jlentini on DSKJ8SOYB1PROD with NOTICES

Federal Register / Vol. 74, No. 159 / Wednesday, August 19, 2009 / Notices 41883 

Dated: August 5, 2009. 

Matthew Leopard, 

Acting Director, Information Management 

Division, Office of Pollution Prevention and 

Toxics. 

[FR Doc. E9–19461 Filed 8–18–09; 8:45 a.m.] 

BILLING CODE 6560–50–S 

ENVIRONMENTAL PROTECTION 

AGENCY 

[EPA–HQ–OW–2009–0297; FRL–8943–9] 

RIN 2040–AF08 

Drinking Water: Perchlorate 

Supplemental Request for Comments 

AGENCY: Environmental Protection 


Agency (EPA). 


ACTION: Notice. 


SUMMARY: The Agency is seeking 

comments on additional approaches to 

analyzing data related to EPA’s 

perchlorate regulatory determination. 

These additional comments are sought 

in an effort to ensure consideration of 

all the potential options for evaluating 

whether there is a meaningful 

opportunity for human health risk 

reduction of perchlorate through a 

national primary drinking water rule. 

EPA will make a final regulatory 

determination for perchlorate after 

considering comments and information 

provided in the 30-day comment period 

following this notice. 

DATES: Comments must be received on 

or before September 18, 2009. 

ADDRESSES: Submit your comments, 

identified by Docket ID No. EPA–HQ– 

OW–2009–0297, by one of the following 

methods: 

• http://www.regulations.gov: Follow 

the online instructions for submitting 

comments. 

• Mail: Water Docket, Environmental 

Protection Agency, Mailcode: 2822T, 

1200 Pennsylvania Ave., NW., 

Washington, DC 20460. 

• Hand Delivery: Water Docket, EPA 

Docket Center (EPA/DC) EPA West, 

Room 3334, 1301 Constitution Ave., 

NW., Washington, DC. Such deliveries 

are only accepted during the Docket’s 

normal hours of operation, and special 

arrangements should be made for 

deliveries of boxed information. 

Instructions: Direct your comments to 

Docket ID No. EPA–HQ–OW–2009– 

0297. EPA’s policy is that all comments 

received will be included in the public 

docket without change and may be 

made available online at http:// 

www.regulations.gov, including any 

personal information provided, unless 

the comment includes information 

claimed to be Confidential Business 

Information (CBI) or other information 

whose disclosure is restricted by statute. 

Do not submit information that you 

consider to be CBI or otherwise 

protected through http:// 

www.regulations.gov or e-mail. The 

http://www.regulations.gov Web site is 

an ‘‘anonymous access’’ system, which 

means EPA will not know your identity 

or contact information unless you 

provide it in the body of your comment. 

If you send an e-mail comment directly 

to EPA without going through http:// 

www.regulations.gov your e-mail 

address will be automatically captured 

and included as part of the comment 

that is placed in the public docket and 

made available on the Internet. If you 

submit an electronic comment, EPA 

recommends that you include your 

name and other contact information in 

the body of your comment and with any 

disk or CD–ROM you submit. If EPA 

cannot read your comment due to 

technical difficulties and cannot contact 

you for clarification, EPA may not be 

able to consider your comment. 

Electronic files should avoid the use of 

special characters, any form of 

encryption, and be free of any defects or 

viruses. For additional instructions on 

submitting comments, go to Unit I.A of 

the SUPPLEMENTARY INFORMATION section 

of this document. 

Docket: All documents in the docket 

are listed in the http:// 

www.regulations.gov index. Although 

listed in the index, some information is 

not publicly available, e.g., CBI or other 

information whose disclosure is 

restricted by statute. Certain other 

material, such as copyrighted material, 

will be publicly available only in hard 

copy. Publicly available docket 

materials are available either 

electronically in http:// 

www.regulations.gov or in hard copy at 

the Water Docket, EPA/DC, EPA West, 

Room 3334, 1301 Constitution Ave., 

NW., Washington, DC. The Public 

Reading Room is open from 8:30 a.m. to 

4:30 p.m., Monday through Friday, 

excluding legal holidays. The telephone 

number for the Public Reading Room is 

(202) 566–1744, and the telephone 

number for the EPA Docket Center is 

(202) 566–2426. 

FOR FURTHER INFORMATION CONTACT: Eric 

Burneson, Office of Ground Water and 

Drinking Water, Standards and Risk 

Management Division, at (202) 564– 

5250 or e-mail burneson.eric@epa.gov. 

For general information, contact the 

EPA Safe Drinking Water Hotline at 

(800) 426–4791 or e-mail: hotlinesdwa@epa.gov. 

Abbreviations and Acronyms 

>—greater than 

<—less than 

BW—body weight 

CBI—confidential business information 

CDC—Centers for Disease Control and 

Prevention 

DWI—drinking water intake 

EPA—U.S. Environmental Protection Agency 

FDA—U.S. Food and Drug Administration 

FR—Federal Register 

HA—Health Advisory 

HRL—health reference level 

IRIS—Integrated Risk Information System 

kg—kilogram 

L—liter 

mg/kg—milligram per kilogram of body 

weight 

mg/L—milligrams per liter (equivalent to 

parts per million [ppm]) 

MRL—Method Reporting Limit 

NAS—National Academy of Science 

NHANES—National Health and Nutrition 

Examination Survey 

NOAEL—no observed adverse effect level 

NOEL—no observed effect level 

NRC—National Research Council 

OW—Office of Water 

PBPK—Physiologically-Based 

Pharmacokinetic 

POD —point of departure 

RAIU—Radioactive Iodide Uptake 

RfD—reference dose 

RSC—relative source contribution 

SDWA—Safe Drinking Water Act 

UCMR—Unregulated Contaminant 

Monitoring Regulation 

μg—microgram (one-millionth of a gram) 

US—United States 

USDA—U.S. Department of Agriculture 

SUPPLEMENTARY INFORMATION 

I. General Information 

A. What Should I Consider as I Prepare 

My Comments for EPA? 

You may find the following 

suggestions helpful for preparing your 

comments: 

1. Explain your views as clearly as 

possible. 

2. Describe any assumptions that you 

used. 

3. Provide any technical information 

and/or data you used that support your 

views. 

4. If you estimate potential burden or 

costs, explain how you arrived at your 

estimate. 

5. Provide specific examples to 

illustrate your concerns. 

6. Offer alternatives. 

7. Make sure to submit your 

comments by the comment period 

deadline. 

8. To ensure proper receipt by EPA, 

identify the appropriate docket 

identification number in the subject line 

on the first page of your response. It 

would also be helpful if you provided 

the name, date, and Federal Register 

(FR) citation related to your comments. 

jlentini on DSKJ8SOYB1PROD with NOTICES

41884 Federal Register / Vol. 74, No. 159 / Wednesday, August 19, 2009 / Notices 

II. Background 

The statutory and regulatory 

background for this action is described 

in detail in the October 10, 2008, FR 

notice discussing EPA’s initial 

regulatory determination for perchlorate 

(USEPA, 2008a). Briefly, the Safe 

Drinking Water Act (SDWA) section 

1412, as amended in 1996, requires EPA 

to make a determination whether to 

regulate at least 5 contaminants from its 

contaminant candidate list (CCL) every 

5 years. Once EPA determines to 

regulate a contaminant in drinking 

water, EPA must issue a proposed 

national primary drinking water 

regulation (NPDWR) and final NPDWR 

within certain set time frames. To 

regulate a contaminant in drinking 

water, EPA must determine that it meets 

three criteria: (1) The contaminant may 

have an adverse effect on human health, 

(2) the contaminant is known to occur 

or there is a substantial likelihood that 

the contaminant will occur in public 

water systems with a frequency and at 

levels of public health concern, and (3) 

regulation of such contaminant presents 

a meaningful opportunity for health risk 

reduction for persons served by public 

water systems. To date, EPA has made 

final regulatory determinations for 20 

contaminants from CCL1 and CCL2 and 

has not found that any of these 

contaminants meet all three criteria. 

On October 10, 2008, EPA published 

a preliminary regulatory determination 

for perchlorate, requesting public 

comment on its determination that 

perchlorate did not meet the second and 

third criteria for regulation. The October 

2008 notice describes in detail the bases 

for EPA’s determination (USEPA, 

2008a). EPA received extensive public 

comment on that notice. 

Today, the Agency is seeking 

comments on additional approaches to 

analyzing data related to EPA’s 

perchlorate regulatory determination. 

The EPA is requesting the additional 

comments in an effort to ensure that the 

Agency considers the potential options 

for evaluating whether there is a 

meaningful opportunity for human 

health risk reduction from perchlorate 

through a national primary drinking 

water rule. EPA’s final decision may be 

a determination to regulate. As 

discussed below, the additional 

alternatives under consideration could 

result in health reference levels which 

are much lower than the level identified 

in the October 2008 notice. The public 

comments EPA received pursuant to the 

October 10, 2008, notice of preliminary 

regulatory determination 1 and from the 

1 On November 12, 2008, EPA extended the 

comment period for 15 days regarding EPA’s 

peer review of the supporting 

documents underscore the complexity 

of the scientific issues regarding the 

regulatory determination for perchlorate 

in drinking water. 

EPA received 32,795 comment letters 

of which 31,632 (96%) letters were from 

seven different apparent mass mailing 

letter writing campaigns that did not 

support the preliminary determination. 

Of the remaining 1,163 comment letters 

that would be considered ‘‘unique,’’ 30 

commenters provided EPA with 

detailed comments. Of those 30 

comment letters, six supported EPA’s 

preliminary determination. These 

comments and other docket materials 

are available electronically at http:// 

www.regulations.gov (Docket ID No. 

