Page 2 of 63 Pentachlorophenol Regist ration Review Team

Human Health & Environmental Effects Jonathan Chen Nathan Mottl Bill Erickson Najm Shamim Siroos Mostaghimi

Health Effects Division Jaclyn Pyne

Risk Management Sandra O’Neill Rose Kyprianou Tom Luminello

Office of General Counsel Philip RossDocket Number EPA-HQ-OPP-2014-0653 www.regulations.gov

Page 3 of 63 TERMS, ABBREVIATIONS AND SYMBOLS

X,3,7,8 TCDD 2, 3, 7, 8-tetrachlorodibenzo-p-dixoin AD Antimicrobials Division A.I. or a.i. active ingredient aPAD acute population adjusted dose ASRI activated sludge respiration inhibition
atm-m 3 /mole atmospheric pressure-cubic meter per mole BCF bioconcentration factor °C degrees Celsius CAS Chemical Abstracts Service CDD chlorodioxin CDF chlorofuran CFR Code of Federal Regulations CHO Chinese hamster ovary CMA Chemical Manufacturers Association CO 2 carbon dioxide COC concentration-of-concern cPAD chronic population adjusted dose DCI data call-in EC 50 median (or 50 percent) effect concentration EC 05 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, Dr ug, and Cosmetic Act FGD flue-gas desulfurization FIFRA Federal Insecticide, Fungicide, and Rodenticide Act FQPA Food Quality Protection Act FWP Final Work Plan g/mol grams per mole GLN guideline number HCB hexachlorobenzene HPV high production volume HxCDD hexachlorodibenzo-p-dioxin IDS Incident Data System Koc organic carbon normalized soil-water partition coefficient Kd soil-water partition coefficient Kow octanol-water partition coefficient LC 50 median (or 50 percent) lethal concentration LD 50 median (or 50 percent) lethal dose LOAEC lowest-observed-adverse-effect-concentration LOEC lowest-observed-effect-concentration LOAEL lowest-observed-adverse-effect-level Log K ow logarithm of the octanol-water partition coefficient μg microgram ml/g milliliter per gramPage 4 of 63 mg/kg milligram per kilogram mg/kg/day milligram per kilogram per day mg/L milligram per liter mm Hg millimeter of mercury 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 PCP Pentachlorophenol PAD population adjusted dose PAI pure active ingredient PDM Probabilistic Dilution Model % percent PC Code Pesticide Chemical Code PCA pentachloroanisole 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 plantsPage 5 of 63 

### Table of Contents
1 Introduction .................................................................................................................. ........... 7 1.1 Statutory and Regulatory Authority ................................................................................. 7 1.2 Case Overview ................................................................................................................. 7 1.3 Chemical Identification and Properties ............................................................................ 9 1.4 PCP and Contaminants ................................................................................................... 11 1.5 Use/Usage Description ................................................................................................... 12 1.5.1 Registrations ........................................................................................................... 12 1.5.2 Summary of Regist ered Uses .................................................................................. 13 1.5.3 Usage Information .................................................................................................. 13 1.6 Regulatory History ......................................................................................................... 13 1.6.1 Tolerance Information ............................................................................................ 14 1.7 Incidents ..................................................................................................................... .... 14 1.7.1 Human Health ......................................................................................................... 14 1.7.2 Ecological ............................................................................................................... 14 2 Anticipated Data Needs ........................................................................................................ 15 3 Human Health Risk Assessment ........................................................................................... 16 3.1 Existing Toxicological Endpoints .................................................................................. 16 3.1.1 PCP ......................................................................................................................... 1 6 3.1.2 Contaminants .......................................................................................................... 18 3.2 Dietary Exposure ............................................................................................................ 1 9 3.2.1 Food ........................................................................................................................ 2 0 3.2.2 Drinking Water ....................................................................................................... 20 3.3 Occupational and Residential Exposures ....................................................................... 20 3.3.1 Occupational Exposure ........................................................................................... 21 3.3.2 Residential Handler Exposures ............................................................................... 21 3.3.3 Residential Post-Applic ation Exposures ................................................................. 22 3.3.4 Aggregate Exposures .............................................................................................. 22 3.3.5 Cumulative Exposures ............................................................................................ 22 4 Environmental Risk Assessment........................................................................................... 22 4.1 Environmental Fate Assessment .................................................................................... 23 4.1.1 Water Quality .......................................................................................................... 24 4.2 Environmental Exposure Pathways ................................................................................ 24 4.3 Ecological Effects Analysis ........................................................................................... 25 4.3.1 Mechanism of Action .............................................................................................. 25 4.3.2 Measures of Effect (Ecotoxicology Endpoints) ...................................................... 26 4.3.3 Ambient Water Quality Criteria for PCP ................................................................ 27 4.3.4 Open literature ........................................................................................................ 28 4.4 Exposure Analysis Plan .................................................................................................. 28 4.4.1 Aquatic and Terrestrial Wild life Exposure Estimates ............................................ 28 4.4.2 Screening Level Down-the-Drain Analysis ............................................................ 28 5 Endocrine Disruptor Screen ing Program (EDSP) ................................................................. 28 6 Optional Label Changes ........................................................................................................ 29 7 Guidance for Commenters .................................................................................................... 29 7.1 Preliminary Work Plan ................................................................................................... 29 7.1.1 Trade Irritants .......................................................................................................... 30Page 6 of 63 7.1.2 Water Quality .......................................................................................................... 30 7.1.3 Environmental Justice ............................................................................................. 30 7.1.4 Additional Information ........................................................................................... 30 8 Next Steps .................................................................................................................... ......... 31 9 References .................................................................................................................... ......... 32

Appendix A Toxicology Profile ............................................................................................... 34 Appendix B Environmental Fate ............................................................................................. 42 Appendix C Ecotoxicology Profile .......................................................................................... 49 Appendix D Product Chemistry ............................................................................................... 62

List of Tables Table 1 – Summary of Anticipated Risk Assessments and Data Needs for Registration Review: PCP ........................................................................................................................... ...................... 8 Table 2 – Anticipated Regist ration Review Schedule .................................................................... 9 Table 3 – Chemical Identification of PCP ...................................................................................... 9 Table 4 – Physical-Chemical and Envir onmental Fate Properties for PCP .................................. 10 Table 5 – The Maximum Concentrations of Cont aminants in Technical PCP Detected in 2013 12 Table 6 – Characterization of Contaminants ................................................................................ 12 Table 7 – Summary of PCP Registered Uses ................................................................................ 13 Table 8 – Studies Anticipated as Needed for the Registration Review of PCP ............................ 15 Table 9 –Data Required by the September 21, 2011 Data Call-In for the PCP RED ................... 15 Table 10 – Toxicological Endpoints Selected fo r Risk Assessment of PCP (2008, RED) .......... 17 Table 11 – Toxicological Endpoints Selected fo r Risk Assessment of HCB (2008, RED) ......... 19 Table 12 – Occupational Exposure Scen arios for Workers Using PCP ....................................... 21 Table 13 – PCP Ecological Effects Endpoints for the Ecological Risk Assessment .................... 26Page 7 of 63 

## 1 Introduction

This document is the United States Environmen tal Protection Agency’s (USEPA, EPA or “the Agency”) Preliminary Work Plan (PWP) for pent achlorophenol, herein refe rred to as PCP. The PWP document explains what EPA's Office of Pesticide Programs (OPP) knows about PCP, highlighting anticipated data and assessment need s, identifying the types of information that would be especially useful to the Agency in conducting the review, and providing an anticipated timeline for completing PCP’s review.

The registration review process was designed to include a publi c participation component to solicit input from interested stak eholders. The Agency intends, by sharing this information in the docket, to inform the public of what it knows ab out PCP and what types of new data or other information would be helpful for the Agency to receive as it moves toward a decision on PCP. The Agency encourages all interested stakeholde rs to review the PWP and to provide comments and additional information that will help th e Agency’s decision-making process for this chemical.



## 1.1 Statutory and Regu latory Authority
The Food Quality Protection Act (FQPA) of 1996 mandated a regi stration review program. All pesticides distributed or sold in the United Stat es generally must be registered by EPA based on scientific data showing that th ey will not cause unreasonable risks to human health or the environment when used as directed on produc t labeling. The registrati on 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 environm ent. Changes in scien ce, 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. Inform ation on this program is provided at http://www2.epa.gov/pesticide-reevaluation

. The Agency is implementing the registration revi ew 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 th e FIFRA standard for registration. The regulations governing registra tion 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 registrati on review decision. After reviewing and responding to comments and data received in the docke t during this initial comment period, the Agency will develop and commit to a Final Work Plan (FWP) and anticipated schedule for the PCP case.



## 1.2 Case Overview
The docket for the PCP (case 2505) has been established at http://www.regulations.gov in docket number EPA-HQ-OPP-2014-0653. Docume nts associated with this registration review can bePage 8 of 63 viewed at this docket. Tables 1 and 2 below summarize the issues relevant to this registration review case and the anticipated registration review schedule.

Table 1 – Summary of Anticipated Risk Asse ssments and Data Needs for Registration Review: PCP

Risk Assessment Assessment Necessary to

Support Registration Review Date of Most Recent Assessment Type of Assessment

Required (New/Updated) *Data Anticipated as Needed (See Table 8 for details)

Dietary (food) No 1 9/25/2008 None None Dietary (drinking water) No 1 9/25/2008 None None Occupational Handler Yes 9/8/2008 Updated None 2

Residential Handler No (see Section 3.3.2) N/A None None

Residential Post Application - Incidental Oral and Dermal Yes 1 9/8/2008 Updated None

Residential Post Application No (see Section 3.3.3) N/A None None

Aggregate Yes 9/25/2008 Updated None 1

Cumulative No (see Section 3.3.5) N/A None None

Tolerance Review No (see Section 0) N/A None None

Ecological Yes 9/8/2008 Updated Aquatic invertebrates, semi-aquatic plants, benthic organisms N/A = Not applicable * Table 1 is a summary of the anticipated risk assessments and data needs for Registration Revi ew. For data called in through t he postReregistration Eligibility Decision (RED) Data Call-In (DCI), see Table 9.

1 Dietary (food and drinking water) and residen tial exposure are part of the general popul ation biological monitoring data from N HANES and will be accounted for in the anticip ated aggregate assessment.

2 Data already required by the 2011 post-RED PCP DCI.Page 9 of 63 Table 2 – Anticipated Registration Review Schedule
Anticipated Activity Target Date* Completion Date Phase 1: Openin g the Docket Open Docket and 60-Day Comment Period for Preliminary Work Plan 2014-12 2014-12 Close Public Comment Period 2015-02 Phase 2: Case Development

Issue Final Work Plan 2015-06

Issue Data Call-In (DCI) 2016-06

Receive Data to be Considered in Risk Assessment 2018-06

Open 30-Day Public Comment Period for Preliminary Risk Assessment(s) 2019-12

Close Public Comment Period 2020-01
Phase 3: Registration Review Decision and Implementation
Open 60-Day Public Comment Period for Proposed Decision 2020-06

Close Public Comment Period 2020-08

Issue Final Decision 2020-12

Begin Post-Decision Follow-up 2020
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 i ngredient in this case).



## 1.3 Chemical Identification and Properties

Table 3 presents the active ingredient to be assessed in case 2505: PCP (PC Code 063001).

Table 3 – Chemical Identification of PCP

Chemical Name PCP Chemical Classification Chlorophenols

PC Code 063001
CAS Number 87-86-5 Molecular Formula C 6 HCl 5 O Molecular Weight (grams/mole) 266.35

Molecular StructurePage 10 of 63 The PCP product chemistry information relevant to risk assessment is summarized in Table 4, and the details of the product chemistry and e nvironmental fate information are discussed in Appendix D and B, respectively.

Table 4 – Physical-Chemical and Envi ronmental Fate Properties for PCP

Guideline No. Parameter PCP Physical/Chemical Properties 830.7000 pH 4.99 830.7050 UV/Visible Absorption NA 830.7200 Melting point ( 25 o C) 191 830.7300 Density 1.987 g/ml 830.7370 Dissociation constant (pKa) 4.74

830.7550 Octanol-water partition coefficient at 25 o C (Log K ow ) 4.75 at pH 5, 5.27 at pH 7, and 5.1 at pH 9

830.7840 Solubility in water (mg/L) 0.3g/L at pH 5; 20 mg/L at pH 7, and 2200 mg/L at pH 9. 830.7950 Vapor pressure (mmHg); 25 o C 1.1 x 10 -4 mm Hg Environmental Fate Properties Mobility 835.1230 Adsorption/desorption study Moderately mobile in sandy loam, immobile in clay loam, moderately mobile in silt loam at low pHs, and mobile at high pH (MRIDs: 42633709, and 43627000) Persistence in Water (half-life) 835.2120 Hydrolysis at 25 o C: pH 5, 7 &9 (days) Hydrolytically stable at all three pHs in abiotic aqueous medium up to 30 days (MRID 42481101) 835.2240 Aqueous photolysis at 25 o C (days) Degrades rapidly at all three pHs at half-life between 13- 30 minutes. (MRID 42885401) 835.3100 Aerobic aquatic metabolism (days) Degrades in aqueous medium flooded with sandy loam soil; half-life of 14 days.(MRID 42288601) Persistence in Soil (half-life) 835.4100 Aerobic soil metabolism at 25 o C (days) Degrades with a half-life of 7-14 days in sandy loam soil (MRID 42594302) 835.4200 Anaerobic soil metabolism (days) Degrades with an observed half-life of 1- 2 months (MRID 42436801)

atm-m 3 /mol = atmosphere cubic meter per mole; o C = degrees Celsius; mg/L = milligrams per liter; mmHg = millimeters of mercury
A potential degradate/metabolite of PCP and other compounds has been identified as pentachloroanisole (PCA), Mol For: C 7 H 3 Cl 5 O; Mol.wt: 280.37, CAS# 1825-21-4. PCA is a derivative of PCP and other chlorinated phenol s found in the environmental media (such as pentachloronitrobenzene).

The Agency has noted that the Stockholm Conve ntion’s Persistent Orga nic Pollutants Review Committee (POPRC) decided in October 2014 to reco mmend to its Conference of Parties (COP) to list PCP and its salts and este r in Annex A to the Convention w ith specific exemptions for the production and use of PCP for utility poles a nd cross-arms. The POPRC considered PCA together with PCP in making this determinati on. The COP has not yet met to decide on this recommendation.Page 11 of 63 Pentachloroanisole (PCA)



## 1.4 PCP and Contaminants
There are three general types of contaminants in PCP. Two types are chlorinated dioxins (CDDs)/chlorofurans (CDFs) compounds: 2, 3, 7, 8-tetrachlorodibenzo-p- dixoin (2,3,7,8 TCDD) and generic HxCDD. The third t ype of contaminant is hexachlorobenzene (HCB). In the past, the Agency has referred to these as “microcontam inants.” For every pesticide product registered at EPA, a confidential statement of formula (CSF) is required to report all the components and their percentage by weight in the product. Contaminants below 0.1% are not reported on the CSF, hence the term microcontaminants - contam inants below the 0.1% reporting limit present at ppm levels (micro levels). These microcontaminan ts are herein referred to as contaminants.

PCP registrants provide monthly reports of analytical data which inform the levels of contaminants in the technical PCP. The sample s of PCP are provided from a manufacturing plant currently in use. Table 5 lists measured value of concentrations in PCP products. The data are presented with written consent from the registrant for the PCP case to demonstrate the extent to which contaminants have decreased from 1986 to 2013.Page 12 of 63 Table 5 – The Maximum Concentrations of Co ntaminants in Technical PCP Detected in 2013

Substance Name 1986 Maximum Concentrations in Technical PCP Levels Detected in 2013 Samples 1 Molecular Structure

HCB 75 ppm 19.33 ppm

2,3,7,8 TCDD Non-detect < 0. 001 mg/kg Non-detect < 0.001 mg/kg

HxCDD 2 ppm 0.554 ppm

1 Registrant’s letter, dated Oct. 6, 2014

Detailed product chemistry characteristics of a ll three contaminants were addressed in the 2008 RED document.

