----- Original Message -----

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Sent: Tuesday, September 29, 2009 12:06 PM

Subject: [DRSG] DRSG Teleconference, 10/6/2009, 12:00 pm

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Society for Risk Analysis
Dose Response Specialty Group

October 2009 Teleconference
Tuesday, October 6, 2009 12:00 pm – 1:00 pm edt

Jeff Gift, Moderator
USEPA, National Center for Environmental Assessment

Presentation: David J. Dix, National Center for Computational
Toxicology, U.S. Environmental Protection Agency
“High Throughput Screening for Hazard and Risk of Environmental
Contaminants”

Call in Number: 1-866-299-3188 Conference Code 9195414155#
(Phone lines will be open 5 minutes before the start of the meeting. We
have added extra lines for this call, but encourage you to join with
nearby colleagues and use speaker-phones to assure as many participants
as possible.)

    Link to access the slides:

PDF version:
    http://www.sra.org/drsg/docs/Dix_6Oct09.pdf

Submit questions and issues for discussion prior to and after the
teleseminar to:
NAS08report@yahoogroups.com


David Dix is the Acting Deputy Director of the National Center for
Computational Toxicology, U.S. Environmental Protection Agency

Abstract:

High throughput toxicity testing provides detailed mechanistic
information on the concentration response of environmental contaminants
in numerous potential toxicity pathways. High throughput screening (HTS)
has several key advantages: (1) expense orders of magnitude less than
animal testing; (2) direct study of human gene, protein and cell targets
is possible; and (3) hundreds to thousands of contaminants can be
studied simultaneously. Quantitative HTS hazard assessment can thus
identify potential mechanisms and pathways by which a contaminant can
lead to specific adverse outcomes. EPA’s ToxCast project is evaluating
the use of HTS for understanding the types of molecular and pathway
perturbations caused by environmental chemicals, and building initial
predictive models of in vivo toxicity for prioritization and hazard
assessment. To date we have tested 309 pesticide active and industrial
chemicals in 467 assays across 9 HTS technologies. These include
cell-free assays, as well as cell-based assays in a variety of human and
rodent primary cells and cell lines. Individual assays and composite
assays for effects on genes and pathways demonstrated a broad spectrum
of chemical activity at the molecular and pathway levels. Many expected
interactions were seen in the data, including endocrine and xenobiotic
metabolism enzyme activity. Chemicals show widely varying promiscuity
across pathways, from no activity to activity in dozens of pathways.
This diversity of behavior is seen even within well-defined chemical
classes. This approach promises to provide meaningful data on thousands
of untested environmental chemicals, and to guide more intelligent,
targeted testing of environmental contaminants in the future. This
abstract may not necessarily reflect Agency policy.



  (See attached file: October 6 2009 Teleseminar.doc)

The point where one mentally or physically is vulnerable in response to provocation or to particular things in general, as in emotions, stress, or pain.

Level at which effect starts

...some dose below which the probability of an individual responding is zero.

• all chemicals have thresholds for adverse effect; the question on which we should focus is whether chemicals have subthreshold doses;
• some chemical’s are hypothesized to have a threshold for adverse effect of only one molecule; these chemicals are likely those where only one molecule can cause self-replicating damage;
• an understanding of the underlying mechanism or mode of action is helpful in determining whether subthreshold doses exist, or whether a chemical can cause self-replicating damage from one molecule.
  

• One often hears that lead does not have a threshold for adverse effects, but this is usually followed up by a supporting statement that existing exposures already put sensitive humans in the range of adverse effect.  This supporting sentence is illogical.  One can hypothesize a threshold of 1 molecule for the adverse effects for lead and then all of us are lead intoxicated, or one can hypothesize a threshold of 10,000,000 molecules for the adverse effect for lead and still be in a range of exposures that exceed this threshold and thereby evoke the adverse effect in sensitive humans.  My judgment is that since the critical effect of lead is unlikely to be self-replicating damage, then more than one molecule of lead is needed to evoke its critical effect.  If this is true, then it is reasonable to task expert groups to estimate a subthreshold dose for lead in sensitive populations, which of course is what government groups have done.