EPA–HQ–OW–2008–0692). 

In its October 2008 FRN, EPA referred 

to a draft report entitled ‘‘Inhibition of 

the Sodium-Iodide Symporter by 

Perchlorate: An Evaluation of Lifestage 

Sensitivity Using Physiologically-Based 

Pharmacokinetic (PBPK) Modeling’’ 

(USEPA, 2008b). This draft report, 

which is described in Section III.A.1, 

was peer reviewed during the comment 

period on the regulatory determination. 

The report (USEPA, 2008c) and a 

summary of significant comments made 

by the external peer reviewers and 

EPA’s responses (USEPA, 2008e) can be 

found at http://cfpub.epa.gov/ncea/cfm/ 

recordisplay.cfm?deid=212508. The 

peer review comments were 

complimentary and supportive of EPA’s 

modeling analysis and support 

document. 

On January 8, 2009, EPA issued an 

interim health advisory (HA) to provide 

guidance to state and local officials in 

their efforts to address perchlorate 

contamination while EPA was 

reviewing scientific issues. A draft of 

the HA was peer reviewed by four 

external peer reviewers. The HA peer 

reviewers comments are discussed in 

Section III.A.2 of this notice. The 

Interim Health Advisory (USEPA. 

2008d) can be found at http:// 

www.epa.gov/safewater/contaminants/ 

unregulated/perchlorate.html and the 

summary of significant comments made 

by the external peer reviewers (USEPA. 

2008e) can be found at http:// 

www.epa.gov/ogwdw/contaminants/ 

unregulated/pdfs/ 

perchlorate_ha_comment_response.pdf. 

In January of this year, EPA 

announced that we planned to seek 

additional input from the National 

Research Council (NRC) on perchlorate. 

The NRC previously studied perchlorate 

health implications from March, 2003 

preliminary regulatory determination for 

perchlorate. 

until they issued their report in January, 

2005 (NRC, 2005). EPA has compiled 

and evaluated additional scientific 

studies relevant to perchlorate health 

effects and exposure available since 

publication of the 2005 NRC report. As 

previously stated, EPA also has obtained 

peer review and public comment on the 

Agency’s analysis of a number of these 

studies. The Agency believes that 

further review by the NRC would 

unnecessarily delay regulatory decision 

making for perchlorate. Therefore, EPA 

is not, at present, planning to request 

additional NRC review of issues related 

to perchlorate. Instead, EPA is issuing 

this notice and seeking comment on a 

broad range of alternative approaches to 

the interpretation of the scientific data 

relevant to a regulatory determination 

for perchlorate in drinking water. 

However, EPA requests comment upon 

whether further review by the NRC is 

warranted. EPA also notes that if the 

Agency were to make a final 

determination to regulate perchlorate, 

the Agency, in accordance with the 

SDWA, would seek review by the 

Science Advisory Board prior to 

proposal of any maximum contaminant 

level goal and national primary drinking 

water rule.2 

In issuing this supplemental notice, 

EPA is not making a final regulatory 

determination for perchlorate nor are we 

changing the Interim Health Advisory 

Level of 15 μg/L. EPA will consider 

comments on the information received 

on this notice, as well as those received 

on the October 10, 2008, FR notice, and 

those received on the peer review of 

supporting documents before 

completing its regulatory determination 

for perchlorate. EPA may also revise the 

Interim Health Advisory as part of this 

process. 

III. Alternative Approaches To 

Analyzing Scientific Data Related to 

Perchlorate in Drinking Water 

EPA is requesting comment on key 

issues related to the regulatory 

determination for perchlorate in 

drinking water. EPA is now considering 

a broader range of alternatives for 

interpreting the available data on: the 

level of health concern, the frequency of 

occurrence of perchlorate in drinking 

water, and the opportunity for health 

risk reduction through a national 

2 The requirement for national drinking water 

regulations are in SDWA Section 1412. EPA’s Web 

page describes the regulatory development process 

(see http://www.epa.gov/safewater/standard/ 

setting.html). SDWA section 1412.e requires that 

EPA request comment from the Science Advisory 

Board prior to proposal of a maximum contaminant 

level goal and national primary drinking water 

regulation. 

jlentini on DSKJ8SOYB1PROD with NOTICES

Federal Register / Vol. 74, No. 159 / Wednesday, August 19, 2009 / Notices 41885 

primary drinking water standard. These 

alternative interpretations may impact 

the Agency’s final regulatory 

determination for perchlorate. 

Therefore, EPA seeks comment on these 

issues and the alternative approaches 

the Agency is considering. 

A. Interpretation of the PhysiologicallyBased Pharmacokinetic (PBPK) 

Modeling 

1. EPA’s PBPK Modeling Analysis in the 

October 2008 FR Notice 

The NRC (NRC, 2005) found that the 

inhibition of iodide uptake by the 

thyroid should be used as the basis for 

a perchlorate risk assessment. In the 

October, 2008, FR notice, EPA describes 

a Physiologically-Based 

Pharmacokinetic (PBPK) modeling 

analysis prepared by the Agency 

utilizing a series of papers (e.g., Clewell 

et al., 2007) discussing PBPK models 

that estimated the effect of perchlorate 

on iodide uptake for the pregnant 

woman and fetus, the lactating woman 

and neonate, and the young child. EPA 

used the PBPK modeling analysis to 

estimate the iodide uptake inhibition for 

these sensitive life stages consuming 

food containing perchlorate at mean 

levels, and drinking water containing 

perchlorate at an HRL of 15 μg/L at the 

90th percentile consumption rate. 

EPA found that the predicted 

radioactive iodide uptake (RAIU) 

inhibition for all subgroups was 

comparable to, or less than, the RAIU at 

the no observed effect level (NOEL) 

selected by the NRC. Based on this 

outcome, EPA concluded that by 

protecting the fetus of the hypothyroid 

or iodide-deficient woman from the 

effects of perchlorate on the thyroid, all 

other life stages and subgroups would 

be protected. 

EPA requested comment on the model 

in the October 2008 FR notice in 

addition to conducting a peer review on 

the application of the model to nonadult life stages. 

2. What Were the Key Scientific Issues 

Raised by Commenters 

Many of the public comments EPA 

received on the PBPK model in response 

to the October 2008 FR notice objected 

to the Agency’s use of a model that had 

not been peer reviewed. Concurrently 

with the public comment period, the 

PBPK model analysis underwent a 

rigorous peer review by eight experts. 

Response by the PB model analysis peer 

reviewers indicated that the 

modifications made to the model and 

the changes to physiological parameters 

were an improvement over the Clewell 

model, and all reviews were generally 

supportive of the analysis. Based on the 

external peer review comments, the 

models and the report entitled, 

‘‘Inhibition of the Sodium-Iodide 

Symporter by Perchlorate: An 

Evaluation of Lifestage Sensitivity Using 

Physiologically-Based Pharmacokinetic 

(PBPK) Modeling’’ were revised. 

As previously discussed, comments 

were also received from four peer 

reviewers for the Interim Drinking 

Water Health Advisory (HA) on the 

application of the model in identifying 

sensitive life stages. One HA peer 

reviewer noted that the use of the PBPK 

model did ‘‘provide an estimate of 

perchlorate exposure to average weight 

babies of healthy breastfeeding women.’’ 

However, this HA peer reviewer 

continued on to recommend that the 

exposure estimate be expanded to 

include consideration of small birth 

weight and preterm infants. 

Another peer reviewer recommended 

that the uncertainty inherent in the 

modeling exercise should be made more 

transparent to the public. This 

uncertainty was linked to the modeling 

code, the availability of data for the 

many variable parameters in the model, 

the combination and handling of the 

data selected for use in simulations, 

and, in particular, the lack of human 

data for specific life stages including 

pregnant women and their fetuses, 

lactating women and their babies, and 

bottle-fed infants for which rat data 

were adapted. The inability of the 

model to reflect iodide nutritional status 

also was cited by three peer reviewers 

as an important limitation. 

Individual peer reviewers raised two 

additional concerns: (1) That the use of 

animal data to predict human responses 

appears to run counter to the NRC 

finding that animal data cannot be used 

to quantitatively predict the response of 

humans due to species differences, and 

(2) that EPA appeared to use the PBPK 

model to modify the reference dose 

(RfD) for infants, justifying the 

allowance of exposures that clearly 

exceeded the RfD established by the 

NRC. 

Peer reviewers further noted that the 

PBPK model and the EPA assessment 

did not account for the activity of other 

compounds with similar actions on the 

thyroid. This issue was also raised by 

EPA’s Office of Inspector General (OIG) 

in reference to EPA’s perchlorate risk 

assessment (see section III.C.2 for more 

information). One reviewer stated that 

the application of the PBPK model by 

the Agency as cited in the Interim 

Health Advisory implied an 

inappropriate certainty in the results 

that was not warranted. This reviewer 

recommended confining the use of the 

PBPK model to exploring the impact of 

varying physiological parameters and 

exposure data among life stages. 

3. Alternative Approaches EPA Is Also 

Now Considering 

Based on the comments received on 

the application of the PBPK model as 

described in the October 2008 notice 

and the Interim HA, EPA is reevaluating how best to incorporate the 

PBPK modeling analysis into its 

evaluation of perchlorate, if at all. 

One approach might be to use the 

PBPK modeling analysis to explore the 

relative sensitivity of the various life 

stages of concern to a fixed dose such 

as the point of departure (POD) or the 

reference dose (RfD). For example, EPA 

has examined the effect of a dose equal 

to the POD on RAIU for a number of 

different life stages. The POD for the 

perchlorate risk assessment (7 μg/kg/ 

day) was recommended by the NRC. 