Some physical chemical characte ristics are shown in Table 6.

Table 6 – Characterization of Contaminants

Substance Water solubility Vapor pressure Log K ow

HCB (CAS# 118-74-1) 6000 mg/L 1.1 x 10 -5 mm Hg 6.18

CDDs and CDFs (including HxCCD) Varies from 1.18 x 10 -4 mg/L to 7.4 x 10 -8 mg/L Varies from 1.4 x 10 -8 mm Hg to 3.75 x 10 -12 mm Hg Varies from 6.1 to 8.1



## 1.5 Use/Usage Description

1.5.1 Registrations There are four EPA-registered products that cont ain PCP as an active ingr edient (a.i.). One of these products is a technical/formulation intermed iate product, and the other three products are end-use products. The formulations include ready-to-use solutions and soluble concentrates. The technical/manufacturing use product contains a nominal concentra tion of 86 percent PCP (other chlorophenols listed as an addi tional 10 percent). The nominal c oncentrations of the three enduse products range from 4.3 percen t (other chlorophenols listed as an additional 0.5 percent) to 86 percent (other chlorophenols listed as an additional 10 percent).Page 13 of 63 PCP is classified as a restricted use pesticide (R UP) for sale and use by ce rtified applicators only. Indoor applications of PCP are prohibited as we ll as application to wood intended for use in interiors (with certain ex ceptions) or for use in contact with food, feed, or drinking water. These restrictions were imposed on PCP registrations as part of the Ag ency’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)

.



### 1.5.2 Summary of Registered Uses

Table 7 presents a summary of the registered uses of PCP that will be assessed in this registration review case. PCP is applied using specialized high pressure treatment cylinders (also called “retorts”) by pressure and thermal treatment. The target rate of retention is not currently specified on labels because it varies with respec t to the petroleum solven t used, species of wood treated, type of wood product and specific Am erican Wood Protection Association (AWPA) standards. For specific retenti ons, refer to AWPA standards.

Table 7 – Summary of PCP Registered Uses

Use Application Method Application Rate

Wood or Wood Structure Protection Treatments

Pressure Treatment to Forest Products Pressure Treatment NR

NR: Not reported on existing labels.



### 1.5.3 Usage Information

According to the Kline Biocides Report fo r 2004/2005, PCP is one of the leading wood preservatives for poles and is preferred by many utility companies. In 2004, U.S. consumption of PCP was estimated at 24.5 million pounds, and wa s forecasted to grow at an average volume rate of 1.6 percent. In 2004, there were onl y two major suppliers of PCP (Kline, 2005).



## 1.6 Regulatory History

PCP has been used as a wood preservative si nce 1936; however, the first pesticidal product containing PCP was registered by the United Sa tes Department of Agriculture (USDA) on December 1, 1950. In 1970, EPA was established and was charged with protecting human health and the environment, and assumed all pesticide registrations from USDA.

In October 1978, an administrative review process was initiated to consider whether the pesticide registration of the three heavy duty wood preservative uses (inclu ding PCP) should be canceled or modified. The Federal Register (Vol.49, No.139) of July 13, 1984 concluded that process and announced that certain changes in the terms and conditions of registrati on were required if registrants and applicants wi shed to avoid cancellation.Page 14 of 63 After evaluating the risk s to public health posed by these three heavy duty wood preservative chemicals (including PCP) along with the significan t economic benefits resulting from their use, the Agency determined that the use of PCP as a wood preservative chemical in accordance with certain modifications to terms of registration would satisfy the st atutory standard for registration. These modifications (classification as restricted use pesticide, worker protection/protective clothing and equipment label requirements, restrict ed to non-residential uses, etc.) are identified and described in the Federal Register of Ja nuary 13, 1986 (Vol.51, No. 7). Additionally, all nonpressure treatment and non-thermal treatments fo r PCP products have been voluntarily deleted.

The Agency completed a Reregistration Elig ibility Decision (RED) for PCP in 2008. EPA determined that PCP products contribute benefits to society and are elig ible for reregistration provided the mitigation measures and associated label changes identified in the 2008 RED are implemented and required data are submitted. A post-RED Generic-Data Call-In (GDCI) and Product-Specific-Data-Call-In (PDCI) were issued on September 21, 2011.



### 1.6.1 Tolerance Information For the active ingredient PCP, EP A has not established tolerances or exemptions from tolerances in raw agricultural commodities or processed food and feed products under the Federal Food, Drug and Cosmetic Act (FFDCA) Section 408 for pentachlorophenol. PCP has been cleared as a food additive by the US Food and Drug Admini stration (US FDA) under FFDCA Section 409 for use as a component in adhesives in 21 CFR 175.105 and is also a component in wood preservatives in 21 CFR 178.105. There are no existing food uses for the wood preservative use.



## 1.7 Incidents

1.7.1 Human Health
Based on a search conducted on October 29, 2014 , covering the period from January, 1905 to January, 2008, over 300 incident re ports exist in the EPA’s In cident Data System (IDS) associated with human PCP exposures. No PCP incidents have been re ported after this time period. In addition, the number of incidents and ep idemiological studies published in scientific literature addressing possible associations between expos ure to PCP and subsequent development of disease is large. The associated concerns include chloracn e, tremors, allergies, insomnia, twitching, diarrhea, dizziness, soft tissue sarcoma, non-Hodgkin’s lymphoma and possibly abnormal births. Whether these deleteri ous health effects result from exposure to PCP specifically, or to one or more other chemicals typically found as contaminants, is not clear.



### 1.7.2 Ecological

No ecological incidents exist in the IDS as of August 12, 2014.Page 15 of 63 

## 2 Anticipated Data Needs

Several studies were required by the DCI followi ng the assessment of PCP in the 2008 RED. In addition to the already-required post-RED DCI data , the following studies as listed in Table 8 are expected to be needed for the registration review of PCP. Table 9 outlin es the data requirements required by the post-RED DCI issued on Septembe r 21, 2011. The Agency anticipates reviewing data received in response to the post-RED DCI as well as data requested for this registration review prior to conducting the registrati on review risk assessments for PCP.

Table 8 – Studies Anticipated as Needed for the Registration Review of PCP

GLN Study Name Test Substance Time Frame (Measured in months from DCI Receipt) Risk Assessment(s)

Data Will Support Use Site(s) Triggering Anticipated Data

Requirement Applicable Exposure Scenario

850.1300 1 Freshwater invertebrate, life cycle TGAI 12 Ecological Wood preservatives Aquatic environment – Aquatic invertebrates

850.4225 2 Seedling emergence, rice TGAI 12 Ecological Wood preservatives Aquatic environment - Semi-aquatic plants

-No GLN 3 Whole sediment, chronic, freshwater (2 spp.) TGAI 24 Ecological Wood preservatives Aquatic environment - Benthic organisms

No GLN 3 Whole sediment, chronic, estuarine/marine TGAI 24 Ecological Wood preservatives Aquatic environment - Benthic organisms

1 The anticipated DCI will require that testing be conducte d with the most sensitive organism (either freshwater or estuarine/marine vertebrates, or freshwater or estuarine/marine invertebrates), as determined from the results of the existing acute toxicity tests.

2 Data on only one plant species (rice, Oryza sativa ) are anticipated to be required.
3 The anticipated DCI will require that a protocol must be a pproved by the Agency prior to the initiation of the study.
Table 9 –Data Required by the Septemb er 21, 2011 Data Call-In for the PCP RED

GLN Study Name Status of DCI 835.6100 Terrestrial field dissipation Waiver request granted. 875.1100 Dermal exposure – outdoor The 2011 DCI specified that the registrant is only required to perform two of the four exposure tests listed, one dermal and one inhalation. In place of these studies, the registrant submitted a biomonitoring protocol study for review (MRID 49278800). The Agency is reviewing the protocol for this observational study. If the protocol and results from the ensuing study are approved, this study would satisfy the exposure study requirements for the PCP 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 Application exposure monitoring data reporting

875.1700 Product use information No data have been submitted; this study is outstanding.Page 16 of 63 

## 3 Human Health Risk Assessment

The Agency anticipates the need to conduct an updated human health risk assessment for PCP based upon the updated exposure study data from the 2011 post-RED DCI. PCP contains CDDs, CDFs, and HCB as contaminants formed dur ing the manufacturing process. Direct measurements of CDDs/CDFs and HCBs for the gene ral population attributed to pressure treated wood are not available for this assessment. Theref ore, to be inclusive of determining potential exposures to PCP contaminants, the amount of H CB and the toxicity equivalents (TEQ) of the CDDs/CDFs in the PCP during manufacturing will be used to extrapolat e equivalent HCB and dioxin exposures for PCP in treated wood. The Agency will use the latest manufacturing reporting information about how much HCB and dioxin are present in PCP samples from the PCP task force, which was created to respond to data requirements and other reevaluation information for the PCP case.

Population-based biological monitoring data fr om the National Health and Nutrition Surveys (NHANES) are available to assess the exposure of the general population to PCP. The NHANES data provides an encompassing review of a ll PCP exposures; the specific PCP treated wood contribution to total PCP exposure cannot be differentiated. The Agency used 2001–2002 NHANES data to inform the 2008 RED and will upda te the registration review risk assessment with the latest available NHANES data from 2003-2004 or a more recent NHANES dataset should one become available at the time of risk assessment. Because NHANES does not include exposures to children under the age of 6 years old, the Children’ s Total Exposure to Persistent Pesticides and Other Persistent Organic Pollu tants (CTEPP) study (Wilson, et al. 2007) will be used to include estimates of exposur es to children under 6 years old.



## 3.1 Existing Toxicological Endpoints

3.1.1 PCP In preparation for the reregistration risk as sessment in 2008, the Agency selected a set of toxicological end-points (2008 RE D). Subsequent to the RED, the Agency’s Integrated Risk Information System (IRIS) program released a PCP reassessment in 2010. The updated Cancer Potency Factor for PCP is 4 × 10 -1 per mg/kg-day compared to th e cancer slope factor (CSF) of 7× 10 -2 per mg/kg-day used in 2008 RED representi ng an almost 5.7-fold increase in cancer potency (IRIS, 2010, http://www.epa.gov/IRIS/subst/0086.htm ). The revised hazard information will be used in the final risk assessment process. The existing database of studies is tabulated in Appendix APage 17 of 63 Table 10 – Toxicological Endpoints Selected for Risk Assessmen t of PCP (2008, RED)

Exposure Scenario Dose (mg/kg/day) Endpoint Study

Acute Dietary Developmental NOAEL = 30 Increased resorptions,reduced fetal weight, and skeletal malformations Developmental toxicity - rat

MRID # 43091702

UF = 100 a Acute RfD = 0.3 mg/kg/day
Chronic Dietary

LOAEL = 1.5 Incr. liver weight and alk. phos. activity; increased incidence of granular cytoplasmic pigment accumulation in the liver Chronic Toxicity - Dog

MRID # 43982701

UF = 300 a Chronic RfD = 0.005 mg/kg/day
Carcinogenicity (dietary) Classified as a B2 (probable human carci nogen) carcinogen by the Health Effects Division Carcinogenicity Assessment Review Committee and EPA’s Science Advisory Board. An oral cancer risk estimate (q1*) of 7.0 x 10 -2 per mg/kg-day was calculated based on the incidences of hepatocellular neoplasms, adrenal medullary neoplasms, and hemangiosarcomas that developed in female mice treated with technical grade PCP or Dowicide EC-7 (NTP, 1989). The slope factor was calculated as the geometric mean of the individual slope factors derived from two data sets: female mouse data for techni cal grade and Dowicide EC-7 PCP. This slope factor may change based on a more recent analysis of the NTP dataset by EPA’s National Center for Environmental Assessment (NCEA) pending peer review of the updated Toxicological profile for the IRIS database.

Short and Intermediate - term (Dermal) a NOAEL = 30 a MOE = 100 Increased resorptions, reduced fetal weight, skeletal malformations Developmental - Rat

Long-term (Dermal) LOAEL = 1.5 a MOE = 300 Incr. liver weight and alk. phos. activity; increased incidence of granular cytoplasmic pigment accumulation in the liver Chronic Toxicity - Dog

Inhalation No inhalation data available for PC P. Inhalation risks for occupational exposure were not performed because most inhalati on values derived from the biomonitoring study in workers were below the level of quantitation, thus implying that the majority of worker exposure is through dermal contact with PCP.

a All exposure scenarios are based on absorbed dose from the biological monitoring studies (oral short- and

intermediate-term NOAEL and oral long-term LOAEL are used to estimate risks with the Target MOEs of 100 and 300, respectively).

PCP also contains CDDs/CDFs and HCB as c ontaminants formed during the manufacturing process. HCB is present in PCP at a concentratio n of 19 ppm. TEQ dioxin is present in PCP at a concentration of 0.413 ng TEQ dioxin/mg PCP (Van den Berg et al, 2006). To estimate the TEQ dioxin lifetime average daily dose (LADD), th e LADD for PCP is multiplied by the TEQ dioxin conversion factor (i.e., 1 mg/kg/day PCP x 0.413 ng TEQ di oxin/mg PCP x 1 mg/1,000,000 ng unit conversion = 4.13E-7).To estimate the HCB exposure dose, the exposure dose for PCP is multiplied by the HCB conversion factor (i .e., 1 mg/kg/day PCP x 19 ng HCB/mg PCP x 1 mg/1,000,000 ng unit conversion = 0.000019).Page 18 of 63 

### 3.1.2 Contaminants

CDD and CDFs

Acute and Chronic Toxicity

The concept of toxic equivalency factors (TEFs) has been develope d to facilitate risk assessment of exposure to chemical mixtures of CDDs a nd CDFs. In this procedure, individual TEFs are assigned to the various congeners of CDDs and CDFs. These values have been published by both the USEPA and the World Health Organiza tion (Younes, 1998) and are based on assigning relative values in re lation to 2,3,7,8-TCDD, which is assigne d a TEF value of 1.0, it being the most potent congener. Multiplying the exposure c oncentration of indivi dual congeners by their respective TEFs yields a toxic equivalency, whic h, when summed for all the components of the mixture, gives the TEQ for that mixture and is an indication of the additional exposure from the PCP contaminants. Recent developments in science policy in the Agency ha ve resulted in a shift towards calculation of non-cancer risk from di oxins and furans using a body burden approach rather than a dose or intake approach. This is appropriate for dioxin/furan contaminants of PCP due to the long half-life of these chemicals. Th e Agency’s Office of Research and Development (ORD) has led the effort in characterizing hazards and risks from exposur e to dioxins and dioxinlike compounds, and OPP, in its assessment of non-cancer risks posed by the dioxin/furan contaminants in PCP, is working with ORD to express these risks using the methodologies developed in ORD for calculation of body burdens from exposure to the contaminants in PCP treated wood.

Carcinogenicity

A carcinogenic endpoint related to absorbed doses of CDD and CDF contaminants has been identified. At this time, for purposes of cancer risk assessment, the Agency is using the currently published sl ope factor of 1.0 x 10 5 per mg/kg-day for the 2,3,7,8 congener.

HCB

As summarized in Table 11, the Agency selected a set of HCB toxicological end-points for the reregistration risk assessment in 2008 (2008 RED) . No additional toxicological information was identified in the draft 2013 ATSDR Toxicologi cal Profile for HCB which summarizes existing literature information for HCB.

