DRAFT AGENDA

FIFRA SCIENTIFIC ADVISORY PANEL (SAP)

OPEN MEETING

April 26 – 29, 2010

FIFRA SAP WEB SITE http://www.epa.gov/scipoly/sap/

OPP Docket Telephone: (703) 305-5805

Docket Number: EPA-HQ-OPP-2010-0125

The Hamilton Crowne Plaza Hotel

The Hamilton Ballroom

1001 14th Street, NW

Washington, DC 20005

202-682-0111

Reevaluation of the Human Health Effects of Atrazine: Review of Experimental 

Animal and In Vitro Studies and Drinking Water Monitoring Frequency

Please note that all times are approximate (see note at end of Agenda).

Monday, April 26, 2010

1:00 P.M. Opening of Meeting and Administrative Procedures – Joseph Bailey, 

Designated Federal Official, Office of Science Coordination and Policy, 

EPA

1:05 P.M. Introduction and Identification of Panel Members – Kenneth Portier, 

Ph.D., FIFRA Scientific Advisory Panel Session Chair

1:15 P.M. Welcome and Opening Remarks – Steven Bradbury, Ph.D., Acting 

Director, Office of Pesticide Programs, EPA

1:25 P.M. Welcome and Introductions – Tina Levine, Ph.D., Director, Health Effects 

Division, Office of Pesticide Programs, EPA

1:30 P.M. EPA Presentation – Experimental Animal and In Vivo Studies

3:00 P.M. Break

3:15 P.M. Experimental Animal and In Vivo Studies Presentation Continued

4:30 P.M. EPA Presentation – Drinking Water Monitoring Frequency

5:30 P.M. Adjourn
2

DRAFT AGENDA

FIFRA SCIENTIFIC ADVISORY PANEL (SAP)

OPEN MEETING

April 26 – 29, 2010

FIFRA SAP WEB SITE http://www.epa.gov/scipoly/sap/

OPP Docket Telephone: (703) 305-5805

Docket Number: EPA-HQ-OPP-2010-0125

The Hamilton Crowne Plaza Hotel

The Hamilton Ballroom

1001 14th Street, NW

Washington, DC 20005

202-682-0111

Reevaluation of the Human Health Effects of Atrazine: Review of Experimental 

Animal and In Vitro Studies and Drinking Water Monitoring Frequency

Please note that all times are approximate (see note at end of Agenda).

Tuesday, April 27, 2010

8:30 A.M. Opening of Meeting and Administrative Procedures – Joseph Bailey, 

Designated Federal Official, Office of Science Coordination and Policy, 

EPA

8:35 A.M. Introduction and Identification of Panel Members – Kenneth Portier, 

Ph.D., FIFRA Scientific Advisory Panel Session Chair

8:45 A.M. Follow-up from Previous Day’s Presentations

9:15 A.M. Public Comments

10:30 A.M. Break

10:45 A.M. Public Comments

12:15 P.M. Lunch Break

1:30 P.M. Charge to Panel – Question 1

In Vivo & In Vitro Experimental Toxicology in Mammals

In 2003, the human health risk assessment was based on a mode of action in which 

exposure to atrazine leads to a reduced release of gonadotropin releasing hormone 

(GnRH) from the hypothalamus thereby lessening the afternoon pituitary luteinizing 

hormone (LH) surge in female Sprague Dawley rats. As a result, the estrus cycle 

lengthens. This, in turn, leads to increased estrogen levels and an increased incidence 

of mammary tumors in female Sprague Dawley rats. EPA determined that atrazine’s 

cancer mode of action (i.e., premature reproductive aging) in the Sprague-Dawley rat is 

not likely to be operative in humans (a conclusion consistent with the SAP 

recommendation in 2000). The Agency will be evaluating the cancer classification 
3

further as the experimental toxicology data are integrated with the epidemiology 

literature; new experimental toxicology studies (Section 3.6 of the draft issue paper) do 

not suggest a change to the Agency’s previous conclusion that atrazine is “not likely to 

be carcinogenic to humans.” 

Although the cancer mode of action may not be operative in humans, it is not 

unreasonable to assume that atrazine might cause adverse effects on hypothalamicpituitary function in humans. Thus, the same endocrine perturbations that induce 

tumors in rats may play a role in at least some reproductive/developmental effects (not 

associated with reproductive aging) that may be relevant to humans. Accordingly, the 

Agency identified disruption of estrous cyclicity and delays in puberty onset (males and 

females) occurring as a consequence of disruptions to the hypothalamic-pituitarygonadal (HPG) axis as the critical endpoints of concern (Sections 2.0 & 3.2 of the draft 

issue paper). 