The POD is the lowest dose 

administered in the Greer et al. (2002) 

clinical study, and resulted in a ‘‘very 

small decrease (1.8%) in radioiodide 

uptake * * * well within the variation 

of repeated measurements of normal 

subjects (NRC, 2005).’’ The POD used 

was determined by NRC to be a No 

Observed Effect Level (NOEL). The NRC 

stated that use of a NOEL differs from 

the traditional approach to deriving an 

RfD, which bases the critical effect on 

an adverse outcome, and that using a 

nonadverse effect that is upstream of the 

adverse effect is a more conservative 

and health-protective approach to 

perchlorate hazard assessment. The 

NRC also recommended that EPA derive 

an RfD by applying a 10-fold 

uncertainty factor to the POD to account 

for differences between healthy adults 

and the most sensitive population, 

fetuses of pregnant women who might 

have hypothyroidism or iodide 

deficiency. When compared to the 

average adult, the 7-day old breast-fed 

infant and the fetus of the pregnant 

woman at gestation week 40 were 

identified by EPA’s analysis as the most 

sensitive subgroup with respect to 

percent RAIU inhibition at a dose to the 

lactating or pregnant women equal to 

the POD. (See Table 1 for the modelpredicted RAIU inhibition and relative 

sensitivity at the POD of different 

subgroups compared to the average 

adult, based on EPA’s modified PBPK 

model.) 

The predicted percent RAIU 

inhibition is approximately 7.8-fold 

higher for the 7-day old breast-fed infant 

and 6.7-fold higher for the fetus (at 

gestational week 40) than for the average 

adult. (Simulations at earlier gestation 

weeks indicate that the fetus is more 

jlentini on DSKJ8SOYB1PROD with NOTICES

41886 Federal Register / Vol. 74, No. 159 / Wednesday, August 19, 2009 / Notices 

sensitive than the adult throughout inhibition is approximately one and a III.B.3 show that infants less than six 

pregnancy, but data available for half-fold higher for the bottle-fed infant months in age generally consume five to 

validation of these parameters are (7–60 days) compared to the average eight times more water than pregnant 

minimal and are considered too adult, and is approximately equal for women or women of child bearing age 

quantitatively uncertain to assign exact the 1–2 year old child and the average on a per body weight basis, and so will 

relative sensitivities.) The same analysis adult. However, the drinking water receive a higher dose for any given 

shows that the predicted percent RAIU exposure data discussed in section drinking water concentration. 

TABLE 1—MODEL-PREDICTED RADIOACTIVE IODIDE UPTAKE (RAIU) INHIBITION AND RELATIVE SENSITIVITY OF DIFFERENT 

SUBGROUPS COMPARED TO THE AVERAGE ADULT AT A DOSE EQUAL TO THE POINT-OF-DEPARTURE (POD) BASED 

ON THE EPA’S MODIFIED PBPK MODELS 

Population or life stage Body weight (kg) Dose i 

(μg/kg-d) RAIU inhibition 

Relative 

sensitivity vs. 

average adult 

Average Adult a ............................................................ 70 ..................................... 7 ....................................... 1.6% 1 

Woman (child-bearing age) ......................................... 68 ..................................... 7 ....................................... b 3.0% 1.8 

Pregnant woman and Fetus (Gestation Week 40) ..... Mom: 79 ........................... 7 ....................................... c 6.1% 3.7 

Fetus: 3.5 ......................... .......................................... c 11% 6.7 

Lactating woman and Breast-fed infant (7 d) ............. Mom: 74 ........................... 7 ....................................... d 2.1% 1.3 

Infant: 3.6 ......................... Mom = 7 .......................... d,e 12.5% 7.8 

Infant = 7 ......................... d,e,f 5.4% 3.3 

(Mom = 2.7) ..................... 

Lactating woman and Breast-fed infant (30 d) ........... Mom: 73 ........................... 7 ....................................... d 2.0% 1.2 

Infant: 4.2 ......................... Mom = 7 .......................... d,e 9.8% 6.1 

Infant = 7 ......................... d,e,f 4.4% 2.7 

(Mom = 3.0 ) .................... 

Lactating woman and Breast-fed infant (60 d) ........... Mom: 72 ........................... 7 ....................................... d 2.0% 1.2 

Infant: 5.0 ......................... Mom = 7 .......................... d,e 7.9% 4.9 

Infant = 7 ......................... d,e,f 4.2% 2.7 

(Mom = 3.6 ) .................... 

Bottle-fed infant (60 d) ................................................ Infant: 5.0 ......................... 7 ....................................... e 2.5% 1.5 

Child (0.97 yr) g ........................................................... Child: 10 .......................... 7 ....................................... h 1.7% 1.1 

Child (2 yr) ................................................................... Child: 14 .......................... 7 ....................................... h 1.7% 1.1 

a The body weight (70 kg) for the average adult is the default weight used by EPA for past regulatory determinations. All other body weights 

are generated by the model. b Maternal body weight was held at the value defined at the start of pregnancy (BW = 67.77 kg), and the ‘‘average adult’’ urinary clearance values as published by Merrill et al. (2005) were used. c Results are based on using the maternal urinary clearance as published in Clewell et al. (2007), which equal about half of the average adult 

clearance. d Results are based on setting the maternal clearance rates of both perchlorate and iodide during lactation equal to that of the average adult. 

Clewell et al. (2007) used an iodide clearance rate equal to that of an average adult, but a perchlorate rate only half that of the average adult. e %RAIU inhibition given for the infant is provided based upon a value of urinary clearance scaled from the adult by BW 2⁄3 to approximate surface-area scaling, and then multiplied by a rising fraction vs. age based on data (DeWoskin and Thompson, 2008) to reflect the reduction in glomerular filtration rates. Clewell et al. (2007) scaled urinary clearance by BW 0.75, rather than adjusting based on GFR. f These %RAIU inhibition values are based on an internal dose to the breast-fed infant of 7 μg/kg-day, the same as for the other subgroups. 

Maternal dose rates lower than the POD are needed to provide 7 μg/kg-day to the infant as shown in the table. These doses differ due to 

changes in body weights and other PK factors with age. g Because EPA typically uses a 10 kg child as a default assumption for its drinking water health advisories, the model was run for a child at 

0.97 yr, the age at which the model-simulated body weight for a child is 10 kg. h Results were obtained by setting urinary clearance constants for the older child equal to the average adult (Merrill et al., 2005) and scaling by 

BW 1. i The dose equal to the POD is 7 μg/kg-day which is 10-fold greater than the RfD. The predicted RAIU inhibition at the RfD would be less than 

those shown in Table 1. 

The modeling analysis may be used as sensitive life stages to develop separate sensitive life stages to inform HRL 

a tool to predict the impact of different HRLs for these life stages as described selection. 

perchlorate drinking water in Section III.B. c. EPA requests suggestions for ways 

concentrations on RAIU across life to use the PBPK modeling analysis to 4. Request for Comment on Alternative stages. Understanding the potential inform the regulatory determination for Approaches impact of reducing perchlorate perchlorate that are different from those 

concentrations may be especially EPA Seeks Comments on the Following described in this notice or the October

important for considering bottle-fed Issues: 10, 2008, notice. 

infants for whom a major portion of the B. Alternative HRLs Based Upon Body diet may consist of water used to a. EPA requests comment on using the Weight and Water Consumption of rehydrate formula. PBPK model to evaluate the relative Other Life Stages sensitivity of the various life stages to Another approach EPA is also perchlorate exposure in drinking water. 1. Analysis and Interpretations From the considering would be to not use the October 2008 FR Notice PBPK modeling analysis to inform the b. EPA requests comment on the 

selection of the HRL for its regulatory utility of the PBPK model for predicting In our October 2008 FR notice, EPA 

determination but instead apply the RfD the impact of different perchlorate requested comments on an HRL of 15 

directly to the exposures of other drinking water concentrations on μg/L to protect pregnant women and 

jlentini on DSKJ8SOYB1PROD with NOTICES

Federal Register / Vol. 74, No. 159 / Wednesday, August 19, 2009 / Notices 41887 

their fetuses based upon the Agency’s 

RfD, recommended by the NRC, and the 

following exposure estimates: 

HRL = RfD × BW/DWI × RSC 

Where: 

RfD = Reference dose (0.7 μg/kg/day) 

BW = Body weight (70 kg, default value) 

DWI = Drinking water intake (2 L/day, 

default value) 

RSC = Relative source contribution (62% for 

pregnant women) 

In calculating the HRL of 15 μg/L, 

EPA used adult default values for both 

body weight (the mean body weight for 

men and women, 70 kg) and drinking 

water intake (84th percentile, 2 L/day). 

The RSC is the percentage of the 

reference dose remaining for drinking 

water after other sources of exposure to 

perchlorate have been considered (e.g., 

food). EPA used the pregnant women’s 

estimated 90th percentile perchlorate 

intake from food to determine the RSC 

of 62%. In past regulatory 

determinations on most other 

noncarcinogenic contaminants, EPA has 

used an RSC default value of 20% for 

screening purposes to estimate the HRL 

when it has lacked adequate data to 

develop empirical RSCs for those 

contaminants (for sulfate and sodium 

EPA did not use an RSC to determine 

the HRL). For the October 2008 notice, 

the Agency believed that sufficient 

exposure data were available for 

perchlorate to enable EPA to estimate a 

better informed RSC and HRL that is 

more appropriate for fetuses of pregnant 

women (the most sensitive life stage 

identified by the NRC). These exposure 

data include the further analysis by EPA 

of the Unregulated Contaminant 

Monitoring Regulation (UCMR) data and 

the Centers for Disease Control and 

Prevention’s (CDC’s) National Health 

and Nutrition Examination Survey 

(NHANES) biomonitoring data, as well 

as the Food and Drug Administration’s 

(FDA’s) Total Diet Study (TDS) (73 FR 

60269–72, October 10, 2008). The EPA 

analysis provided a distribution of 

exposure (not just a mean) specific to 

almost 100 pregnant women who are 

not likely to have been exposed to 

perchlorate from their drinking water, 

although it did not separate out iodinedeficient pregnant women because of 

data limitations. EPA estimated that for 

90% of the pregnant women, exposure 

to perchlorate from food is equal to, or 

less than, 0.263 μg/kg/day (90th 

percentile). This represents nearly 38% 

of the RfD, leaving an RSC for water of 

62%. 