Acute and Chronic Toxicity

The toxicology of HCB is discussed in deta il within the 1991 “Dri nking Water Criteria Document for Hexachlorobenzene,” prepared by the U.S. EPA’s Office of Health and Environmental Assessment (EPA, 1991) and the “ATSDR Toxicological Profile for Hexachlorobenzene” (ATSDR, 2002). Both assessme nts characterize the acu te toxicity of HCB as low, with oral LD50 values in the range from 3500-10,000 mg/kg in rats, and other data citing 1700 mg/kg in rats, 2600 mg/kg in ra bbits, and 4000 mg/kg in mice.Page 19 of 63 Carcinogenicity

The Agency has classified HCB as a B2 (pr obable human) carcinogen, based on data sets that showed induction of tumors of the thyroid, liver, and kidney in three r odent species (U.S.EPA, IRIS, 1996). In the IRIS database, the oral can cer slope factor was 1.7 (mg/kg/day)-1 based on hepatocellular carcinomas in female Sprague-Dawle y rats using a 2/3's animal to human scaling factor. However, based on current agency policy, a 3/4's scaling factor is applied to adjust the slope factor. The cancer slope factor for HCB was modified by 0.6X to account for the newer factor. For this evaluation, carcinogenic risk was assessed for non-di etary exposure to HCB using the modified cancer slope factor of 1.02 per mg/kg-day.

Table 11 – Toxicological Endpoints Selected for Risk Assessmen t of HCB (2008, RED)

Exposure Scenario Dose (mg/kg/day) Endpoint Study

Incidental Oral: Short-Term NOAEL = 40

Target MOE = 100 Body weight loss, hyperesthesia, tremors, convulsions in maternal rats at 60 mg/kg/day. Developmental toxicity – rat

(Khera, 1974)

Incidental Oral: Intermediate-Term LOAEL = 0.5

Target MOE = 100 Increased incidence of liver porphyrin levels in female rats at 2 mg/kg/day 15 Week OralToxicity- Rat (KuiperGoodman et al, 1977)

Dermal: Short-Term Oral NOAEL = 40 mg/kg/day (a

MOE = 100 Body weight loss, hyperesthesia, tremors, convulsions in maternal rats at 60 mg/kg/day. Developmental toxicity – rat

(Khera, 1974)

Dermal: Intermediate-Term LOAEL = 0.5

Target MOE = 100 Increased incidence of liver porphyrin levels in female rats at 2 mg/kg/day 15 Week OralToxicity- Rat (KuiperGoodman et al, 1977)

Dermal: Long-Term Oral NOAEL =0.08 mg/kg/day

Target Moe = 100 Hepatic centrilobular basophilic chromogenesis at 0.29 mg/kg/day Chronic Toxicity - Rat (Arnold et al., 1985)

Inhalation Short-, Intermediate, and Long-Term No route-specific endpoints are av ailable for HCB. Therefore, in accordance with agency po licy, oral endpoints and route extrapolation are employed to estimate inhalation risks as needed. Target MOE = 1000

Carcinogenicity B2 (probable Human Carcinogen). Q*=1.02 per mg-kg/day. (Extrapolated using a Q*of 1.7(mg/kg/day)-1 derived from a linearized multistage model to which a 3⁄4 scaling factor was applied: 1.7 x 0.6 =1.02) Sourced to EPA REDs for DCPA, November 1998, and Chlorothalonil, April 1999 and EPA’s IRIS Database.
a). Since an oral endpoint was selected for HCB dermal risk assessments, a derm al absorption value of 26.0 % should be used in route-to-route extrapolations.



## 3.2 Dietary Exposure

The most recent dietary exposure assessment fo r PCP was done in support of the 2008 RED using dietary monitoring data assembled by the Food and Drug Admini stration (FDA) fromPage 20 of 63 1991. The dietary monitoring data assembled by FDA for certain food items have been discontinued since 1992 based on a lack of de tectable residues. The 2008 non-occupational exposure and risk assessment for the PCP RED was also based on the NHANES biological monitoring data from the 2001-2002 survey. The NHANES data account for both indirect dietary exposures and exposures through drinking water more effectively than the standard models normally used by the Agency to esti mate exposures. Residues of PCP have been measured in urine by the NHANES data. U pdated 2003-2004 data (or a more recent NHANES dataset) will be included in the aggregate asse ssment (see Section 3.3.4) as part of registration review. A separate dietary asse ssment is not anticipated to be required at this time since the NHANES data reflect any potential dietary exposure to PCP.



### 3.2.1 Food

Dietary exposure to PCP was previously evaluate d as part of the U.S. EPA’s 2008 RED. Given the restrictions on use of this pesticide in place since 1984, a dietary risk assessment is not anticipated to be necessary. As part of the 2008 RED, the Agency conducted a dietary exposure assessment using FDA monitoring data from 1991 th at showed levels of PCP in a few food items as well as NHANES data from 2001-2002.

Since risks of concern were not identified at that time and no addi tional uses that would contribute additional exposure from food contact have been registered, the Agency does not anticipate the need for additional residue chemistry data.



### 3.2.2 Drinking Water

No separate human drinking wate r exposure assessment is expected for PCP. As discussed above, the NHANES biomonitoring data will include any human exposures from drinking water.



## 3.3 Occupational and Re sidential Exposures
The agency anticipates the need to revise the occupational and resident ial assessments conducted in support of the 2008 RED. This is needed to account for new exposure monitoring studies required in the 2011 post-RED DCI and the revised t oxicological endpoints th at are likely to be selected based on the new cancer slop factor fo r PCP. Since no residential handler uses are expected from the use of PCP, a risk assessment is not required. However, EPA will be assessing residential post-application exposures.

As a result of the past RED mitigation, the Agency implemented mitigation measures to reduce exposure to workers in wood treatment facilities. In an effort to determine if those mitigation measures are effective in reducing exposure, th e Agency issued a post-RED DCI notice requiring that new exposure monitoring studies be conducte d at wood treatment fac ilities using the latest personal protective equipment (PPE) and engineeri ng controls to mitigate exposures that were specified in the 2008 RED (e.g. ve ntilation systems, vacuums after treatment, and automated cylinder doors). These mitigation measures are reflected on the PCP product labels. The Agency received a protocol (MRID 49278801) for a wood pressure treatment biomonitoring study andPage 21 of 63 expects to receive a new study during registrati on review that should help the Agency to determine new exposures based on the new exposur e control measures speci fied in the RED.

To assess exposures to pole installers (electrica l utility linemen), a chemical-specific biological monitoring post-application study was used by the Agency (Thind et al. 1991). The purpose of the study was to characterize ch ronic or long-term exposure of PCP to linemen by examining PCP levels in workers’ urine.



### 3.3.1 Occupational Exposure The Agency conducted an occupational asse ssment for the RED for PCP on September 8, 2008 (U.S. EPA, 2008e). The occupational assessment wa s based on absorbed doses for occupational workers using chemical-specific biological monitoring data submitted by the PCP Task Force (MRID 44813701) and the biological monitoring data for electrical utility linemen (Thind et al. 1991).

The Agency anticipates receiving new occupatio nal studies for the wood preservative use (exposure studies to monitor work exposure at pre ssure treatment plant) in order to conduct new occupational risk assessments to assess the de rmal and inhalation routes of exposure from pressure treatment exposure and pole lineman dur ing registration review. The scenarios outlined in Table 12 are the typical wo rker exposure scenarios for a variety of exposures. Studies accounting for these exposure scenarios were required by the 2011 post-RED DCI (see Table 9).

For example, for pressure treatment facilities, workers operate and mon itor application system valves and controls, open and cl ose cylinder doors (automated), 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 fo r shipment. Workers perform various labor and cleanup duties in treatment and dr ip 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 wast e; cleaning cylinders; and, ha ndling hazardous waste.

Table 12 – Occupational Exposure Scenarios for Workers Using PCP

Scenario Exposure Route(s) Duration Occupational Exposures
Pressure Treatment Workers Dermal and Inhalation * Short, Intermediate, and Long- Term

Pole Installers Dermal and Inhalation* Short, Intermediate, and Long- Term
*Biological monitoring data can be used in lieu of dermal and inha lation monitoring studies.



### 3.3.2 Residential Handler Exposures Residential handler exposures ar e not expected based on the labe led use patterns; therefore, a residential assessment is not anticipated as needed for this registration review.Page 22 of 63 

### 3.3.3 Residential Post-Application Exposures Population-based biological mon itoring data from the NHANES data are available to assess the exposure of the general population to PCP. The NHANES data provides an encompassing review of all PCP exposures. Because NHANES do es not include exposures to children under the age of 6 years old, the CTEPP study will also be used to include estimates of exposures to children under 6 years old. EPA will base th e residential exposures based on NHANES and CTEPP data and calculate non-cancer and cancer risks. The amount of HCB and the toxicity equivalents (TEQ) of the CDDs/CDFs in the PC P during manufacturing are used to extrapolate equivalent HCB and dioxin expos ures for PCP in treated wood.


### 3.3.4 Aggregate Exposures EPA anticipates the need to revise the aggr egate assessment conducted in support of the 2008 RED using updated NHANES data. Upon a reeval uation and selection of toxicological endpoints, combined with the human health exposure assessments expected as a part of this registration review case, aggregate exposures will need to be assessed.

This assessment will include dietary (food) expos ures and residential exposures based on the latest NHANES data. EPA believes the NHANES data set provides the most comprehensive data on exposure to PCP from all sources (dietary and non-dietary as well as both EPA- and FDAregistered uses) and is the best dataset for es timating aggregate risk to triclosan. Because NHANES does not include exposures to children under the age of 6 years old, the Children’s Total Exposure to Persistent Pe sticides and Other Persistent Organic Pollutants (CTEPP) study (Wilson, et al. 2007) will be used to include estim ates of exposures to children under 6 years old.



### 3.3.5 Cumulative Exposures With respect to cumulative exposure, unlike other pesticides for which EPA has followed a cumulative risk approach based on a common me chanism of toxicity, EPA has not made a common mechanism of toxicity finding as to PCP. For the purposes of this registration review, therefore, EPA has not assumed that PCP has a common mechanism of toxicity with other substances. For information regarding EPA’s ef forts 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 in registra tion review will allow the Agency to determine potential acute and chronic risk s to non-target organisms and to aquatic organisms exposed to PCP and its degradates and impurities that may be transported from antimicrobial use sites into the terrestrial and aquatic environments (includi ng in-service uses of PCP treated wood). The Agency has not yet conducted a risk assessmen t that supports a complete endangered species determination for PCP. The risk assessment will allow the Agency to determine whether its use has 'no effect' or 'may affect' federally listed th reatened or endangered species (listed species) or their designated critical habita ts. 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.Page 23 of 63 Fish and Wildlife Service and/or National Mari ne Fisheries Services (the Services), as appropriate.

The Agency conducted preliminary environmental risk assessments for the 2008 RED. Ecological risks were assessed separately for PCP (EPA 2008b), for the dioxin/furan (CDDs/CDFs) contaminants (EPA 2008c), and for the HCB contaminants (EPA 2008d). The only use assessed was the in-service use of treated utility poles. Risks from in-service uses of PCP-treated wood in other terrestri al situations (e.g., fences, timb ers, railroad ties) and in the aquatic environment (e.g., pilings, wharves) were not assessed. Risk assumptions from the preliminary assessments are summarized below. Since the time of the RED, EPA has not received information that would alter the ri sk conclusions from 2008. However, in 2013, EPA released new data requirements for antimicrobial pesticides (Subpart W of 40 CFR Part 158) to update scientific framework for identifying a nd assessing risks. In re gistration review, the Agency anticipates the need to request ecotoxicity data to characterize the risks identified in the 2008 RED.

In the RED, based on the moderate toxicity of PCP to the laboratory rat and the low concentration of PCP expected in soil around utility poles, minima l acute risk was presumed for small wild mammals. Due to low estimated en vironmental concentration (EECs) modeled for surface waters, minimal acute risk also was pres umed for birds feeding on aquatic organisms. The potential for chronic risk to birds and mammal s, acute risk to beneficial insects, and acute risk to birds and mammals feeding on contaminat ed foods (e.g., soil invertebrates, seeds, small mammals) was not addressed.

For PCP aquatic organism risk presumptions were based on RQ methodology. Aquatic EECs were modelled based on environmental fate parame ters and resultant esti mates of movement of leachate from utility poles. Based on comparing EECs to ecotoxicity values, minimal acute and chronic risks were presumed for exposure of freshw ater fish and aquatic i nvertebrates. Minimal acute risk also was presumed for estuarine/marine fish and invertebrates, but chronic risk could not be assessed due to lack of chronic toxicity data for estuarin e/marine organisms. Risk to freshwater and estuarine/marine benthic invertebrates was not addr essed due to lack of sedimenttoxicity data. Risk to vascul ar aquatic plants and algae were below the Agency’s LOCs.

The RED also examined risks from the contaminants and determined some potential risks. Since the amount of contaminant levels have been redu ced since the time of th e RED, these risks will be re-evaluated in registration review.



## 4.1 Environmental Fate Assessment
The environmental fate assessment is primarily for PCP and for the contaminants CDDs, CDF, and HCB. Previous analyses have not shown PC A as a major degradate of PCP. However, in light of the recent Stockholm Convention PO PRC analysis of PCP, EPA is reviewing information and data available for PCA to determine if it is appropriate to include PCA in the risk assessment to be conducted in registration review. The Agen cy welcomes the submission of PCA information and data from the public and in terested stakeholders to this PWP during the comment period.Page 24 of 63 PCP is hydrolytically stable at pH, 5, 7, and 9 unde r abiotic conditions. It de grades photolytically in aqueous medium with a half-life of between 13-20 mi nutes (MRID 42481101). Major and minor degradates have been iden tified as tetra and tr ichlorophenols which are discussed in more detail in Appendix B.

PCP degrades in aerobic soils and aquatic syst ems with a half-life of 7-14 days, and under anaerobic conditions with a ha lf-life of 1-2 months.

PCP has a log Kow of 5.05 and may be bioaccumula tive in aquatic animals. PCP adsorption to soils is pH dependent. At acidic pHs, PCP is tightly bound to the soil structure, but as pH increases, adsorption decreases resulting in greater mobility at neutral and higher pHs.

Chlorinated dioxins, HCB, and PCA are relatively in soluble and stable in the environment. They all have characteristics which indicate the potential for bioaccumulation.



### 4.1.1 Water Quality PCP is not identified as a cause of impairment for any water bodies listed as impaired under section 303(d) of the Clean Water Act. 1 In addition, no Total Maximum Daily Loads (TMDL) have been developed for PCP. 2 However, PCP has two types of contaminants: CDDs, and CDFs (abbreviated as dioxins) and HCB. Dioxins are identified as a cause of impairment for 617 water bodies in the United States. Fish is consumed from these impair ed water bodies. Source(s) of origin of these CDDs and CDFs in impaired water bodies and their presence in fish are not identified. HCB is identified as a cause of impair ment for 44 water bodies in the United States. Fish is consumed from these impaired water bodi es. Source(s) of origin of HCB in impaired water bodies and their presence in fish are not identified. It is st ated that no TMDLs are needed for these impairments. More information on im paired water bodies and TMDLs can be found at EPA’s website. 3



## 4.2 Environmental Exposure Pathways
Leachate from treated wood is likely to be the primary source of environmental exposure to nontarget organisms. PCP and its degradates and impurities may leach into the soil surrounding treated utility poles, fences, tim bers, and other treated wood. PC P, CDDs/CFDs, and HCB might be transported into the aquatic environment via various environmental pathways, including runoff and leaching. PCP-treated wood used direc tly in the aquatic envi ronment will leach PCP and its’ degradates and impurities directly into surface waters and sediments. Most material reaching the aquatic environments is expected to bind to organic matter and sediments and expose benthic invertebrates. A soluble fraction of the leachate also will be present in the water column and may expose fish, aquatic invertebrate s, and aquatic plants. In the water column, exposure is expected to be acute , whereas chronic exposure is exp ected in aquatic sediments. Bioconcentration in fish and aquatic invertebra tes may result in exposure and bioaccumulation in predators, such as fish-eating birds an d mammals, larger fish, and reptiles.

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

2 http://iaspub.epa.gov/tmdl_waters10/attains_nation.tmdl _pollutant_detail?p_pollutant_group_id=885&p_pollutant_ group_name=PESTICIDES

3 http://www.epa.gov/owow/tmdl/Page 25 of 63 Terrestrial organisms also may be exposed via va rious environmental pathways. Invertebrates in and around treated wood structures may be exposed from contam inated soil. Contaminated invertebrates may be eaten by other terrestrial animals, including small mammals, birds, and reptiles. Bioaccumulation may l ead to higher trophic levels bei ng exposed as PCP, CDDs/CDFs, and/or HCB move through the food chain.

