan, MI for the Creosote Council II. 

Unpublished. HED document no. 011033. 

MRID 43032301: North American P2 Creosote: Acute Oral Toxicity Study in Rats. Study 

conducted by IRDC, Mattawan, MI for the Creosote Council II. Unpublished. HED document 

no. 011033. 

MRID 43032302: North American P2 Creosote: Acute Dermal Toxicity Study in Rats. Study 

conducted by IRDC, Mattawan, MI for the Creosote Council II. Unpublished. 

MRID 43032303: North American P2 Creosote: Acute Inhalation Toxicity Evaluation in Rats. 

Study conducted by IRDC, Mattawan, MI for the Creosote Council II. 

Unpublished. HED document no. 011033. 

MRID 43032304: North American P2 Creosote:Eye Irritation Study in Rats. Study conducted by 

IRDC, Mattawan, MI for the Creosote Council II. Unpublished. HED document no. 011033. 

MRID 43032305: North American P2 Creosote: Primary Dermal Irritation Test in Rabbits.Study 

conducted by IRDC, Mattawan, MI for the Creosote Council II. Unpublished. HED document 

no. 011033. 

MRID 43032306: North American P2 Creosote: Dermal Sensitization Study (Buehler) in the 

Albino Guinea Pig. Study conducted by IRDC, Mattawan, MI for the Creosote Council II. 

Unpublished. HED document no. 011033. 
Page 41 of 54

MRID 43601001: North American P1/P13 Creosote: Thirteen Week Subchronic Inhalation 

Toxicity Study on North American P1/P13 Creosote CTM in Rats. Study conducted by IRDC, 

Mattawan, MI for the Creosote Council II. Report No. 671-016 (1995). Unpublished. 

MRID 43600901: North American P2 Creosote: Thirteen Week Subchronic Inhalation 

Toxicity Study on North American P2 Creosote CTM in Rats: Study conducted by IRDC, 

Mattawan, MI for the Creosote Council II. Report No. 671-018 (1995). Unpublished. 

MRID 43616101: North American P1/P13 Creosote: 90-Day Subchronic Dermal Toxicity Study 

in Rats. Study conducted by IRDC, Mattawan, MI for the Creosote Council 

II. Report No. 671-013 (1995). Unpublished. 

MRID 43616201: North American P2 Creosote: 90 Day Subchronic Dermal Toxicity Study in 

Rats. Study conducted by IRDC, Mattawan, MI for the Creosote Council II. Report No. 671-

014 (1993). Unpublished. 

MRID 43584201: North American P1/P13 Creosote: Developmental Toxicity Study in Rats. 

Study conducted by IRDC, Mattawan, MI for the Creosote Council 

II. Report No. 671-020 (1995). Unpublished. 

MRID 43584202: North American P2 Creosote: Developmental Toxicity Study in Rats. 

Study conducted by IRDC, Mattawan, MI for the Creosote Council 

II. Report No. 671-022 (1995). Unpublished. 

MRID 44844401: A 6-Month Dermal Oncogenicity Study of Creosote in Mice. Study conducted 

by WIL Research Laboratories, Ashland, OH for Koppers Industries, Pittsburgh, PA. Report no. 

WIL-100005. Unpublished. 

MRID 47179501: Fasano, W. (2007) AWPA P1-P13 Creosote: In vivo dermal absorption in the 

rat. E.I. du Pont de Nemours and Company, HaskellSM Laboratory for Health and Environmental 

Sciences, Newark, Delaware. Laboratory Project ID. DuPont-19622, July 2, 2007. 

MRID 47179502: Fasano, W. (2007) AWPA P1-P13 Creosote: In vitro kinetics in rat and human 

skin. E.I. du Pont de Nemours and Company, HaskellSM Laboratory for Health and 

Environmental Sciences, Newark, Delaware. Laboratory Project ID: DuPont-21647, April 30, 

2007. 

Agency for Toxic Substances and Disease Registry (1990): Toxicological Profile for Creosote. 