2. What Were the Key Issues Raised by 

Public Commenters? 

The comments EPA received 

underscore the complexity of the 

scientific issues and many were critical 

of EPA’s derivation of the HRL. Of those 

that provided detailed comments, many 

were concerned about the adequacy of 

the HRL to address all sensitive life 

stages (e.g., pre-term and full-term 

infants). For example, a number of 

commenters argued that the proposed 

HRL is too high for infants because an 

HRL of 15 μg/L would allow daily 

exposures that are two to five times 

higher than the RfD. 

One commenter cites a March 8, 2006, 

letter from the Children’s Health 

Protection Advisory Committee to the 

EPA Administrator. The commenter 

states, ‘‘* * * [T]he committee 

emphasized the higher exposure of 

infants to perchlorate and greater 

susceptibility to serious negative effects 

associated with perchlorate exposure. 

Neither of these issues, however, was 

given adequate consideration in the 

Preliminary Determination.’’ 

Another commenter addresses EPA’s 

use of default values in deriving the 

HRL stating, ‘‘* * * EPA continues to 

use the obsolete default of 70 kg for 

body weight and 2 L/day of water 

consumption when these values 

certainly do not apply to pregnant 

women. These defaults are specifically 

intended for the population in general, 

and should be superseded by more 

specific and appropriate values when 

risk assessment is being conducted for 

a defined subpopulation (U.S. EPA, 

2004, 2005).’’ 

3. Alternative Approaches for 

Calculating HRLs 

EPA agrees that reassessing exposure 

assumptions and other life stages 

warrants further consideration. The 

NRC (2005) identified ‘‘the fetuses of 

pregnant women who might have 

hypothyroidism or iodide deficiency’’ as 

‘‘the most sensitive population,’’ but 

also identified infants and developing 

children as additional ‘‘sensitive 

populations.’’ Infants and young 

children have greater exposure to 

contaminants in food and water because 

of greater consumption of food and 

water on a per unit body weight basis. 

Therefore, these life stages may be the 

most vulnerable populations when their 

relative exposure is considered. 

Therefore, EPA is considering 

alternative approaches to deriving HRLs 

by evaluating exposures at different life 

stages. EPA is considering alternative 

HRLs that are estimates of the maximum 

concentration of perchlorate that can be 

consumed in drinking water without an 

individual’s total perchlorate dose from 

food and water exceeding the RfD. 

EPA’s Guidance on Selecting Age 

Groups for Monitoring and Assessing 

Childhood Exposures to Environmental 

Contaminants (USEPA, 2005) 

recommends the following 10 age 

groups be considered in exposure 

assessments for children. 

• Less than 12 Months old: birth to < 

1 month, 1 to < 3 months, 3 to < 6 

months and 6 to < 12 months. 

• Greater than 12 months old: 1 to < 

2 years, 2 to < 3 years, 3 to < 6 years, 

6 to < 11 years, 11 to < 16 years, and 

16 to < 21 years. 

EPA’s Guidance for Risk 

Characterization (USEPA, 1995) 

recommends that when considering 

exposure to use both high end (i.e., 90th 

and 95th percentile) and central 

tendency (average or median estimates) 

descriptors to convey the variability in 

risk levels experienced by different 

individuals in the population. 

Table 2 arrays the alternative HRLs at 

the average 90th and 95th percentile 

drinking water ingestion rates for each 

of the 10 childhood life stages (as well 

as for pregnant women and women of 

child-bearing age, 15 to 44). The table 

uses the life stage specific drinking 

water intake data that are adjusted to 

account for the body weight of the 

individual. EPA’s Child-Specific 

Exposure Factors Handbook (USEPA, 

2008f) recommends values for drinking 

water ingestion rates for each of 

recommended children’s life stage based 

on a study of drinking water ingestion 

of the U.S. population by Kahn and 

Stralka (2008). The study reports 

ingestion estimates for ‘‘all individuals’’ 

and for ‘‘consumers only.’’ Estimates 

reported for ‘‘all individuals’’ include 

all survey participants regardless of 

whether they consumed water during 

the 2-day survey period. Ingestion 

estimates for ‘‘consumers only’’ are 

generated from only the respondents 

who reported ingestion of drinking 

water from a community water system 

during the survey period. The authors 

report that this group is often the 

primary focus in analyses of risk due to 

ingestion of water that may be 

contaminated. Consequently, this is the 

only group presented in Table 2. 

In addition to identifying infants and 

developing children as sensitive life 

stages, as noted previously, the NAS 

identified the fetuses of iodide deficient 

pregnant women as the most sensitive 

population (or life stage). To address 

concerns that the default weight and 

ingestion rates provided in the October 

2008 notice do not apply to this group, 

EPA has included an alternative HRL for 

jlentini on DSKJ8SOYB1PROD with NOTICES

41888 Federal Register / Vol. 74, No. 159 / Wednesday, August 19, 2009 / Notices 

this life stage in Table 2. This value is 

calculated based on body weight and 

drinking water ingestion information 

specifically from pregnant women 

(USEPA, 2004). 

EPA notes that for six life stages in 

Table 2 (birth to < 1 month, 1 to < 3 

months, 3 to < 6 months, 16 to 18 years 

and 18 to 21 years and for pregnant 

women), the sample size used to 

estimate some of the drinking water 

ingestion rates (denoted in Table 2 by 

foot note c) do not meet the minimum 

data requirements as described in the 

‘‘Third Report on Nutrition Monitoring 

in the United States’’ (LSRO, 1995). 

However, these are the best available 

data to characterize drinking water 

ingestion for these specific life stages. 

EPA also notes that these data clearly 

show the trend that drinking water 

mean ingestion rate on a per body 

weight basis increases as the life stage 

age decreases. To address this potential 

concern regarding sample size for some 

of these drinking water ingestion rates, 

EPA also aggregated the three youngest 

recommended age groups into one 

category on Table 2 (birth to < 6 

months) based on data from EPA 

(USEPA, 2004). To address women of 

childbearing age, EPA presents HRLs 

calculated based upon drinking water 

ingestion data for women ages 15 to 44. 

To estimate dietary exposure to 

perchlorate and to calculate RSCs, EPA 

used data available from two studies 

previously described by EPA, the FDA’s 

Total Diet Study (Murray et al., 2008) 

and the NHANES–UCMR Analysis (73 

FR 60269–73, October 10, 2008). In 

cases where these studies did not 

provide a dietary exposure estimate for 

one of the recommended child-specific 

life stages/age groups, EPA applied the 

RSC calculated for the age group closest 

to the age group of interest. This meant 

that the RSCs for the age groups 

between birth and 6 months, 59%, were 

based on the mean dietary exposure 

estimate for infants ages 6 through 11 

months, 0.29 μg/kg-day, derived from 

FDA’s Total Diet Study. We understand 

that infant diets vary significantly 

between birth and age 11 months and 

that the TDS mean dietary perchlorate 

exposure estimates for ages 6 through 11 

months consider consumption of baby 

foods that are not consumed by younger 

infants (see http://www.fda.gov/Food/ 

FoodSafety/ 

FoodContaminantsAdulteration/ 

ChemicalContaminants/Perchlorate/ 

ucm077615.htm). Researchers from the 

CDC (Schier et al., 2009) recently 

published a study in which they 

estimated exposures to perchlorate from 

the consumption of infant formula. For 

infants age 1 month, the researchers’ 

central tendency estimate of perchlorate 

daily dose from consumption of bovine 

milk-based infant formula with lactose 

(the type of formula with the highest 

concentrations of perchlorate) was also 

0.29 μg/kg-day, corresponding to an RSC 

of 59%. Thus, EPA’s RSC for young 

infants, 59%, is supported through two 

different estimates of central tendency 

infant dietary perchlorate exposure. 

TABLE 2—ALTERNATIVE HRLS AT THE AVERAGE, 90TH AND 95TH PERCENTILE DRINKING WATER INGESTION RATES FOR
 

VARIOUS LIFE STAGES
 

Life stage RfD 

(μg/kg-day) 

RSC a 

(percent) 

Mean 

ingestion 

rate d 

(mL/kg-day) b 

Alt HRL 

(μg/L) 

90th 

Percentile 

ingestion 

rate d 

(mL/kg-day) b 

Alt HRL 

(μg/L) 

95th 

Percentile 

ingestion 

rate d 

(mL/kg-day) b 

Alt HRL 

(μg/L) 

Birth to < 1 

month ............ 0.7 59 137 3 c 235 2 c 238 2 

1 to < 3 months 0.7 59 119 3 c 228 2 c 285 1 

3 to < 6 months 

Birth to < 6 

0.7 59 80 5 148 3 c 173 2 

months .......... 