Likely pathways for exposure of nontarget organisms are summarized below. All relevant routes of environmental exposure will be co nsidered in the risk assessment.

Terrestrial Organisms • Dietary exposure of small mammals and birds to leachate in soil and food sources (e.g., invertebrates, seeds) on and in the soil surrounding treated wood structures. • Dermal contact of benefi cial insects, birds, and small mammals with treated wood surfaces. • Dietary exposure of predatory mammals , birds, and reptiles to contaminated prey; bioaccumulation may lead to exposure at hi gher trophic levels in the food chain. • Ingestion of residues through drinking wate r sources such as puddles or roadside ditches at the use site.

Aquatic or Semi Aquatic Organisms • Exposure via contaminated surface waters. • Exposure via contam inated aquatic sediments. • Dietary exposure of predatory and herbivor ous fish and reptiles to contaminated prey and aquatic plants; bioaccumulation may lead to e xposure at higher trophic levels in the food chain. • Uptake of residue in surface waters by aquatic plants. • Uptake of residue in surface waters and sediments by rooted semi-aquatic plants.

A conceptual model diagram (CMD) also is av ailable for wood preservative uses. Based on antimicrobial use patterns, the Agency develope d conceptual models fo r 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 Mechanism of Action

The toxicity of PCP to animals is due to th e uncoupling of oxidative phosphorylation in the mitochondria. This results in reduced production of adenosine triphosphate (ATP), accompanied by weight loss due to acce1eration of metabolic ra te and utilization of tissue energy reserves (EPA 1986). Activities of various enzymes also are affected.Page 26 of 63 

### 4.3.2 Measures of Effect (Ecotoxicology Endpoints)

4.3.2.1 Available Ecotoxicity Endpoints Acute and chronic ecotoxicity endpoints are curren tly available for PCP from several sources. Registrants have submitted ecotoxicity studie s conducted in accordance with the 850 OCSPP Harmonized Test Guidelines to address the da ta requirements for pesticide registration. Additional data are available in EPA’s Office of Water Ambient Water Quality Criteria for Pentachlorophenol – 1986 (EPA 1986) and the OPP Pesticid e Ecotoxicity Database. These acute and chronic data will be used to evaluate the potential effects of PCP to terrestrial and aquatic animals and plants. For the CDDs /CDFs and HCB contaminants, which are not registered pesticides, 850 guideli ne studies are not available, but some data were previously compiled from the open literature. See Appendix C for additional information on the ecotoxicity data EPA has for the PCP case.

4.3.2.2 PCP All data requirements (existing database of studi es and studies anticipated to be required) and available ecotoxicity endpoints for PCP are tabu lated in Appendix C . The most sensitive of those endpoints will be used for assessing risk to each receptor group. The endpoints currently available for the risk assessment for PCP are pr ovided in Table 13. Endpoints for mammals are found in section 3.1 (Human Health Risk Asse ssment – Existing Toxicological Endpoints).

Table 13 – PCP Ecological Effects Endpoints fo r the Ecological Risk Assessment

Receptor

Group Test Material Risk Scenario Toxicity Endpoint Reference

Freshwater fish TGAI Acute LC50 = 15 μg ai/L 43485104 Chronic NOAEC = 11 μg ai/L EPA 1986

Freshwater invertebrates TGAI Acute EC50 = 92 μg ai/L EPA 1986 Chronic NOAEC <4.1 μg ai/L 1 EPA 1986
Freshwater benthic invertebrates TGAI Chronic Data gap --

Estuarine/marine fish TGAI Acute LC50 = 31 μg ai/L 40228401 Chronic NOAEC = 6.6 μg ai/L See Appendix C

Estuarine/marine

invertebrates TGAI Acute EC50 = 34 μg ai/L USFWS 1980 Chronic Not required --

Estuarine/marine benthic invertebrates TGAI Chronic Data gap --

Algae TGAI EC 50 NOAEC EC50 = 27 μg ai/L NOAEC = 9 μg ai/L 42633704

Aquatic vascular plants TGAI EC 50 NOAEC EC50 = 250 μg ai/L NOAEC = 32 μg ai/L 42633708

Semi-aquatic plants TGAI EC 50 NOAEC Data gap --

Birds TGAI Acute LD50 = 380 mg ai/kg 160000Page 27 of 63 Dietary LC50 = 3400 ppm 22923 Chronic Not required -- Amphibians TGAI Acute LC50 = 207 μg ai/L OPP database Nontarget insects TGAI Acute LD50 >48.3 μg ai/bee 36935

1 This chronic endpoint is from the Ambient Water Quality Criteria for PCP; however, based on concerns with the study, the Agency anticipates the need to require a new chronic freshwater invertebrate study. See Appendix C for additional detail.

4.3.2.3 Contaminants

Ecotoxicity studies conducted in accordance with the 850 OCSPP Harmonized Test Guidelines are not available. Available ecotoxicity info rmation from the open literature and EPA/OW’s Ambient Water Quality Criteria fo r 2,3,7,8-tetrachlorodibenzo-p-dioxin (EPA 1984) was compiled for the 2008 PCP RED (EPA 2008b). So me selected endpoints are presented in Appendix C and summarized below along with the risk conclusions.

CDDs/CDFs

Data on the ecological effects of CDDs and CDFs are relatively limited. Most effects data are for the 2,3,7,8-chlorinated CDD/CDFs , especially 2,3,7,8-TCDD, which is very highly toxic to birds (LD50 = 15 μg/kg bw), small mammals (LD50=114-284 μg/kg), and aquatic organisms. CDFs are moderately toxic to fish (LC50 = 1140 μg/L) and aquatic invertebrates (LC50 = 1310 μg/L), but TCDD’s are very highly toxic to fish (e.g., coho salmon 96-h LC50 = 0.005 μg/L). However, TCDD-induced mortality often occurs up to 30 to 80 days after exposure, even from durations as short as 6 h. Exposure of coho salmon ( Oncorhynchus kisutch ) to an initial concentration of 0.0056 μg/L resulted in 55% mort ality within 60 days. Sublethal effects have also been reported for polychlorinated dioxins and furans, including: re duced growth; weight loss; abnormal hatching; cellular alterations; numerous types of le sions in numerous organs; and behavioral effects on swimming, reduced feeding, and loss of response to external stimuli.

Despite the reported toxicity of the CDDs/CDFs to aquatic organisms, acute and chronic risks to aquatic organisms were deemed to be low due to low aquatic exposure expected from runoff of leachate from PCP-treated utility poles. However, the assessment also concluded that CDDs/CDFs might eventually reach toxic levels and pose risks to benthic organisms due to accumulation of these compounds in sediments.

HCB

The available information indicates that HCB is less toxic than PCP or the CDDs/CDFs. However, it has shown high toxicity to some fish (LC50s = 140 and 200 μg/L for sole and flounder, respectively) and is mode rately toxic to birds. Toxici ty to freshwater and saltwater benthic invertebrates ranged from 42 to 60 mg/kg sediment.



### 4.3.3 Ambient Water Quality Criteria for PCP The AWQC document contains a review of public li terature on acute and chronic effects of PCP on freshwater and saltwater organisms (EPA 19 86). Some of the more sensitive endpointsPage 28 of 63 provided in that document are include in the Ecot oxicity Profile (Appendix C) and will be used for the risk assessment. The AWQC document also derived wate r quality criteria values. Because the toxicity of PCP varies with pH (i. e., toxicity decr eases as pH increases), values were adjusted to pH 6.5 for developing the crite ria. EPA/OW’s current ambient water quality criteria for PCP are as follows:

Freshwater: Acute: 10.97 μg ai/L Chronic: 3.46 μg ai/L Saltwater: Acute: 25.05 μg ai/L Chronic: 7.91 μg ai/L



### 4.3.4 Open literature Additional open literature studies also w ill be identified through EPA’s ECOTOXicology (ECOTOX) database. The ECOTOX database will be searched when the risk assessment is prepared. Any acute or chronic end points more sensitive than what is currently available will be used in the risk assessment and risk characte rization. Additional information on the Agency’s use of open literature is found on the Agency’s website: http://www.epa.gov/pesticides/science/efed/pol icy_guidance/team_authors/endangered_species_ reregistration_workgroup/esa_ evaluation_open_literature.htm

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## 4.4 Exposure Analysis Plan

4.4.1 Aquatic and Terrestrial Wildlife Exposure Estimates

Available OPP models will be used to determ ine the estimated environmental concentration (EECs) in the aquatic environment. Resulti ng 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 PCP treated wood at the site of the treatment is dried with a dr ain pad underneath and any leaked chemical is recycled for use. Remaining chemi cal 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 num erous studies to asse ss potential adverse outcomes from exposure to chemicals. Collectiv ely, these studies includ e acute, subchronic and chronic toxicity, including asse ssments of carcinogenicity, ne urotoxicity, developmental, reproductive, and general or systemic toxicity. These studies include e ndpoints which may be susceptible to endocrine influe nce, including effects on endocri ne target organ histopathology, organ weights, estrus cyclicity, sexual maturatio n, fertility, pregnancy rates, reproductive loss, and sex ratios in offspring. For ecological hazard assessments, EPA evaluates acute tests andPage 29 of 63 chronic studies that assess gr owth, developmental and reprod uctive effects in different taxonomic groups. As part of the 2008 RED, for PC P, EPA reviewed these data and selected the most sensitive endpoints for relevant risk as sessment scenarios from the existing hazard database. However, as required by FFDCA section 408(p), PCP is subject to the endocrine screening part of the Endocrine Di sruptor Screening Program (EDSP).

EPA has developed the EDSP to determine whet her 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 ot her such endocrine effect s as the Administrator may designate.” The EDSP employs a two-tiered approach to making th e statutorily required determinations. Tier 1 consists of a battery of 11 screening assays to identify the potential of a chemical substance to interact with the estrog en, androgen, or thyroid (E, A, or T) hormonal systems. Chemicals that go th rough Tier 1 screening and are found to have the potential to interact with E, A, or T hormonal systems will proceed to the next stag e of the EDSP where EPA will determine which, if any, of th e Tier 2 tests are necessary base d on the available data. Tier 2 testing is designed to identify a ny adverse endocrine-related eff ects 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 scre en all pesticide chemicals. Between October 2009 and February 2010, EPA issued test orders/dat a call-ins for the firs t group of 67 chemicals, which contains 58 pesticide active ingredients and 9 inert ingredient s. A second list of chemicals identified for EDSP screening was published on June 14, 2013 4 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.

PCP is on List 2. List 2 represents the next set of chemicals for which EPA intends to issue test orders/data call-ins in the near future. For furt her information on the st atus of the EDSP, the policies and procedures, the lists of chemicals, future lists, the test gui delines and the Tier 1 screening battery, plea se visit our website. 5


## 6 Optional Label Changes

The Agency invites comment on any label amendments that could be considered to eliminate the anticipated need for EPA to requi re certain data, reduce the possibi lity 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

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

chemicals.

5 http://www.epa.gov/endo/Page 30 of 63 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 PCP registration review case.



### 7.1.1 Trade Irritants Through the registration review process, the Ag ency intends to solicit information on trade irritants and, to the extent feas ible, 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 fr om lack of MRLs or disparities between U.S. tolerances and MRLs in key export markets, providing as much specificity as possible re garding the nature of the concern.



### 7.1.2 Water Quality The Agency invites submission of wa ter quality data for this pesticide. To the extent possible, data should conform to the qua lity 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 Process 6 in order to ensure they can be used quantitatively or qualitati vely in pesticide risk assessments.



### 7.1.3 Environmental Justice

EPA seeks to achieve environmenta l justice, the fair tr eatment and meaningful involvement of all people, regardless of race, color, national origi n, or income, in the deve lopment, implementation, and enforcement of environmental laws, regulati ons, 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 thei r location, cultural practices, or other factors, may have atypical, unusually high exposure to PCP 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 provid e available information a nd data that will assist the Agency in refining its risk assessments, including any species-spec ific ecological effects determinations.

As mentioned in Section 1.6, the Agency dete rmined in the 2008 RED that PCP products contribute benefits to society a nd were eligible for reregistra tion. In registration review, EPA plans to update the benefits and alternatives a ssessments for PCP. Stakeholders are encouraged to provide updated information on benefits a nd alternatives during th e PWP comment period.

EPA is seeking additional information on PCA, particularly any pert inent monitoring data.

6 http://www.epa.gov/oppsrrd1/registration_review/water_quality_sop.htmPage 31 of 63 Additionally, 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 alr eady reported to the Agency 5. Monitoring data



## 8 Next Steps

After the 60-day comment period closes in February 2015, the Agency will review and respond to any comments received in a timely manner, and then issue a Final Work Plan for the PCP

case.Page 32 of 63 

## 9 References

ATSDR, 2002. Toxicological Profile for Hexachlorobenzene. September, 2002.

EPA, 1986. Ambient Water Qua lity Criteria for Pentachlorophe nol – 1986. USEPA Office of Water, Regulations and Standards Criter ia and Standards Division, Washington DC.

EPA, 1991. Drinking Water Criteria Document for Hexachlorobenzene. Prepared for Office of Water by Environmental Criteria and Assessment Of fice, Office of Health and Environmental Assessment, USEPA, Cincinnati, OH.

EPA, 2008a. Reregistration Eligibility D ecision for Pentachlorophenol. September 25, 2008, Antimicrobials Division, Office of Pesticide Programs, Washington, DC.

EPA, 2008b. Ecological Hazard and Envi ronmental Risk Assessment Chapter – Pentachlorophenol, PC Code: 63001, Case No.: 2505, R. C. Petrie, August 25 2008, Antimicrobials Division, Office of Pe sticide Programs, Washington, DC.

EPA, 2008c. Chlorinated Dibenzo Dioxins (CDDs) and Chlorinated Dibenzo Furans (CDFs) as Contaminants of Pentachlorophenol. Ecological Hazard and Environmental Risk Assessment for the Pentachlorophenol Reregistration Eligibility Decision (RED), PC Code: 63001, Case No.: 2505, R. C. Petrie, September 18 2008, Antimicrobial s Division, Office of Pesticide Programs, Washington, DC.

EPA, 2008d. Hexachlorobenzene (HCB) as a Contaminant of Pentach lorophenol. Ecological Hazard and Risk Assessment – Supplement to the Pentachlorophenol Reregistration Eligibility Decision (RED) Document, PC Code: 63001, Ca se No.: 2505, R. C. Petrie, August 25 2008, Antimicrobials Division, Office of Pesticide Programs, Washington, DC.

EPA, 2008e. Occupational Exposure and Risk A ssessment of Dioxins and Furans (CDD/CDFs) in Pentachlorophenol, August 19, 2008, Antimicrobial s Division, Office of Pesticide Programs, Washington, DC.

Kline, 2005. Specialty Biocides North Ameri ca 2004-2005, Volume II: United States, Kline and Company, Inc.

NTP (National Toxicology Program). (1989) NTP t oxicology and carcinoge nesis studies of two pentachlorophenol techni cal-grade mixtures (CAS No. 87-86-5) in B6C3F1 mice (feed studies). Public Health Service, U.S. Depart ment of Health and Human Services; NTP TR 349. Available from the National Institute of Environm ental Health Sciences, Research Triangle Park, NC.

Thind, K.S., Karmali, S., and House, R.A., 1991. Occupational Exposure of Electrical Utility Linemen to Pentachlorophenol. Am erican Industrial Hygiene A ssociation Journal 52:547-552.Page 33 of 63 Wilson et al., 2007. An observational study of the pot ential exposures of pr eschool children to pentachlorophenol, bisphenol-A, an d nonylphenol at home and daycar e. Environmental Research 103 (2007) 9-20.

Younes, M., 1998. WHO toxic equivalency factor s (TEFs)for dioxin-like compounds for human and wildlife of WHO meeti ng held in Stockholm, Seden on June 15-18. World Health Organization, Internat ional Programme on Chemical Safty.Page 34 of 63 

# Appendix A Toxicology Profile

Toxicology Profile for PCP

The Agency does not anticipate the need to require additional toxi cology data for PCP. 