U.S. Department of Health and Human Services: Public Health Service. McMahon, Timothy F.: 

Creosote: Endpoint Selection Report. February 2008. Unpublished. 

Culp, S.J., Gaylor, D.W., Sheldon, W.G., Goldstein, L.S., and Beland, F.A. (1996): DNA adduct 

measurements in relation to small intestine and forestomach tumor incidence during the chronic 

feeding of coal tar or benzo[a]pyrene to mice. Polycyclic Aromatic Compounds 11, 161-168. 
Page 42 of 54

Culp, S.J., Gaylor, D.W., Sheldon, W.G., Goldstein, L.S., and Beland, F.A. (1998): A 

comparison of the tumors induced by coal tar and benzo(a)pyrene in a 2-year bioassay. 

Carcinogenesis 19:1, pp. 117-124

Gaylor, D.W., Culp, S.J., Goldstein, L.S., and Beland, F.A. (2000): Cancer Risk Estimation for 

Mixtures of Coal Tars and Benzo[a]pyrene. Risk Analysis 20(1): 81-85. 

McMahon, Timothy F.: Creosote: Endpoint Selection Report. February 2008. Unpublished. 

Schneider, K., Roller, M., Kalberlah, F., and Schumacher-Wolz, U. (2002): Cancer Risk 

Assessment for Oral Exposure to PAH Mixtures. J. Appl. Toxicol. 22: 73-83. 

USEPA, 1984: Wood Preservative Pesticides: Creosote, Pentachlorophenol, Inorganic 

Arsenicals. Position Document 4 

York, Raymond G. (1994): Developmental Toxicity Study in New Zealand White Rabbits. Study 

conducted by IRDC, Mattawan, MI for Koppers Industries, Pittsburgh, PA. 

Report no. 672-002. Unpublished. 

York, Raymond G. (1995): Two Generation Reproduction/Fertility Study in Rats. Study 

conducted by IRDC, Mattawan, MI for Koppers Industries, Pittsburgh, PA. 

Report no. 672-006. Unpublished. 

 
Page 43 of 54

Appendix B Environmental Fate 

The agency does not anticipate the need to require environmental fate studies for registration 

review other than a wood leaching study called in through the post-RED DCI in 2011. In the 

RED, the agency conducted an open literature search for environmental fate and transport studies 

on the creosote mixture and based the assessment on the PAH constituents only. In this 

appendix, the agency is summarizing the contents of the RED. 

The environmental fate and transport of creosote as addressed here focuses primarily on the 

likely exposure of PAHs into three environmental compartments: 1) leaching of creosote mixture 

into surface and ground waters from the railroad ties and utility poles; 2) migration into 

soil/sediments from the railroad ties and utility poles, and 3) bioaccumulation into the aqueous 

and benthic organisms. 

The PAHs in creosote are primarily expected to sorb to soil and sediment because of limited 

water solubility and high carbon content. Microbial degradation and volatility are expected to be 

more rapid for those PAHs with fewer rings. Photodegradation in water is also a primary route 

of dissipation for those PAHs in water. 

Water and Sediment 

Hydrolysis 

PAHs are fused aromatic polycyclic rings which have no hydrolyzable hydrogens and the 

solubility of these compounds are very low in water. Therefore, hydrolysis is not an important 

route of dissipation for creosote. 

Aqueous Photolysis 

PAHs can readily photodegrade in water because these compounds absorb UV light. However, 

photooxidized products of PAHs can be stable, and can persist in air/water and soils and become 

an environmental concern as these photooxidized products are also bioaccumulative (Kirso, 

1991). The half-lives in water for various PAHs ranged from 3.6-375 minutes (freshwater, most 

<110 minutes), 28-146 minutes for benzo(a)pyrene (saltwater, most <72 minutes), and 0.58-

9,840 hours (numerous PAHs, most <48 hours). 