---

From: DRSG@yahoogroups.com [mailto:DRSG@yahoogroups.com] On Behalf Of Michael Dourson
Sent: Wednesday, October 07, 2009 4:55 PM
To: DRSG@yahoogroups.com; John Doull
Subject: [DRSG] Threshold for Adverse Effect

 

Dear Colleagues

I thoroughly enjoyed our email discussion of "threshold" for adverse effect last spring and wish for us to continue.  However, let's perhaps restart this email stream with some existing definitions of "threshold."   This will allow our deliberations and conclusions to perhaps be more understandable to our colleagues who have not taken as much time to study this issue.  

One of definition of threshold from Wikipedia is:

The point where one mentally or physically is vulnerable in response to provocation or to particular things in general, as in emotions, stress, or pain.

Another one from the dictionary on my word software is:

Level at which effect starts

Casarett & Doull (2008—page 23) define it as:

...some dose below which the probability of an individual responding is zero.

Other definitions as starting points are of course welcome.  Based on these definitions, and probably ones that we could get elsewhere, one immediately recognizes that all chemicals have a threshold for adverse effect, since at least one molecule of a chemical is needed to evoke the adverse effect.  It is not correct to say that some chemicals do not have a threshold for an adverse effect.

The question before many of us, thus, is not whether a chemical has a threshold---since all chemicals do---but rather can it be that this threshold is one molecule of a chemical.  Another way to state the question is whether a chemical can have a subthreshold dose, that is one molecule or greater.  I am sure that many of us, and perhaps all of us would agree, the answer to this question lies more with a better understanding of the underlying biology, and less with a better understanding of mathematics.

In order to illustrate this potential agreement, let’s start with some examples.

Does water have a threshold of adverse effect?  

Hah!  Trick question, of course it does.  Here is the real question: Can one molecule of water cause an adverse effect?   

All of the biologists are going to answer this question along the following line: Of course not, we exhale a zillion (definition: an indeterminately large number) water molecules each minute.  Adding 1 more to your body is of no biological consequence.   In fact, water is an essential macro-nutrient, although consumption of enough water will do harm, and has caused death on numerous occasions.  Thus, water has a subthreshold dose for adverse effect, the maximum amount which can be, or perhaps has been, estimated.

Next question: Can one molecule of vitamin A cause an adverse effect?   

All of the biologists are going to answer this question along the following line: Of course not, we need zillions of vitamin A molecules to survive (note to my mathematical colleagues---sorry folks, this is just about as quantitative as some of us get).  Adding 1 more to your body is of no biological consequence.  In fact, vitamin A is an essential micro-nutrient, although eating polar bear liver may cause adverse effects in humans, because of its overabundance of vitamin A.  So at some point, vitamin A, like water, is toxic, and like water, vitamin A has a subthreshold dose for adverse effect the upper limit of which has been estimated by the Institute of Medicine as Upper Limits to variously aged humans.

Next question: Can one molecule of lead cause an adverse effect?   

Well, lets scratch our heads on this one.  (Hmm... Just by doing this we just lost about a zillion lead molecules found in the skin cells in our scalp.)  All of the biologists are going to answer this question along the following line: Well, in order to answer this question we need to know the molecular basis of lead’s toxicity, or at least its likely mode of action.  However, if this mechanism or mode does not result in self replicating damage, it is hard to imagine that 1 molecule of lead can cause an adverse effect either since it will likely get excreted or sequestered and the body has repair capabilities.*  

I could go on with other examples.  In fact, you will find some toxicologists able (and some even willing) to make such an argument with any chemical.  In fact, some, and perhaps many of us biologists, would argue that the estimation of subthreshold doses, such as Reference Dose (RfD) is exactly this exercise.  Whether or not one agrees with the last sentence, however, the important points from this email are:

• all chemicals have thresholds for adverse effect; the question on which we should focus is whether chemicals have subthreshold doses;
• some chemical’s are hypothesized to have a threshold for adverse effect of only one molecule; these chemicals are likely those where only one molecule can cause self-replicating damage;
• an understanding of the underlying mechanism or mode of action is helpful in determining whether subthreshold doses exist, or whether a chemical can cause self-replicating damage from one molecule.
  

