Page 3 of 33 

### Table of Contents

1 Introduction

................................ ................................ ................................ ............................. 5

1.1 Statutory and Regulatory Authority

................................ ................................ ................. 5

1.2 Updates to Work Plan

................................ ................................ ................................ ...... 6

1.3 Case Overview

................................ ................................ ................................ ................. 7

1.4 Chemical Ide ntification and Properties

................................ ................................ ............ 7

1.5 Use/Usage Description

................................ ................................ ................................ ..... 9

1.5.1 Registrations

................................ ................................ ................................ ............. 9

1.5.2 Summary of Registered Uses

................................ ................................ .................... 9

1.5.3 Usage Information

................................ ................................ ................................ .. 10

1.6 Regulatory History

................................ ................................ ................................ ......... 10

1.6.1 Recent/Pending Regulatory Actions

................................ ................................ ....... 11

1.6.2 Tolerance Information

................................ ................................ ............................ 11

1.7 Incidents

................................ ................................ ................................ ......................... 11

1.7.1 Human Health

................................ ................................ ................................ ......... 11

1.7.2 Ecological

................................ ................................ ................................ ............... 11

2 Anticipated Da ta Needs

................................ ................................ ................................ ........ 11

3 Human Health Risk Assessment

................................ ................................ ........................... 14

3.1 Existing Toxicological Endpoints

................................ ................................ .................. 14

3.2 Dietary Exposure

................................ ................................ ................................ ............ 15

3.2.1 Food

................................ ................................ ................................ ........................ 15

3.2.2 Drinking Water

................................ ................................ ................................ ....... 16

3.3 Occupational and Residential Exposures

................................ ................................ ....... 16

3.3.1 Occupational Handler Exposure

................................ ................................ ............. 16

3.3.2 Residential Handler Exposures

................................ ................................ ............... 17

3.3.3 Residential Post

- Application Exposures

................................ ................................ . 17

3.4 Aggregate and Cumulative Exposure

................................ ................................ ............. 17

3.4.1 Aggregate Exposures

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

3.4.2 Cumulative Exposures

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

4 Environmental Risk Assessment

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

4.1 Environmental Conceptual Model Exposure Pathways

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

4.2 Ecological Effects Assessment

................................ ................................ ....................... 19Page 4 of 33 5 Endocrine Disruptor Screening Program (EDSP)

................................ ................................ . 20

6 Next Steps

................................ ................................ ................................ ............................. 20

7 References

................................ ................................ ................................ ............................. 21

Appendix A T oxicology Profile

................................ ................................ ............................... 24
Appendix B Ecotoxicology Profile

................................ ................................ .......................... 29

List of Tables Table 1

- Summary of Anticipated Risk Assessments and Data Needs: Phenol

............................ 6 Tabl e 2

- Anticipated Registration Review Schedule

................................ ................................ ..... 6 Table 3

- Chemical Facts of Phenol and Salt

................................ ................................ .................. 7 Table 4

- Physical

- Chemical and Fate Properties for Phenol and Salt

................................ ........... 8 Table 5

- Summary of Phenol and Salt Registered Uses

................................ .............................. 10 Table 6

– Studies Anticipated as Needed fo r the Registration Review of Phenol and Salt

.......... 12 Table 7

– Existing Toxicological Endpoints

................................ ................................ ................. 14 Table 8

– Occupational Handler Exposure Scenarios for Phenol and Salt

................................ ... 16 Table 9

– Residential Post

- Application Exposure Scenarios for Phenol and Salt

........................ 17 Table 10

- A cute Toxicity for Freshwater Fish

................................ ................................ ............. 29 Table 11

– Acute Toxicity for Aquatic Invertebrates

................................ ................................ ... 31
Table 12

- A c ut e T o x i c i t y o f P h e no l t o M a r i n e / Es t ua r i n e I nv e r t e b r a t e s

................................ ...... 33
Table 13

- C h r o ni c T o x i c i t y o f P h e no l t o M a r i n e / Es t ua r i n e I nv e r t e b r a t e s

................................ ... 33

List of Figures Figure 1

- Conceptual Model for Ecological Exposure and Effects of Phenol and Salt to Aquatic and Terrestrial Organisms

................................ ................................ ................................ ............. 19Page 5 of 33 

## 1 Introduction

This document is the Environmental Protection Agency’s (EPA or “the agency”) Final Work Plan (FWP) for the registration review of the Phenol and Salt Case. The FWP document explains what EPA's Office of Pesticide Programs knows about the chemicals

, highlighting anticipated data and assessment needs, identifying the types of information that would be especially useful to the Agency in conducting the review, and providing an anticipated timeline for completing their review. There were no public comments received concerning the Preliminary Work Plan (PWP), which was posted in the Phenol and Salt registration review docket (EP A

- HQ

- OPP

201 2

- 0810 ). In the PWP, the Agency solicited comments on specific topics: environmental justice, water body impairment, trade irritants, and structure activity relationships. No comments or information were received during the public comment period concerning these issues. Therefore, the data needs, work plan, and timeline described in the PWP remain as they were presented initially. Further, this document makes final the work plan for the Phenol and Salt registration review process.



## 1.1 Statutory and Regulatory A uthority

The Food Quality Protection Act (FQPA) of 1996 mandated a registration review program. All pesticides distributed or sold in the United States generally must be registered by the U.S. Environmental Protection Agency (USEPA, EPA, or the Agency) bas ed on scientific data showing that they will not cause unreasonable risks to human health or the environment when used as directed on product labeling. The registration review program is intended to make sure that, as the ability to assess risk evolves and as policies and practices change, all registered pesticides continue to meet the statutory standard of no unreasonable adverse effects to human health or the environment. Changes in science, public policy, and pesticide use practices will occur over time. Through the registration review program, the Agency periodically reevaluates pesticides to make sure that as change occurs, products in the marketplace can be used safely. Information on this program is provided at http://www.epa.gov/oppsrrd1/registration_review/

.
The Agency is implementing the registration review program pursuant to Section 3(g) of the Federal Insecticide, Fungicide, and Rodenticide Act (F IFRA) and will review each registered pesticide every 15 years to determine whether it continues to meet the FIFRA standard for registration. The regulations governing registration review begin at 40 CF R 155.40. The Agency will consider benefits informatio n and data as required by FIFRA. The public phase of registration review begins when the initial docket is opened for each case. The docket is the Agency’s opportunity to state what it knows about the pesticide and what additional risk analyses and data or information it believes are needed to make a registration review decision. The Phenol and Salt Preliminary Work Plan (PWP) was published on December 19 , 2012 and the 60

- day comment period ended on February 12 , 2013

.
Documents associated with this registration review can be viewed at http://www.regulations.gov in docket EPA

- HQ

- OPP

- 2012

- 0810

. Below is a summary of the issues relevant to this registration review case.Page 6 of 33 

## 1.2 Updates to Work Plan

Since the publication of the P WP, the agency has made the following updates:

• The akgency will conduct a tolerance review for indirect

- food contact uses

• Corrected formatting and typographical errors

Table 1

- Summary of Anticipated Risk Assessments and Data Needs : Phenol

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 6 for more detail about anticipated data needs)

Dietary (food) No 5/26/2005 None None
Dietary (drinking water) No 5/26/2005 None None

Occupational Handler Yes 5/26/2005 Updated Indoor Exposure Data Inhalation Toxicity Study

Residential Handler No 5/26/2005 None None

Residential Post Application

- Incidental Oral and Dermal Yes 5/26/2005 Updated Surface Residue Data

Residential Post Application

- Inhalation Yes 5/26/2005 Updated Indoor Exposure Data Inhalation Toxicity Study

Aggregate Yes 5/26/2005 Updated Dietary, Residential Handler and Residential Post Application

Cumulative No N/A None None

Tolerance Review Yes N/A New None
Ecological No N/A None None

N/A = Not applicable

Table 2

- Anticipated Registration Review Schedule

Anticipated Activity Target Date 1 Completion Date Phase 1: Opening the Docket Open Docket and 60

- Day Comment Period for Preli minary Work Plan 2012

- 12 2012

- 12

- 18
Close Public Comment Period 2013

- 0 2 2013

- 02

- 12 Phase 2: Case Development
Issue Final Work Plan 2013

- 06 2013

- 05
Issue Data Call

- In (DCI) 2014

- 06
Receive Data to be Considered in Risk Assessment 2016

- 06 Open 30

- Day Public Comment Period for Preliminary Risk Assessment(s) 2017

- 12
Close Public Comment Period 2018

- 01

1 The anticipated schedule will be revised as necessary ( e.g ., on any need arising under the Endocrine Disruptor Screening Program with respect to the active ingredients in this case).Page 7 of 33 Phase 3: Registration Review Decision and Implementation Open 60

- Day Public Comment Period for Pro posed Decision 2019

- 06
Close Public Comment Period 2019

- 08
Issue Final Decision 2019

- 12 Begin Post

- Decision Follow

- up 2019 Total (years) 7



## 1.3 Case Overview

The docket for the Phenol & Salt Case (Case 4074 ) has been established at http://www.regulations.gov in docket number EPA

- HQ

- OPP

- 2012

- 0810



## 1.4 Chemical Identification and Properties

Table 3 presents the two active ingredient s to be assessed in C ase 4074 : p henol (PC Code
064001 ) and s odium phenate (PC Code 064002 )

. P henol and sodium phenate are considered to
be toxicologically and ecologically equivalent for the purposes of registration revie w; and e xcept where otherwise noted, the two active ingredients in this case will be referred to collectively as “phenols”.