Octanol-Water Partition Coefficient and Bioconcentration in Aquatic Organisms 

Based on the log Kow (Log P) value of creosote of 3.25 (Table 4), bioconcentration of PAHs in 

aquatic organisms is a significant route of dissipation. In general, the potential for 

bioconcentration of PAHs increases as the number of rings increases, but sorption to sediment 

and the lack of water solubility may limit the actual bioconcentration of higher molecular weight 

compounds. Most of the bioconcentration data for creosote PAHs was associated with 

Superfund sites and environmental spills and not laboratory studies that were specifically 

targeted to measure bioconcentration based on known water concentrations. Southworth et al. 
Page 44 of 54

(1978) measured the bioconcentration in clams near a creosote spill. For the 2-ring and 4-5 ring 

PAHs, concentrations in clams increased while the concentrations of 3-ring compounds were 

stable or declined slightly. The concentration of 4-5 ring PAHs were the highest in clams. 

Creosote Behavior with Sediment and Ground Water 

Mueller et al. (1993) studied the removal of Group 1, 2, and 3 PAHs8 from contaminated 

groundwater in Florida over 32 days. Group 1 PAHs include known carcinogens (only member 

is benzo(a)pyrene (5-rings), Group 2 PAHs include “probable carcinogens” which range from 3-

5 rings, and Group 3 PAHs include numerous 4- and 5-ring compounds. Overall, 89.4-98 % of 

PAHs were removed by biodegradation and only 3.5-9.2 % remained at the end of the study. 

Over a 28-day period, Bouwer et al. (1996) studied the removal of 2-3 ring PAHs in sediment 

ground water and determined the effect of oxygen on mineralization. Mineralization for 

anthracene and phenanthrene ranged from 4 to 23 percent, ranged from 4 to 42 percent for 

benzene, and from 8 and 55 percent for naphthalene. Shocken and Gibson (1984) demonstrated 

degradation of acenaphthene and acenaphthalene (3-ring compounds) into acenaphthenequinone 

(parent compound plus two ortho keto groups). Godsy et al. (1992) demonstrated lateral 

movement of <150 meters in ground water from an abandoned wood treatment site for most 

PAHs. Goerlitz et al. (1985) demonstrated that PAHs were not detected in ground water at 

depths >12 meters at the same abandoned wood treatment site. Mueller et al. (1991) determined 

that lower-molecular weight PAHs in groundwater degraded faster (half-lives of ~3 days) while 

higher molecular-weight PAHs degraded slower (half-lives of ~14 days). 

Soil 

Soil Leaching/Adsorption/Desorption Batch Equilibrium 

Some of the PAHs, particularly those that have a high molecular mass (higher number of the 

fused aromatic rings) have a higher tendency to adsorb to soil organic carbon. Such adsorption 

coefficients (KOC) have been reported in literature (Knightes and Peters, 2003). The log Koc 

values range from 3.36 for naphthalene (2-rings) to 5.18 for pyrene (4 rings). Some PAHs with a 

high Koc can bind strongly with the organic carbon of the soils/sediments and may not be 

bioavailable to the aquatic organisms. However, if the octanol/ water coefficients (Kow) is high, 

and if the PAHs are desorbed from the soils/sediments to which they are bound, some of these 

PAHs can become bioaccumulative to the benthic organisms. 

Volatility from Soil 

Few studies are reported in the open literature on field volatilities for PAHs present in creosote. 

Lindhardt and Christensen (1996) measured the volatility of 11 PAHs from contaminated soil 

and determined that steady-state concentrations of naphthalene and methyl naphthalene (2-ring 

PAHs) were observed at 10-20 days, and measurable fluxes of acenaphthene and fluorene (3-ring 

PAHs) were only detected using a soil cover with low organic content, indicating sorption. 