The Agency continues to believe that this disruption of the HPG axis is critical to affecting 

estrous cyclicity and delayed puberty onset. However, as discussed in Questions 1.2-1.6

(See Figure 3 of the draft issue paper), new information has been published that indicates

a more expanded understanding of how atrazine may perturb the pathway leading to

reproductive effects. These new data indicate that atrazine disrupts the hypothalamicpituitary-adrenal (HPA) axis altering the central nervous system’s control of the pituitary 

and adrenal which, in turn, disrupts the HPG axis. Furthermore, a hypothesis for a direct

effect of atrazine on the adrenal cortex and the gonads which may impact steroidogenesis 

directly is also supported by the available data.

Question 1.1 – With the caveat that the review of the epidemiological literature is still 

on-going, please comment on the Agency’s preliminary conclusion that new 

experimental data from in vitro and in vivo laboratory animal studies do not support a 

change in the conclusions from the 2003 risk assessment that atrazine is unlikely to be 

a human carcinogen.

2:15 P.M. Charge to Panel – Question 1(continued)

Question 1.2 – Based on an evaluation of the studies examining the mode of action of 

atrazine on neuroendocrine function (Section 3.2 of the draft issue paper), the Agency 

has preliminarily concluded that atrazine affects both the HPG axis and the HPA axis. 

With respect to the temporal concordance, recent studies show that atrazine induces a 

rapid (within minutes) increase in ACTH and adrenal cortical hormones (corticosterone 

and progesterone) in both male and female rats (Fraites et al., 2009; Laws et al., 2009; 

Pruett et al., 2009), while changes in the HPG axis, such as the suppression of the LH 

surge, may take up to 2-3 days (Cooper et al., 2009). This sequence of HPA alterations

followed by HPG changes indicates that the suppression of the surge may be, in part, 

mediated by activation of the HPA axis (i.e., a corticosterone suppression of the GnRH 

and LH release). In addition, with respect to dose-response concordance, atrazineinduced increases in ACTH, corticosterone and adrenal progesterone are seen 

following a single dose of atrazine (50 mg/kg). In contrast, the HPG is not altered 

following a single dose up to 200 mg/kg. However, when treated for multiple days, the 
4

dose necessary to alter the HPA axis is lower than or equal to the one needed to affect 

the HPG axis. 

Please comment on the Agency’s preliminary hypothesis for the mode of action 

involving atrazine’s alteration of both the HPA and HPG axes. Does the document 

adequately and clearly describe the hypothesis in the context of a “toxicity pathway” (i.e. 

cellular response pathways that, when sufficiently perturbed, are expected to result in 

adverse health effects)? Does the document clearly describe the data used to test the 

proposed hypothesis? To what extent do the available data establish key events in the 

proposed mode of action hypothesis? What are the strengths and limitations of the data 

available on this hypothesis? 

Please include in your comments a discussion of the Agency’s interpretations of the 

data linking the initial perturbations in HPA axis to changes in the HPG axis. 

Please comment on the evidence that the initial perturbations in the HPA axis may lead 

to impairment in reproductive function and/or developmental consequences. Which 

event(s) is/are viewed as critical in leading to health consequences? Are there data on 

other substances that would inform this question?

3:15 P.M. Break

3:30 P.M. Charge to Panel – Question 1 (continued)

Question 1.3 – The Agency has preliminarily concluded that atrazine directly targets 

cells within the HPA axis (Sections 3.2 & 3.3.2.3 of the draft issue paper) and that the 

increased activity of the adrenal axis does not reflect nonspecific stress. Evidence for 

this conclusion is based on the following observations. 

a. Several studies report increased adrenocorticotropic hormone (ACTH) 

and corticosterone levels immediately following a single exposure to 

atrazine and its two metabolites (deisopropyl-atrazine, DIA; deethylatrazine, DEA) but not diamino-s-chlorotriazine (DACT; Laws et al., 

2009; Fraites et al., 2009; Pruett et al., 2009). 

b. A single intravenous administration of DEA in vivo (Fraites et al., 

2009) also causes an immediate increase in ACTH and adrenal 

hormone release, indicating that a chlorotriazine-induced 

gastrointestinal distress is not driving the hormonal response.

c. The adrenal corticosterone response to continued oral exposure to 

atrazine did not habituate in rats (Fraites et al., 2009; Laws et al., 

2009) or mice (Pruett et al., 2009). 

d. Although, atrazine induced a rapid increase in ACTH, prolactin 

secretion was not affected in the same animals (Laws et al., 2009). 