## Acute Toxicity for Product Labeling

Acute toxicity studies available for labeling purposes have been summarized in Table A1. The acute toxicity database for PCP is considered complete. The acute toxicity of PCP is low for dermal toxicity (Toxicity Category IV) and primar y dermal irritation (Toxicity Category III) but shows higher toxicity for acute oral toxicity and primary eye irritation (Toxi city Category II). No dermal sensitization was observed with the tec hnical test material. Acceptable acute inhalation toxicity data for PCP were not available, but waivers were gran ted for these data. No additional data are anticipated to be required. Table A1 – Acute Toxicity Studies for PCP

Guideline No./ Study Type MRID No. Results Toxicity Category

870.1100/ Acute oral toxicity 00101715 LD50 = 155 mg/kg (M); and LD50 = 137 mg/kg (F) II

870.1200/ Acute dermal toxicity 00101715 LD50 > 3980 mg/kg IV

870.1300/ Acute inhalation toxicity N/A Waiver granted (a) I

870.2400/ Primary eye irritation 00101715 Corneal involvement at day 7 postinstillation II

870.2500/ Acute dermal irritation 46616602 Moderate irritation at 72 hours postapplication III

870.2600/ Skin sensitization 42594301 No sensitization observed using Buehler method N/A

Note: N/A=Not available (a) The PCP Task Force previously submitted data to the Agency on efforts to develop methods to conduct inhalation

studies. This effort was without success, based on an inability to generate consistent chamber concentrations of PCP. The Task Force also cited label instructions (based on EPA Position Document 4 for Wood Preservatives) requiring the use of respirators and pr otective clothing for applicators enteri ng pressure treatment cylinders and other related equipment contaminated with wood treatment formulation. On this basis, waivers were requested by the Task Force for inhalation toxicity data. The Agency granted these waiver requests and a Toxicity Category I for inhalation hazard will be assigned.Page 35 of 63 

## Subchronic Toxicity

There is one 90-day dermal toxicity study (MRID # 43182301). In the study, PCP (88.9% a.i.) was administered by dermal occlusion to groups of 10 male and female Sprague-Dawley rats for 6 hours/day, 5 days/week, at doses of 0, 100, 500, or 1000 mg/kg/day. No stat istically significant differences in group mean body weight or weight gain were observed at any treatment level, nor were there any treatment related mortalities or clinical signs of toxicity. Dermal irritation consisting of erythema (grade 1-2) at 100 mg/ kg/day and erythema (grade 1-4) at 500 and 1000 mg/kg/day was observed during we eks 2-5 of the study. The magnit ude of the dermal irritation decreased after week 5. There was no dermal i rritation observed in control rats. At the 500 and 1000 mg/kg/day dose levels, incr eased total white blood cell c ounts and absolute lymphocyte counts were observed in female ra ts. Decreased platelet count was observed at all dose levels in female rats. The hematological e ffects were ascribed to dermal irritation and not to systemic effects of the test chemical. Significant increas es in alanine and aspartate aminotransferase activities were observed in male and female rats at the 500 and 1000 mg/kg/day dose levels, while increased cholesterol was observed at th ese dose levels in fe males only. Significant increases in absolute liver wei ght were observed at the 1000 mg/ kg/day dose level for both males and females. The increase in liver weight was thought to be the result of enzyme induction. Kidney weights were increased at the 1000 mg/k g/day dose in males, and at the 500 and 1000 mg/kg/day dose levels in females. At necropsy, ta n crusty areas, acanthosis of the epidermis, and chronic inflammation of the dermis was noted at th e treatment site in all treatment groups of both sexes. An increased incidence of hepato cellular degeneration accompanied by chronic inflammation was observed at 500 and 1000 mg/kg/da y in both males and females. Based on the results of this study, the Systemic LOAEL = 50 0 mg/kg/day (enzyme induction and minimal to mild hepatocellular degeneration and chronic inflammation in males and females), and the Systemic NOAEL = 100 mg/kg/day. This study is classified as acceptable and satisfies the guideline requirement ('82-3) for a subchronic derm al toxicity study in rats. No additional data are anticipated to be required. 

## Developmental Toxicity

In a developmental toxicity study (MRID # 43091702), pregnant Crl: CD BR VAF/plus rats (25/dose) received oral admini stration of PCP (88.9%) at doses of 0, 10, 30 or 80 mg/kg/day during gestation days 6 through 15. Developmental toxicity observ ed at 80 mg/kg/day included: significant increase in the number of resorptions (mainly early) w ith a corroborativ e decrease in litter size; reduced mean fetal weights; signif icant increase in the number of fetuses with external, visceral and/or skelet al malformation/variations (hyd rocephaly, diaphragmatic hernia, and dilation of the renal pelvis); and significant increase in th e number of litters (22 of 23) that contained fetuses (6 of 22) with skeletal anoma lies. The most common were vertebral structural variations and incomplete o ssification. For developmental to xicity, the NOAEL was 30 mg/kg and the LOAEL was 80 mg/kg/day based on incr eased resorptions, reduced fetal weight and skeletal malformations/variations.Page 36 of 63 In a study conducted by Schwetz et al. (Toxicol. Appl. Pharmacol 28: 151-161, 1974), doses of 0, 5, 15, 30, and 50 mg/kg/day commercial grade (88.4% a.i.) or purif ied (>98% a.i.) PCP prepared in corn oil were administered to groups of pregnant Sprague-Daw ley rats on gestation days 6-15 inclusive. For purifie d PCP, the number of rats per group was as follows: control, 33 rats; 5 mg/kg, 15 rats; 15 mg/kg, 18 rats; 30 mg/kg/, 20 rats; 50 mg/kg, 19 rats. For the commercial grade of PCP: 5 mg/kg, 18 rats; 15 mg/kg, 17 rats; 30 mg/kg, 19 rats; 50 mg/kg, 15 rats. Additional groups of rats were administer ed 0 or 30 mg/kg/day PCP (type of a.i. not specified) on days 8-11 or 12-15 of gestati on. Maternal toxicity from purified PCP was evidenced by decreased maternal weight gain at the 30 and 50 mg/kg dose groups for days 6-21 of gestation (74% decrease vs. control). For the commercial grade, weight gain was decreased 43% at the 50 mg/kg dose, and by 22% at the 30 mg/kg dose. Weight gain appeared more significantly affected by purified PCP. No other significant signs of mate rnal toxicity were observed. Fetal incidence of resorption was signi ficantly increased at 30 and 50 mg/kg purified and commercial grade PCP. The report stated that the fetal and litter incidence was also significantly increased at 15 mg/kg commercial grade PCP, but the fetal incidence (7 and 8% at control and 15 mg/kg/day) as we ll as the litter incidence ( 55 and 64% at control and 15 mg/kg/day) did not appe ar biologically meaningful. Fetal bod y weight was reported significantly decreased for commercial grade PCP at 30 and 50 mg/kg/day and at 30 mg/kg/day for purified PCP, but actual values were not reported. Crown- rump length was significa ntly decreased at 30 mg/kg/day purified PCP. The litter incidence of subcutaneous edema, lumber spurs, and supernumerary, lumber or fused ribs was signifi cantly increased at 30 and 50 mg/kg commercial grade PCP, but the data did not indicate a dose-re sponse, i.e. the number of litters affected with subcutaneous edema, rib and vertebral abnormalit ies were greater at 30 mg/kg than at 50 mg/kg for the commercial grade of PCP and for the purified PCP. The number of litters at the high dose of purified PCP was also severely limited (onl y 2 litters at this dose). Resorptions were significantly increased when PCP (both grades) wa s administered on gestation days 8-11, but not on gestation days 12-15. Based on the results of this study, the Maternal NOAEL can be considered as 15 mg/kg/day, based on body wei ght effects, for both grades of PCP. The Developmental NOAEL would appear to differ according to grade of PCP used. Limited data for purified PCP at the 50 mg/kg/dose hampers eval uation of a NOAEL and LOAEL for this grade. For the commercial grade of PCP, the NOAEL ca n be considered as 15 mg/kg/day, and the LOAEL as 30 mg/kg/day, based on decreased fetal body weight and crown-rump length. The responses observed at the low dose of commerci al grade PCP for fetal anomalies (i.e. lumber spurs, anomalous ribs, subcutaneous edema) do not show a dose-response pattern at the higher doses of PCP, and are also limited by reduced number of litters at the high dose.

In a study conducted by Welsh et al. (Fd. Chem . Toxic. 25(2): 163-172, 1 987), groups of male and female Sprague-Dawley rats (20/group) were placed on diets cont aining purified PCP at dose levels of 0, 60, 200, or 600 ppm (0, 4, 13, an d 43 mg/kg/day reported for females; no actual intake data for males). These test diets were administered for 181 days. At the end of the subchronic phase, male and female rats were mated for teratological evaluation following subchronic exposure to PCP. Body weight gain in maternal rats exposed to PCP was significantly decreased at the high dose (76% from control). Pregna ncy rates were low in all dose groups (77.5, 55, 84.2, and 85 for the 0, 60, 200, a nd 600ppm dose groups, respectively) but,Page 37 of 63 according to the report, there was no effect on fer tility. Decreased number of viable fetuses (due to early death) was observed at the 600 ppm dose level of PCP, as well as an increase in total litter resorptions. Body weight of fetuses appear ed decreased at the 200 ppm dose level; analysis at the 600 ppm dose level was not complete, due to an alteration in the sex ratio at this dose (100% male sex ratio at this dos e as reported). There were no repor ted alterations in external or sternebral observations at any dose level tested in this study. In creased incidence of misshapen centra was reported at 200 ppm PCP, but the high dose could not be analyzed due to inadequate numbers of fetuses. The inciden ce of total skeletal variations was reported increased at the 200 ppm dose level for PCP. The results of this st udy demonstrate toxicity of PCP at 200 ppm (13 mg/kg/day) in the form of incr eased percentage of female rats with 2 or more resorptions. However, this study is hampered by a lack of feta l data at the high dose, and inconsistent and low percentages of pregnancy at each dose level of PCP tested. The data appear to point to a definitive toxic effect of PCP at the 43 mg/kg/day dose level on both maternal and fetal rats, with decreased weight gain in maternal rats, and decreased viable fetu ses, increased early deaths, and increased resorptions at the high dose.

In a developmental toxicity study (MRID # 43091701), inseminated New Zealand White rabbits (20 rabbits/dose) were administered PCP by ga vage at doses of 0, 7.5, 15, and 30 mg/kg/day on gestation days 6-18 inclusive. Cesarean secti on examinations were performed on all surviving does on gestation day 29, followed by external, viscer al, and skeletal examination of all fetuses. There were no maternal deaths or signs of mate rnal toxicity at any dose level. Significantly reduced weight gain was observed in the high do se group on gestation days 6-9 (loss of 40g vs. gain of 20 g in controls), and in the mid and high dose groups for gestatio n days 9-12 (gain of 20 g at the mid and high dose vs. gain of 50 g in c ontrols). These changes were considered minimal as the differences in weight gain were e quivalent to only 0.5-1% of mean body weight. A consistent reduction in mean food consumption ( 71-90% of control value on gestation days 9-12) was observed at the high dose. Weight gain wa s comparable for treate d and control rabbits following the treatment interval. A slight but non-s ignificant dose-related decrease in litter size was observed, corresponding to a decrease in implan tations/litter for the tr eated does. There were no statistical differences in the number of treated litters vs. control when the incidences for all observations of external, visceral , and skeletal effects were co mbined. Although the incidence of affected litters was not statis tically significant, a significantly greater (p < 0.01) number of individual fetuses in the 15 mg/ kg litters contained interfrontal ossification sites compared to controls. Based on the results of this study, the Maternal to xicity NOAEL = 15 mg/kg/day, and the Maternal toxicity LOAEL = 30 mg/kg/day, based on minimally reduced body weight gain and consistent reductions in food consumption during treatment. The Developmental toxicity NOAEL = 30 mg/kg/day; a Developmental toxicity LOAEL was not identified. This study is classified as acceptable and satisfies the guide line requirement (83-3b) for a developmental toxicity study in non-rodents. No additional data are anticipated to be required. 

## Reproductive Toxicity

In a 2-generation reproducti on study (MRID 44464101), PCP (88.9% a.i.; lot no. EL-604) in corn oil was administered to 30 male and female Sprague-Dawley rats/sex/dose by gavage atPage 38 of 63 dose levels of 0, 10, 30, and 60 mg/kg/day. P1 male a nd female rats were given the test material once daily at least 70 days prior to cohabitation and continuing th rough the day before sacrifice. F1 generation rats may have been exposed in ut ero during gestation and vi a maternal milk during the postpartum period. The day afte r weaning, F1 generation rats were administered the test material by gavage at the same dose levels as P1 rats and were continued until one day prior to sacrifice. F2 pups were exposed possibly indirect ly during maternal gestation or via maternal milk. In addition to standard parameters, es trous cycling and sper m morphology and function were measured. At 60 mg/kg/day PCP, body weight and body weight gain of P1 and F1 parental rats was significantly decreased from contro l over the period of treatment pre-mating. Gestational and lactational body weights of P1 a nd F1 female rats were also significantly decreased. Fertility index and number of litters were decrea sed in both generations at 60 mg/kg/day PCP. Days to vaginal patency were si gnificantly increased in P1 female pups, as was days to preputial separation in P1 male pups. Es trous cycling was not sign ificantly affected in either P1 or F1 females, but in F1 males, th e number of sperm observed with a broken flagellum was significantly increased at 60 mg/kg/day, and the average te sticular spermatid count was significantly decreased at 60 mg/kg/day. Testis weight in F1 generation males was also decreased. Decreased brain weight (4-8%) and incr eased liver weight (20- 33%) were observed in both P1 and F1 male and female rats at 60 mg/kg/day. Macroscopic pa thology (enlarged liver) and microscopic pathology (centrilobular hypertrophy, subacute inflammation, single cell necrosis, pigment deposition) were observed in increased incidence at 60 mg/kg/day. The single cell necrosis and pigment deposi tion were considered related to treatment. Mean litter size, number of live pups, and viability index were significantly reduced in the P1 and F1 pups. Decreased weight of the liver, brain, splee n, and thymus were observed in F2 pups at 60 mg/kg/day. At 30 mg/kg/ day, body weight and weight gain decreases of approximately 11% were observed in F1 female pare ntal rats. Significant decreases in average testicular spermatid count and testis weight were observed in F1 male parental rats. Based on the data in this study, the Systemic NOAEL = 10 mg/kg/day for male and female parental rats. The Systemic LOAEL = 30 mg/kg/day for male and female rats, based on decreased body weight a nd weight gain in F1 generation parental rats, and advers e testicular effects in F1 male rats (decreased testis weight, decreased spermatid count). The reproductiv e NOAEL = 10 mg/kg/day in this study. The reproductive LOAEL = 30 mg/kg/day, based on decreased group mean litter weight. This reproductive study in the rat is classified acceptabl e and satisfies the guid eline requirement for a 2-generation reproductive study (OPPTS 870.3800) in ra ts. No additional data are anticipated to be required. 

## Chronic Toxicity

In a chronic toxicity study, (MRID 43982701) PCP (90.9% a.i.) was fed (gelatin capsules) to four beagle dogs/sex/dose at dose levels of 0, 1.5, 3.5, or 6.5 mg/kg/day for 52 weeks. At 6.5 mg/kg/day, one male and one female dog were sacrificed in extrem is on days 247 and 305, respectively, due to significan t clinical toxicity (significan t weight loss, lethargy, marked dehydration, vomiting, icterus). The LOAEL was 1.5 mg/kg-day (lowest dose tested), based on liver pathology consisting of dose-related increa ses in incidence and seve rity of hepatocellularPage 39 of 63 pigmentation, cytoplasmic vacuolation, and chro nic inflammation, and significant increases in relative liver weight and increases in absolute liver weight (significant in females), and increased serum enzyme activity. The NOAEL could not be established. This study is considered acceptable and satisfies the guideline requi rement ('83-1; OPPTS 870.4100) for a chronic toxicity study in non-rodents. No additional data are anticipated to be required. 