Aerobic Soil Metabolism 

 

8

 Carex Canada, http://www.carexcanada.ca/en/polycyclic_aromatic_hydrocarbons/ 
Page 45 of 54

Most of the PAHs have a tendency to biodegrade under aerobic conditions. It has been reported 

that over eighty percent of biodegradation occurs in the first month after the wood preservative 

application, with the exception of benz[a]pyrene and benzo[k]fluoranthene, which have shown 

resistance to biodegradation. A number of aerobic soil metabolism studies on PAHs conducted 

at various contaminated sites as well as in simulated microcosms reported that low molecular 

weight PAHs generally metabolized in aerobic conditions and the greater the oxic environment, 

the higher the biodegradation level. Chapman et al. (1995) determined that 72 % of lowmolecular weight PAHs were degraded after washing creosote-contaminated soil. Hurst et al. 

(1996) found that after 7 days, 45 and 55 % of PAHs mineralized in 2 and 21 % oxygen, 

respectively. 

Anaerobic Soil Metabolism 

Genther et al. (1997) studied the anaerobic soil metabolism of PAHs and demonstrated that only 

anthraquinone (3-rings) and 2-methyl anthracene (3-rings) demonstrated any degradation under 

anaerobic conditions. 

Volatility from Treated Wood 

Exposure to air does not seem to be an important factor in the environmental behavior for most 

PAHs. While Gevao et al. (1998) showed that acenaphthene, fluorene, phenanthrene, 

anthracene, and fluoranthene volatilized at a faster rate at 30 C than at 4 C, 85 percent of these 

components remained in the wood after seven weeks. The rate of volatilization was slow for 

acenaphthene (half-life, one year) and fluoranthene (half-life, one year). In most cases, the initial 

rates of dissipation are caused by partitioning between the wood and air and biodegradation in 

the presence of microbial populations. 

Leaching from Treated Wood 

Guideline data on leaching of creosote components from treated wood were required in a postRED DCI (GDCI-025004-30249) and have not been submitted. The agency still anticipates the 

submission of these leaching data. Literature data indicate that leaching occurs primarily in the 

first 7 days in flooded conditions (Bestari et al., 1998a). In a terrestrial microcosm, 95 % of 

PAHs in Ponderosa pine blocks were present in wood after 2.5 months. In an aquatic 

microcosm, a leaching rate of 50 ug/cm2/day in freshwater was observed from marine-grade 

Douglas fir pilings (Bestari et al, 1998b). This study measured 15 of the 16 priority pollutant 

PAHs. In a terrestrial setting (Mississippi State University, 1981), 2-ring compounds were not 

found in soil around stakes but 3, 4, and 5-ring compounds were found in soil. 

 
Page 46 of 54

Environmental Fate References for Appendix B 

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Bauer, J.E. et al. 1985. Appl. Environ. Microbiol. 81-90. 

Bauer, J.E. et al. 1988. Appl. Environ. Microbiol. 1649-1655. 

Behymer, T.D. and R.A. Hites. 1985. Environ. Sci. Technol. 19(10):1004-1006. 

Bestari, K.T. Jim et al. 1998b. Distribution and composition of polycyclic aromatic 

hydrocarbons within experimental microcosms treated with creosote-impregnated 

douglas fir pilings. Environ. Toxicol. Chem. 17(12):2369-2377. 

Bieri, R.H. et al. 1986. Polycyclic aromatic hydrocarbons in surface sediments from the 

Elizabeth River subestuary. Int. J. Environ. Anal. Chem. 26:97-113. 

Bouwer, E.J. and P.L. McCarty. 1983. Appl. Environ. Microbiol. 45:1295-1299. 

Bruner, K.A. et al. 1994. J. Great Lakes Research. 20:725-734. 

Callahan, M.A. et al. 1979. Water Related Environmental Fate of 129 Priority Pollutants, EPA440-4-79-029a,b. 

Elder, J.F. and P. Dresler. 1988. Accumulation and bioconcentration of polycyclic aromatic 

hydrocarbons in a nearshore estuarine environment near a Pensacola (Florida) creosote 

contamination site. Environmental Pollution. 49:117-132. 

Electric Power Research Institute (EPRI). 1992. Document EPRI TR-01000870. 