This is unusual in that an increase in both ACTH and prolactin are 

typically observed in response to a number of physiological and 

psychological stressors.
5

Please comment on the extent to which the available evidence supports the preliminary 

conclusion that atrazine and its intermediate metabolites (DIA and DEA) induce 

changes in the HPA axis as a result of a direct action on the HPA tissue and such 

changes are not due to a generalized or non-specific stress response. Are there data 

on other substances that would support this conclusion?

4:15 P.M. Charge to Panel – Question 1 (continued)

Question 1.4 – Based on a review of in vitro studies evaluating the effects of atrazine 

on estrogen production, the Agency has preliminarily concluded that atrazine does not 

have a direct effect on the catalytic activity of aromatase. However, with continued 

exposure (> 24 hrs) atrazine can cause increased estrone and estradiol production in 

the H295R and JEG-3 cell lines (Sanderson et al., 2000; Laville 2006; Higley et al., 

2010). These changes in estrogen production have been associated with increased 

cAMP and CYP19 mRNA (Sanderson et al., 2000, 2001) that are part of a complex 

mode of action through which atrazine up-regulates the gene expression of aromatase 

and possibly other enzymes within the steroidogenic pathway (Section 3.3.2.3 & Figure 

3, Arrow 7of the draft issue paper). The hypothesis that atrazine alters multiple steroids 

is supported by increased testosterone concentrations in H295R cells following 

exposure to atrazine (Higley et al., 2010), and in vitro studies demonstrating that 

atrazine affects a number of signal transduction pathways and/or transcription factors in 

a variety of cell lines (Suzawa and Ingraham, 2008; Albanito et al., 2008). Upregulation of the expression of a group of major steroidogenic genes has been observed 

in JEG-3 cells (Suzawa and Ingraham, 2008). In vivo, there is little evidence that 

atrazine alters aromatase per se (Modic, 2004) and the evidence associating atrazine 

exposures to increases in serum estrogens appears to be related to a general increase 

in gonadal and adrenal progesterone and androstanedione (Modic 2004; Laws et al., 

2009). 

Please comment on the extent that the available data do or do not support the Agency’s 

preliminary conclusion that atrazine has a general stimulatory effect on steroidogenesis, 

as opposed to a direct effect on aromatase.

5:00 P.M. Adjourn
6

DRAFT AGENDA

FIFRA SCIENTIFIC ADVISORY PANEL (SAP)

OPEN MEETING

April 26 – 29, 2010

FIFRA SAP WEB SITE http://www.epa.gov/scipoly/sap/

OPP Docket Telephone: (703) 305-5805

Docket Number: EPA-HQ-OPP-2010-0125

The Hamilton Crowne Plaza Hotel

The Hamilton Ballroom

1001 14th Street, NW

Washington, DC 20005

202-682-0111

Reevaluation of the Human Health Effects of Atrazine: Review of Experimental 

Animal and In Vitro Studies and Drinking Water Monitoring Frequency

Please note that all times are approximate (see note at end of Agenda).

Wednesday, April 28, 2010

8:30 A.M. Opening of Meeting and Administrative Procedures – Joseph Bailey, 

Designated Federal Official, Office of Science Coordination and Policy, 

EPA

8:35 A.M. Introduction and Identification of Panel Members – Kenneth Portier, 

Ph.D., FIFRA Scientific Advisory Panel Session Chair

8:45 A.M. Charge to Panel – Question 1 (continued)

Question 1.5 – A series of studies evaluating the effect of either peripubertal or 

gestational exposure of atrazine in the male rat indicate that atrazine decreases 

testosterone concentrations and may lower androgen dependent tissue weights but that 

it has little effect on basal LH secretion in the male. This response generally occurs at 

doses of 50 mg/kg and above. In contrast, atrazine in vitro has been found to 

consistently increase steroid hormone production. Thus, there is an apparent 

discrepancy between the in vivo and in vitro data. However, our understanding of the 

interplay between the adrenal and the gonadal axes may provide an explanation. At 

the doses used in the in vivo studies, atrazine induces an activation of the adrenal axis 

(increased ACTH and corticosterone) and the increase in corticosterone does not 

habituate (i.e., it does not lessen with repeated dosing). There are a number of studies 

in the literature demonstrating that prolonged corticosterone stimulation will impair 

testosterone production by a direct action on steroidogenesis in the Leydig cells. 

