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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).

Day 1

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. Introduction: Status of the Reevaluation of the Health Effects of 

Atrazine – Anna Lowit, Ph.D., Health Effects Division, Office of Pesticide 

Programs, EPA

1:45 P.M. Reevaluation of Human Health Effects of Atrazine: Review of 

Experimental Animal and In Vitro Studies and Drinking Water 

Monitoring Frequency – Elizabeth Mendez, Ph.D., Health Effects 

Division, Office of Pesticide Programs, EPA
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2:00 P.M. A Proposed MOA for Atrazine and Atrazine Metabolites – Ralph L. 

Cooper, Ph.D., Endocrinology Branch, Toxicity Assessment Division, 

National Health and Environmental Effects Research Laboratory, EPA.

3:00 P.M. Break

3:15 P.M. Review of Atrazine Immunotoxicity – Robert Luebke, Ph.D., 

Cardiopulmonary and Immunotoxicity Branch, Environmental Public 

Health Division, National Health and Environmental Effects Research 

Laboratory, EPA.

3:45 P.M. Neurological Effects of Atrazine – John Liccione, Ph.D., Health Effects 

Division, Office of Pesticide Programs, EPA

4:15 P.M. Summary of Non-Cancer Mammalian Toxicity Reevaluation –

Elizabeth Mendez, Ph.D., Health Effects Division, Office of Pesticide 

Programs, EPA

4:30 P.M. Approaches to Evaluating Water Sampling Strategies and Frequency

of Monitoring – Nelson Thurman, M.S., Environmental Fate and Effects 

Division, Office of Pesticide Programs, EPA

5:00 P.M. Evaluating the Performance of Sampling Strategies for Estimating 

Maximum Concentrations of Different Durations – Mary Frankenberry, 

Environmental Fate and Effects Division, Office of Pesticide Programs, 

EPA

5:25 P.M. Artificial Neural Network Modeling of Atrazine Occurrence Patterns –

Michael J. Messner, Ph.D., Standards and Risk Reduction Branch, Office 

of Ground Water and Drinking Water, EPA

5:50 P.M. Water Sampling Summary – Nelson Thurman, M.S., Environmental Fate 

and Effects Division, Office of Pesticide Programs, EPA

5:55 P.M. Summary and Conclusion – Anna Lowit, Ph.D., Health Effects Division, 

Office of Pesticide Programs, EPA

6:00 P.M. Adjourn

Day 2

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

10:00 A.M. Break

10:15 A.M. Public Comments

12:15 P.M. Lunch Break

1:30 P.M. Charge to Panel – Question 1
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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 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 hypothalamic-pituitary 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-pituitary-gonadal 

(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

hypothalamic-pituitary-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 doseresponse concordance, atrazine-induced 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 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 
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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; deethyl-atrazine, DEA) but not diamino-schlorotriazine (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.

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). Up- regulation 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 
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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

Day 3

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 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 
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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)

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 endocrine-related 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
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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 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 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 
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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

Day 4

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 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
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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