Table 3

- Chemical Facts of Phenol and Salt

Chemical Name Phenol Sodium phenate

Classification Phenol Phenoxy

PC Code 064001 064002

CAS No. 108

- 95

- 2 139

- 02

- 6

Molecular Formula C 6 H 5 OH C 6 H 5 ONa Molecular Weight 94.11 g/mol 116.10 g/mol First registered in US as a pesticide 1969 1969

RED issued 2004 2004 RED updated 2009 2009

EPA Registered Products 4 3

Tolerances None 2 None 2

Molecular Structure

2 See Section 1.5.2 Tolerance Information for further informationPage 8 of 33 The phenol and sodium phenate product chemistry information (source: MRIDs 41443603 and 42930901; EPI Suite v 4.10; TOXNET) relevant to risk assessment is summarized in Table 4

.

Table 4

- Physical

- Chemical and Fate Properties for Phenol and Salt

OPPTS Guideline
No. Physical and Chemical Properties Phenol Sodium P henate

830.1550 Product identity and composition Refer to Table 3

. Refer to Table 3

.

830.1800 Enforcement analytical
method Gas Chromatography, FID de tector GC MS

830.6302 Color Colorless to slight pink crystalline solid White to reddish rods or granules

830.6303 Physical State Solid

. Pure phenol absorbs easily water from air and liquefies. Crystalline needles or rods

830.6304 Odor Sharp medicinal, sweet odor Slight phenolic odor

830.6313 Stability to sunlight, normal and elevated temperature, metals/metal ions Stable under ordinary conditions of use and storage. Heat will contribute to instability. May discolor in light.

Substances to be avoided include strong oxidizing agents, str ong bases, strong acids, alkali s, calcium hypochlorite. Not highly flammable and not explosive. No oxidizing properties.

Conditions to Avoid: Heat, flames, ignition sources and incompatibles. Stable under no rmal temperatures and pressures.

Deliquescent

830.7000 pH About 6.0 (aq ueous sol utio n) Alkaline in aqueous

830.7050 UV/Visible Absorption UV: 258 nm; photo

- degrade, especially in air. N/A

830.7200 Melting point 40.5

- 41.5°C; 43°C 174.06 ◦ C

830.7220 Boiling point 182°C @ 760 mmHg 439.17 ◦ C

830.7300 Density 1.071 g/ cm3 @ 20°C N/A

830.7370 Dissociation Constant Phenol is a weak acid. pKa = 9.89 at 20°C; pKa 9.95 (in water); N / A

830.7550 Partition coefficient ( n

octanol/water) Log Kow is 1.46 at 25°C Log Kow is

- 1.170 at 25°C

830.7840 Solubility in water 84 g/l at 20°C;
1 gram/9 grams of water. Highly soluble in water.
1 ,000 gm /L at 25°C.

830.7860 Solubility in organic solvents Very soluble in alcohol , chloroform, ether, glycerol, carbon disulfide Soluble in alcohol

830.7950 Vapor pressure 0.4mm Hg at 20°C 0.341 mm Hg at 25°C 2.60E

- 08 mm Hg at
25 °C

N/A Henry's Law Constant 3.33X10

- 7 atm

- cu m/mol @ 25 °C 1.529E

- 006 atm

- m 3 /mole 3.972E

- 015 atm

- m 3 /mole

N/A Log K
oc (organic carbon ratio in soil) 3 1.21

- 1.96 N/A

3 Source: EPI

- Suite v4.1Page 9 of 33 N/A Photolysis 3 Absorbs light in the region of 290

- 330 nm, likely photodegrade directly in surface water. N/A

N/A Half

- life in freshwater 3 <1 day N/A

N/A Biodegradability 3 Completely biodegrades in soil within 5 days N/A

N/A Estimated half

- life in air 3 <1 day N/A

N/A Log bioconcentration factor (BCF ) 3 0.28 in goldfish and 1.3 for golden orf N/A



## 1.5 Use/Usage Description

Products containing phenol and sodium phenate are registered for use as a hard surface disinfectant s , deodorizer s and cleaner s on the following hard non

- porous surfaces: agricultural premises and equipment ; HVAC systems ; food handling/storage establishment premises and equipment ; residential and public access premises ; and medical/dental/veterinary premises ; and

e qui pment

.



### 1.5.1 Registrations

There are four EPA

- register ed products that contain phenol as an active ingredient (a.i. ). Three of the four product s also contain the alkali metal salt of phenol, sodium phenate, as an active ingredient . The percent a.i. of phenol ranges from 0. 6 percent to 7.8 percent and the formulations include ready to use liquid, as a wipe and as a liquid concentrate

. The percent a.i. of sodium phenate ranges from 0.06 percent to 0.3 percent and the formulations include ready to use liquid,

as a wipe and liquid concentrate. The amo unt of the active phenol moiety in formulations containing both phenol and sodium phenate is expressed as the total phenol acid equivalent 4 (a.e.). Products containing phenol and sodium phenate range from 1.61 to 8.04 percent a.e.

There is no registered manufacturing use product or registered technical grade active ingredient. There are eight products containing phenol as an inert ingredient (PC Code 800189).



### 1.5.2 Summary of Registered Uses

Table 5 presents a summary of the registered uses of phenols that will be assessed in this registration review

. Phenols can be applied by the following application methods: ready to use liquid, mop, soaking, fogging, spray, wipe and liquid concentrate.

4 The phenol acid equivalent content for sodium phenate is 80 percent:

; therefore

1.56% phenol (acid) content + (0.06% sodium phenate x 80% a.e.) = 1.61% phenol a.e. and 7.8% phenol (acid) content + (0.3% sodium phenate x 80% a.e.) = 8.04% phenol a.e. contentPage 10 of 33 Table 5

- Summary of Phenol and Salt Registered Uses

Use Application Method Application Rate

Agricultural Premises and Equipment

– Indirect Food Contact

Farm Equipment, Animal and Poultry Housing Spray, Mop, Wipe, Soak 1.56 percent phenol (1.61 percent phenol a.e.)

Commercial, Industrial, Institutional, Premises and Equipment

HVAC systems in commercial, industrial, institutional areas Fogging 1.56 percent pheno l (1.61 percent phenol a.e.)

Food Handling/Storage Establishments Premises and Equipment

– Indirect Food Contact

Food Processing Plants Spray, Mop, Wipe, Soak 1.56 percent phenol (1.61 percent phenol a.e.)

Residential and Public Access Premises

HVAC systems in residential areas (including cruise ships) Fogging 1.56 percent phenol (1.61 percent phenol a.e.)

Day Care Centers, Schools, Health Clubs Trigger Spray 1.56 percent phenol (1.61 percent phenol a.e.)

Medical/Dental/Veterinary Premises and Equipment

Hospital Disinfection Spray, Mop, Wipe, Soak 1.56 percent phenol (1.61 percent phenol a.e.)

Clean Room Production Are a s Fogging 1.56 percent phenol (1.61 percent phenol a.e.)



### 1.5.3 Usage Information

The Kline Biocides Report does not mention phenol s

.



## 1.6 Regulatory History

Phenol and sodium phenate (PC Codes 064001 and 064002) were first registered as pesticide active ingredients by the United Sates Department of Agriculture (USDA) on June 11, 1969. In 1970, the Environmental Protection Agency ( EPA) was established and assumed all pesticide registration responsibilities from USDA. Phenol and sodium phenate are currently regulated by both the U.S. EPA and the U.S. Food and Drug Administration (FDA). EPA regulate s the pesticidal uses of phenols summarized in Table 5 and FDA regulates uses of phenols such asPage 11 of 33 those found in over

- the

- counter drugs used for the treatment of various conditions including
insect bit es, poison ivy, diaper rash, antiseptics and acne (21 CFR §310.531 and §310.545). Prior to April 12, 2005

, phenols were registered for use as a materials preservative in paints; however,
this use was terminated in response to the risks identified in the “P henol/Sodium Phenate Reregistration Decision” memorandum dated September 30, 2004. EPA completed a RED
addendum for Phenols and Salt on March 30, 2009 to include the use of fogging in clean rooms and HVAC ductwork uses that were inadvertently omitted from 2004 “Phenol/Sodium Phenate Reregistration Decision” memorandum. The post

- RED data call

- in (DCI) has not been issued.



### 1.6.1 Recent/Pending Regulatory Actions

There are no recent regulatory actions for phenol and salt case. E PA anticipates issuing the post

RED DCI in the near future.



### 1.6.2 Tolerance Information

No tolerances have been established for phenol or sodium phenate. T wo tolerance exemptions have been established for phenol as an inert ingredient (solvent/ co solvent ) in pesticide products used on growing crops ( 40 CFR 180.920 ) or on livestock (40 CFR 180.930 ). The Agency will assess the need for a tolerance during registration review.



## 1.7 Incidents

1.7.1 Human Health

EPA identified 1 0 incidents in the OPP Incident Data System associated with dermal and inhalation exposure from the period 1989 to 2012

. M ost of the dermal incidents resulted in skin irritation , rash, itchin g and skin discoloration

. I nhalation exposure resulted in respira tory irritation, difficult breathing, throat and chest congestion and sore throat

. In i ncidents where dermal and inhalation exposure occurred

, the following symptoms were reported : h eadache, dizziness , night sweats

, and heart palpitation

.



### 1.7.2 Ecological

No phenol ecological incidents resulting from its use as a registered antimicrobial have been reported to the Agency’s Ecological Incide nt Information System (EI I S , v 2.11 ) from the period
1970 to 2012.