Therefore, the in vivo effects on testosterone synthesis are likely the result of an adrenal 

hormone-mediated down regulation of HPG axis (through corticotropin releasing 
7

hormone [CRH] modulation of GnRH pulsatility) or directly on the testis (through a 

glucocorticoid receptor mediated change in steroidogenesis). 

Please comment on the degree to which the proposed mode of action (Figure 3 of the 

draft issue paper) provides a biologically plausible explanation for the decrease in serum

and testicular testosterone identified in the in vivo studies. Please comment on the extent 

that the available data do or do not support this hypothesis.

10:00 A.M. Break

10:15 A.M. Charge to Panel – Question 1(continued)

Question 1.6 - Based on a review of the neurotoxicity studies (Section 3.4 of the draft 

issue paper), the Agency has preliminarily concluded that several recent studies 

provided further support for the concern that dopaminergic neurotransmission may be 

affected by atrazine, a concern that was raised by studies prior to 2003. However, the 

Agency has also concluded that several aspects of these studies of the dopaminergic 

neuronal pathways, in particular the changes noted in stereological evaluations and the 

observed changes in behavior, should be considered as preliminary findings. This 

conclusion is based on the notable limitations identified in the data including: (1) lack of 

clear dose-response relationships, (2) lack of inclusion of suitable positive controls to 

confirm the competency and reliability of the procedures utilized in examining 

dopaminergic systems in the brain, (3) limited data to corroborate stereological findings, 

(4) limited or no supporting histological and behavioral assessments, and (5) no 

consideration of the potential role of the HPA axis (e.g. alterations in corticosterone). 

EPA has further determined that two non-dopaminergic neurotoxicity studies--one on 

brain somatostatinergic systems and the other on neurobehavior in mice -- also have 

significant limitations (e.g., lack of details on source and purity of atrazine, and age and 

body weights of the mice; poor quality of amino cupric silver staining photomicrographs; 

limited presentation of reverse-transcriptase polymerase chain results; lack of data to 

corroborate conclusion of neuronal degeneration; reference citations did not support 

statements made in the text; no explanation of biological plausibility of alterations in 

somatostatinergic receptor subtypes; inappropriate statistical evaluation of data (litter 

vs. pup); discrepancies in number of pups examined for behavioral endpoints, and lack 

of objective and validated behavioral tests). Please comment on these preliminary 

conclusions regarding the neurotoxicity findings. 

The Agency has preliminarily concluded that the available studies indicate that the 

neurotoxicity endpoints examined are not more sensitive than those evaluated for

neuroendocrine function following atrazine exposure (e.g., attenuation of LH surge and

estrous cycle disruptions in female Sprague-Dawley rats which form the basis for the 

current chronic RfD). In addition, the Agency has concluded that there is no association

between atrazine exposure and development of Parkinson’s Disease on the basis of nonspecificity of effects on brain dopaminergic systems, lack of histological and behavioral

features characteristic of Parkinson’s Disease, and results of epidemiological studies. 

Please comment on this preliminary conclusion.

11:00 A.M. Charge to Panel – Question 1(continued)
8

Question 1.7 – Based on a review of two studies of the potential effects of atrazine on 

the prostate (Section 3.3.2.2 of the draft issue paper), the Agency has concluded that 

the results of the Rayner et al. (2007) study of pregnant rats treated during gestation 

support previous observations (Stoker et al., 1999) that atrazine treatment to the rat 

dam either perinatally or early postnatally can increase prostate weights (due to an 

increase in inflammatory infiltrate) in the male offspring. This effect on the offspring was 

shown to be due to a suppression of prolactin in the atrazine-exposed dams during 

lactation, and is consistent with the mode of action of atrazine on neuroendocrine 

function. The Agency also preliminarily concluded that further research is needed to 

provide more convincing evidence that atrazine-mediated suppression of prostate 

cancer in the probasin/SV40T antigen transgenic rat (androgen-dependent prostate 

cancer rodent model) may possibly be due to caloric restriction rather than endocrinerelated as postulated by Kandori et al. (2005). Please comment on these preliminary 

conclusions regarding the recent prostate findings.