6 to < 12 

0.7 59 95 4 184 2 221 2 

months .......... 0.7 59 53 8 112 4 129 3 

1 to < 2 years ... 0.7 44 27 11 56 6 75 4 

2 to < 3 years ... 0.7 44 26 12 52 6 62 5 

3 to < 6 years ... 0.7 60 24 18 49 9 65 6 

6 to < 11 years 0.7 71 17 29 35 14 45 11 

11 to < 16 years 0.7 84 13 45 26 23 34 17 

16 to < 18 years 0.7 80 12 47 24 23 c 32 18 

18 to < 21 years 

Pregnant 

0.7 80 13 43 29 19 c 35 16 

Women e ....... 

Women Ages 

0.7 c 62 c 14 31 c 33 13 c 43 10 

15–44 ............ 0.7 80 15 37 32 18 39 14 

a RSC calculated for nearest age range based on the mean dietary intake from TDS (see Table 5 at 73 FR 60275, October 10, 2008), RSC for 

pregnant women and women ages 15–44 based on the 90th percentile dietary intake from NHANES–UCMR analysis (see Table 6 at 73 FR 

60276, October 10, 2008). b Drinking Water Ingestion Rates for consumers only in Community Water Systems taken from EPA’s ‘‘Child-Specific Exposure Factors Handbook’’ (USEPA, 2008e). Except for values for infants from birth to 6 months, which are taken from Tables 5.2.A2 of EPA’s ‘‘Estimated Per Capita 

Water Ingestion and Body Weight in the United States—An Update’’ (USEPA, 2004), and for Pregnant Women and Women Ages 15–44 which 

are taken from Table 6.2.A2 of EPA’s ‘‘Estimated Per Capita Water Ingestion and Body Weight in the United States—An Update’’ (USEPA, 

2004). c The sample sizes for the estimates of ingestion rates for these life stages do not meet the minimum data requirements as described in the 

‘‘Third Report on Nutrition Monitoring in the United States’’ (LSRO, 1995). d Ingestion rate is adjusted for the self-reported body weights from the CFSII. 

e The most sensitive population identified by the NRC are the fetuses of pregnant women who might have hypothyroidism or iodide deficiency. 

jlentini on DSKJ8SOYB1PROD with NOTICES

Federal Register / Vol. 74, No. 159 / Wednesday, August 19, 2009 / Notices 41889 

4. Request for Comments 

EPA Seeks Comments on the Following 

Issues: 

a. EPA requests comment on whether 

the alternative HRLs described in this 

notice appropriately take into account 

specific and appropriate exposure 

values for all potentially sensitive life 

stages, including infants, children and 

the fetuses of pregnant women (rather 

than the 70 kg body weight and 2 liter 

per day consumption used for past 

regulatory determinations). b. EPA requests comment on the 

alternative HRLs in Table 2 and which 

of these values would be appropriate 

levels of health concern against which 

to compare the levels of perchlorate 

found in public water systems. c. EPA requests comment on whether 

EPA used the best available and most 

appropriate data to estimate alternative 

HRLs in Table 2. EPA specifically 

requests comment on the drinking water 

ingestion rates in Table 2 (denoted by 

footnote c) where the sample size does 

not meet the minimum data 

requirements as described in the ‘‘Third 

Report on Nutrition Monitoring in the 

United States’’ (LSRO, 1995). Does 

aggregating life stages (birth to 6 

months, and women ages 15–44) 

address sample size limitation and still 

provide an accurate representation of 

the exposure to the most vulnerable life 

stages? d. EPA requests comment on the 

merits of the approach described here of 

deriving HRLs for sensitive life stages 

based on the RfD combined with the life 

stage specific exposure data and 

whether there are other approaches that 

may be useful for deriving HRLs. 

C. Occurrence Analysis 

1. Occurrence Analysis in the October 

2008 Federal Register Notice 

In the October 2008 FR notice, EPA 

presented information on the drinking 

water occurrence of perchlorate. The 

data source was EPA’s UCMR 1 and the 

samples were collected between 2001 

and 2005. A total of 34,331 samples 

were collected from 3,865 public water 

systems. EPA found that 1.9% of the 

samples (637 out of 34,331) had 

perchlorate at, or above, the minimum 

reporting level (MRL = 4 μg/L) and that 

4.1% of the systems (160 out of 3,865 

systems) reported perchlorate at, or 

above, the MRL in at least one sample. 

The average perchlorate concentration 

among systems that detected perchlorate 

was 9.85 μg/L and the median was 6.40 

μg/L.

Table 3 presents EPA’s estimates of 

the population served by water systems 

for which the highest reported 

perchlorate concentration was greater 

than various threshold concentrations 

ranging from 4 μg/L (MRL) to 25 μg/L. 

The fourth column presents a high end 

estimate of the population served 

drinking water above a threshold. This 

column presents the total population 

served by those drinking water systems 

in which at least one sample was found 

to contain perchlorate above the 

threshold concentration. EPA considers 

this a high-end estimate because it is 

based upon the assumption that the 

entire system population is served water 

from the entry point that had the highest 

reported perchlorate concentration. In 

fact, many water systems have multiple 

entry points into which treated water is 

pumped for distribution to their 

consumers. For the systems with 

multiple entry points, it is unlikely that 

the entire service population receives 

water from the one entry point with the 

highest single concentration. Therefore, 

EPA also is providing a less 

conservative estimate of the population 

served water above a threshold in the 

fifth column in Table 3. EPA developed 

this estimate by assuming the 

population was equally distributed 

among all entry points. For example, if 

a system with 10 entry points serving 

200,000 people had a sample from a 

single entry point with a concentration 

at or above a given threshold, EPA 

assumed that the entry point served 

one-tenth of the system population, and 

added 20,000 people to the total when 

estimating the population in the last 

column of Table 3. This approach may 

provide either an overestimate or an 

underestimate of the population served 

by the affected entry point. In contrast, 

in the example above, EPA added the 

entire system population of 200,000 to 

the more conservative population 

served estimate in column 4, which is 

most likely an overestimate. EPA noted 

that the population estimates in Table 3 

are for people at all life stages and 

estimated that at any one time, 1.4 

percent of the population in Table 3 are 

pregnant women based upon data from 

the U.S. Census Bureau. 

TABLE 3—UCMR 1 OCCURRENCE AND POPULATION ESTIMATES FOR PERCHLORATE ABOVE VARIOUS THRESHOLDS 

Thresholds a PWSs with at least 1 detection > 

threshold of interest 

PWS entry or sample points with at 

least 1 detection > threshold of 

interest b 

Population served 

by PWSs with at 

least 1 detection > 

threshold of 

interest c 

Population 

estimate for entry 

or sample points 

having at least 1 

detection > 

threshold of 

interest d 

4 μg/L ..................... 4.01% .................................................. 

(155 of 3,865) ...................................... 

2.48% .................................................. 

(371 of 14,987) .................................... 

16.6 M e ................ 5.1 M. 

5 μg/L ..................... 3.16% .................................................. 

(122 of 3,865) ...................................... 

1.88% .................................................. 

(281 of 14,987) .................................... 

14.6 M .................. 4.0 M. 

7 μg/L ..................... 2.12% .................................................. 

(82 of 3,865) ........................................ 

1.14% .................................................. 

(171 of 14,987) .................................... 

7.2 M .................... 2.2 M. 

10 μg/L ................... 1.35% .................................................. 

(52 of 3,865) ........................................ 

0.65% .................................................. 

(97 of 14,987) ...................................... 

5.0 M .................... 1.5 M. 

12 μg/L ................... 1.09% .................................................. 

(42 of 3,865) ........................................ 

0.42% .................................................. 

(63 of 14,984) ...................................... 

3.6 M .................... 1.2 M. 

15 μg/L ................... 0.80% .................................................. 

(31 of 3,865) ........................................ 

0.29% .................................................. 

(44 of 14,987) ...................................... 

2.0 M .................... 0.9 M. 

17 μg/L ................... 0.70% .................................................. 

(27 of 3,865) ........................................ 

0.24% .................................................. 

(36 of 14,987) ...................................... 

1.9 M .................... 0.8 M. 

20 μg/L ................... 0.49% .................................................. 

(19 of 3,865) ........................................ 

0.16% .................................................. 

(24 of 14,987) ...................................... 

1.5 M .................... 0.7 M. 

25 μg/L ................... 0.36% .................................................. 

(14 of 3,865) ........................................ 

0.12% .................................................. 

(18 of 14,987) ...................................... 

1.0 M .................... 0.4 M. 

Footnotes: 


a All occurrence measures in this table were conducted on a basis reflecting values greater than the listed thresholds. 


jlentini on DSKJ8SOYB1PROD with NOTICES

41890 Federal Register / Vol. 74, No. 159 / Wednesday, August 19, 2009 / Notices 

b The entry/sample-point-level population served estimate is based on the system entry/sample points that had at least 1 analytical detection 

for perchlorate greater than the threshold of interest. The UCMR 1 small system survey was designed to be representative of the nation’s small 

systems, not necessarily to be representative of small system entry points. c The system-level population served estimate is based on the systems that had at least 1 analytical detection for perchlorate greater than the 

threshold of interest. d Because the population served by each entry/sample point is not known, EPA assumed that the total population served by a particular system is equally distributed across all entry/sample points. To derive the entry/sample point-level population estimate, EPA summed the population 

values for the entry/sample points that had at least 1 analytical detection greater than the threshold of interest. e This value does not include the population associated with 5 systems serving 200,000 people that measured perchlorate at 4 μg/L in at least 

one sample because the table only shows population estimates greater than each of the thresholds in the first column. 

The Agency also evaluated 

supplemental drinking water 

monitoring data for perchlorate in 

California and Massachusetts. EPA 

believes these States’ monitoring results 

are generally consistent with the results 

collected by EPA under UCMR 1. 