## 2 Anticipated Data Needs

Table 6 presents a summary of the data anticipated as being needed to support this registration
review.Docket Number EPA

- HQ

- OPP

- 2012

- 0810 www.regulations.gov

Page 12 of 33 Table 6

– Studies Anticipated as Needed for the Registration Review of Phenol and Salt

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

Studies Anticipated to be Required through the Registration Review DCI
8 75.14 00 Indoor Exposure,
Inhalation TGAI 24 Occupational and
Residential Hard Surface
Disinfection 1. Trigger pump sprayer, low pressure handwand , mop , and wipe 5 2. Hand held fogg ing of clean rooms 6

3. HVAC treatment

875.1700 Product Use
Information TGAI 12 All All All scenarios.

875.2300 7 Indoor Surface
Residue Dissipation TGAI 24 Residential Surface disinfection of
household floors and carpets Dermal and incidental exposures to phenol are expected for toddlers who sit or play on household floors or carpets after they are disinfected with phenol products.

875.2500 Post Application Exposure, Inhalation TGAI 24 Residential Air Deodorization

, HVAC Treatments Inhalation exposure following the use of air deodorizers or HVAC treatments.

Studies Expected to be Required through the Anticipated Post

- RED DCI 8

875.1200 Dermal exposure

-- Indoor TGAI 24 Occupational and Residential Hard Surface Disinfection
Air Deodorization
HVAC Treatment 1. Trigger pump sprayer, low pressure handwand , mop , and wipe 5 2. Hand held fogg ing of clean rooms 6

3. HVAC treatment

5 It may be possible to use proprietary surrogate expo sure data if data compensation issues can be addressed.

6 If the labels are modified to require automatic foggers in place of hand held foggers, then the study likely would not be needed.

7 If surface residue data are not available, then the standard assum ption of 100 percent transferable surface residue will be used which might overestimate the risk.

8 The 850.1010 Aquatic invertebrate acute toxicity, test, freshwater daphnids , 850.1075 Fish acute toxicity test, freshwater and marine , and 850.2100 Avian ac ute oral toxicity test were anticipated as being required as a result of the RED. The Agency now believes that these data are not anticipated to be necessary to support Registration Review because of the low environmental exposure to non

- target organisms. Therefore, these studies will not be required through the post

- RED DCI.Page 13 of 33 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

875. 14 00 a 9 , 10 Indoor Inhalation Exposure

- whole building TGAI 12 Occupational and
Residential Air Deodorization

, HVAC Treatment HVAC treatment

875. 14 00 b 10

, 11 Indoor Inhalation Exposure

- chamber study TGAI 12 Occupational and
Residential Air Deodorization

, HVAC Treatments HVAC treatment

9 A whole building study is anticipated as needed as confirmatory data for the HVAC ductwork treatment use. The anticipated DCI will provide that the whole building study is to be based on OPPTS Guideline 875.1 4 00 Indoor Inhalation Exposure

, and conducted at a representative application site during an actual application or at a simulated application site that is configured to match the characteristics of a representative applicatio n. The anticipated DCI will provide that the specific conditions such as ventilation rate, air temperature, application method and application rate must match the conditi ons of the labeled use and will recommend that a study protocol be submitted for revi ew by the Agency prior to the initiation of the actual study.

10 Due to a typographical error, guideline 875.1400 was incorrectly presented as 875.1200 in the RED.

11 A chamber study is anticipated as needed as confirmatory data for the HVAC ductwork treatme nt use. The anticipated DCI will provide that the chamber study
is to be based on OPPTS Guideline 875.1 4 00 Indoor Inhalation Exposure and ASTM D5116

- 06 Standard Guide for Small

- Scale Environmental Chamber Determinations of Organic Emissions from Indoor Mat erials/Products . The anticipated DCI will provide that the specific conditions of the chamber study such as ventilation rate, air temperature, application method and application rate must match the conditions of the labeled use and recommend that a study protocol be submitted for review by the Agency prior to the initiation of the actual study.Docket Number EPA

- HQ

- OPP

- 2012

- 0810 www.regulations.gov

Page 14 of 33 

## 3 Human Health Risk Assessment

The Agency anticipates the need to conduct a human health risk assessment for phenols . The Agency expects to require additional data for use in conducting the registration review.



## 3.1 Existing Toxicological Endpoints

On March 9, 2004, the Antimicrobials Divis ion Toxicology Endpoint Selection Committee (ADTC) reviewed the available toxicology data for phenols and selected the toxicological doses and endpoints listed in Table 7 . These endpoints as well as the associated data base uncertainty factors, the FQPA safety factor and targets for margin of exposure (MOE) are subject to reevaluation during registration review, particularly if any new toxicity data via future
submiss ions and/or literature publicati ons become available for phenols

.

Table 7

– Existing Toxicological Endpoints

Exposure Scenario Dose Used in Risk Assessment (mg/kg/day) Target Margin of Exposure (MOE) , UF, Special FQPA SF, for Risk Assessment Study and Toxicological Effects

Acute Dietary (gen population) An acute dietary endpoint has not been identified for phenol.

Acute Dietary (females 13

- 49) An acute dietary endpoint has not been identified for phenol.

Chronic Dietary (all populations) NOAEL = 60 mg/kg/day
UF = 100

Chronic RfD = 0.6 mg/kg/day UF = 100 FQPA SF = 1 Developmental toxicity study in rats (MRID No. 43735402) Based on significant reductions from the control in mean fetal body weight/litter at 120 mg/kg/da y.

Incidental Oral
Short

- Term (1

- 30 Days)

Residential Only NOAEL= 60 mg/kg/day MOE = 100 FQPA SF = 1 Developmental toxicity study in rats (MRID No. 43735402) Based on significant reductions from the control in mean fetal body weight/litter at 120 mg/kg/day.

Incidental Oral
Intermediate

Term (1

- 6 Months)

Residential Only NOAEL= 60 mg/kg/day MOE = 100 FQPA SF = 1 Developmental toxicity study in rats (MRID No. 43735402) Based on significant reductions from the control in mean fetal body weight/litter at 120 mg/kg/day.Page 15 of 33 Exposure Scenario Dose Used in Risk Assessment (mg/kg/day) Target Margin of Exposure (MOE) , UF, Special FQPA SF, for Risk Assessment Study and Toxicological Effects

Dermal 12

Short and intermediate

term NOAEL = 60 mg/kg/day MOE = 100 Developmental toxicity study in rats (MRID No. 43735402). Based on significant reductions from the control in mean fetal body weight/litter at 120 mg/kg/day.

Inhalation (All durations ) LOAEL = 0.1 mg/L MOE = 300 (ST, IT)

MOE = 1000 (LT) Dalin and Kristofferson: Physiological Effects of a Sub

- lethal Concentration of Inhaled
Phenol on the Rat. Ann. Zool. Fennici 11:
193

- 199, 1974
LOAEL of 0.1 mg/L, based on alterations in sliding angle from tilting plane test, and significant increases in liver enzymes

Cancer Data are inadequate for classification of human carcinogenic potential (U

. S

. EPA, 200 5 ) . No additional carcinogenicity data will be nee ded. 13



## 3.2 Dietary Exposure

The Agency does not anticipate the need to revise the dietary assessments conducted in support of the 2004 RED.



### 3.2.1 Food

There are no chronic dietary risks of concern associated with the approved uses of phenol and sodium phenate and no additional residue chemistry data are expected to be needed.

Human dietary exposure to phenol and sodium phenate residues may occur as a re sult of the use of products on food contact surfaces of food processing plants and any food

- handling facilities including public eating places. After treatment, all food contact surfaces must be washed with soap or detergent and rinsed with potable water p rior to reuse. In the RED, use of these products to disinfect food contact surfaces was assessed based on use on kitchen countertops. EPA believes the results to be conservative. A n acute dietary assessment was not conducted because phenol and s odium phena te do not elicit adverse systemic effects resulting from a single dose

. Chronic dietary risks were below the Agency’s level of concern ( 7.5% of the cPAD for adult males, 9.0% for adult females

, and 36% for children ). A t ransfer efficiency of 10% was assume d in the RED due to the high vapor pressure of phenol (0.35 mmHg at 25 C). Use of the 10%

t ransfer efficiency is considered appropriate due to volatilization of phenol and reduction of residues on the treated surface following the required washing and rins ing steps prior to reuse.

12 From the available data, dermal absorption percentages of 20

- 50% have been observed from in vivo and in vitro studies. The ADTC selected the 50% dermal absorption value for phenol for use as a conservative value in risk assessments. This value also takes into account the irritant properties of phenol which may increase its dermal absorption. Phenol is not expect ed to result in chronic dermal exposure due to its volatile nature and short half

- life. Therefore, the ADTC did not select a long

- term d ermal endpoint for phenol, and the dermal exposure risk assessment is not required.

13 See Appendix A Carcinogenic Pote ntial of Phenol for further explanation

.Page 16 of 33 

### 3.2.2 Drinking Water

The Agency does not anticipate the need to revise the drinking water assessment conducted in support of the 2004 RED. Phenol and sodium phenate are registered only for indoor uses. Although minimal, some surface water contamination could occur resulting from washing down

the

- drain or running off from livestock premises. P henol has a high water solubility (8.3 g/100 ml at 20 ◦ C) and low adsorption to soil (log K OC = 1.21

- 1.96) both of which favor leaching to ground water. However, as the half

- life in water is less than one day (0.6 days), bio degradation in soil is complete within five days, and photodegradation in water is likely, neither surface water

nor groundwater contamination is likely

. Therefore, at this time, phenol and sodium phenate are not expected to reach wastewater treatment plants or to contaminate drinking water and a drinking water assessment is not deemed to be necessary

.



## 3.3 Occupational and Residential Exposures

The Agency anticipates the need to revi se the occupational and residential assessments conducted in support of the 2004 RED. Uses of phenols that may result in occupational handler and residential post

- application exposure are presented in Table 8 and Table 9

.