This email would not be complete without reference to a lot of good thoughts by others, including, but not limited to, the postings by Kenny Crump, Kevin Brand, Jim Wilson, Clark Carrington, Paul Schlosser, John Frangos, Harlee Strauss, Rory Conolly, Janus Byczkowski, John Lipscomb and Wout Slob, and Wout’s letter to the editor (see email dated 5-6-09), and internal discussions with Andy Maier and Lynne Haber.  How we collectively approach the area of subthreshold dose needs first and foremost a biological underpinning, but also mathematical prowess based on such understanding, a prowess, unfortunately, that most of the biologists (including me) lack.   Paul Price’s recent telecon sponsored by the DSRG on September 1st was a nice foray into this joint area.  I look forward to other efforts as well.

Cheers!

Michael

Toxicology Excellence for Risk Assessment (TERA),
improving the practice of risk assessment through independent and objective guidance and advice. See www.tera.org

P.s.  I apologize if I missed anyone on the email postings.  They made excellent reading.

---

• One often hears that lead does not have a threshold for adverse effects, but this is usually followed up by a supporting statement that existing exposures already put sensitive humans in the range of adverse effect.  This supporting sentence is illogical.  One can hypothesize a threshold of 1 molecule for the adverse effects for lead and then all of us are lead intoxicated, or one can hypothesize a threshold of 10,000,000 molecules for the adverse effect for lead and still be in a range of exposures that exceed this threshold and thereby evoke the adverse effect in sensitive humans.  My judgment is that since the critical effect of lead is unlikely to be self-replicating damage, then more than one molecule of lead is needed to evoke its critical effect.  If this is true, then it is reasonable to task expert groups to estimate a subthreshold dose for lead in sensitive populations, which of course is what government groups have done.

When the point came up during the teleseminar on Tuesday, it was
reference to specific, in vitro dose-response data, one figure of which
is copied below.  That there is an *apparent* threshold in these data is
in high probability an artifact of the use of a log scale on the x axis:
that was Dale Hattis' point.  When examining the biochemical mechanisms
in well-defined, fairly uniform cell culture system, the arguments about
population variability are really irrelevant.

** There are known cellular/biochemical processes which are at least
highly non-linear: a Hill model with a coefficient of 2 or greater is
the best representation of the data.  In those cases (if the coefficient
is a good bit greater than 2) referring to the response in that defined
system as having a "threshold" strikes me as appropriate.

The problem is, you cannot distinguish a process with a hill coefficient
equal to 1 from one in which it is, say 4, by visual examination of data
plotted with a log-x-axis.

The discussion of what happens in the variable human population is also
important, and I can believe that a "threshold" observed in a cellular
system does not necessarily mean there's effectively zero risk below a
finite exposure level in that population.  That's a critical
consideration when one is translating mechanistic data and models to
population-based risk assessment.  But let's please not mix up that
population-risk-assessment activity with attempts to understand and
incorporate mechanistic data, where you really have to start by
understanding the individual.

When we are talking about methods for elucidating and incorporating
cellular and biochemical mechanisms into our analysis of dose-response,
being accurate in our discussion of the characteristics of the mechanism
is important.  And looking at a plot like this and saying that it shows
a "threshold" because of the *apparent* non-linearity represents a
simple failure to recognize what happens when you plot linear functions
on semi-log plots.  It is inaccurate.

-Paul


(Embedded image moved to file: pic21543.jpg)

---

From: Kenny Crump [mailto:KennyCrump@...]
Sent: Thursday, October 08, 2009 9:16 AM
To: Price, Paul (S); 'Michael Dourson'; DRSG@yahoogroups.com
Subject: RE: [DRSG] Threshold for Adverse Effect

Paul,

 

That is a very nice example.  But not of a threshold.  If we are going to define doses that cause small but positive consequences thresholds then “threshold” becomes a vacuous concept.

 

Regards,

 

Kenny

 

  

 

 

Kenny S. Crump

Louisiana Tech

P.O. Box 10348

Ruston, LA 71272-0046

Direct Dial: 318-257-4051

Cell: 318-278-9426

FAX: 318-257-2182

KennyCrump@...

Web Page:  http://www2.latech.edu/~kcrump/

 

Home:

Kenny and Shirley Crump

2220 S. Vienna

Ruston, LA 71270

318-255-7058

 

From: DRSG@yahoogroups.com [mailto:DRSG@yahoogroups.com] On Behalf Of Price, Paul (S)
Sent: Wednesday, October 07, 2009 9:11 PM
To: Michael Dourson; DRSG@yahoogroups.com
Subject: RE: [DRSG] Threshold for Adverse Effect

 

 

Mike and the group:

 

I have been thinking about one of the counter arguments to the existence of thresholds. This argument is the idea that in any population where some small fraction displays an adverse effect that any dose of an agent that causes the adverse effect will push a small but finite number of individuals from the category of "unaffected" to the category of "affected". This model is quite attractive for continuous variables (IQ, liver functions, height, lung function, etc.).