Perchlorate occurrence analysis from 

California and Massachusetts can be 

found online at: http:// 

www2.cdph.ca.gov/certlic/ 

drinkingwater/Pages/Perchlorate.aspx 

and http://www.mass.gov/dep/water/ 

drinking/percinfo.htm# sites 

respectively. 

2. What Were the Key Issues Raised by 

Commenters? 

EPA received comments on the 

proposed decision not to regulate 

perchlorate based on the population 

exposed above the HRL. Some 

comments objected to the Agency’s 

proposed HRL as being ‘‘inappropriately 

high’’ thereby ‘‘greatly reducing the size 

of the population predicted to be 

exposed at a level of public health 

concern * * * and significantly 

minimizing the need for regulation of 

perchlorate from an occurrence 

standpoint.’’ 

One commenter believes that, 

‘‘Approximately 4% of public water 

supplies serving 17 million Americans 

would be in exceedance of an HRL 

between 2 and 6 μg/L. This is 15 million 

more at risk individuals than currently 

estimated by the Agency.’’ 

Another commenter believes that at 

an HRL of 2 μg/L, 16.6 million would 

be exposed, and another commenter 

states that if EPA set the HRL at 5 μg/ 

L, then 5–7 times more individuals 

would be exposed above the HRL than 

at 15 μg/L. 

However, one commenter points out 

that, ‘‘An MCL of 2 μg/L could impact 

approximately 4% of public water 

systems nationally. At this level, 

regional impacts in California and Texas 

would be greater due to the higher 

geographical concentration of detections 

in those states. Yet it should be noted 

that water systems in Massachusetts, 

New Jersey and California have already 

established regulatory limits of 2 μg/L, 

5 μg/L and 6 μg/L respectively, thereby 

capping the population exposure 

potential from community drinking 

water sources in those States.’’ 

3. Numbers of Systems and Populations 

That Would Be Exposed at Levels 

Exceeding the Alternative Approaches 

the Agency Is Considering 

EPA plans to use the UCMR 1 

perchlorate data to conduct analyses to 

estimate the number of systems and 

populations served by systems that 

would be exposed to the various 

alternative HRL concentrations of 

perchlorate. Estimates will be made of 

the populations served by systems for 

which the highest reported perchlorate 

concentration exceeds the various 

threshold concentrations ranging from 1 

μg/L to 25 μg/L. One limitation to the 

UCMR 1 data is that the perchlorate 

analytical method MRL is 4 μg/L; only 

perchlorate sample detections greater 

than or equal to 4 μg/L can be 

dependably quantified and reported. 

Any perchlorate sample concentration 

with a value between 0 and 4 μg/L is 

recorded in the UCMR 1 data as a ‘‘nondetection.’’ Therefore, to estimate 

perchlorate occurrence relative to 

concentrations both above and below 

the MRL of 4 μg/L, while fully using all 

perchlorate detection and non-detection 

data, it is necessary to estimate 

occurrence using modeling techniques 

EPA is considering using a Bayesian 

hierarchical model (a form of 

probabilistic model that uses maximum 

likelihood estimation techniques) to 

estimate perchlorate occurrence and to 

estimate the uncertainty and variability 

of those occurrence estimates. For this 

modeling effort, EPA could use the basic 

assumption that the national 

distribution of perchlorate sample 

concentrations can be modeled as a 

lognormal distribution. The lognormal 

distribution is a fundamental 

probability distribution that is used 

commonly and effectively to 

characterize environmental contaminant 

occurrence. The basic characteristic of a 

lognormal distribution is that the 

logarithms of the values being evaluated 

(in this case, the perchlorate 

concentrations of UCMR 1 samples of 

drinking water) are normally 

distributed. One property of the 

lognormal distribution that makes it 

particularly well-suited to describing 

phenomena like environmental 

contaminant occurrence data is that it is 

bounded by zero on the low end and it 

reflects a ‘‘right-skewed’’ distribution— 

that is, it has a tail in the upper end— 

that is consistent with having a small 

proportion with relatively high values. 

The Bayesian model could estimate 

the number of public water systems, and 

populations served by systems, with at 

least one estimated sample detection 

greater than 1, 2, 3, 4, 5, 7, 10, 12, 15, 

17, 20, and 25 μg/L. EPA notes that 

systems or entry/sample points with at 

least one detect above the threshold may 

not expose the population to this level 

at all times. At any particular time, 

perchlorate levels may be lower or 

higher than the highest estimated 

sample detection. However, EPA 

believes this approach more closely 

reflects the short term exposure during 

life stages of concern (i.e., fetuses, preterm newborns, infants and young 

children) than does the estimated mean 

concentration of perchlorate at a system. 

EPA underscores the fact that the 

estimated total population exposed at 

thresholds that lie below the perchlorate 

MRL of 4 μg/L would be equal to, if not 

greater than, the corresponding high end 

estimate of 16.8 million people. To 

estimate the portion of the total 

population that is at a childhood life 

stage potentially exposed at these 

thresholds, EPA could use U.S. Census 

data as it did in the October 2008 FR 

notice to estimate the number of 

pregnant women potentially exposed 

above the HRL and could also estimate 

the number of infants and children 

potentially exposed above the HRL 

Perchlorate monitoring data from the 

State of Massachusetts could be used to 

help characterize the distribution of 

very low perchlorate concentration 

occurrence. Massachusetts monitoring 

uses a modified version of the EPA 

laboratory analytical method for 

perchlorate that has a MRL of 1 μg/L. 

This is the only known, state-wide 

monitoring program that uses an 

analytical method with an MRL lower 

than 4 μg/L. Bayesian hierarchical 

modeling can use the Massachusetts 

data to improve the model estimates in 

the lower concentration ranges. 

jlentini on DSKJ8SOYB1PROD with NOTICES

Federal Register / Vol. 74, No. 159 / Wednesday, August 19, 2009 / Notices 41891 

4. Request for Comment on Alternative 

Approaches 

EPA Seeks Comments on the Following 

Issues: 

a. EPA requests comment on the 

potential use of a Bayesian model to 

estimate the number of public water 

systems, and populations served by 

such systems, with at least one 

estimated sample detection greater than 

1, 2, 3, 4, 5, 7, 10, 12, 15, 17, 20, and 

25 μg/L. 

b. EPA requests comment on using 

U.S. Census data to estimate the 

portions of the population that are in 

the sensitive life stage at any one time. 

c. EPA requests comment on how the 

Agency should account for the variation 

of perchlorate levels over time in public 

water systems. EPA believes that 

estimating the number of systems, entry 

points and populations with at least one 

detection above the HRL is appropriate 

for the perchlorate regulatory 

determination because a single quarterly 

or semi-annual sample more closely 

reflects the short term exposure during 

life stages of concern (i.e., fetuses, preterm newborns, infants and young 

children). However, EPA requests 

comment on whether the Agency should 

consider other approaches such as 

estimating the number of systems, entry 

points and populations with two or 

more detections above HRL or some 

other approach. 

IV. Consideration of Studies Published 

Since EPA Adopted the NAS RfD for 

Perchlorate 

EPA’s preliminary regulatory 

determination is based on NRC’s (NRC, 

2005) recommendation to use data from 

the Greer et al. (2002) study as the basis 

for the perchlorate RfD/risk assessment. 

Since the publication of the NRC 

report, researchers have investigated 

perchlorate occurrence in humans by 

analyzing for perchlorate in urine and 

breast milk—such biomonitoring data 

has the potential to better inform EPA’s 

analysis of exposure to perchlorate 

through food and water and to provide 

insight into the possible interactions of 

other physiologic conditions (e.g., 

iodine deficiency) with perchlorate 

ingestion. EPA’s preliminary regulatory 

determination described the 

consideration of these studies, many of 

which were published after the NRC 

report (including, but not limited to, 

Blount et al. (2006 and 2007), 

Steinmaus et al. (2007), and Amitai et 

al. (2007)) (73 FR 60267–68, October 10, 

2008). 

CDC researchers published two 

biomonitoring papers using CDC’s 

2001–2002 NHANES data—the first 

study measured perchlorate in urine 

(Blount et al., 2006) and the second 

examined the relationship between 

urinary perchlorate and thyroid 

hormone levels (Blount et al., 2007). In 

the urinary biomonitoring study, the 

authors found perchlorate in all samples 

tested (2,820 survey participants ages 

six and older) and estimated a total 

daily perchlorate dose for adults (doses 

for children were not calculated). The 

median dose was about one tenth (0.066 

μg/kg/day) of the RfD, while the 95th 

percentile dose was about one third of 

the RfD (0.234 μg/kg/day). In the second 

study, which examined the relationship 

between urinary levels of perchlorate 

and blood serum levels of thyroid 

hormones, Blount et al. (2007) found 

that for women with low iodine levels 

(urinary iodide levels less than 100 μg/ 

L) urinary perchlorate is associated with 

a decrease in (a negative predictor for) 

T4 levels and an increase in (a positive 

predictor for) thyroid stimulating 

hormone levels. The perchlorate 

exposures at which this association was 

observed are lower than anticipated 

based on other studies. The study 

authors indicated that further research 

needs to be performed to confirm these 

findings. The subsequent Steinmaus 

(2007) analysis of the same NHANES 

2001–2002 epidemiological data 

concluded that thiocyanate in tobacco 

smoke and perchlorate interact in 

affecting the thyroid function in lowiodine women. The Amitai et al. study 

assessed thyroid hormone (thyroxine) 

values in newborns in different 

perchlorate exposure groups (low, high 

and very high) and found no significant 

differences. 

In studies analyzing breast milk for 

perchlorate, Pearce et al. (2007) and 

Kirk et al. (2005, 2007) all found 

perchlorate in study samples. The 

objective of the Pearce et al. (2007) 

study was ‘‘to determine whether breast 

milk iodine concentrations in Bostonarea women are adequate for infant 

nutrition, and whether breast milk 

iodine concentrations may be associated 

with environmental perchlorate or 

cigarette smoke exposure.’’ Pearce et al. 