### 3.3.1 Occupational Handler Exposure

The Agency anticipates the need to revise the occupational handler assessment conducted in support of the 2004 RED. Occupational handler dermal and inhalation exposures were assessed in the RED for hard surface disinfection using aerosol spray and towelette, loading foggers for clean room fogging and application of disinfectant to HVAC ductwork

– fogging. The dermal
M OEs were assessed using an oral NOAEL of 60 mg/kg/day from a developmental toxicity study in rats along with a dermal absorption factor of 50 percent. Inhalation MOEs were assessed using a LOAEL of 0.1 mg/liter from an inhalation toxicity study in rats. W ith the exception of the dermal MOE of 70 for surface disinfection using towelettes (while wearing gloves), all of the dermal and inhalation MOEs exceeded the target MOEs and were not of concern

. Occupational post application inhalation exposures were asse ssed in the RED for general cleaning solution vapor exposures and re

- entering clean rooms after fogging treatment. The MOEs were above target MOE of 300 and were not of concern.

If new endpoints are identified from the toxicology studies that are anticip ated to be required for registration review, then exposures to phenol will need to be re

- assessed during registration review. The exposure routes could include dermal and inhalation for occupational exposures. Occupational handler scenarios to be assesse d are presented in Table 8

.

Table 8

– Occupational Handler Exposure Scenarios for Phenol and Salt

Scenario Exposure Route(s) Duration Occupational ExposuresPage 17 of 33 Spray, mop and wipe for hard surface disinfection Dermal and Inhalation Short and Intermediate Term

Fog clean rooms for adjunct treatments Dermal and Inhalation Short and Intermediate Term

ULV applications for HVAC treatments Dermal and Inhalation Short and Intermediate Term



### 3.3.2 Residential Handler Exposures

Residential handler exposure is not expected based on currently registered uses. Based on the
information av ailable, the Agency believes that an occupational user will apply phenol pesticide products in residential settings.



### 3.3.3 Residential Post

- Application Exposures

The Agency anticipates the need to revise the residential post

- application assessment conducted in support of the 2004 RED once the d ata to be required through the post

- RED DCI are received and reviewed

. Residential post

- application exposures could result when bystanders (adults and children) who come in contact with phenols products applied to HVAC systems or when children have contac t with floors treated with phenol disinfectant products

. The exposure routes could include dermal, inhalation and incidental oral. The r esidential post

- application exposure scenarios applicable to phenol are listed in Table 9

.

Table 9

– Residential Post

- Application Exposure Scenarios for Phenol and Salt

Scenario Exposure Route(s) Duration

Residential Exposures

Toddlers playing on phenol disinfected floors Dermal and Incidental Oral Short and Intermediate Term

Post application exposure following HVAC treatments Inhalation Short and Intermediate Term

Post application inhalation exposures following the application of Sporicidin , a pesticide product containing phenol, to HVAC ductwork were previously assessed in the M emorandum: Occupational and Residential Exposure and Risk Assessment for the Duct Cleaning Use of Phenol (Sporicidin) of December 12, 2009 (D313122). The results of these assessments indicated the estimated risks would be below EPA’s level of concern if re

- entry were delayed for 16 or 24 hours after application, depending upon which model is used. The registrant has since voluntar ily amended the registration and label to change the application rate for the HVAC use to 4 ounces per 2,000 square feet of building area to reduce the re

- entry interval to 3 hours. The Agency will be assessing the new application rate as a part of registr ation r eview.



## 3.4 Aggregate and Cumulative ExposurePage 18 of 33 

### 3.4.1 Aggregate Exposures

The Agency anticipates the need to revise the aggregate assessment conducted in support of the
2004 RED. Upon reevaluation and selection of toxicological endpoints, combined with the hum an health exposure assessments expected as a part of this registration review case, aggregate exposures will need to be assessed.



### 3.4.2 Cumulative Exposures

With respect to cumulative exposure, unlik e other pesticides for which the Agency has followed
a cumula tive risk approach based on a common mechanism of toxicity, EPA has not made a common mechanism of toxicity finding as to phenol and any other substances and phenol does not appear to produce a toxic metabolite produced by other substances. For the purpose s of this registration review, therefore, EPA has not assumed that phenol has a common mechanism of toxicity with other substances. For information regarding EPA’s efforts to determine which chemicals have a common mechanism of toxicity and to evaluate the cumulative effects of such chemicals, see the policy statements released by EPA’s Office of Pesticide Programs at http://www.epa.gov/pesticides/cumulative/

. 

## 4 Environmental Risk Assessment

The Agency does not anticipate conducting an environmental risk assessment because of the low environmental exposure to non

- target organisms. The wipe use pattern is not expected to result in any exposure of fish and wildlife because used wipes will be disposed of i n the trash. Disposal of used solution down the drain is not expected to result in exposure of fish and wildlife to phenol or toxic degradates because of the short half lives in various environmental media like water, soils, and air. The half life of phe nol in air is less than a day (0.6 days), its half life in water is less than a day and it degrades in aerobic and anaerobic soil systems in less than five days. Due to low K OW ( 1.46 at 25°C ), it is not likely to bioaccummulate in aquatic organism s

. For those uses which would result in down

- the

- drain disposal of used solutions, it is unlikely that environmental exposure of fish and wildlife would occur because phenols degrade rapidly in the environment and are not expected to bioaccumulate. If exposure we re to occur, phenols have a low toxicity to fish, aquatic invertebrates and aquatic plants which would indicate a low potential for risk. No avian studies were available, so the toxicity of phenols to avian species could not be assessed. However, since t he exposure to avian species is considered to be very low, risk to avian species is unlikely. Therefore, since the environmental exposure to non

- target organisms is considered to be low from registered antimicrobial uses, no environmental risk assessment will conducted for this chemical (see Appendix B) . The available ecological data are summarized in the Tables 12

- 15 in Appendix B

.



## 4.1 Environmental Conceptual Model Exposure Pathways

Phenol has many degradation pathways as shown in Figure 1

. The short half l ives in various environmental media like water, soils, and air, make contamination of the surface water, soils,
and sediments is unlikely

. The half life of phenol in air is less than a day (0.6 days), and itPage 19 of 33 degrades in aerobic and anaerobic soil systems in less than five days. The dashed lines in the conceptual model below emphasize that the adverse eco

- effects are unlikely for phenol s

.

Figure 1

- Conceptual Model for Ecological Exposure and Effects of Phenol and Salt to Aquatic and Terrestrial Organisms



## 4.2 Ecological Effects Assessment

EPA does not anticipate conducting an ecological risk assessment because of the low environmental exposure to non

- target organisms. Based on the low likelihood of exposure due to the short half life of phenol in various environment al media like water, soils, and air

, the Agency intends to conclude that the registered uses of phenol and sodium phenate will have 'no effect' on endangered or threatened terrestrial or aquatic species, or their designated critical habitats, as listed by the U.S. Fish and Wildlife Service (USFWS) and the National Oceanic and Atmospheric Administration's (NOAA) National Marine Fisheries Service (NMFS). EPA anticipates conducting no further analysis of potential r isks to endangered or threatened species unless public comment or other submissions provide data or information that would otherwise inform the Agency's determination.Page 20 of 33 

## 5 Endocrine Disruptor Screening Program (EDSP)

As required by FIFRA and FFDCA, EPA reviews numerous studies to assess potential adverse outcomes from exposure to chemicals. Collectively, these studies include acute, sub chronic and chronic toxicity, including assessments of carcinogenicity, neurotoxici ty, developmental, reproductive, and general or systemic toxicity. These studies include endpoints which may be susceptible to endocrine influence, including effects on endocrine target organ histopathology, organ weights, estrus cyclicity, sexual maturati on, fertility, pregnancy rates, reproductive loss, and sex ratios in offspring. For ecological hazard assessments, EPA evaluates acute tests and chronic studies that assess growth, developmental and reproductive effects in differe nt taxonomic groups. As part of its reregistration decision , for phenol s , EPA reviewed these data and selected the most sensitive endpoints for relevant risk assessment scenarios from the existing hazard database. However, as required by FFDCA section 408(p), phenol and sodium phenate is subject to the endocrine screening part of the Endocrine Disruptor Screening Program (EDSP).

EPA has developed the EDSP to determine whether certain substances (including pesticide active and other ingredients) may have an effect in humans or wildlife similar to an effect produced by a “naturally occurring estrogen, or other such endocrine effects as the Administrator may designate.” The EDSP employs a two

- tiered approach to making the statutorily required determinations. Tier 1 consists of a b attery of 11 screening assays to identify the potential of a chemical substance to interact with the estrogen, androgen, or thyroid (E, A, or T) hormonal systems. Chemicals that go through Tier 1 screening and are found to have the potential to interact wi th E, A, or T hormonal systems will proceed to the next stage of the EDSP where EPA will determine which, if any, of the Tier 2 tests are necessary based on the available data. Tier 2 testing is designed to identify any adverse endocrine

- related effects ca used by the substance, and establish a dose

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

Under FFDCA section 408(p), the Agency must screen all pesticide chemicals. Between October 2009 and February 2010, EPA issued test orders/data c all

- ins for the first group of 67 chemicals, which contains 58 pesticide active ingredients and 9 inert ingredients. Phenol and sodium phenate are not among the group of 58 pesticide active ingredients on the initial list to be screened under the EDSP. Acc ordingly, as part of registration review, EPA will issue future EDSP orders/data call

- ins, requiring the submission of EDSP screening assays for phenol and sodium phenate.

For further information on the status of the EDSP, the policies and procedures, the list of 67 chemicals, future lists, the test guidelines and the Tier 1 screening battery, please visit our website: http://www.epa.gov/endo/

. 