 

The conceptual problem with this model is that it relies on the arbitrary nature of crossing a bright line criterion as the only the only definition of what is an effect.  At large doses a large fraction of the population will be moved across the criterion value.  But in addition many will be pushed well past the criterion. This will not occur at low doses.

 

Consider a chemical that reduces the height of children. Assume that a dose A of a chemical that causes loss of height of 6 inches and assume that the criterion for an adverse effect is having a height of less than 4 ft. (My apologies to those who are below 4 ft in height.) This reduction in height will cause X% of the population to move from "unaffected" (height > 4 ft) to "affected" (height < than 4 ft). But it also will cause the affected population (those who would have been above 4 ft but are now less than 4 ft) to have heights that range from just below 4 ft to a height of 3 ft 6 in. Thus some of the affected individuals will be well below the criterion.

 

Now assume that at a lower dose B, the loss of height is 0.06 inches. The fraction that crosses the 4 ft is reduced but is still non zero. If we make the assumption that the distribution of heights in the population between 4 and 4.5 ft is uniform (this is incorrect but let’s ignore this fact) then the response will be X/100%, or a 100 fold change in response.  If X were 10^-1 then dose B would be 10^-3 or still quite significant.

 

But the difference between the two scenarios is not fully captured but just saying that the response is X% at dose A and X/100% at the dose B.  At B the affected individuals who would have been above 4 ft will have heights ranging from just less than 4 ft to a height of 3 ft 11.94 in. Thus none of the affected individuals will be significantly below the criterion of 4 ft. This clearly is a different effect than the first case. 

 

To put it another way, if my child were ill and I was given the choice of a drug that as a side effect would reduce his/her height by six inches versus one that would reduces it by 0.06 inches, I would not consider the side effects posed by the drugs equivalent. But by only counting the number pushed over the criterion of 4 ft the model ignores this difference.    

 

This suggests that on top of the measure of the fraction of the population pushed across a bright line criterion that their also needs to be some measure of how far they are pushed passed the criterion. So if we were to give a larger weight to the importance of the effects that occur at the first dose and lower weight to the second dose, the difference between the dose A and B would be X*(Weight 1) and X/100*(Weight 2).

 

I would argue that in this case the weight that should be given to the second dose would be zero. Thus even though the number who responded would be non-zero, a threshold would have occurred.

 

I have glossed over a number of additional issues in this analysis (such as multiple stressors that could add up to some significant risk or if the impact on health of the continuous variable were non linear) but the basic point of the argument I think remains valid.

 

 

Paul Price

 

An exposure level at which there are no statistically or biologically significant increases in the frequency or severity of adverse effect between the exposed population and its appropriate control; some effects may be produced at this level, but they are not considered adverse, nor precursors to adverse effects (EPA’s IRIS archived glossary),

 

---

From: Kenny Crump  [mailto:KennyCrump@...]
Sent: Thursday, October 08, 2009 9:16  AM
To: Price, Paul (S); 'Michael Dourson';  DRSG@yahoogroups.com
Subject: RE: [DRSG] Threshold for Adverse  Effect

 
 
 

Paul,



That  is a very nice example.  But not of a threshold.  If we are going to  define doses that cause small but positive consequences thresholds then  “threshold” becomes a vacuous concept.



Regards,



Kenny



   





 

Kenny S.  Crump

Louisiana  Tech

P.O. Box  10348

Ruston, LA  71272-0046

Direct Dial:  318-257-4051

Cell:  318-278-9426

FAX:  318-257-2182

KennyCrump@... <mailto:KennyCrump@...>

Web  Page:  http://www2.latech.edu/~kcrump/



Home:  

Kenny and  Shirley Crump

2220 S.  Vienna

Ruston, LA  71270

318-255-7058



 
 

From:  DRSG@yahoogroups.com [mailto:DRSG@yahoogroups.com] On Behalf Of Price,  Paul (S)
Sent: Wednesday, October 07, 2009 9:11 PM
To:  Michael Dourson; DRSG@yahoogroups.com
Subject: RE: [DRSG] Threshold  for Adverse Effect
 
 
 
  
 
 
 
 

Mike  and the group:



I have  been thinking about one of the counter arguments to the existence of  thresholds. This argument is the idea that in any population where some small  fraction displays an adverse effect that any dose of an agent that causes the  adverse effect will push a small but finite number of individuals from the  category of "unaffected" to the category of "affected". This model is quite  attractive for continuous variables (IQ, liver functions, height, lung  function, etc.).