Ehrlich, G.G. et al. 1982. Groundwater. 20(4):703-710.

Flyvberg, J.E. et al. 1993. J. Contamin. Hydrology. 12:133-150. 

Fowler, M.G. et al. 1993. Preliminary results from a field experiment investigating the fate of 

some creosote components in a natural aquifer. Org. Geochem. 22:641-649. 

Fukuda, K. et al. 1988. Chemosphere. 17(4):651-659.

Gevao, B. and K.C. Jones. 1998. Kinetics and potential significance of polycyclic aromatic 

hydrocarbon desorption from creosote-treated wood. Environ. Sci. Tech. 32:640-646. 

Gile, J.D. et al. 1982. J. Agric. Food Chem. 30:295-301. 

Goerlitz, D.F. et al. 1985. Environ. Sci. Tech. 19(10):955-961. 

Grbic-Galic, D. et al. 1991. Anaerobic degradation of aromatic hydrocarbons and aerobic 

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Harris, J.C. 1982. Handbook of Chemical Property Estimation Methods. W.J. Lyman, W.F. 

Reehl, D.H. Rosenblatt, Eds. McGraw-Hill Book Company, New York: Chapters 7-8. 

Hellou, J.G. et al. 1990. Polycyclic aromatic hydrocarbons in muscle tissue of marine mammals 

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Mattraw, H.C. and B.J. Frank. 1986. Movement and fate of creosote waste in ground water, 

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Mississippi State University. 1981. Cooperative Agreement Number 12-156. 
Page 48 of 54

Mueller, J.G. et al. 1991. Biodegradation of creosote in contaminated groundwater: chemical 

and biological assessment. Applied and Environmental Microbiology. 57(5):1277-1285. 

Mueller, J.G. et al. 1993. Strategy using bioreactors and specially selected microorganisms for 

bioremediation of groundwater contaminated with creosote and pentachlorophenol. 

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National Oceanic and Atmospheric Administration (NOAA). 1988. A Selected Summary of 

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Shocken, M.J. et al. 1984. Bacterial oxidation of the polycyclic aromatic hydrocarbons 

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Eds., American Society for Testing and Materials: 359-380, Philadelphia. 

Southworth, G.R., J.J. Beauchamp, and P.K. Schmieder, 1978. Water Research. 12:973-977. 

Spacie, A. et al. 1983. Uptake, depuration, and biotransformation of anthracene and 

benzo[a]pyrene in bluegill sunfish. Ecotoxicology and Environmental Safety. 7:330-

341. 

Stegman, J.J. and J.M. Teal. 1973. Marine Biology. 22:37-44. 

Tay K.L. et al. 1992. Sediment bioassessment in Halifax Harbour. Environmental Toxicology 

and Chemistry. 11:1567-1581. 

Verasani, U. et al. 1978. Toxicol. Appl. Pharmacol. 44:277-289. 
Page 49 of 54

Wan, M.T. 1994. Utility right-of-way contaminants: polycyclic aromatic hydrocarbons. J. 

Environ. Quality. 23:1297-1304. 

Wendt, P.H. et al. 1996. Wood preservatives leachates from docks in an estuarine environment. 

Arch. Environ. Contamin. Toxicol. 31:24-37. 

Zepp, R.G. et al. 1980. Assessing the photochemistry of organic pollutants in aquatic 

environments. In, Dynamics, Exposure and Hazard Assessment of Toxic Chemicals. R. 

Haque, Ed. Ann Arbor Sci. Publ. Inc., Ann Arbor, Michigan: 69-110. 
Page 50 of 54

Appendix C Ecotoxicology Profile 

The ecotoxicity database is incomplete. The agency anticipates the need to require ecotoxicity 

data for registration review (for a complete list of the anticipated data, see Table 6). 

 Terrestrial Organisms 

Birds, acute oral 

No data are available. A study is anticipated to be needed to determine the toxicity of creosote to 

birds. The guideline (850.2100) is not satisfied. 