## 6 Next Steps

A DCI will be developed regarding the data needs listed under t he “ Anticipated Data Needs” section of this document. The Agency expects to issue the DCI in June 2014. The Agency will

conduct an human health hazard assessment for all uses.Page 21 of 33 

## 7 References

A

r a m b a s i c, M

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. ( 1995 )

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, P h e n o l a n d S o d i um o n A llium ce pa L

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Behl, C.R., et al. (1983)

. Permeation of Skin and Eschar by Antiseptics I: Baseline Studies With Phenol. J Pharm Sci 72.4:391

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Bishop, J.B., et al. (1977)

. Alterations in the Reproductive Patterns of Female Mice Exposed to Xenobiotics. Fundamental and Applied Toxicology 40:191

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Boutwell, R.K. and D.K . Bosch

. (1959)

. The Tumor

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Brown VKH, VL Box, BJ Simpson (1975) Decontamination Procedures for Skin Exposed to Phenolic Compounds." 1975. Arch. Environ. Health, Vol 30.1

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Capel, I.D., et al. (1971) The Fate of [ 14 C] Phenol in Various Species. Xenobiotica 2:25

- 34; 1971.

Carpenter, C.P. (1948) "Skin Absorption and Irritation of Sodium Phenate." Mellon Institute of Industrial Research, University of Pittsburgh. May 5, 1948 (unpublished, U.S. EPA/OPTS Public Files Fiche OTS0515564/ 86

- 870001402).

Carpenter, C.P. (1949) "The Acute Toxicity of Phenol." Mellon Institute of Industrial Research, University of Pittsburgh. May 6, 1949 (Unpublished, U.S. EPA/OPTS Public Files F iche OTS0515567/ 86

- 870001405).

ClinTrials BioResearch (1998) A 13

- week neurotoxicity study of phenol administered in the drinking water to the rat. Volumes 1 and 2. Senneville, Quebec, Canada. Project I.D.: 97439. P. Beyrouty, study director.

Conning DM, Hayes MJ (1970) The dermal toxicity of phenol: An investigation of the most effective first

- aid measures. Br J Ind Med 27: 155

- 159

Dalin, N.M. and R. Kristoffersson (1974) Physiological effects of a sub

- lethal concentration of inhaled phenol on the rat. Ann Zool Fennici 11: 193

- 199.

Dow Chemical Co., (1994) Hiser, M.F., B.E. Kropscott, R.J. McGuirk, and J.S. Bus (1994) Pharmacokinetics, metabolism, and distribution of C 14 phenol in Fischer 344 rats after gavage, drinking water, and inhalation exposure, w ith cover letter dated 07/13/1994. Dow Chemical Co., (U.S. EPA/OPTS Public Files Fiche OTS0557473/86940001296).

H o d s o n , P

. V

. , D i x o n D

. G

. , a n d K

. L

. K a i s e r

. ( 1984 )

. M ea s u r e m e n t o f M e d i an L e t h al D o s e as a R a p i d I n d i ca t i o n o f C o n t a mi n a n t T o x i c it y t o F i s h

. E nv i r o n

. T o x i c o l

. C h e m

. 3 ( 2 ) :243

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Hoffman et al. ( 2001 ) . Two

- week (ten

- day) inhalation toxicity and two

- week recovery study of phenol vapor in the rat. Int. J. Toxicol. 20: 45

- 52.Page 22 of 33 Hughes, M.F. and L.L. Hall (1995) Disposition of Phenol in Rat after Oral, Dermal, Intravenous, and Intratracheal Administration. Xenobiotica 25, 873

- 883, cited in ATSDR, 1998.

IARC, International Agency for Research on Cancer (1999) Phenol. In IARC Monographs on the Evaluation o f Carcinogenic Risks to Humans. Vol. 71, Re

- Evaluation of Some Organic Chemicals, Hydarzine and Hydrogen Peroxide (Part 1

- 3). WHO, World Health Organization, Geneva, Switzerland. Pp. 749

- 768.

Kavlock, R.J. (1990) Structure

- Activity Relationships in the Developmental Toxicity of Substituted Phenols: In Vivo Effects. Teratology 41:43

- 59.

Moser, V.C., B.M. Cheek and R.C. MacPhail (1995) A multidisciplinary approach to toxicological screening: III. Neurobehavioral toxicity. J Toxicol Environ Health. 45(2):
173

- 210.

Narotsky M,G. and R.J. Kavlock (1995) A multidisciplinary approach to toxicological screening: II. Developmental Toxicity. J Toxicol Env Health 45: 145

- 171.

NCI (1980) Bioassay of Phenol for Possible Carcinogenici ty. U.S. National Cancer Institute, Bethesda, M.D., U.S. Department of Health and Human Services. Technical Report Series
No. NCI

- CG

- TR

- 203 (cited in BUA, 1998), Hazleton Laboratories Americal Inc., Vienna, VA, NIH publication No. 80

- 1759, August 1980, 1 23 pp.

NRC (2004) National Academy of Sciences Spacecraft Water Exposure Guidelines for Selected Contaminants, Volume 1, Phenol. Board of Environmental Studies and Toxicology Division on Earth and Life Sciences, National Research Council (NRC) Committee on Toxicology, The National Academies Press, Washington, D.C., 2004

Ryan et al. (2001) Two

- generation reproduction study and immunotoxicity screen in rats dosed with phenol via the drinking water. International Journal of Toxicology 20: 121

- 142.

Salaman, M. H. and O.M. Glendenning (1957) Tumor promotion in mouse skin by sclerosing agents. Br. J. Cancer. 11: 434

- 444.

Stenius U., M. Warholm, A. Rannug, et al. (1989) The role of GSH depletion and toxicity in hydroquinone

- induced development of enzyme

- altered foc i. Carcinogenesis. 10:593

- 599.

T i s l e r , T

. a n d J

. Z a g o r c

- K o n ca n

. ( 1995 )

. R e l a t i v e Se n s it i v it y o f s o m e Se l ec t ed A qua t i c O r ga n i s m s t o P h e n o l

. B u ll e t i n o f E nv i r o n m e n t a l C o n t a mi n a t i o n a n d T o x i c o l o g y , 54: 717

- 723.

U

. S. E nv i r o n m e n t a l P r ot ec t i o n A ge n cy (E P A )

. ( 1980 )

. A m b i e n t W a t e r Qua li t y C r i t e r i a f o r P h e n o l

. U

. S. E P A 440/5

- 80

- 066. Oc to b e r , 1980.

U

. S. E nv i r o n m e n t a l P r ot ec t i o n A ge n cy (E P A )

. (1986) Guidelines for carcinogen risk assessment. Federal Register 51(185):33992

- 34003.

U

. S. E nv i r o n m e n t a l P r ot ec t i o n A ge n cy (E P A )

. ( 2002 )

. E C O T OX U s er Gu i de: E C O T OX i c o l o gy Da t a b a s e S y s t e m

. Ve r s i o n 3

. 0. Av a il a b l e: h tt p://www

. epa

. g o v /ec oto x /Page 23 of 33 U.S. E nvironmental P rotection A gency (EPA). (2002) Toxicological Review of Phenol. Integrated Risk Information System (IRIS).

U

. S. E nv i r o n m e n t a l P r ot ec t i o n A ge n cy (E P A )

. (2004) Incident Reports Associated with Phenol

, Antimicrobials Division, July 27, 2004.

U.S. Environmental Protection Agency (EPA). (2005) Guidelines for Carcinogen Risk Assessment, Risk Assessment Forum, U.S. Environmental Protection Agency, Washington, DC, EPA/630/P

- 03/001F, March, 2005.

Wynder, E.L. and D. Hoffmann (1961) A study of tobacco carcinogenesis. VIII. The role of the aci dic fractions as promoters. Cancer. 14(6): 1306

- 1315.Page 24 of 33 

# Appendix A T oxicology Profile

The following is a summary of the toxicology information for phenol and sodium phenate taken from the AD Memorandum: PHENOL AND SALT ( Phenol; hydroxybenzene, carbolic acid, phenyl hydroxide and Sodium Phenate; phenol sodium salt, phenoxy ) : Hazard Characterization for the Human Health Assessment Scoping Document in Support of Registration Review of Phenol and Salt . DP403983, TXR Number 1003265



## Ac ute Toxicity for Product Labeling

The acute toxicity database for registration review of phenol and sodium phenate is considered incomp l ete. Acute toxicity studies (OTS0515567) submitted to satisfy toxicology guideline requirements in support of registra tion of phenol and sodium phenate

- containing pesticide products were determined to be unacceptable for regulatory purposes. In addition

, studies reporting LC 50 inhalation values or test results addressing the skin sensitizing potential of the technical gr ade active ingredient

, phenol or sodium phenate

, have not been submitted to the Agency.

Currently, no registrations exist for a phenol or sodium phenate technical grade active ingredient and therefore, no registered source has been identified for any of the registered phenol and sodium phenate end

- use products. In the absence of a registered source as well as no manufacturing limitations in producing a phenol and sodium phenate technical grade active ingredient, each end

- use product registrant is respon sible for citing and/or submitting acute toxicity data. These data include acute oral, dermal, inhalation, eye irritation and dermal irritation toxicity studies and a skin sensitization study.

Data which fully characterizes the acute toxicity of phenol and/or sodium phenate may be available in the published literature. T he Agency will accept submission of published literature addressing acute toxicity of phenol and / or sodium phenate for review and determination of the regulatory acceptability of these d ata

. 

## Subchronic Toxicity

The database for subchronic toxicity is considered complete. Although oral range

- finding studies in both the rat and the mouse were reviewed and classified non

- guideline (due to the lack of subchronic parameter measurements) , systemic toxicities were noted at 10,000 ppm in both species, based on a decrease in mean body weight gain ( NCI, 1980 ). In a two

- week (whole

body, chamber) inhalation study ( Dalin and Kristoffersson, 1974 ), rats had elevated plasma K 1+ and Mg 2+ levels, increased activities of plasma enzymes LDH, GOT, GPT, and GLDH and exhibited toxic effects in the central nervous system (muscle tremors, twitching, abnormal gait and posture) up to 5 days following continuous exposure at 26 ppm for a 15

- day period (24 hou rs/day). In contrast, a two

- week (nose

- only) inhalation study conducted in rats (Hoffman, etPage 25 of 33 al. 2001) did not result in any portal of entry adverse toxic effects, or any other toxicity, at any exposure level up to and including 25 ppm following intermitt ent exposure for 6 hours/day, 5 days/week (for a total of 10 exposures) to the vapors of phenol. The results from this second inhalation study also indicated that there was no delayed occurrence of toxic effects following a
14

- day follow

- up recovery period

. 