(2007) did not find a significant 

correlation with either breast milk 

perchlorate or urinary perchlorate levels 

with breast milk iodine concentrations. 

The objective of the Kirk et al. (2005) 

study was to determine the amount of 

perchlorate to which children are 

exposed by measuring perchlorate and 

iodide levels in cow and human breast 

milk and then comparing these numbers 

to corresponding levels of perchlorate in 

drinking water in the area. Kirk et al. 

(2005) did not find a correlation 

between the levels of perchlorate in 

breast milk and perchlorate in drinking 

water, but speculated that there was a 

correlation between higher levels of 

perchlorate and lower levels of iodine in 

breast milk. The objective of the Kirk et 

al. (2007) study was to determine the 

variability of perchlorate, thiocyanate, 

and iodide in breast milk in serially 

collected samples (6 samples on each of 

the 3 study days) involving 10 women. 

The authors concluded that ‘‘Iodine 

intake may be inadequate in a 

significant fraction of this study 

population. Perchlorate and thiocyanate 

appear to be common in human milk. 

The role of these chemicals in reducing 

breast milk iodide is in need of further 

investigation.’’ 

Blount et al. (2007) suggested breast 

milk as an excretion pathway and 

Dasgupta et al. (2008) compared a 

woman’s daily intake of iodine and 

perchlorate with the concentrations of 

each in her breast milk. The Dasgupta et 

al. study found that a higher proportion 

of perchlorate enters the breast milk 

compared with a small proportion of 

iodine. 

Of those commenters that provided 

detailed comments to the October 2008 

FR notice, many commenters believe 

that EPA’s RfD is not adequately 

protective of human health. One 

commenter stated that ‘‘[T]he EPA 

reference dose for perchlorate is based 

on data from Greer et al. (2002) that 

observed the inhibition of radioiodide 

uptake. Ginsberg and Rice (2005) 

identified several problems with the 

Greer et al. study that suggest the need 

for reevaluation of the value that serves 

as the foundation for regulatory 

decision-making,’’ and that, ‘‘* * * the 

results of the Blount study more closely 

reflect our understanding of the 

biological and toxicological processes 

pertaining to thyroid homeostasis, both 

in terms of thyroid hormone variability 

and the role of iodine.’’ The commenter 

‘‘[S]trongly recommends that the CDC 

data analyzed in the study of Blount et 

al. (2006) and Blount et al. (2007) be 

used as the basis for the derivation of a 

new reference dose.’’ 

Other commenters agree, stating that 

the use of the Greer et al. (2002) study 

‘‘* * * is based on a limited clinical 

study of short duration and small 

sample size not representative of the 

variability in the human population,’’ 

and the ‘‘[U]se of these limited data to 

calculate a regulatory trigger level has 

been widely criticized as inadequate 

* * * and no longer reflects the best 

available data.’’ 

Another commenter believes that 

‘‘[A]dditional important data on 

pregnant women and their offspring 

jlentini on DSKJ8SOYB1PROD with NOTICES

41892 Federal Register / Vol. 74, No. 159 / Wednesday, August 19, 2009 / Notices 

have become available since the time of 

development of the EPA RfD in 2005 

which would necessitate a 

reconsideration of the existing value 

* * * in addition EPA has discussed 

other data relevant to deriving an 

updated RfD in this Federal Register 

notice including Amitai et al., 2007, 

Blount et al., 2006, and studies 

discussing PBPK models.’’ 

One commenter concludes by stating, 

‘‘* * * [T]hat EPA has based its 

argument for not regulating perchlorate 

contamination in public water systems 

on a literature that is both limited and 

ill focused. We believe that EPA has not 

performed a sufficiently ‘thorough 

review’ of the literature, that it has 

omitted important information, and that 

it has failed to perform its due diligence 

in the interpretation and analysis of the 

information that it did present. To 

correct this, EPA must employ the CDC 

study (Blount et al., 2006a) as the point 

of departure for RfD determination, and 

must focus on the neonate and infant as 

the most sensitive population.’’ 

One commenter does not believe that 

additional analysis is warranted and 

that EPA should issue a final 

determination as soon as possible, 

stating that ‘‘EPA has an extraordinary 

wealth of comprehensive, authoritative 

scientific information relating to 

perchlorate’s health effects, 

supplemented by extensive occurrence 

and exposure data. The Agency is 

therefore exceptionally well-positioned 

to issue a well-considered regulatory 

determination.’’ The commenter 

continues by stating, 

* * * EPA has ample scientific and 

technical data to make a final determination 

on or before the planned date of December 

2008 * * *. [P]erchlorate is one of the most 

well-studied chemicals with detailed 

information on the mechanism of action, 

dose-response, and health effects. This issue 

also is not new. EPA released its first draft 

risk assessment on perchlorate in 1998, 

followed by a second in 2002. The 2005 NAS 

report was a comprehensive review of the 

science. The animal and human studies that 

have been published since the NAS report 

reduce the uncertainty and reinforce the NAS 

panel’s finding that there will not be any 

adverse health effects from perchlorate at 

environmentally-relevant concentrations. 

New studies published since the NAS 

report increase the weight of evidence that 

the current RfD protects human health 

including the most sensitive members of our 

population. In addition, testimony by 

Congressional members and witnesses alike 

have discussed the lengthy amount of time 

that EPA has spent studying the health 

effects, urging the agency to issue a 

determination as soon as practicable. We join 

them in urging EPA to issue the final 

determination promptly. 

An additional key scientific issue was 

raised by EPA’s OIG in the report 

released for public comment ‘‘OIG 

Scientific Analysis of Perchlorate 

(External Review Draft)’’ (EPA, 2008g). 

The report states, 

The OIG Analysis concludes that a single 

chemical risk assessment of perchlorate is 

not sufficient to assess and characterize the 

combined human health risk from all four 

NIS stressors, (i.e., thiocyanate, nitrate, 

perchlorate and lack of iodide) and that 

* * * Only a cumulative risk assessment can 

fully characterize the nature and sources of 

risk affecting this public health issue. 

Furthermore, a cumulative risk assessment 

allows an informed environmental decision 

to be made on how to mitigate the risk 

effectively. 

The report goes on to say, 

Potentially lowering the perchlorate 

drinking water limit from 24.5 ppb to 6 ppb 

does not provide a meaningful opportunity to 

lower the public’s risk. By contrast, 

addressing moderate and mild iodide 

deficiency occurring in about 29% of the U.S. 

pregnant and nursing population appears to 

be the most effective approach of increasing 

TIU [total iodide uptake] to healthy levels 

during pregnancy and nursing, thereby 

reducing the frequency and severity of 

permanent mental deficits in children. 

The draft report, and comments 

submitted by EPA’s Office of Water and 

Office of Research and Development, 

can be found in the Docket to this 

notice. 

EPA agrees that additional important 

data have become available since the 

RfD was derived in 2005. However, EPA 

has evaluated the new data and has 

decided to make the regulatory 

determination based upon the current 

RfD. EPA will continue to evaluate any 

new perchlorate data to determine its 

relevance to the regulatory 

determination in accordance with the 

SDWA. 

V. Next Steps 

The Agency will consider the 

information and comments submitted in 

response to this supplemental notice, as 

well as comments received on the 

October 10, 2008, FR notice, and all 

peer review comments before issuing a 

final regulatory determination for 

perchlorate and intends to do so as 

expeditiously as possible. EPA believes 

that the alternative analyses presented 

in this notice could lead the Agency to 

make a determination to regulate 

perchlorate. 

VI. References 

Amitai Y, Winston G, Sack J, Wasser J, Lewis 

M, Blount BC, Valentin-Blasini L, Fisher 

N, Israeli A, and Leventhal A. (2007). 

Gestational exposure to high perchlorate 

concentrations in drinking water and 

neonatal thyroxine levels. Thyroid. 17(9): 

843–850. 

Blount, B.C., J.L. Pirkle, J.D. Osterloh, L. 

Valentı ́n-Blasini, and K.L. Caldwell. 

2006. Urinary perchlorate and thyroid 

hormone levels in adolescent and adult 

men and women living in the United 

States. Environmental Health 

Perspectives. Vol. 114, No. 12. pp. 1865– 

1871. 

Blount, B.C., L. Valentı ́n-Blasini, J.D. 

Osterloh, J.P. Mauldin, and J.L. Pirkle. 

2007. Perchlorate Exposure of the US 

Population, 2001–2002. J. Exposure Sci. 

Environ. Epidemiol. (2007) 17, 400–407. 

Dasgupta, P.K., A.B. Kirk, J.V. Dyke, and 

S.I. Ohira. 2008. Intake of Iodine and 

Perchlorate Excretion in Human Milk. 

Environ. Sci. Technol. Advance online 

publication accessed September 18, 

2008. 

DeWoskin R. and C. Thompson. 2008. 

Renal clearance parameters for PBPK 

model analysis of early lifestage 

differences in the disposition of 

environmental toxicants. Regul Toxicol 

Pharmacol. 2008 Jun;51(1):66–86. 

Ginsberg G, Rice D, 2005. The NAS 

Perchlorate Review: Questions Remain 

about the Perchlorate RfD. Environ 

Health Perspectives 113(9):1117–1119. 

Greer, M.A., G. Goodman, R.C. Pleuss, and 

S.E. Greer. 2002. Health effect 

assessment for environmental 

perchlorate contamination: the dose 

response for inhibition of thyroidal 

radioiodide uptake in humans. Environ 

Health Perspect Vol. 110. pp. 927–937. 