Please comment on the extent to which the available data support the proposed mode of 

action for prostatitis and the appropriateness of the rodent model in the context of human

health.

12:00 noon Lunch

1:15 P.M. Charge to Panel – Question 1 (continued)

Question 1.8 – Based on data obtained in studies to assess the effects of atrazine on 

the immune system following developmental and adult exposure, as well as in vitro

mechanistic studies, EPA concluded that atrazine has the potential to affect the immune 

system (Section 3.5 of the draft issue paper). However, the Agency has also concluded 

that underlying mechanisms of atrazine-mediated immunotoxicity and its relevance to 

potential adverse health effects in humans are still not thoroughly understood. It is well 

established that products of the endocrine system modulate immune function. 

However, adult rodent studies have not determined whether immune system effects are 

caused by direct effects of atrazine and/or its metabolites or whether they are the result 

of modulated endocrine hormone production, which in turn affects immune cells. Two 

published studies indicate that exposure to atrazine during immune system 

development may result in altered immune function in offspring, although no 

conclusions were drawn on the potential adversity of the effects, because 

immunosuppression was observed in one study and immunoenhancement was 

observed in the other. Please comment on potential explanations for the disparate 

findings reported by Rooney et al. and Rowe et al. Many immunotoxicologists consider 

immunomodulation, i.e., suppression or enhancement of immune function, as a 

potentially adverse alteration of homeostasis, because both have been associated with 

disease states. Thus, while the results Rooney et al. and Rowe et al. may appear to be 

contradictory, together the data indicate unintended immunomodulation at 

approximately the same dose in two species. Please comment on characterizing the 

effects of gestational atrazine exposure as immunomodulation, when describing the 

immunotoxicological outcome of developmental immunotoxicity studies.

Appendix B of the draft issue paper describes experiments conducted by EPA scientists 

on the potential developmental immunotoxicity of atrazine. The results of the 
9

experiments provide conflicting results. Additional studies did not provide a suitable 

explanation of the differences. The Agency believes both sets of data are of high 

quality. However, in the context of hazard assessment, such differences are difficult to 

interpret. Please comment on the information contained in Appendix B and provide 

suggestions for interpreting such data as part of the atrazine re-evaluation.

The available data do not indicate that atrazine-induced immunotoxicity is a more 

sensitive endpoint than the atrazine-induced effects on neuroendocrine function, (e.g.,

attenuation of LH surge and estrous cycle disruptions which form the basis for the current 

chronic RfD) in female Sprague-Dawley rats. Please comment on the degree to which 

these preliminary conclusions are supported by the available data.

2:00 P.M. Charge to Panel – Question 1(continued)

Question 1.9 – After the April 2010 SAP, the Agency will evaluate the weight of 

evidence (WOE) for atrazine by integrating the experimental toxicology data with the 

epidemiological studies. As part of this work, the Agency will consider the available 

data on hormonal changes and functional outcomes that may be used as endpoints for 

deriving PoDs across different durations of exposure and for different populations 

(including potentially sensitive ones). Important studies evaluating the dose-response 

relationships for hormones involved in the HPA axis are still on-going. These studies 

are expected to provide high quality data that can be used to characterize the entire 

dose response curve. With the caveat that these data are not available now, given the 

current understanding of atrazine’s mode of action, please comment on what would be 

appropriate endpoints to consider for use in deriving points of departure in a possible 

future risk assessment.

Given that the duration of the toxicological concern is a key factor in evaluating the 

frequency of drinking water monitoring, please include in your response a consideration 

of the magnitude and duration of changes in key events in the toxicity pathway that are 

sufficient perturb normal function and comprise human health. In defining the exposure 

window of interest, please comment on the toxicokinetic/dynamic considerations with 

respect to atrazine's effects on the HPA/HPG axis. 

3:00 P.M. Break

3:15 P.M. Charge to Panel – Question 2

Approaches to Evaluating Water Sampling Strategies & Frequency of Monitoring

In conjunction with the toxicological review presented in the issue paper, the Agency 

has also discussed methods for re-evaluating the sampling frequency that is necessary 

for determining, with confidence, concentrations of the pesticide in water that sources 

drinking water. These have included different methods for estimating pesticide 

concentrations between known sampling events and examining the performance of 

different sampling strategies for averaging periods of different durations. The Agency 

seeks feedback from the Panel with regard to how the uncertainty and variability in both 

the monitoring data and in the toxicity data (i.e., point of departure) can be integrated to 
10

characterize and to interpret the potential significance of atrazine concentrations in

drinking water. 