## Developmental Toxicity

The database for developmental toxicity is considered complete. Phenol was administered in two developmental guideline studies in rats (MRID 43735402) and mice (MRID 43735401) at concentrations of 30, 60, or 120 mg/kg/day and 70, 140, or 280 mg/kg/day, respectively. There was no evidence of toxicity in these animals at concentrations below the high

- dose. Fetal body weight was significantly reduced at 120 and 280 mg/kg/day in rat and mouse studies, respectively. Additionally, fe male mice experienced increased mortality and clinical signs of CNS toxicity (tremors, ataxia, lethargy) at the high

- dose (280 mg/kg/day). S ignificant weight loss in dams and clinical signs of toxicity in pups (paralysis and/or palsy of the hind limbs) we re observed in animals administered phenol in a non

- guideline developmental study (Kavlock, 1990), at the two highest doses of 667 and 1000 mg/kg/day. In a non

- guideline special study (Nartosky and Kavlock, 1995) maternal and developmental toxic effects w ere observed at the 2 doses (40 and 53.3 mg/kg/day).



## Reproductive Toxicity

The database for reproductive toxicity is considered complete. In a two

- generational reproductive study ( Ryan et al., 2001 ), rats were exposed to 200, 1

, 000, or 5

, 000 ppm phenol (equivalent to 0, 14, 70, and 310 mg/kg/day in males and 0, 20, 93, and 350 mg/kg/day in females) for 10 weeks/generation. There were significant reductions in food and water consumption, body weight and body weight gain in dams and F1 generation dams at 5

, 000 ppm (potential flavor aversion). The decreased birth weight, and body weight gains observed in the F1 generation pups at 5

, 000 ppm occurred concomitantly with maternal toxicity (decreased maternal body weight) as a result of decreased maternal food and water consumption during lactation. Decreases in body weight as well as litter survival were observed at 5

, 000 ppm in the F1 and more so in the F2 generation offspring. The increased mortality in the pups occurred concurrently with maternal toxicity (decreased maternal body weight). Similarly to the F1 generation offspring, decreased maternal body weight (F1 dams) and reduced palatability were likely significant factors that contributed to the decreased body weights in the high

- dose F2 generation. I n a non

- guideline reproductive study ( Bishop, et al. 1997 ) phenol was administered to mice at a concentration of 350 mg/kg. There were no treatment

- related clinical signs or mortality observed in maternal, developmental, or reproductive parameters and a L OAEL was

not established (highest dose tested, 350 mg/kg).



## Chronic Toxicity and Carcinogenicity

C hronic toxicity/carcinogenicity studies in rats and mice were performed by the National Cancer Institute (NCI, 1980) to examine the carcinogenicity of phenol. Phenol was administered inPage 26 of 33 drinking water to male and female rats at doses of (M/F) 0, 322/360, and 645/721 mg/kg/day for 103 weeks. In mice, phenol was administered in drinking water at doses of (M/F) 0, 590/60 2, and 1180/1204 mg/kg/day for 103 weeks. There was no evidence of carcinogenicity in any dose group except low dose male rats, where a statistically significant increase in the occurrence of leukemia, lymphoma, or interstitial

- cell tumors was observed

. A lthough there was an increased incidence of these tumor types at the low dose, there was also a high spontaneous tumor rate in matched control rats, as well as a lack of carcinogenicity at the high dose. Therefore, it was concluded in this study that phenol was not carcinogenic in male or female rats and mice

.

A 20

- week dermal study in the rat showed chronic irritation and hair growth inhibition with administ ration of 3 mg phenol (in 200 uL acetone). A single papilloma was found 7 weeks into the study, but there was no evidence that it was significantly increased or treatment

- related. In a special, mechanistic study (Stenius, et al. 1989) there was no eviden ce of tumor initiation or hepatocyte GSH depletion following administration of 100 mg/kg/day phenol.



## Carcinogenic Potential of Phenol

Several epidemiology studies have evaluated the carcinogenesis of phenol, but they have not found a consistent dose

- relate d association. Because all of the subjects were also exposed to other chemicals and there was no correction for smoking, these studies are not adequate to reach conclusions on the carcinogenic potential of phenol in humans.

Phenol was negative for carc inogenicity in drinking water studies conducted in rats and mice (NCI, 1980), although an increased incidence of leukemias was observed only in low

- dose male rats. In short

- term dermal assays, tumorigenicity (production of papillomas in the absence of

tre atment by an initiating agent) was observed only at a dose/concentration combination that produced ulceration and thus was well above the MTD (Salaman and Glendenning, 1957). Similarly, although phenol was a promoter when tested in initiation/promotion st udies, the doses tested typically caused ulceration (Salaman and Glendenning, 1957; Boutwell and Bosch, 1959) and death (Boutwell and Bosch, 1959). There were two exceptions. First, the low concentration tested by Salaman and Glendenning) caused promotion as well as "transient light crusting." Because the site of the weekly treatment was rotated across four sites on the body, it is unclear whether more severe effects would have been observed if the same site had been treated for the entire study. The sec ond exception was that the low concentration tested by Wynder and Hoffmann (1961) was reported as causing no toxicity, although the sensitivity of the evaluation is unclear. On the basis of the high observed toxicity, it is not clear whether the promoting activity observed for phenol in several dermal studies was secondary to the repeated injury and healing of the skin.

Evaluations conducted by the Agency (U.S. EPA, 2002) have concluded that there is inadequate evidence in humans and animals to classify phenol as a carcinogen. Similar conclusions have been reached by other groups in assessments of potential carcinogenic risk to humans for phenol. For example, IARC (1999) concluded that there is inadequate evidence in humans and animals to conduct an asse ssment of carcinogenicity for phenol and therefore, phenol is not classifiable as to its carcinogenicity to humans (Group 3).Page 27 of 33 Although the available data for carcinogenicity do not permit a definitive classification for the carcinogenic potential of phen ol, additional data on carcinogenicity will not be needed. This is due to the selection of a chronic Reference Dose value of 0.6 mg/kg/day for phenol and phenol salts for non

- carcinogenic effects that may occur over a lifetime. This value of 0.6 mg/kg/day, when compared to the dose level that caused an increased incidence of tumors in male rats (322 mg/kg/day) is orders of magnitude lower and is considered protective as a regulatory endpoint against any potential carcinogenic effects of phenol.



## Mutagenicit y

The results of the mutagenicity studies indicated that phenol was not mutagenic in Salmonella typhimurium or Drosophila melanogaster and did not induce micronuclei or bone marrow chromosomal aberrations in mice. However, mutagenic effects were observed in Chinese Hamster Ovary (CHO) cells and spermatocytes in mice and HL60 cells. The genotoxic potential of phenol appears to depend on the competing processes of activation to a genotoxic form and metabolic inactivation (e.g., via conjugation). Phenol ten ded to be negative in bacterial gene mutation assays but was positive or equivocal in mammalian cell gene mutation assays. Phenol tended to induce micronuclei in mice when administered intraperitoneally but was negative (or positive only at very high doses ) when administered orally. This difference is likely due to the first

- pass conjugation and inactivation of orally administered phenol. Phenol was also positive in
in vitro micronucleus tests with human lymphocytes and CHO cells. Results from DNA damage assays are inconsistent, but they tend to show that phenol can cause sister chromatid exchanges or cell transformation if it is not metabolically inactivated. Overall, phenol did not exhibit strong mutagenic effects.



## Other Toxicological Effects

Neurotoxicity

Neurotoxic signs were observed in an acute dermal toxicity studies (at concentrations ranging from 0.625 to 0.68 mL/kg) and included convulsions ( Brown, et al., 1975), tremors ( Carpenter, 1949), and stimulation of motor nerve endings or spin al motor centers (Conning, 1970). Impaired balance, involuntary muscle twitches, jerkiness, and increased sluggishness were observed in rats exposed continuously to 26 ppm (100 mg/m 3 ) phenol in air for 15 days (Dalin and Kristoffersson, 1974). The IRIS T oxicological Profile for Phenol (US EPA, 2002) reports numerous nervous system effects (tremors, decreased motor activity and increased rearing post

exposure) following phenol dosing in animals

. Studies performed by ClinTrials BioResearch presented one ani mal with tremors that later died (apparently of dehydration) following dosing in drinking water (1998). Additionally, several gavage studies have shown rats and mice with phenol

- related tremors ( 43735402; Dow Chemical Co., 1994; Moser et al., 1995 ) . Howe ver, in a specialized 13

- week neurotoxicity study in male and female rats that included a Functional Observational Battery (FOB) and a detailed neurohistopathology evaluation ( ClinTrials BioResearch, 1998 ), nervous system effects were observed as tremors i n one animal and decreased motor activity in females. A short

- term gavage screening study ( Moser et al., 1995 )Page 28 of 33 found that the only effect in an FOB was a marginal decrease in motor activity and increased rearing post

- exposure. Part of this could be attri buted to the dehydration observed in the study, but it was also concluded that phenol contributed to the decreased motor activity.