 
 
The  conceptual problem with this model is that it relies on the arbitrary nature  of crossing a bright line criterion as the only the only definition  of what is an effect.  At large doses a large fraction of the  population will be moved across the criterion value.  But in  addition many will be pushed well past the criterion. This will not occur at  low doses.

 
 
Consider  a chemical that reduces the height of children. Assume that a dose A  of a chemical that causes loss of height of 6 inches and assume  that the criterion for an adverse effect is having a height of less than 4  ft. (My apologies to those who are below 4 ft in height.) This reduction  in height will cause X% of the population to move from "unaffected"  (height > 4 ft) to "affected" (height < than 4 ft). But  it also will cause the affected population (those who would have been  above 4 ft but are now less than 4 ft) to have heights that range  from just below 4 ft to a height of 3 ft 6 in. Thus some of the affected  individuals will be well below the criterion.

 
 
Now  assume that at a lower dose B, the loss of height is 0.06 inches. The fraction  that crosses the 4 ft is reduced but is still non zero. If we make the  assumption that the distribution of heights in the population between 4 and  4.5 ft is uniform (this is incorrect but let’s ignore this fact) then the  response will be X/100%, or a 100 fold change in response.  If X  were 10-1 then dose B would be 10-3 or still quite  significant.

 
 
But  the difference between the two scenarios is not fully captured but just saying  that the response is X% at dose A and X/100% at the dose B.   At B the affected individuals who would have been above 4 ft  will have heights ranging from just less than 4 ft to a height of 3 ft  11.94 in. Thus none of the affected individuals will be significantly below  the criterion of 4 ft. This clearly is a different effect than the  first case.

 
 
To put  it another way, if my child were ill and I was given the choice of a  drug that as a side effect would reduce his/her height by six inches  versus one that would reduces it by 0.06 inches, I would not consider the  side effects posed by the drugs equivalent. But by only counting the  number pushed over the criterion of 4 ft the model ignores this  difference.    

 
 
This  suggests that on top of the measure of the fraction of the population pushed  across a bright line criterion that their also needs to be some measure  of how far they are pushed passed the criterion. So if we were to  give a larger weight to the importance of the effects that occur at  the first dose and lower weight to the second dose, the difference  between the dose A and B would be X*(Weight 1) and X/100*(Weight 2).  

 
 
I  would argue that in this case the weight that should be given to the  second dose would be zero. Thus even though the number who responded  would be non-zero, a threshold would have occurred.

 
 
I have  glossed over a number of additional issues in this analysis (such as  multiple stressors that could add up to some significant risk or if the impact  on health of the continuous variable were non linear) but the basic point  of the argument I think remains valid.



 
 
Paul  Price

 

Hello BMDS User:

You are receiving this BMDS News announcement because you are a
registered user of the EPA benchmark dose software (BMDS).  As a member
of the BMDS-News list you will periodically receive news and information
related to BMDS.

BMDS-News Announcement #10:    EPA will be conducting the following full
day BMDS workshop on December 5 in conjunction with the December 6-9,
2009 Society for Risk Analysis (SRA) conference.  The cost is $250 for
those who preregister by Friday, November 6, 2009 ($300 thereafter).  To
learn more about the SRA conference go to
http://www.sra.org/events_2009_meeting.php.  To register online for the
BMDS workshop go to
https://ssl4.westserver.net/birenheide.com/secure/sra/

   Introduction to the Benchmark Dose Methodology and Interactive
   Application of EPA’s Benchmark Dose Software (BMDS), Version 2.1.1


   SRA 2009 Annual Meeting (Baltimore MD, Dec 5, 2009)