## Carcinogenicity

The Agency’s IRIS program (2010, http://www.epa.gov/IRIS/subst/0086.htm ) classified PCP as “likely to be carcinogenic to humans.” This can cer weight of evidence determination is based on: (1) evidence of carcinogenicity from oral studies in male mice exhibiting hepatocellular adenomas and carcinomas, and pheochromocytomas and malignant pheochromocytomas, and in female mice exhibiting hepato cellular adenomas and carcino mas, pheochromocytomas and malignant pheochromocytomas, and hemangiomas and hemangiosarcomas (NTP, 1989); (2) some evidence of carcinogenicity from oral st udies in male rats exhibiting malignant mesotheliomas and nasal squamous cell carci nomas (Chhabra et al., 1999; NTP, 1999); (3) strong evidence from human epidemiologic stud ies showing increased risks of non-Hodgkin’s lymphoma and multiple myeloma, some evidence of soft tissue sarcoma, and limited evidence of liver cancer associated with PCP exposure (D emers et al., 2006; Ha rdell et al., 1995, 1994; Kogevinas et al., 1995); and (4) positive evidence of hepatoce llular tumor-promoting activity (Umemura et al., 2003a, b, 1999) and lymphoma a nd skin-adenoma promoting activity in mice (Chang et al., 2003). For more detail on Charact erization of Hazard and Dose Response, see the toxicological review, Section 6 (PDF). No additional data are anti cipated to be required. 

## Mutagenicity

The available evidence for gene mutations in bacterial systems suggest s that PCP is largely devoid of positive effects with the exception of one published report, in which a positive response was noted. PCP is also observed to be weakly clastogenic, with chromosomal aberrations observed using Chinese hamster ovary cells in the presence of rat liver S9. In contrast to the data for PCP, data for the metabolit e tetrahyhdroquinone (THQ) show positive effects on Chinese hamster V79 cells (increase in frequency of thioguanine-resistant mutants; Jansson and Jansson, Mutation Res. 260: 83-87), increase in micronuclei using V79 cells (Jansson and Jansson, Mutation Res. 279: 205-208), covalent binding to DNA (Witte et al., Mutation Res. 145: 71-75), and induction of DNA single-strand breaks (Witte et al., Mutation Res. 145: 71-75; Ehrlich, W.: Mutation Res. 244: 299-302). THQ has b een thought to be invol ved in some or all of the mutagenic and carcinogenic effects of PC P. No additional data are anticipated to be required.



## Neurotoxicity

Although a vailable data on PCP i ndicate the potential for nervous system effects in vitro (decrease in neuromuscular and ganglionic conduction, inhibition of human red cellPage 40 of 63 cholinesterase) and in vivo animal data Clin ical signs associated with PCP exposure are suggestive of neurotoxicity, based on the av ailable data, there is no evidence of frank, unequivocal neurotoxicity in the database, includi ng changes in brain weight or incidence of neuropathology in the central nervous system tis sues (nonperfused). Therefore, nervous system has not been generally considered as a target ti ssue from PCP exposure. No additional data are anticipated to be required.


## Immunotoxicity

The immunotoxic effects of PCP have been st udied by the U.S. Department of Health and Human Services’ National Toxicology Program (NTP ) and others. The data appear to indicate that the immunotoxic effects of PCP are la rgely mediated by the chlorinated dioxin contaminants. Although data from human studies are limited, it is likely that the immune effects observed are also due in part to the contaminants present w ithin PCP. No additional data are anticipated to be required.



## Dermal Absorption

For PCP, a dermal absorption factor of 40% is used for correction of oral to dermal dosing. This value is based on a dermal absorption study (MRID # 00259257) in which radiolabelled PCP (5% solution in P-9 oil) was applied to the skin of young adult Sprague-Dawley rats for 0.25, 1, 4, 8, and 24 hours. At 8 hours post-applica tion, the calculated absorption was 40%. At 24 hours post-application, th e calculated absorption was 60%. This risk
assessment is required for PCP, all of the human expos ures are measured with biological monitoring data, and therefore no additional derm al absorption data are anticipated to be required.



## Metabolism

PCP has been shown to be readily absorbed by oral, inhalation, and derm al routes of exposure (Reigner et al., Pharmaceut. Res. 9: 1053-1057, 1992; Yuan, JH et al., Xenobiotica 24(6): 553- 560, 1994; Hoben, Bull. Environ.Contam. Toxicol 15: 466-474, 1976). Peak plasma levels have been shown to occur in the range of 1.3-6 hours in experimental animals in an oral dose range of 0.1-15 mg/kg, while in humans, ma ximum plasma concentration of PCP occurred at 4 hours following a single 0.1 mg/kg oral dose. Absorpti on from dermal exposure has been shown to range from 24% in rhesus monkeys (Wester et al., Fundam. Appl. Toxicol. 20: 68-71, 1993) to 40% in rats (EPA MRID # 00259257).

Biotransformation of PCP has also been examined in several studies published in the scientific literature. Reigner et al. (Xenobiotica 21( 12): 1547-1558, 1991) observed a 60% recovery in urine from i.v. or oral administration of 2.5 mg/kg PCP, mainly as conjugated PCP and conjugated tetrahydroquinone. In two earlier studies by Ahlbor g (Arch. Toxicol 40: 45-53, 1978)Page 41 of 63 and Braun (Toxicol. Appl. Pharmacol. 41: 395- 406, 1977), glucuronides of PCP were the major urinary metabolites observed after oral dos es of 10 mg/kg and 100 mg/kg respectively. Pretreatment with phenobarbital in the study by Ahlborg et al . enhanced the formation of tetrahydroquinone. In other work by Rener and H opfer (Renner, G. And Hopfer, C.: Xenobiotica 20: 573-582, 1990), 24 female Sprague-Dawley rats were treated with PCP at 53 mg/kg/day for 28 days. The results of this study indicated that PCP leads to tetrahydroquinone via 2,3,5,6- tetrachlrophenol as a main degradative pathway, and to trichlorohydroquinone via 2,3,4,6- tetrachlorophenol and 2,3,4,5-tetr achlorophenol via a minor pathwa y. PCP, tetrachlrophenol, and trichlorophenol can become conjuga ted with glucuronic acid or sulf ate. While previous work in humans has shown the absence of formati on of the tetrahydroquinone metabolite, newer published literature indicates formation of th is metabolite both in vitro (Mehmood et al., Chemosphere 33(4): 759-769, 1996) as well as in vi vo. The kinetics of elimination of PCP have been published, with half-lives of elimination ranging from 5-6 hours in mice ( Reigner et al., Pharmaceut. Res. 9: 1053-1057, 1992), 2-11 hours in rats (Reigner et al., Xenobiotica 21(12): 1547-1558, 1991; Braun et al., Toxicol. Appl. Ph armacol. 41: 395-406, 1977) and 72-84 hours in monkeys (Braun and Sauerhoff, Toxicol. Appl . Pharmacol. 38: 525-533, 1976). In humans, mean plasma half-life was calculated to be 30.2 ± 4.0 hours following a 0.1 mg/kg oral dose to four male volunteers (Braun et al., in Toxicology and Occupational Me dicine [W.B. Diechmann, ed.], pp. 289-296). Limited data on the volume of distributi on of PCP indicate that in contrast to rats, where the volume of distribution ranges from 116-268 ml/kg, humans s how a higher volume of distribution (348 ml/kg). One study was available with human data on volume of distribution. No additional data are antici pated to be required.Page 42 of 63 

# Appendix B Environmental Fate

Environmental Fate and Transport Properties of PCP

The Agency does not anticipate the need to requi re environmental fate studies for registration review.

Water and Sediment

Hydrolysis (MRID 42481101)

PCP was hydrolytically stable in sterile aqueous pH 5, 7 and 9 buffer solutions incubated at 25°C for up to 30 days.

Photodegradation in Water (MRID 42855401)

PCP photodegraded rapidly with ha lf-lives of 13-20 minutes in sterile aqueous pH 5, 7 and 9 buffer solutions irradiated with natural sunli ght at 42°N (in MA) on different days and at different times of the day in August/September, a nd was stable in dark controls under similar conditions; air temperatures during the studies ranged from approximately 8 to 36°C. Dichloromaleic anhydride (more likely present as dichloromaleic acid) was reported to be the major degradate at all pHs, and reached resp ective maximums of 64.5-67.5% (80 minutes posttreatment), 100% (110 minutes), a nd 98.9% (90 minutes) of the applie d radioactivity at pH 5, pH 7 and pH 9. Tetrachlororesorcinol was a majo r degradate at pH 5 (maximum of 34.8-36.1%) and pH 7 (maximum of 15.7%) and was a minor de gradate at pH 9. Tetrachlorohydroquinone and tetrachlorocatechol were minor de gradates at pH 5 and pH 7, but were not detected at pH 9.

Aerobic Aquatic Metabolism (MRID 42288601)

PCP degraded in a flooded sandy loam soil with an observed half- life of approximately 14 days (calculated first-order half-lif e of 4.9 days) in flooded sandy lo am soil incubated aerobically (under continuous airflow) at 25°C for up to 30 days. Initial PCP degr adation was less rapid (52% of the applied radioactivity remained as parent at 14 days ) than that observed after an apparent acclimation period; only 7% of the applie d was present as parent compound at 21 days. The major degradate 3,4-dichlorophenol was 0.30% of the applied prior to 30 days and was 36.6% at day 30. Various isomers of tetrachlo rophenol (maximum of 10%) and trichlorophenol (maximum of 82.2%) were also formed as ma jor degradates; indivi dual isomers were not identified. Volatiles were negl igible (0.9%), and nonextractable [14C] residues were 41% of the applied at 30 days. The soil:water distributi on ratio for PCP was approximately 1:32 initially, then changed to approximately 1:1 by 14 days, and was 2.5:1 at 30 days.Page 43 of 63 Anaerobic Aquatic Metabolism (MRID 42436801)

PCP degraded with an observed half-life of 1- 2 months (calculated firs t-order half-life of 34 days) in flooded sandy loam soil incubated anaero bically (nitrogen atmosphere) at 25C for up to one year. Initial PCP degradati on was relatively slow (84% and 72% of the applied remained as parent at 14 days and 1 month, respectively), then accelerated after an apparent acclimation period; only 5% of the applied wa s present as parent compound at 2 months. Various isomers of tetrachlorophenol (maximum of 9.7%) and trichl orophenol (maximum of 82.7%) were formed as major degradates; individual isomers were not iden tified. Volatiles were negligible (1.4%), and nonextractable [14C] residues were 7.8% of th e applied at 12 months. The soil:water distribution ratio for PCP was a pproximately 1:13 initially, then changed to 1:1 by 7 days, and was 4:1 at 1-12 months.

Soil

Soil Leaching/Adsorption/Desorption Batch Equilibrium (MRID 42633709 and 43627000)

Based on batch equilibrium studies, PCP, at a pproximately 1-14 ppm, was determined to be moderately mobile in one sandy lo am soil and slightly mobile in two sandy loam soils, and was immobile in a clay loam soil. In silt loam soils designated as “high” organic matter soils, PCP was moderately mobile in the lower pH soil and m obile in the higher pH so il. In silt loam soils designated as “low” organic matter soils, PCP wa s slightly mobile in the lower pH soil and mobile in the higher pH soil. The soil properties and the Freundlich adsorption coefficients (K ads ) and associated exponents are listed in the fo llowing table. Desorption coefficients were not reported for the sandy loam or clay loam soils . Data were not provided for a coarse-textured soil such as loamy sand or sand.

Table B1: Soil-water Partition Coefficient (Kds) in Various Soils

Soil Series or Origin Texture % OM pH K ads 1/N (ads)

Georgia Sandy loam 0.4 5.9 5.72 0.81
Nebraska 1 Sandy loam 1.2 6.9 9.96 0.86 California Sandy loam 2.6 7.9 10.8 0.87

Ohio Clay loam 3.7 5.3 74.6 0.88 Silt loam High 5.8 8.3 - Silt loam High 7.5 2.0 -
Silt loam Low 4.2 18 -
Silt loam Low 6.6 1.3 -

1 Indicates the same “blue sandy loam” soil utili zed in all other guide line laboratory studies.Page 44 of 63 Kd values were also obtained in a second acceptable study on the major PCP degradates 2,3,4- trichlorophenol and 2,3,4,5-tetr achlorophenol in a sandy loam soil (pH 6.3, 1.6% organic). Based on batch equilibrium studies, the PCP degradates 2,3,4-trich lorophenol and 2,3,4,5- tetrachlorophenol were both determined to be sli ghtly mobile in one sandy loam soil. No data were submitted for the PCP degradates dichloromaleic acid, tetrachlororesorcinol, or other isomers of tri- a nd tetrachlorophenol.

Table B2: Kds for the PCP Degradates

Kds 2,3,4-trichlorophenol 2,3,4,5-tetrachlorophenol

K ads 10.2 14.6
K oc 1080 1550
1/N 0.78 0.78

Aerobic Soil Metabolism (MRID 42594302)

PCP degraded with an observed half-life of 7-14 days (calculated first-or der half-life of 63 days) in sandy loam soil maintained at 75% of 0.33 bar moisture and incubated at 25  C for up to one year. An acclimation period for the microbial degradation was not observed. The degradation rate was observed to decrease with time; at 7 da ys, 54.7% of the applied radioactivity remained present as parent, while 23.5% was present as parent at 61 days (the interval closest to the calculated first-order half-life). No major degrad ates were observed. The minor degradates were various isomers of tetrachlorophenol (maximum of 2.3-2.4% of the applied) and trichlorophenol (maximum of 4.4%); indi vidual isomers were not identified. By 12 months post-treatment, 25.7% of the applied radioactivity had volatilized as CO 2 and 1.3% had volatilized as a trichlorophenol. Nonextractable [ 14 C] residues increased throughout the study and were a maximum of 64.0% of the applied at 12 months, w ith the majority (76%) associated with the humic fraction of the soil organic matter.

Bioaccumulation in Fish (165-4) 42633710, 42855402

PCP residues bioaccumulated in bl uegill sunfish exposed to PCP, at a nominal concentration of 2.5 ug/L in a flow-through system (pH 6.7-7.2) for 28 days, with bioconcen tration factors (BCF) of 190x for the edible tissue, 790x for the nonedible tissue and 490x for the whole fish. Maximum mean concentrations of [ 14 C] residues were 640 ppb, 2800 ppb and 1500 ppb in edible, nonedible and whole fish tissues, respectively. Total [ 14 C] residues at exposure day 28 were 170 ppb in edible tissues, 930 ppb in nonedibl e tissues and 500 ppb in whole fish tissues. At day 28, all of the residues in the edible ti ssues were identified as PCP; in the nonedible tissues, 87-94% of the accumulated [ 14 C] residues were identifie d as PCP and 6-13% as glucoronide conjugates of PCP. Depuration was rapid, with over 97% of the accumulated residues eliminated from all tissues by day 14. The exposure to the parent may not have beenPage 45 of 63 constant. [ 14 C]Residues in the water were not adequate ly characterized; approximately 24% of the [ 14 C] residues in the water at da ys 26 and 28 (the only water sa mples characterized) were not present as the parent compound.

Aqueous Availability from Treated Wood (MRID 43205001)

Maximum and average leaching rates for southern pine wood (11-inch length and 1-inch in diameter) treated with PCP at 0.50 lbs/ft 3 are reported in the following table. Reported data indicated that the average leaching rate and th e maximum leaching rate of PCP increased with increased pH.