## Metabolism

The database for Phenol metabolism is considered to be complete. Phenol is readily absorbed by the inha lation, o ral, and dermal routes and is completely metabolized within 24 hours following administration. The portal

- of

- entry metabolism for the inhalation and oral routes appears to be extensive and involves sulfate and glucuronide conjugation and, to a lesser exte nt, oxidation. Once absorbed, phenol is widely distributed in the body, although the levels in the lung, liver, and kidney are often reported as being higher than in other tissues (on a per

- gram

- tissue basis). Elimination from the body is ra pid and p heno l does not appear to accumulate significantly in the body. Phenol was predominantly conjugated with sulfate and lower amounts of glucuronic acid and the metabolites were rapidly excreted in the urine, regardless of the route of administration. The major urinary metabolites identified include phenyl sulfate, quinol sulfate, phenyl glucuronide, and quinol glucuronide ( Capel et al., 1971; Hughes and Hall, 1995).



## Dermal Absorption

Dermal penetration studies were available from the open literature and IRIS Toxicological profile (Behl, 1983; Hughes and Hall, 1995; US EPA, 2002) for phenol. Phenol is readily absorbed via the dermal route and systemic effects can result from dermal exposure. Age and hydration seemed to have little effect on the perme ability of phenol through human and mouse skin. Permeation and chemical denaturation of skin by phenol were found to be similar between mouse and human skin tissue; indicating that the hairless mouse is an adequate model for chemical permeability in human s. The effects on the skin were apparently a result of destroyed barrier integrity and the results suggest that the stratum corneum is proportionally impaired as the phenol concentration is increased. Dermal absorption is considered the primary route of entry for vapor, liquid, and solid phenol. The skin has relatively low potential to detoxify phenol. Therefore, absorption through the skin may represent the greatest hazard from phenol because it readily passes through the skin and there is no first

- pas s metabolic effect as is observed following oral

exposure

.Page 29 of 33 

# Appendix B Ecotoxicology Profile

Toxicity to Terrestrial Receptors

No data have been submitted for acute or chronic effects of phenols on avian species.



## Toxicity to Aquatic Receptors

1. Ac u t e To x i c i t y o f P h e n o l t o F r es h w a t e r F i sh

A s s h o wn i n the following Table 10

, acu t e to x i c it y f o r f r es h w a t e r f i s h r a n g e d f r o m 5 m g/L (r a i nb o w t r o u t ) t o 23

. 9 m g/L ( b l u e g ill )

, w i t h a v e r a ge v a l u e s o f 9

. 1 m g/L f o r r a i nb o w t r o ut a n d
17

. 1 m g/L f o r b l u e g ill

. T h e s e d a t a i n d i ca t e t h a t p h e n o l i s m o d e r a t e l y to x i c t o c o l dw a t e r s p ec i e s ,
s u c h a s t h e r a i nb o w t r o u t

, a n d s li g h t l y to x i c t o w a r m w a t e r s p ec i e s , s u c h a s t h e b l u e g ill.

Table 10

- Acute Toxicity for Freshwater Fish

O r g a n i sm Res u l t s - LC 50 ( m g/ L ) ( 95% C o n f i d e n ce T o x i c i t y Ca t e g o r y C o mm e n t s R e f e r e n ce
R ai n bo w t r o ut ( O n c o r h y n c hus

m

yki ss ) 5

. 02 (4

. 23

- 7

. 49) m o d e r at e ly

t o x i c - 96h t e s t du r ati o n ;

- j u v e n il e o r g a n i s m s ;

- r e n e w a l s y s t e m E P A A W Q C, 1980;

a n d U

. S

. E PA

, 2002

R ai n bo w t r o ut ( O n c o r h y n c hus

m

yki ss ) 11

. 6 s li g h tly

t o x i c - 96h t e s t du r ati o n ;

- f

l o w

- t hr o ugh s y s t e m

- u s e d a c ti v e i n g r e d i e n t

c o n ce n t r ati o n E P A A W Q C, 1980;

a n d U

. S

. E PA

, 2002

R ai n bo w t r o ut ( O n c o r h y n c hus

m

yki ss ) 13

. 1 (11

. 9

- 14

. 1) s li g h tly

t o x i c - 48h t e s t du r ati o n ;

- s y s t e m t y pe n o t r e p o r t e d;

- u s e d a c ti v e i n g r e d i e n t

c o n ce n t r ati o n Ti s l e r a n d Z a g o r c

K o n c a n , 1995

R ai n bo w t r o ut ( O n c o r h y n c hus

m

yki ss ) 6

. 1 (5

. 5

- 6

. 8) m o d e r at e ly

t o x i c - 96h t e s t du r ati o n ;

- f

l o w

- t hr o ugh s y s t e m;

- u s e d a c ti v e i n g r e d i e n t

c o n ce n t r ati o n U

. S

. E PA

, 2002

R ai n bo w t r o ut ( O n c o r h y n c hus

m

yki ss ) 8

. 9 m o d e r at e l y
t o x i c - 96h t e s t du r ati o n ;

- f

l o w

- t hr o ugh s y s t e m U

. S

. E PA

, 2002

R ai n bo w t r o ut ( O n c o r h y n c hus

m

yki ss ) 9

. 7 m o d e r at e l y
t o x i c - 96h t e s t du r ati o n ;

- f

l o w

- t hr o ugh s y s t e m;

- u s e d a c ti v e

- i n g r e d i e n t H o d s o n e t al.

, 1984.
U

. S

. E PA

, 2002Page 30 of 33 O r g a n i sm Res u l t s - LC 50 ( m g/ L ) ( 95% C o n f i d e n ce T o x i c i t y Ca t e g o r y C o mm e n t s R e f e r e n ce

c o n ce n t r ati o n
R ai n bo w t r o ut ( O n c o r h y n c hus

m

yki ss ) 10

. 5 (9

. 1

- 12

. 2) s li g h tly

t o x i c - 96h t e s t du r ati o n ;

- f

l o w

- t hr o ugh s y s t e m;

- u s e d a c ti v e

- i n g r e d i e n t

c o n ce n t r ati o n U

. S

. E PA

, 2002

R ai n bo w t r o ut ( O n c o r h y n c hus

m

yki ss ) 7

. 7 m o d e r at e l y
t o x i c - 96h du r ati o n ;

- f

l o w

- t hr o ugh s y s t e m U

. S

. E PA

, 2002

R ai n bo w t r o ut ( O n c o r h y n c hus

m

yki ss ) 8

. 9 m o d e r at e l y
t o x i c - 96h du r ati o n ;

- f

l o w

- t hr o ugh s y s t e m U

. S

. E PA

, 2002

B l u e g il l ( L e po m i s

m a c r o c h i r u s ) 17

. 4 (11

. 9

- 25

. 3) s li g h tly

t o x i c - 96h t e s t du r ati o n ;

- f

l o w

- t hr o ugh s y s t e m

- u s e d a c ti v e i n g r e d i e n t

c o n ce n t r ati o n

. U

. S

. E PA

, 2002

B l u e g il l ( L e po m i s

m a c r o c h i r u s ) 13

. 5 s li g h tly

t o x i c - 96h t e s t du r ati o n ;

- s tati c s y s t e m E P A A W Q C, 1980;

a n d U

. S

. E PA

, 2002

B l u e g il l ( L e po m i s

m a c r o c h i r u s ) 19

. 3 s li g h tly

t o x i c - 96h t e s t du r ati o n ;

- j u v e n il e o r g a n i s m s ;

- r e n e w a l s y s t e m E P A A W Q C, 1980;

a n d U

. S

. E PA

, 2002

B l u e g il l ( L e po m i s

m a c r o c h i r u s ) 11

. 5 s li g h tly

t o x i c - 96h t e s t du r ati o n ;

- r e n e w a l s y s t e m;

- u s e d a c ti v e i n g r e d i e n t

c o n ce n t r ati o n

. E P A A W Q C, 1980;

a n d U

. S

. E PA , 2002

B l u e g il l ( L e po m i s

m a c r o c h i r u s ) 23

. 9 (20

. 2

- 31

. 5) s li g h tly

t o x i c - 96h t e s t du r ati o n ;

- s tati c s y s t e m E P A A W Q C, 1980;

a n d U

. S

. E PA

, 2002

2. Ac u t e To x i c i t y o f P h e n o l t o F r es h w a t e r I n ve r t e b r a t e s

A s s h o wn i n the following Table 11

, acu t e to x i c i t y f o r aqua t i c i nv e r t e b r a t e s ( Daphnia magna )

r a n g e d f r o m 4

. 2 m g/L t o 88 m g/ L

. T h e e n dp o i n t f o r t h e s e s t ud i es i s t h e E C 50 f o r imm o b ili za t i o n o r t h e L C 50 . T h e a v e r ag e v a l ue f o r t h e e n dp o i n t c o n ce n t r a t i o n s s h o wn i n T a b l e 2 i s 18

. 8 m g/ L

. N ota b l y , w h e n c o n s i d e r i n g o n l y t h e s t ud i e s w h e r e t h e e n dp o i n t i s r ep o r t e d t o b e b ase d o n t h e ac t i v e i n g r ed i e n t c o n ce n t r a t i o n (T a b l e 2 )

, t h e a v e r ag e c o n ce n t r a t i o n i s r e l a t i v e l y l o we r a t 14

. 6 m g/ L

. T h e s e d a t a r e s u l t s i n d i ca t e t h a t p h e n o l i s m o d e r a t e l y t o s li g h t l y to x i c t o

a qu a t i c i nv e r t e b r a t e s

.Page 31 of 33 Table 11

– Acute Toxicity for Aquatic Invertebrates

O r g a n i sm Res u l t s - E C 50 ( m g/ L ) ( 95% C o n f i d e n c e T o x i c i t y Ca t e g o r y C o mm e n t s R e f e r e n ce
W at e r f l ea ( D aphn i a m agna ) 9 .6 m o d e r at e ly

t o x i c - 48h t e s t du r ati o n ;