   This daylong course is designed to provide participants with an
   interactive training workshop on the use of the U.S. EPA’s Benchmark
   Dose Software, BMDS 2.1.1 and its application to risk assessment. The
   course will provide instruction in changes that have been implemented
   in version 2.1.1, including a new user interface that allows multiple
   run processing, the ability to save model option choices, summary
   sheets for side-by-side comparison of model results, and enhanced
   export to spreadsheet functionality. The course will provide an
   overview of the BMD process, including determination of data adequacy,
   model fitting, model comparison, selection of a benchmark response
   level, and modeling linear verses nonlinear responses. Attendees will
   also work on examples from chemical assessments and learn how to take
   advantage of the new features offered by version 2.1.1 of BMDS to
   prepare summary reports for insertion in their assessments. This
   workshop will cover all the BMD models available in the current
   version of BMDS—including the recently added dichotomous hill,
   background dose, and continuous exponential models. This course is an
   interactive training workshop in the features of BMDS 2.1.1 and it is
   therefore recommended that prior to this training students who are not
   familiar with BMD modeling take the online BMD training course (
   http://www.epa.gov/ncea/bmds/training/index.html) in order to ensure
   that they receive the maximum benefit from participating in the
   workshop. Participants need to bring their own laptops to the workshop
   with the latest version of BMDS 2.1.1 installed (with necessary
   administrative rights). BMDS 2.1.1 should be available for download
   from http://epa.gov/ncea/bmds/ by Friday, November 6, 2009.

--------------------------------------------------------------
J. Allen Davis, MSPH
Biologist
National Center for Environmental Assessment
U.S. Environmental Protection Agency
109 T.W. Alexander Dr, MC B243-01
RTP, NC 27711
phone: 919-541-3789
fax: 919-541-0245
email: davis.allen@...


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Hi DRSG,
We are putting on 2 cumulative risk assessment workshops at SRA this
year on Sunday 12/6/09.  Please feel free to sign up and/or pass this
along to others who many be interested!  Information attached.
Thanks,
LT
(See attached file: SRA 09 Cume RA Part 1 Handbook for web.pdf)(See
attached file: SRA 09 Cume RA Part 2 Handbook for web.pdf)
Linda K. Teuschler
U.S. EPA/NCEA-Cin
26 W. ML King Dr. (MSA-110)
Cincinnati, OH 45268
513-569-7573
fax: 513-487-2539
teuschler.linda@...


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   |[DRSG] DRSG Teleconference, 11/3/2009, 12:00 pm
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  Reminder      DRSG Yahoo! Group
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  Title:        DRSG Teleconference



  Date:         Tuesday November 3, 2009

  Time:         12:00 pm - 1:00 pm

  Repeats:      This event repeats every month on the first Tuesday.

  Notes:        Our next teleconference will be noon to 1 pm EST, on the first
Tuesday of the month. We have
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----- Original Message -----

From: DRSG@yahoogroups.com

To: DRSG@yahoogroups.com

Sent: Monday, November 02, 2009 11:56 AM

Subject: [DRSG] DRSG Teleconference, 11/3/2009, 12:00 pm

Reminder from:		DRSG Yahoo! Group
Title:		DRSG Teleconference
Date:		Tuesday November 3, 2009
Time:		12:00 pm - 1:00 pm
Repeats:		This event repeats every month on the first Tuesday.
Notes:		Our next teleconference will be noon to 1 pm EST, on the first Tuesday of the month. We have 25 lines available for the call. CALL IN NUMBER: 513-569-7897 CONFEREE CODE: 7217 plus the # sign. For problem resolution during the call, contact the Help Desk at 513-569-7754.
Get reminders on your mobile, Yahoo! Messenger, and email. Edit reminder options

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The BMDS course at SRA will be offered on Sunday, December 6, not
December 5.

Jeff Gift, Ph.D.
National Center for Environmental Assessment
EPA (B243-01)
RTP, NC 27711
919-541-4828
919-541-0245 (fax)
gift.jeff@...

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   |Jeff Gift/RTP/USEPA/US@EPA
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   |11/02/2009 12:04 PM
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   |BMDS-News Announcement #10 - December 5, 2009 SRA Workshop for BMDS 2.1.1 -
Preregister by November 6 and Save                            |
  
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Hello BMDS User:

You are receiving this BMDS News announcement because you are a
registered user of the EPA benchmark dose software (BMDS).  As a member
of the BMDS-News list you will periodically receive news and information
related to BMDS.