Table B3: Leaching Rates at Various Conditions

Final Concentration mg/L Max. Leaching Rate x 10 -2 mg/kg leachate/in 2 /day Average Leaching Rate x 10 -3 mg/kg leachate/in 2 /day pH 5 5.73 1.04 0.51 pH 7 36.2 2.28 3.27 pH 9 65.5 3.32 6.33
0.1 N HCl 1.73 0.6 0.17
Seawater 22.7 3.11 2.21
Purified water 6.57 0.66 0.61

Degradates of PCP in Environmental media

Environmental fate studies on PCP have shown that a number of degradates are formed in aquatic and soil metabolism studies as shown below.

Table B4: Degradates of PC P in Environmental media

Study Type Degradates Characterized

Hydrolysis No degradate formed in pHs 5, 7, and 9 under abiotic conditions

Aqueous Photolysis Dichloromaleic anhydride (formed at pHs 5, 7, and 9

Tetrachlororescorcinol, major at pH5

Minor at pHs 7, and 9

Tetrachlorohydroquinone and tetra chlorocatchechol: minor at pH 5, and 7. None at pH 9

Aerobic Aquatic metabolism 3,4-dichlorophenol: < 30% up to 30 days; 36.6% at day 30 Major degradate

Isomers of tetrachloro and trichloro formed also as major degradates.Page 46 of 63 Anaerobic aquatic metabolism Tetrachlorophenol (9.7%) a nd trichlorophenol (82.7%). Isomers were not identified

Aerobic soil metabolism Tetrachorophenol (2.3-2.4%); trichlorophenol (4.4%) as minor degradates. No isomers were identified

Adsorption/ Desorption/ batch equilibrium study 2,3,4 trichlorophenol, and 2,3,4,5-tetrachlorophenol were identified in sandy loam soil (pH 6.3, 1.6 organic matter). These degradates were slightly mobile in the sandy loam soilPage 47 of 63 Environmental Fate References for Appendix B

42481101 Blumhorst, M. (1993) Aqueous H ydrolysis of Pentachlorophenol Project ID 156001 EPL Bi o Analytical Services, Inc.

42855401 Connor, S. (1993) Pentachlor ophenol-Determination of Aqueous Photolysis Ra te Constant and Half-Life: Final Report: Lab Proj ect Number: 12836.0692.6112.720: 93- 1-4568. Unpublished study prepared by Springborn Labs, Inc. 68 p.

41969201 Schmidt, J. (1991) Determination of the Photolysis Rate of [carbon 14]-Pentachloro -phenol on the Surface of Soil: Final Report: Lab Project Number : 38440. Unpublished study prepared by ABC Labor- atories, Inc. 32 p.

41969201 Schmidt, J. (1991) Determination of th e Photolysis Rate of [carbon 14]-Pentachloro-phenol on the Surface of Soil: Final Report: Lab Project Number: 38440. Unpub lished study prepared by ABC Laboratories, Inc. 32 p. 0 42594302 Schmidt, J. (1992) Aerobic Soil Metabolism of (carbon 14)-Pentachlorophenol: Lab Project Number: 38353. Unpublished study prepared by ABC Labs, Inc. 41 p.

42288601 Schmidt, J. (1992) Aerobic Aquatic Metabolis m of [carbon 14] Pentachlo rophenol: Lab Project Number: 38354. Unpublished study prepared by ABC Labs, Inc. 38 p.

42436801 Schmidt, J. (1992) An aerobic Aquatic Metabolism of 14C-Pentachlorophenol: Lab Project Number: 38355. Unpublished study prepared by ABC Laboratories, Inc. 37 p.

42633709 Weeden, D. (1993) Pentachlo rophenol: Determination of the Sorption an d Desorption Properties: Lab Project Number: 92-12-4536: 12836.0692.6113.710. Unpublished study prepared by Springborn Laboratories, Inc. 69 p.

43627001 Christensen, K. (1995) Me tabolites of Pentachlorophenol- Determination of Adsorption/Desorption Coeffecients: Final Report: Lab Project Number: 95-3-5756: 12836.0195.6117.710. Unpublished study prepared by Springborn Labs, Inc. 68 p.

42633710 Dionne, E. (1993) Pentachl orophenol: Bioconcentration and Elimination of (carbon 14)-residues by Bl uegill Sunfish: LabPage 48 of 63 Project Number: 92-12-4532: 12836.0692.6114.140. Unpublished study prepar ed by Springborn Laboratories, Inc. 90 p.

42855402 Dionne, E. (1993) Pentachl orophenol-Bioconcentration and Eliminati on of (carbon 14)--Residues by Bluegill Sunfish (Lepomis m acrochirus): Amended Fina l Report: Lab Project Number: 12836.0692.6114.140: 92-12-4532. Unpublished study prepared by Springborn Labs, Inc. 83 p.

43205001 Connor, S. (1994) Pentachl orophenol-Leaching from Utility Poles Exposed to the Aquatic Environment: Final Report: Lab Proj ect Number: 12836.1293.6116.795: 94- 3-5201. Unpublished study prepared by Springborn Labs., Inc. 66 p.

43214601 Schocken, M. (1994) Pentachlorophenol: Determination of Photodegrada tion in Air: Amended Final Report: Lab Project Number : 12836/0692/6115/722: 94/4/5226. Unpublished study prepared by Springborn Lab., Inc. 90 p.

40924102 Banerji, S.; Piontek, K.; O'c onnor, J. (1986) (Pen tachlorophenol)- pentachloro phenol adsorption on soils and its potential for migration into groundwater.

41995201 Schmidt, J. (1991) Anaerobic Soil Metabolism of [Carbon 14]-Penta- chlorophenol: Lab Project Number: 38437. Unpublished study
prepar ed by ABC Laboratories, Inc. 46 p.

Unacceptable studies submitted to OPP to satisfy guideline requirements:

43214601 Schocken, M. (1994) Pentachlorophenol: Determination of Photodegrada tion in Air: Amended Final Report: Lab Project Number : 12836/0692/6115/722: 94/4/5226. Unpublished study prepared by Springborn Lab., Inc. 90 p.Page 49 of 63 

# Appendix C Ecotoxicology Profile

Ecotoxicity data for PCP are available from severa l sources. In addition to the guideline studies submitted by registrants, data also are available in the EPA Office of Water’s Ambient Water Quality Criteria for Pentachlorophenol – 1986 (EPA 1986), and the EPA/OPP Pesticide Ecotoxicity Database. The ecotoxicity databa se is compiled from actual studies reviewed by EPA in conjunction with pestic ide registration or reregistra tion and studies performed by USEPA, USDA and USFWS laboratories which have been reviewed by agency biologists and judged acceptable for use in the eco logical risk assessment process. Some ecotoxicity data also are available for the PCP contaminants (dioxins/furans and HCB). The data for these contaminants is from the OPP/AD risk assessm ents conducted in conjunction with the 2008 PCP RED as compiled by Petrie (EPA 2008a,b).


### PCP Ecotoxicity Profile

Terrestrial Organisms

Birds, acute oral

Three available acute-oral (LD50) studies categorize PCP as being sl ightly to moderately toxic to birds. The guideline (850.2100) is satisfied. No additional acute oral toxicity data are anticipated to be needed.

Table C1: Avian Acute-oral Toxicity

Test Species Test Material (% ai) LD50 (mg ai/kg bw) Toxicity Category EPA Study
ID

Northern bobwhite ( Colinus virginianus ) 88.9 627 Slightly toxic 42633701 Acceptable

Mallard ( Anas platyrhynchos) 99.6 380 Moderately toxic 160000 Supplemental Ring-necked pheasant ( Phasianus colchicus ) 99.6 504 Moderately toxic 160000 Supplemental

Birds, dietary

Six available studies categorize PCP as being sl ightly to practically nontoxic to birds when provided in their diet. The guide line (850.2200) is satisfied. No a dditional dietary toxicity data are anticipated to be needed.Page 50 of 63 Table C2: Avian Dietary Toxicity

Test Species Test Material (% ai) LC50 (ppm) Toxicity Category EPA Study
ID

Northern bobwhite ( Colinus virginianus ) 88.9 5581 Practically nontoxic 42633702 Acceptable

40 3400 Slightly toxic 22923 Supplemental

Mallard ( Anas platyrhynchos) 88.9 3763 Slightly toxic 42633703 Acceptable

40 4500 Slightly toxic 22923 Supplemental Ring-necked pheasant ( Phasianus colchicus ) 40 5204 Practically nontoxic 22923 Supplemental Japanese quail (Coturnix japonica) 40 22923 Practically nontoxic 22923 Supplemental

Nontarget Insects

Additional toxicity data are not an ticipated to be needed for beneficial insects. One acceptable study is available. The guideline for an acute toxicity test (85 0.3020) is satisfied. For PCP, the Agency does not anticipates needing a honeyb ee study for toxicity of residues on wood (850.3030) to support wood preservative uses.

Table C3: Honeybee Toxicity

Test Species Test Material (% ai) LD50 (μg ai/bee) Toxicity Category EPA Study
ID
Honeybee (Apis mellifera) Tech. > 48.3 Not determined - slightly toxic at most 36935 Acceptable



### Aquatic Organisms

Freshwater Fish, acute

The 21 acute toxicity studies tabulated below cate gorize PCP as being highly to very highly toxic to a variety of freshwater fis h. The guideline (850.1075) for acute toxicity testing is satisfied. No additional acute toxicity data are anticipated to be needed.Page 51 of 63 Table C4: Freshwater Fish Acute Toxicity

Test Species Test Material (% ai) LC50 (μg ai/L) Toxicity Category EPA Study ID

Rainbow Trout ( Oncorhynchus mykiss) 100 15 Very highly toxic 43485104 Acceptable
100 75 Very highly toxic Bionomics 1977 1 Acceptable
96 34 Very highly toxic 40098001 Acceptable
37 76 Very highly toxic TN0918 Supplemental
88 86 Very highly toxic 63572 Acceptable
15.7 370 Very highly toxic 00090429 Acceptable
96 115 Highly toxic 40098001 Acceptable

Bluegill ( Lepomis macrochirus ) 96 32 Very highly toxic 40098001 Acceptable

100 60 Very highly toxic Bionomics NR 1 Acceptable

37 150 Highly toxic TN0943 Supplemental

96 215 Highly toxic 40098001 Acceptable

15.7 345 Highly toxic 00033067 Acceptable

Fathead minnow ( Pimephales promelas ) 96 205 Highly toxic 40098001 Acceptable

100 600 Highly toxic 00033067 Acceptable
Chinook salmon ( Oncorhynchus tshawytscha ) 96 31 Very highly toxic 40098001 Acceptable
Channel catfish ( Ictalurus punctatus ) 88 <53 Very highly toxic EPA 1986 Supplemental

96 66 Very highly toxic 40098001 Acceptable
White sucker ( Catostomus commersoni ) Tech 85 Very highly toxic USFWS 2 Supplemental Largemouth Bass ( Micropterus salmoides ) Tech 136 Highly toxic USFWS 2 Supplemental
Brook trout ( Salvelinus fontinalis ) 99 138 Highly toxic EPA 1986 Supplemental
Atlantic salmon

( Salmo salar ) Tech 500 Highly toxic USFWS 2 SupplementalPage 52 of 63 1 OPP reviewed data cited in the OPP Pesticide Ecotoxicity Database

2 US Fish and Wildlife Service reviewed data c ited in the OPP Pesticide Ecotoxicity Database

Freshwater Fish, chronic

Two early life-stage studies are available. The guideline (850.1400) for a fish early life-stage toxicity test is satisfied. No additional acute toxicity data are anticipated to be needed.

Table C5: Freshwater Fish Early Life-Stage Toxicity

Test Species Test Material (% ai) NOAEC and LOAEC (μg ai/L) Endpoints Affected EPA Study ID

Rainbow Trout ( Oncorhynchus mykiss) 99 NOAEC = 11 LOAEC = 19 Survival and Growth (length, weight) EPA 1986 Acceptable

Fathead minnow ( Pimephales promelas ) 88 NOAEC = 16 LOAEC = 34 Survival 40924115 Supplemental

Freshwater Invertebrates, acute

The 12 acute toxicity studies tabulated below cate gorize PCP as being moderately to very highly toxic to freshwater invertebrates. The guideline (850.1010) for acute toxicity testing is satisfied. No additional acute toxicity data are anticipated to be needed.

Table C6: Freshwater Invertebrate Acute Toxicity

Test Species Test Material (% ai) EC50 (μg ai/L) Toxicity Category EPA Study ID

Waterflea ( Daphnia magna ) 93.7 134 Highly toxic EPA 1986 Supplemental
99 145 Highly toxic EPA 1986 Supplemental
96 240 Highly toxic 40098001 Supplemental
86 410 Highly toxic 40098001 Supplemental
88 450 Highly toxic 00063572 Acceptable

88 480 Highly toxic 00085230 Acceptable

37 1350 Moderately toxic TN0952 Acceptable
Cladoceran ( Simocephalus vetulus ) 93.7 160 Moderately toxic EPA 1986 SupplementalPage 53 of 63 Amphipod ( Hyalella azteca ) 99 239 Highly toxic EPA 1986 Supplemental Amphipod ( Gammarus pseudolimnaeus ) 88 92 Very highly toxic EPA 1986 Supplemental

Bladder snail ( Aplexa hypnorum ) 88 142 Highly toxic EPA 1986 Supplemental

Snail ( Gillia altilis ) 99 300 Highly toxic EPA 1986 Supplemental

Freshwater Invertebrates, chronic

Four supplemental life cycle tests are availabl e. However, an NOAEC for the most sensitive species ( Ceriodaphnia reticulata ) was not determined. Although an NOAEC was reported for Daphnia magna , the invertebrate species most commonly tested, the test material for that study is unknown. Therefore, an additional study using a daphnid species is anticipated to be needed for the TGAI. The guideline (850.1300) for a freshwater invertebrate life cycle is not satisfied.

Table C7: Freshwater Invertebrate Life Cycle Toxicity

Test Species Test Material (% ai) NOAEC and LOAEC (μg ai/L) Endpoints Affected EPA Study ID

Cladoceran ( Ceriodaphnia

reticulata ) 93.7 NOAEC <4.1 LOAEC = 4.1 Reduction in offspring EPA 1986 Supplemental

Snail ( Physa gyrina ) 93.7 NOAEC <26 LOAEC = 26 Embryo production EPA 1986 Supplemental

Waterflea ( Daphnia magna ) NR NOAEC = 180 LOAEC = 320 Survival EPA 1986 Supplemental

Cladoceran ( Simocephalus vetulus ) 93.7 NOAEC = 119 LOAEC = 264 Survival EPA 1986 Supplemental

Estuarine/Marine Fish and Invertebrates, acute

The available acute toxicity studies categorize PCP as being highly toxic to estuarine/marine fish and moderately to very highly toxic to estuarin e/marine invertebrates. No additional acute toxicity data are needed. The guidelines for fish (850.1075), bivalve (850.1025 or 850.1055), and one additional invertebrate sp. (850.1035) are satisfied.Page 54 of 63 Table C8: 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 ) 100 240 Highly toxic 43485104 Acceptable
96 220 Highly toxic 40228401 Acceptable
96 330 Highly toxic 40228401 Acceptable
Pinfish ( Lagodon rhomboides ) 96 31 Very highly toxic 40228401 Acceptable Mysid shrimp ( Americamysis bahia ) 96 320 Highly toxic 40228401 Acceptable Pacific oyster ( Crassostrea gigas ) 100 48 Very highly toxic 43485104 Acceptable Eastern oyster ( Crassostrea virginica ) 98 49 Very highly toxic EPA 1986 Supplemental
Tech. 34 Very highly toxic USFWS 2 Supplemental Shrimp ( Palaemon elegans ) 100 84 Very highly toxic 43485104 Acceptable Grass shrimp ( Palaemonetes pugio ) 96 2500 (LC50) Moderately toxic 40228401 Acceptable

1 Office of Water reviewed data cited in the OPP Pesticide Ecotoxicity Database

2 US Fish and Wildlife Service reviewed data c ited in the OPP Pesticide Ecotoxicity Database

Estuarine/Marine Fish and Invertebrates, chronic

One supplemental life cycle test is available fo r fish. However, because the NOAEC of 47 μg ai/L for the sheepshead minnow is a higher value th an the LC50 for the pinfish (31 μg ai/L), an acute-to-chronic ratio (ACR) is used to estimate an NOAEC for the more sensitive pinfish. Based on the sheepshead LC50 (220 μg ai/L) and NOAEC, an ACR of 4.68 (220 μg ai/L /47 μg ai/L) is derived. The extrapolat ed NOAEC for the pinfish is then calculated as 31 μg ai/L/4.68 = 6.6 μg ai/L. That value will be used for the risk assessment. No additional data are anticipated to be needed. The guideline (850.1400) for an estuarin e/marine fish early life-stage toxicity test is satisfied.