Question 2.1 – Given the nature of the temporal patterns of pesticide occurrence in 

surface waters described in Section 5.2, including serial correlations from day to day, 

periodicity in elevated concentrations within seasons and from year to year, below 

quantitation data, and uncertainty in the shape of the pesticide distributions in surface 

waters--what statistical approaches should the Agency consider in determining 

confidence bounds on exposure estimates from monitoring data? Please comment on 

how the approach may vary depending on the duration of concern.

4:00 P.M. Charge to Panel – Question 2 (continued)

Question 2.2 – The first two simulation methods presented in Section 5.5 are 

applicable to the specific data sets they describe, although some generalities regarding 

shape patterns appear to exist. Given this information, please comment on the 

strengths and weaknesses of the approaches and on the practical merits of pursuing 

them or some other numerical approach with a larger set of higher concentration 

systems. Please comment on how the methods for determining confidence bounds 

might apply given these considerations. 

5:00 P.M. Adjourn
11

DRAFT AGENDA

FIFRA SCIENTIFIC ADVISORY PANEL (SAP)

OPEN MEETING

April 26 – 29, 2010

FIFRA SAP WEB SITE http://www.epa.gov/scipoly/sap/

OPP Docket Telephone: (703) 305-5805

Docket Number: EPA-HQ-OPP-2010-0125

The Hamilton Crowne Plaza Hotel

The Hamilton Ballroom

1001 14th Street, NW

Washington, DC 20005

202-682-0111

Reevaluation of the Human Health Effects of Atrazine: Review of Experimental 

Animal and In Vitro Studies and Drinking Water Monitoring Frequency

Please note that all times are approximate (see note at end of Agenda).

Thursday, April 29, 2010

8:30 A.M. Opening of Meeting and Administrative Procedures – Joseph Bailey, 

Designated Federal Official, Office of Science Coordination and Policy, 

EPA

8:35 A.M. Introduction and Identification of Panel Members – Kenneth Portier, 

Ph.D., FIFRA Scientific Advisory Panel Session Chair

8:45 A.M. Charge to Panel – Question 2 (continued)

Question 2.3 – As described in Section 5.4.2, the Agency is considering the use of a 

confidence interval or prediction interval approach to characterize the uncertainty of 

exposure estimates derived from monitoring data of varying sampling frequencies. 

Please comment on the strengths and weaknesses of either placing confidence bounds 

on the rolling average estimates and comparing the upper limit from monitoring against 

the level of concern (LOC) or, conversely, placing confidence bounds on the LOC. 

9:45 A.M. Charge to Panel – Question 2 (continued)

Question 2.4 – Please comment on the relative merits of the various modeling 

approaches the Agency described in Section 5.4.1 and 5.6 for interpolating pesticide 

concentrations between sampling points and, in particular, on the strengths and 

weaknesses of these methods as the frequency of samples decreases. Considering the 

health endpoint(s) being considered for atrazine, particularly data for the HPA axis, and 

the exposure time frame needed to induce the health effect(s) which is shorter than that 
12

used in the 2003 risk assessment, please comment on the advantages and 

disadvantages of each model for evaluating the likely occurrence and exposure via 

drinking water of short, moderate, and long duration concentrations. Please comment 

on the Agency’s proposed approach for evaluating these methods, as described in 

Section 5.7.1. To what extent should the Agency consider other factors, such as the 

shape of the chemograph (Section 5.5.3), weather patterns, stream flow, and/or 

pesticide use patterns in evaluating the modeling approaches?

10:30 A.M. Break

10: 45 A.M. Charge to Panel – Discussion continued as needed

12:00 noon Lunch

1:15 P.M. Charge to Panel – Discussion continued as needed

3:00 P.M. Break

3:15 P.M. Charge to Panel – Discussion continued as needed

5:00 P.M. Adjourn

Please be advised that agenda times are approximate; when the discussion for 

one topic is completed, discussions for the next topic will begin. For further 

information, please contact the Designated Federal Official for this meeting, 

Joseph Bailey, via telephone: (202) 564-2045; fax: (202) 564-8382; or email: 

bailey.joseph@epa.gov