Nontarget Insects 

Toxicity data are needed for beneficial insects to support the use of creosote as a wood 

preservative. The guideline for an acute toxicity test (850.3020) is not satisfied. At this time, the 

agency does not anticipate needing a honeybee study for toxicity of residues on wood (850.3030) 

to support the heavy duty wood preservative uses. 

 Aquatic Organisms 

Freshwater Fish, acute 

No guideline data are available. Supplemental data available in the OPP chemical files for 

creosote indicate that creosote is moderately to highly toxic to fish. The guideline (850.1075) for 

acute toxicity testing with freshwater fish (cold-water and warm-water species) is not satisfied. 

Data are anticipated to be needed for the ecological risk assessment for listed and nonlisted 

freshwater fish. 

Freshwater Fish Acute Toxicity

Test Species Test Material 

(% ai) 

LC50 

(μg ai/L) 

Toxicity 

Category 

EPA Study 

ID 

Rainbow Trout 

(Oncorhynchus mykiss)

Coal tar creosote 

(97) 600 Highly toxic TN 0571 Supplemental 

Marine grade creosote 

(nr) 570 Highly toxic TN 2401 Supplemental 

Bluegill 

(Lepomis macrochirus) 

Coal tar creosote 

(97) 1600 Moderately toxic TN 0542 Supplemental 

Freshwater Invertebrates, acute 

No guideline data are available. Supplemental data available in the OPP chemical files for 

creosote indicate that the material tested (marine creosote) is highly to very highly toxic to 
Page 51 of 54

daphnids. The guideline (850.1010) for acute toxicity testing with a freshwater invertebrate is 

not satisfied. The data are anticipated to be needed for the ecological risk assessment for listed 

and nonlisted freshwater invertebrates. 

Freshwater Invertebrate Acute Toxicity

Test Species Test Material 

(% ai) 

EC50 

(μg ai/L) 

Toxicity 

Category 

EPA Study 

ID 

Waterflea 

(Daphnia magna) 

Marine creosote 

(nr) 76 Very highly toxic TN 2392 Supplemental 

Marine creosote 

(nr) 240 Highly toxic TN 2393 Supplemental 

Estuarine/Marine Fish and Invertebrates, acute 

No guideline data are available. Supplemental data available in the OPP chemical files for 

creosote indicate that creosote is highly to very highly toxic to estuarine/marine organisms. 

These data can be used to help characterize the toxicity of creosote to estuarine/marine 

organisms, but they do not satisfy the guidelines for fish (850.1075), bivalve (850.1025 or 

850.1055), and one additional invertebrate sp. (850.1035). These data are anticipated to be 

needed for the ecological risk assessment for listed and nonlisted estuarine/marine fish and 

invertebrates. 

Estuarine/Marine Fish and Invertebrate Acute Toxicity

Test Species Test Material 

(% ai) 

EC50 

(μg ai/L) 

Toxicity 

Category 

EPA Study 

ID 

Sheepshead minnow 

(Cyprinodon variegatus) 

Coal tar creosote 

(97) 

720 (juv.) 

3500 (adult) Highly toxic 40228401 Supplemental 

Mysid shrimp 

(Americamysis bahia) 

Coal tar creosote 

(97) 18 Very highly toxic 40228401 Supplemental 

Eastern oyster 

(Crassostrea virginica) 

Coal tar creosote 

(97) 710 (adult) Highly toxic 40228401 Supplemental 

Pink shrimp 

(Penaeus duorarum) 

Coal tar creosote 

(97) 240 (adult) Very highly toxic 40228401 Supplemental 

Fish and Aquatic Invertebrates, chronic 

No data are available. Chronic data are anticipated to be needed for one fish and one 

invertebrate species. The expected DCI will provide that testing must be done with the most 

sensitive species (either freshwater or estuarine/marine) as determined from the results of the 

acute toxicity tests (acute EC50 freshwater invertebrates; acute LC50 freshwater fish; 

LC50/EC50 estuarine/marine species). The guideline for a freshwater or estuarine/marine fish 

early life-stage toxicity test (850.1400) is not satisfied. The guideline for a freshwater 

invertebrate life cycle test (850.1300) or estuarine/marine mysid life cycle test (850.1350) is not 
Page 52 of 54

satisfied. These data are included as studies anticipated to be required in registration review (see 

Table 6). 