- s tati c s y s t e m E P A A W Q C, 1980;

a n d U

. S

. E PA

, 2002

W at e r f l ea ( D aphn i a m agna ) 7 m o d e r at e ly

t o x i c - 50h t e s t du r ati o n ;

- j u v e n il e o r g a n i s m s ;

- s tati c s y s t e m E P A A W Q C, 1980;

a n d U

. S

. E PA

, 2002

W at e r f l ea ( D aphn i a m agna ) 88 s li g h tl y t o x i c - 48h t e s t du r ati o n ;

- s tati c s y s t e m E P A A W Q C, 1980;

a n d U

. S

. E PA

, 2002

W at e r f l ea ( D aphn i a m agna S t. ) 0

. 102 ( mm o l/ L ) (= 9

. 6 m g / L ) m o d e r at e ly

t o x i c - 48h t e s t du r ati o n ;

- r e n e w a l s y s t e m A r am b a s i c a t al.,
1995

W at e r f l ea ( D aphn i a m agna S t r au ss ) 33

. 9 (30

- 39

. 2) s li g h tl y t o x i c - 24h t e s t du r ati o n ;

- s y s t e m t y pe n o t

r e p o r t e d

- u s e d a c ti v e i n g r e d i e n t

c o n ce n t r ati o n Ti s l e r a n d Z a g o r c

K o n c a n , 1995

W at e r f l ea ( D aphn i a m agna ) 23

. 5 ( 21

- 26

. 3) s li g h tl y t o x i c - 48h t e s t du r ati o n ;

- s tati c s y s t e m U

. S

. E PA

, 2002

W at e r f l ea ( D aphn i a m agna ) 6 .6 m o d e r at e ly

t o x i c - 48h t e s t du r ati o n ;

- s tati c s y s t e m ;

- u s e d a c ti v e i n g r e d i e n t

c o n ce n t r ati o n U

. S

. E PA

, 2002

W at e r f l ea ( D aphn i a m agna S t r au ss ) 4

. 2 m o d e r at e l y
t o x i c - 48h t e s t du r ati o n ;

- s tati c s y s t e m ;

- u s e d a c ti v e i n g r e d i e n t

c o n ce n t r ati o n U

. S

. E PA

, 2002

W at e r f l ea ( D aphn i a m agna ) 30 s li g h tl y t o x i c - 48h t e s t du r ati o n ;

- s tati c s y s t e m ; U

. S

. E PA

, 2002

W at e r f l ea ( D aphn i a m agna ) 12

. 6 s li g h tl y t o x i c - 48h t e s t du r ati o n ;

- f

l o w

- t hr o ugh s y s t e m ; U

. S

. E PA

, 2002Page 32 of 33 O r g a n i sm Res u l t s - E C 50 ( m g/ L ) ( 95% C o n f i d e n c e T o x i c i t y Ca t e g o r y C o mm e n t s R e f e r e n ce (10

. 2

- 15

. 5)

- u s e d a c ti v e i n g r e d i e n t

c o n ce n t r ati o n
W at e r f l ea ( D aphn i a m agna ) 10 (8

. 8

- 12) m o d e r at e l y to

s li g h tl y t o x i c - 48h t e s t du r ati o n ;

- s tati c s y s t e m ; U

. S

. E PA

, 2002

W at e r f l ea ( D aphn i a m agna ) 15 s li g h tl y t o x i c - 48h t e s t du r ati o n ;

- s tati c s y s t e m ; U

. S

. E PA

, 2002

W at e r f l ea ( D aphn i a m agna ) 5

. 5 (4

. 9

- 6

. 3) m o d e r at e ly

t o x i c - 48h t e s t du r ati o n ;

- s y s t e m t y pe n o t

r e p o r t e d;

- u s e d a c ti v e i n g r e d i e n t

c o n ce n t r ati o n U

. S

. E PA

, 2002

W at e r f l ea ( D aphn i a m agna ) 12* (7

. 3

- 20) s li g h tl y t o x i c - 48h t e s t du r ati o n ;

- s tati c s y s t e m U

. S

. E PA

, 2002

W at e r f l ea ( D aphn i a m agna ) 30

. 1* s li g h tl y t o x i c - 48h t e s t du r ati o n ;

- s y s t e m t y pe n o t

r e p o r t e d U

. S

. E PA

, 2002

W at e r f l ea ( D aphn i a m agna ) 32* (24

- 43) s li g h tl y t o x i c - 48h t e s t du r ati o n ;

- s tati c s y s t e m U

. S

. E PA

, 2002

W at e r f l ea ( D aphn i a m agna ) 8

. 6* (7

. 2

- 10

. 2) m o d e r at e ly

t o x i c - 48h t e s t du r ati o n ;

- s tati c s y s t e m U

. S

. E PA

, 2002

W at e r f l ea ( D aphn i a m agna ) 19

. 8* (18

- 22) s li g h tl y t o x i c - 48h t e s t du r ati o n ;

- s tati c s y s t e m ;

- u s e d a c ti v e i n g r e d i e n t

c o n ce n t r ati o n U

. S

. E PA

, 2002

W at e r f l ea ( D aphn i a m agna ) 23* s li g h tl y t o x i c - 48h t e s t du r ati o n ;

- s tati c s y s t e m ;

- u s e d a c ti v e i n g r e d i e n t

c o n ce n t r ati o n U

. S

. E PA

, 2002

W at e r f l ea ( D aphn i a m agna ) 13* (10

- 17) s li g h tl y t o x i c - 48h t e s t du r ati o n ;

- s tati c s y s t e m U

. S

. E PA

, 2002

W at e r f l ea ( D aphn i a m agna ) 11

. 2* (9

. 8

- 12

. 6) s li g h tl y t o x i c - 48h t e s t du r ati o n ;

- s tati c s y s t e m ;

- u s e d a c ti v e i n g r e d i e n t

c o n ce n t r ati o n U

. S

. E PA

, 2002

W at e r f l ea ( D aphn i a m agna ) 8

. 3* (5

. 8

- 12

. 5) m o d e r at e ly

t o x i c - 48h t e s t du r ati o n ;

- s y s t e m t y pe n o t

r e p o r t e d U

. S

. E PA

, 2002

* E n dp o i n t i n s t udy i s i de n t i f i ed as L C 50Page 33 of 33 3. Tox i c i t y t o Es tu a r in e a n d M a r i n e O r ga ni s m s

A cu t e to x i c it y t e s t i n g w i t h e s t u a r i n e a n d m a r i n e o r ga n i s m s u s i n g t h e T G A I i s n o t r equ i r e d f o r
t h e i n d oo r use s o f p h e n o l or s o d i um p h e n a t e

. S e v e r a l s t ud i e s o n m a r i n e / es t ua r i n e i nv e r t e b r a t e s

we r e f o u n d i n t h e E C O T OX da t a b a s e (E P A

, 2002 )

. T h e e n dp o i n t s f r o m t h e s e s t ud i es a r e

su mm a r i ze d i n t h e Table 12 b e l o w:

Table 12

- A c ut e T o x i c i t y o f P h e no l t o M a r i n e / Es t ua r i n e I nv e r t e b r a t e s

O r g a n i sm Res u l t s - LC 50

o r E C ( fl g/ L ) ( 95% C o n f i d e n c e T o x i c i t y Ca t e g o r y C o mm e n t s R e f e r e n ce
M y s i d ( A r c ha e o m y s i s k o k ubo i ) 96

- h r L C50 = 260

- 4530 ( fo r m u lati o n ) h i g h l y t o

m o d e r at e ly

t o x i c - 96h t e s t du r ati o n ;

- s tati c s y s t e m U

. S

. E PA

, 2002

O p o ss um s hr im p ( A m e r ic a m y s is
bah i a ) 96

- h L C50 = 12500 (10700

- 15600)

( fo r m u lati o n ) s li g h tl y t o x i c - 96h t e s t du r ati o n ;

- s tati c s y s t e m U

. S

. E PA

, 2002

D a gg e r b la de g r a s s

s hr imp ( P a l a e m on etes

pug i o ) 96

- h r L C50 = 5800 (4330

- 7770) m o d e r at e ly

t o x i c - 96h t e s t du r ati o n ;

- s tati c s y s t e m U

. S

. E PA

, 2002

Table 13

- C h r o ni c T o x i c i t y o f P h e no l t o M a r i n e / Es t ua r i n e I nv e r t e b r a t e s

O r g a n i sm Res u l t s - L O E C, NO E C , M A T C ( fl g/ L ) C o mm e n t s R e f e r e n ce
O p o ss um s hr im p ( A m e r ic a m y s is
bah i a ) m o r tality
27

- d NO E C = 2410

L O E C = 6880
MA T C = 4080 - 27 d a y t e s t du r ati o n ;

- f

l o w

- t hr o ugh s y s t e m U

. S

. E PA

, 2002

4. T o x i c i t y t o P l a n ts

T e rr e s t r i al a n d aqua t i c p l a n t t e s t i n g i s n o t r e qu i r e d f o r t h e r e g i s t e r ed i n d oo r u s es o f p h e n o l or

s o d i um p h e n a t e

. T h e r e we r e aqua t i c p h y toto x i c it y e n dp o i n t s r ep o r t e d i n t h e E C O T OX da t a b a s e (E P A

, 2002 )

. W h il e t h e s e da t a we r e r e p o r t ed i n s u mm a r y f o r m , t h ey i n d i ca t e t h at p h e n o l
de m o n s t r a t e s l o w to x i c i t y t o v a r i o us aqua t i c p l a n t spec i es , w i t h 4

- da y E C 50 v a l u e s r a n g i n g f r o m 12

, 000 ppb ( duckweed, Lemna mino r ) t o 370

, 000 ppb ( g r ee n a l ga , C hlo r e lla v ulga r i s ).