Kahn, H.D., and K. Stralka. 2008. Estimated 

daily average per capita water ingestion 

by child and adult age categories based 

on USDA’s 1994–1996 and 1998 

continuing survey of food intakes by 

individuals. Journal of Exposure Science 

and Environmental Epidemiology (2009) 

19(4):396–404. 

Kirk, A.B., P.K. Martinelango, K. Tian, A. 

Dutta, E.E. Smith, and P.K. Dasgupta. 

2005. Perchlorate and iodide in dairy 

and breast milk. Environmental Science 

and Technology. Vol. 39, No. 7. pp. 

2011–2017. 

Kirk, A.B., J.V. Dyke, C.F. Martin, and P.K. 

Dasgupta. 2007. Temporal patterns in 

perchlorate, thiocyanate and iodide 

excretion in human milk. Environ Health 

Perspect Online Vol. 115, No. 2. pp. 182– 

186. 

Life Sciences Research Office, Federation 

of American Societies for Experimental 

Biology Prepared for the Interagency 

Board for Nutrition Monitoring and 

Related Research. 1995. Third Report on 

Nutrition Monitoring in the United 

States: Volume 1. U.S. Government 

Printing Office, Washington DC. 

Murray, C.W III, S.K. Egan, H. Kim, N. 

Beru, P.M. Bolger. 2008. US Food and 

Drug Administration’s Total Diet Study: 

Dietary Intake of Perchlorate and Iodine. 

Journal of Exposure Science and 

Environmental Epidemiology, advance 

online publication January 2, 2008. 

National Research Council (NRC). 2005. 

Health Implications of Perchlorate 

Ingestion. National Academies Press, 

jlentini on DSKJ8SOYB1PROD with NOTICES

Federal Register / Vol. 74, No. 159 / Wednesday, August 19, 2009 / Notices 41893 

Board on Environmental Studies and 

Toxicology. January 2005. 276 p. 

Pearce, E.N., A.M. Leung, B.C. Blount, H.R. 

Bazrafshan, X. He, S. Pino, L. ValentinBlasini, L.E. Braverman. 2007. Breast 

milk iodine and perchlorate 

concentrations in lactating Boston-area 

women. J Clin Endocrin Metab Vol. 92, 

No. 5, pp. 1673–1677 

Schier, J.G., A.F. Wolkin, L.ValentinBlasini, M.G. Belson, S.M. Kieszak, C.S. 

Rubin, B.C. Blount. Journal of Exposure 

Science and Environmental 

Epidemiology, advance online 

publication 18 March 2009; doi: 10.1038/ 

jes.2009.18. 

Steinmaus, C., M.D. Miller, R. Howd. 2007. 

Impact of smoking and thiocyanate on 

perchlorate and thyroid hormone 

associations in the 2001–2002 National 

Health and Nutrition Examination 

Survey. Environ Health Perspect 

115(9):1333–8. 

USEPA. 1995. Guidance for Risk 

Characterization. Science Policy Council, 

February, 1995. 

USEPA. 2004. Estimated Per Capita Water 

Ingestion and Body Weight in the United 

States—An Update. Office of Science 

and Technology, Washington, DC; EPA/ 

822/R–00–001. 

USEPA. 2005. Guidance on Selecting Age 

Groups for Monitoring and Assessing 

Childhood Exposures to Environmental 

Contaminants. National Center for 

Environmental Assessment, Washington, 

DC; EPA/630/P–03/003F. 

USEPA. 2008a. Drinking Water: 

Preliminary Regulatory Determination on 

Perchlorate, Federal Register, Vol. 73, 

No. 198. p. 60262, October 10, 2008. 

USEPA. 2008b. Inhibition of the SodiumIodide Symporter by Perchlorate: An 

Evaluation of Lifestage Sensitivity Using 

Physiologically-Based Pharmacokinetic 

(PBPK) Modeling. Office of Research and 

Development, Washington, DC; EPA/ 

600/R–08/106A. 

USEPA. 2008c. External letter peer review 

of EPA’s draft report, Inhibition of the 

Sodium-Iodide Symporter by 

Perchlorate: An Evaluation of Lifestage 

Sensitivity Using Physiologically-based 

Pharmacokinetic (PBPK) Modeling. 

National Center for Environmental 

Assessment, Washington, DC; November 

12, 2008. 

USEPA. 2008d. Interim Drinking Water 

Health Advisory for Perchlorate. Office 

of Science and Technology, Washington, 

DC; EPA 822–R–08–025. 

USEPA. 2008e. Comment Response 

Summary Report, Peer Review of 

Drinking Water Health Advisory for 

Perchlorate. Office of Science and 

Technology, Washington, DC; December 

2008. 

USEPA. 2008f. Child-Specific Exposure 

Factors Handbook. National Center for 

Environmental Assessment, Washington, 

DC; EPA/600/R–06/096F. 

USEPA. 2008g. Scientific Analysis of 

Perchlorate (External Review Draft). 

Office of Inspector General, Washington, 

DC; Assignment No. 2008–0010. 

Dated: August 5, 2009. 

Peter S. Silva, 

Assistant Administrator, Office of Water. 

[FR Doc. E9–19507 Filed 8–18–09; 8:45 am] 

BILLING CODE 6560–50–P 

ENVIRONMENTAL PROTECTION 

AGENCY 

[EPA–HQ–OPPT–2009–0496; FRL–8429–5] 

National Advisory Committee for Acute 

Exposure Guideline Levels for 

Hazardous Substances; Notice of 

Public Meeting 

AGENCY: Environmental Protection 


Agency (EPA). 


ACTION: Notice. 


SUMMARY: A meeting of the National 

Advisory Committee for Acute Exposure 

Guideline Levels for Hazardous 

Substances (NAC/AEGL Committee) 

will be held on September 9–11, 2009, 

in Research Triangle Park, NC. At this 

meeting, the NAC/AEGL Committee will 

address, as time permits, the various 

aspects of the acute toxicity and the 

development of Acute Exposure 

Guideline Levels (AEGLs) for the 

following chemicals: Cadmium; 

carbofuran; carbon dioxide; dichlorovos; 

dicrotophos; dimethyl phosphate; 

fenamiphos; gasoline; hydrogen 

selenide; lead; methamidophos; methyl 

iodide; mevinphos; monocrotophos; 

nerve agent GB; phosgene; 

phosphamidon; red phosphorus; ricin; 

tetrachloroethylene; 1,1,1-

trichloroethylene; and 

trimethylphosphite. 

DATES: A meeting of the NAC/AEGL 

Committee will be held from 10 a.m. to 

5 p.m. on September 9, 2009; from 8 

a.m. to 5 p.m. on September 10, 2009; 

and from 8 a.m. to noon on September 

11, 2009. 

ADDRESSES: The meeting will be held at 

the EPA Main Campus, 109 T.W. 

Alexander Dr., Research Triangle Park, 

NC 27711. 

FOR FURTHER INFORMATION CONTACT: Paul 

S. Tobin, Designated Federal Officer 

(DFO), Risk Assessment Division 

(7403M), Office of Pollution Prevention 

and Toxics, 1200 Pennsylvania Ave., 

NW., Washington, DC 20460–0001; 

telephone number: (202) 564–8557; email address: tobin.paul@epa.gov. 

To request accommodation of a 

disability, please contact the DFO, 

preferably at least 10 days prior to the 

meeting, to give EPA as much time as 

possible to process your request. 

SUPPLEMENTARY INFORMATION: 

I. General Information 

A. Does this Action Apply to Me? 

This action is directed to the public 

in general. This action may be of 

particular interest to anyone who may 

be affected if the AEGL values are 

adopted by government agencies for 

emergency planning, prevention, or 

response programs, such as EPA’s Risk 

Management Program under the Clean 

Air Act and Amendments Section 112r. 

It is possible that other Federal agencies 

besides EPA, as well as State agencies 

and private organizations, may adopt 

the AEGL values for their programs. As 

such, the Agency has not attempted to 

describe all the specific entities that 

may be affected by this action. If you 

have any questions regarding the 

applicability of this action to a 

particular entity, consult the person 

listed under FOR FURTHER INFORMATION 

CONTACT. 

B. How Can I Get Copies of this 

Document and Other Related 

Information? 

1. Docket. EPA has established a 

docket for this action under docket 

identification (ID) number EPA–HQ– 

OPPT–2009–0496. All documents in the 

docket are listed in the docket index 

available at http://www.regulations.gov. 

Although listed in the index, some 

information is not publicly available, 

e.g., Confidential Business Information 

(CBI) or other information whose 

disclosure is restricted by statute. 

Certain other material, such as 

copyrighted material, will be publicly 

available only in hard copy. Publicly 

available docket materials are available 

electronically at http:// 

www.regulations.gov, or, if only 

available in hard copy, at the OPPT 

Docket. The OPPT Docket is located in 

the EPA Docket Center (EPA/DC) at Rm. 

3334, EPA West Bldg., 1301 

Constitution Ave., NW., Washington, 

DC. The EPA/DC Public Reading Room 

hours of operation are 8:30 a.m. to 4:30 

p.m., Monday through Friday, excluding 

legal holidays. The telephone number of 

the EPA/DC Public Reading Room is 

(202) 566–1744, and the telephone 

number for the OPPT Docket is (202) 

566–0280. Docket visitors are required 

to show photographic identification, 

pass through a metal detector, and sign 

the EPA visitor log. All visitor bags are 

processed through an X-ray machine 

and subject to search. Visitors will be 

provided an EPA/DC badge that must be 

visible at all times in the building and 

returned upon departure. 

2. Electronic access. You may access 

this Federal Register document 

electronically through the EPA Internet