BMDS-News Announcement #10:    EPA will be conducting the following full
day BMDS workshop on December 5 in conjunction with the December 6-9,
2009 Society for Risk Analysis (SRA) conference.  The cost is $250 for
those who preregister by Friday, November 6, 2009 ($300 thereafter).  To
learn more about the SRA conference go to
http://www.sra.org/events_2009_meeting.php.  To register online for the
BMDS workshop go to
https://ssl4.westserver.net/birenheide.com/secure/sra/

   Introduction to the Benchmark Dose Methodology and Interactive
   Application of EPA’s Benchmark Dose Software (BMDS), Version 2.1.1


   SRA 2009 Annual Meeting (Baltimore MD, Dec 5, 2009)


   This daylong course is designed to provide participants with an
   interactive training workshop on the use of the U.S. EPA’s Benchmark
   Dose Software, BMDS 2.1.1 and its application to risk assessment. The
   course will provide instruction in changes that have been implemented
   in version 2.1.1, including a new user interface that allows multiple
   run processing, the ability to save model option choices, summary
   sheets for side-by-side comparison of model results, and enhanced
   export to spreadsheet functionality. The course will provide an
   overview of the BMD process, including determination of data adequacy,
   model fitting, model comparison, selection of a benchmark response
   level, and modeling linear verses nonlinear responses. Attendees will
   also work on examples from chemical assessments and learn how to take
   advantage of the new features offered by version 2.1.1 of BMDS to
   prepare summary reports for insertion in their assessments. This
   workshop will cover all the BMD models available in the current
   version of BMDS—including the recently added dichotomous hill,
   background dose, and continuous exponential models. This course is an
   interactive training workshop in the features of BMDS 2.1.1 and it is
   therefore recommended that prior to this training students who are not
   familiar with BMD modeling take the online BMD training course (
   http://www.epa.gov/ncea/bmds/training/index.html) in order to ensure
   that they receive the maximum benefit from participating in the
   workshop. Participants need to bring their own laptops to the workshop
   with the latest version of BMDS 2.1.1 installed (with necessary
   administrative rights). BMDS 2.1.1 should be available for download
   from http://epa.gov/ncea/bmds/ by Friday, November 6, 2009.

--------------------------------------------------------------
J. Allen Davis, MSPH
Biologist
National Center for Environmental Assessment
U.S. Environmental Protection Agency
109 T.W. Alexander Dr, MC B243-01
RTP, NC 27711
phone: 919-541-3789
fax: 919-541-0245
email: davis.allen@...


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Hello BMDS User:

You are receiving this BMDS News announcement because you are a
registered user of the EPA benchmark dose software (BMDS).  As a member
of the BMDS-News list you will periodically receive news and information
related to BMDS.

BMDS-News Announcement #11: EPA is now distributing Version 2.1.1 (Build
55) of the Benchmark Dose Software (BMDS). BMDS 2.1.1 (Build 55)
contains a flexible new feature that allows users to export select BMDS
summary report data and plots to Excel. It also contains a comprehensive
set of sample session and model option files to assist users in running
batch operations, and several improvements to the ten Berge model that
were not available in version 2.1. The Readme.rtf file distributed with
BMDS provides details on the improvements made in Version 2.1.1 (Build
55), installation requirements, and known problems.

IF YOU ALREADY HAVE BMDS 2.1 (BUILD 52) INSTALLED, you need only
download and unzip a SMALL PATCH FILE, which should allow you to upgrade
BMDS without the need for assistance from your local IT/computer support
department.

TO DOWNLOAD BMDS 2.1.1 go to the BMDS website at
http://www.epa.gov/ncea/bmds

Jeff Gift, Ph.D.
National Center for Environmental Assessment
EPA (B243-01)
RTP, NC 27711
919-541-4828
919-541-0245 (fax)
gift.jeff@...


Here are some useful addresses for managing your subscription:

UNSUBSCRIBE: Send a blank message to:
BMDS-News-unsubscribe@...

SUBSCRIBE: Send a blank message to: BMDS-News-subscribe@...

WEB INTERFACE: https://lists.epa.gov/read/?forum=BMDS-News
You can visit this address to change your subscription email address,
read and send mail, unsubscribe, read and search archives, or change
your settings at any time.


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