Aquatic and Semi-aquatic Plants 

No data are available. Data for vascular and non-vascular aquatic plants are anticipated to be 

needed to support wood preservative uses. The guidelines for testing with duckweed, a vascular 

sp. (850.4400), three algal spp. (850.4500), and cyanobacteria (850.4550) are not satisfied. A 

seedling emergence toxicity test with rice also is needed; the guideline (850.4225) is not 

satisfied. These data are anticipated to be needed for the ecological risk assessment for listed 

and nonlisted plants. 

Benthic Invertebrates, chronic 

No sediment-toxicity data are available for creosote. Based on environmental fate properties 

discussed in Appendix B, creosote is expected to accumulate and persist in aquatic sediments. 

Because creosote persists in sediments (half-life > 10 days), chronic testing is anticipated to be 

needed for freshwater (2 spp.) and estuarine/marine (1 sp.) benthic invertebrates. There currently 

is no guideline number for this test. 

 
Page 53 of 54

Ecotoxicity References for Appendix C

40228401 EPA. 1986. Acute Toxicity Handbook of Chemicals to Estuarine Organisms. F.L. 

Mayer, Jr., Environmental Research Laboratory, Office of Research and 

Development, Gulf Breeze, FL. EPA/600/X-86/231 

TN 0571 EPA. 1973. Toxicity of C & P Creosote to rainbow trout. Fish Toxicity Lab. 

Report, Animal Biology Lab., EPA-PR, ARC, Beltsville, MD. ID No. MB 189. 

TN 0542 EPA. 1973. Toxicity of C & P Creosote to bluegill. Fish Toxicity Lab. Report, 

Animal Biology Lab., EPA-PR, ARC, Beltsville, MD. ID No. MB 189. 

TN 2392 EPA. 1979. Marine Creosote: Daphnia magna Static Jar Test #2392. Biological 

Report of Analysis, Animal Biology Lab., Washington, DC. 

TN 2393 EPA. 1979. Creosote: Daphnia magna Static Jar Test #2393. Biological Report of 

Analysis, Animal Biology Lab., Washington, DC. 

TN 2393 EPA. 1979. Marine Grade Creosote: Rainbow trout (Salmo gairdneri) Static Jar 

Test #2401. Biological Report of Analysis, Animal Biology Lab., Washington, DC. 

 
Page 54 of 54

Appendix D Physical and Chemical 

Properties 

The creosote product chemistry information is summarized in Table D1. 

Table D-1 - Physical-Chemical Properties for Creosote 

Guideline No. Parameter Creosote Reference/Comments 

830.7050 UV/Visible Absorption Not available 

for mixture 

PAHs absorb UV light but no 

spectrum available for 

mixture 

830.7200 Melting point (oC) Not applicable MRID 48480902 

Product is liquid 

830.7220 Boiling point (oC) >180 MRID 48490902 

830.7370 Dissociation constant (pKa) Not applicable

MRID 48480902 

No acid or base functional 

groups 

830.7550 Octanol-water partition coefficient 

at 25 o

C (Log Kow) 3.25 MRID 48480902 

830.7840 Solubility in water (mg/L) 313 MRID 48480902 

830.7950 Vapor pressure (mmHg) 11.1 MRID 48480902 

24.4 o

C 

 None Henry's law constant at 25 o

C 

(atm-m3

/mol) Not calculated 

Product is a mixture with 

various chemical and physical 

properties 

atm-m3/mol = atmosphere cubic meter per mole; oC = degrees Celsius; mg/L = milligrams per liter; mmHg = 

millimeters of mercury.