Table C9: Estuarine/Marine Fish Early Life-Stage Toxicity

Test Species Test Material (% ai) NOAEC and LOAEC (μg ai/L) Endpoints Affected EPA Study ID Sheepshead minnow ( Cyprinodon variegatus ) 100 NOAEC = 47 LOAEC = 88 Survival of 1 st generation fish EPA 1986 Supplemental

Pinfish -- NOAEC = 6.6 1
-- --

1 extrapolated value based on the ACR as described abovePage 55 of 63 Aquatic and Semi-aquatic Plants

Five acceptable studies are available for aquatic plants, but none are available for semi-aquatic plants. The guidelines for testing with duckw eed, a vascular sp. ( 850.4400), three algal spp. (850.4500), and cyanobacteria (850.4550) are satisfie d. No additional aquatic plant data are needed. A seedling emergence toxicity test with rice is anticipated to be needed; the guideline (850.4225) is not satisfied.

Table C10: Aquatic and Semi-aquatic Plant Toxicity

Test Species Test Material (% ai) EC50 (μg ai/L) NOAEC (μg ai/L) EPA Study ID

Aquatic species:

Duckweed ( Lemna gibba ) 88.9 250 32 42633708 Acceptable Green algae ( Selanastrum capricornutum ) 88.9 50 9 42633706 Acceptable

Marine diatom ( Skeletonema costatum ) 88.9 27 9 42633704 Acceptable

Freshwater diatom ( Navicula pelliculosa ) 88.9 124 28 42633705 Acceptable Cyanobacteria ( Anabaena flos-aquae ) 88.9 50 6 42633707 Acceptable

Semi-aquatic species:

Rice ( Oryza sativa ) Data gap --

Sediment-dwelling Invertebrates

Sediment toxicity data are not available. Based on its enviro nmental fate properties (e.g., log
K ow = 4.7 at pH 5), PCP is expected to accumulate in aquatic sediments. Because PCP 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.

Amphibians

Amphibian data are not required, but acute toxicity endpoints are av ailable for two species in the OPP Pesticide Ecotoxicity Database. These stud ies demonstrate that PCP is highly toxic to amphibians.Page 56 of 63 Table C11: Amphibian Acute Toxicity

Test Species Test Material (% ai) LC50 (μg ai/L) Toxicity Category EPA Study ID Bullfrog ( Rana catesbeiana ) 99 207 Highly toxic OPP 1 Supplemental
Salamander ( Ambyystoma mexicanum) Tech. 300 Highly toxic OPP 1 Supplemental

1 OPP Pesticide Ecotoxicity Database



### Ecotoxicity Profile - Dioxins/Furans

The data tabulated below are from the 2008 Chlorinated Dibenzo Dioxins (CDDs) and Chlorinated Dibenzo Furans (CDFs) as C ontaminants of Pentachlorophenol – Ecological Hazard and Risk Assessment for the Pentachl orophenol Reregistrati on Eligibility Decision (RED) Document , R.C. Petrie, Antimicrobials Division, USEPA Office of Pesticide Programs, Washington, DC. These data were selected fo r use in that risk assessment. Additional ecotoxicity data are available in the appendices of that document. Additional ecotoxicity data for dioxins and furans are not an ticipated to be required.

Table C12: Selected Avian and Mammalian Toxicity Values for Dioxins (2,3,7,8-TCDD)

Species Test Toxicity Toxicity Category

Northern bobwhite Acute oral LD50 = 15 μg/kg Very highly toxic
8-day dietary LC50 = 167 ppt Very highly toxic

Ringneck pheasant Reproduction (10 week) NOAEL= 0.014 μg/kg-day (fertility, embryo mortality) NA

Mouse acute oral LD50=114-284 μg/kg Very highly toxic

Rat Reproduction (exposed days 6-15 of gestation) NOAEL = 0.125 μg/kg-day (litter size and pup weight) NA

Table C13: Selected Aquatic Toxici ty Values for Dioxins (CDDs/CDFs)

Compound/ Test species Test Toxicity Toxicity Category

2,3,7,8-TCDD: Coho salmon 96-h acute LC50=5.60 ppt very highly toxic

Rainbow trout (sac fry) 96-h acute LC50=1.83 ppt very highly toxic

Rainbow trout 28-day early life-stage LC50=0.046 ppt very highly toxicPage 57 of 63 (swim-up fry) NOEC=0.0011 ppt

fathead minnow 28-day LC50=1.7 ppt very highly toxic Daphnia magna 48-h acute EC50>1020 ppt very highly toxic Annelid worm 55 days NOEC = 200 ppt NA
Snail 12 days NOEC = 200 ppt NA
Dibenzofuran:

Sheepshead minnow 96-h acute LC50=1800 ppb moderately toxic

fathead minnow 96-h acute LC50=1140 ppb moderately toxic Daphnia magna 48-h acute LC50=1340 ppb moderately toxic Mysid 96-h acute LC50=1310 ppb moderately toxic
Diatom, Skeletonema

costatum 96-h acute EC50=1500 ppb NA

2,3,7,8-TDCF: Medaka 13-day LC50=16 ppb very highly toxic



### Ecotoxicity Profile HCB

The data tabulated below are from the 2008 Hexachlorobenzene (HCB) as a Contaminant of Pentachlorophenol – Ecological Hazard and Ri sk Assessment for th e Pentachlorophenol Reregistration Eligibility Decision (RED) Document , R.C. Petrie, Antimicrobials Division, USEPA Office of Pesticide Programs, Washingto n, DC. Additional ecotoxicity data for HCB are not anticipated to be required.

Table C14: Selected Aquati c Toxicity Values - HCB

Species Test Endpoint/Effect Toxicity Category

Acute and Subchronic Toxicity:

Flounder ( Platichthys flesus) 96 h LC50 – 200 μg/L Highly toxic

Sole ( Solea solea ) 96 h LC50 – 140 μg/L Highly toxic

Channel catfish ( Ictalurus punctatus ) Static – 24 h LC50 – 6400 μg/L Moderately toxic

Bluegill ( Lepomis

macrochirus ) Static – duration not reported LC50 – 12,000 μg/L Slightly toxic

Largemouth bass (Micropterus salmoides ) Static – 96 h LC50 – 12,000 μg/L Slightly toxicPage 58 of 63 Coho salmon Static – 96 h. LC50 – 50,000 μg/L Slightly toxic

Largemouth bass 10 days 3.5 μg/L (liver and kidney damage) NA

Diatom ( Cyclotella meneghiniana ) Static - 48 h EC50 - 2 μg/L (genetic effect) NA

Freshwater green algae ( Selanastrum capricornutum ) Static - 96 h EC50 > 30 μg/L NA

Chronic Toxicity:

Water flea ( Daphnia magna) 14 days EC50 – 16 μg/L (50% reduction in fertility) NA

Cladoceran, ( Ceriodaphnia dubia ) Life cycle/partial life cycle – 7 days NOEC > 7 μg/L NA

Rainbow trout ( Salmo gairdneri) Early life stage – 90 days NOEC > 3.68 μg/L NA

Fathead minnow ( Pimephales promelas ) Early life stage – 32 days NOEC > 4.8 μg/L NA

Snail ( Lymnaea palustris ) 10-12 weeks 0.5 μg/L, 5 μg/L (significantly reduced growth rate) NA

Crab ( Portunus pelagicus ) 6 weeks 5 μg/L (reduction in carapace growth rate) NA

Table C15: Whole Sediment Acute Toxicity - HCB

Species NOAEC (mg/kg) Test duration/ type

Freshwater amphipod

(Hyalella azteca) 42 14-day test (spiked sediment)

60 10-day test (spiked sediment)

Midge ( Chironomus tentans) 42 14-day test (spiked sediment)

60 10-day test (spiked sediment)

Estuarine amphipod ( Leptochirus plumulosus ) 60 10-day test (spiked sediment)Page 59 of 63 Table C16: Selected Avian Toxicity Values for HCB

Species Test Method/Duration Endpoint

Ring-necked Pheasant ( Phasianus colchicus ) 5 days LC50 – 617 ppm

Japanese Quail 5-day LC50 – 568 ppm

Bobwhite Quail NR LD50 -- 575 mg/kg

Mallard NR LD50 -- 1450 mg/kg

Mallard Duck ( Anas platyrhynchos ) 8 days LC50 > 5000 ppm

Herring gull ( Larus argentatus ) Egg injection study LD50 – 4300 μg/kg (embryo mortality)

Herring gull Egg injection study 1500 μg/kg – significant reduction in embryonic weight

Japanese Quail ( Coturnix japonica ) 90 days NOEL – 5 ppm LOEL – 20 ppm

(egg volume)
NOEL – 1 ppm LOEL – 5 ppm (morphology, organ weight)Page 60 of 63 Ecotoxicity References for Appendix C

42633701 Campbell, S.; Jaber, M. (1993) Pentac hlorophenol: An Acute Oral Toxicity Study with the Northern Bobwhite: Lab Pr oject Numbner: 345-103. Unpublished study prepared by Wildlife International Ltd. 18 p. 42633702 Campbell, S.; Jaber, M. (1993) Pentac hlorophenol: A Dietary LC50 Study with the Northern Bobwhite: Lab Project Numb er: 345-101. Unpublished study prepared by Wildlife International Ltd. 37 p. 42633703 Campbell, S.; Jaber, M. (1993) Pentac hlorophenol: A Dietary LC50 Study with the Mallard: Lab Project Number: 345-102. Unpublished study prepared by Wildlife International Ltd. 36 p. 00033067 Mattson, V.R.; Arthur, J.W.; Walbridge, C. T. (1976) Acute Toxicity of Selected Organic Compounds to Fathead Minnow s: EPA-600/3-76- 097. (Unpublished study received May 2, 1980 under 32240-2; prepared by U.S. Environmental Protection Agency, Office of Re- search and De velopment, Environmental Research Laboratory, sub- mitted by Domain Industr ies, Inc., New Richmond, Wis.; CDL: 099418-G) 00063572 McCarty, W.M.; Alexander, H.C. (1977) Toxi city of Dowicide EC-7 to Freshwater Organisms. (Unpublished study received May 16, 1978 under 464-431; submitted by Dow Chemical U.S.A., Mi dland, Mich.; CDL:234322-A) 42633704 Hoberg, J. (1992) Pentachlorophenol Techni cal: Toxicity to the Marine Diatom: Lab Project Number: 92-12- 4540: 12836.0692.6109.450. Unpublished study prepared by Springborn Labor atories, Inc. 61 p. 42633705 Hoberg, J. (1993) Pentachlorophenol Technica l: Toxicity to the Freshwater Diatom: Lab Project Number: 92-12- 4521: 12836.0692.6108.440. Unpublished study prepared by Springborn Labor atories, Inc. 62 p. 42633706 Hoberg, J. (1993) Pentachlorophenol Techni cal: Toxicity to th e Freshwater Green Alga: Lab Project Number: 92- 10-4481: 12836.0692.6107.430. Unpublished study prepared by Springborn Labor atories, Inc. 62 p. 42633707 Hoberg, J. (1993) Pentachlorophenol Techni cal: Toxicity to th e Freshwater Bluegreen Alga: Lab Project Numb er: 92-11-4502: 12836.0692.6110.420. Unpublished study prepared by Springborn Laboratories, Inc. 61 p. 42633708 Hoberg, J. (1993) Pentachlorophenol Tec hnical: Toxicity to the Duckweed: Lab Project Number: 93-1-4560: 12836.0692.6111.410. Unpublished study prepared by Springborn Laboratories, Inc. 66 p.

00022923 Hill, E.F. et al. 1975. Leth al Dietary Toxicities of Envir onmental Pollutants to Birds. U.S. Fish and Wildl. Serv., Sp ecial Scientific Re port – Wildlife No. 191. Washington, DC.Page 61 of 63 00160000 Hudson, R.H. et al. 1984. Handbook of Toxicity of Pesticides to Wildlife (2 nd edition). U.S. Fish and Wildl. Serv., Resource Publ. 153. Washington, DC.

00085230 McCarty, W.M. (1977) Toxicity of Dowicide^(TM)I EC-7 to Daphnids. (Unpublished study received Oct 28, 1977 under 464-31; submit- ted by Dow Chemical U.S.A., Midland, Mich.; CDL:232112-A) 40098001 Mayer, F.L., Jr. and M.R. Elle rsieck. 1986. Manual of Acute Toxicity: Interpretational Data Base for 410 Chemical s and 66 Species of Freshwater Animals. US Fish and Wildlife Service, Res. Publ. 160, Washington, DC

40924115 Spehar, R.; Nelson, H.; Swanson, M.; et al (1985) Pentachlorophenol toxicity to amphipods and fathead minnows at differe nt test pH values. Environmental Toxicology and Chemistry 4:389-397. 40228401 Mayer, F.L., Jr. 1986. Acute Toxi city Handbook of Chemicals to Estuarine Organisms. EPA/600/X-86/231. Envi ron. Res. Lab., Gulf Breeze, FL

EPA 1986 Stephen, C. 1986. Ambient Aquati c Life Water Quality Criteria for Pentachlorophenol. USEP A/ORD. EPA-440/5-86-009.

TN0918 Report of Analysis: Certox P- 40 Wood Preserver. Rainbow trout. EPA Animal Biology Lab., Washington, D.C. January 19, 1976.

TN0952 Report of Analys is: Certox P-40 Wood Preserver. Daphnia magna . EPA Animal Biology Lab., Washington, D.C. March 1, 1976.Page 62 of 63 

# Appendix D Product Chemistry

The PCP product chemistry information is summar ized in Table D1 (source: EPA RED, 2008).

Table D1 – Product Chemistry of PCP.

Guideline Numbers PCP Source

830.1550 Product identity and composition Refer to Table 4

830.1600 Description of materials used to produce the product CBI A

830.1620 Description of production process CBI

830.1650 Description of Formulation Process CBI

830.1670 Description of Formulation Process CBI

830.1700 Preliminary analysis CBI

830.1750 Certified limits CBI

830.1800 Enforcement analytical method MRID 41002702

830.1900 Submittal of samples CBI

830.6302 Color Light brown/tan TGAI: White needle-like crystals EPA RED, 2008

830.6303 Physical State Solid EPA RED, 2008

830.6304 Odor Phenolic EPA RED, 2008

830.6313 Stability Stable for a year EPA RED, 2008

830.6314 Oxidation/Reduction Not applicable

830.6315 Flammability Not applicable

830.6316 Explodability Not applicable

830.7000 pH at25 °C 4.99 EPA RED, 2008

830.7050 UV/Visible Absorption Not applicable

830.7200 Melting point (°C) 190-191 o C EPA RED, 2008Page 63 of 63 Guideline Numbers PCP Source

830.7220 Boiling point (°C) Not applicable

830.7300 Density (g/cm 3 ) 1.979 g/ml EPA RED, 2008

830.7370 Dissociation Constant pKa(s) 4.74 EPA RED, 2008

830.7520 Particle size, fiber length, & diameter distribution Not applicable

830.7550 Log Kow 5.05 at pH 5 EPA RED, 2008

830.7840 Solubility in water (mg/L) at 25 o C 0.3 g/L at pH 5 20 ppm at pH 7 2200 ppm at pH 9 EPA RED, 2008

830.7860 Solubility in organic solvents Not applicable

830.7950 Vapor pressure (mm Hg) at 25 °C 1.1 x 10 -4 mm Hg at 25 o C EPA RED, 2008

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