Organophosphorus Cumulative Risk Assessment


Organophosphorus
Cumulative Risk
Assessment - 2006
Update
PRO^
— Continuation —
August 2006
Appendices have been separated from the original PDF
into individual PDF documents for viewing on-line.
This PDF contains the C, D, E, and G appendices

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C-1. The Sources of Residue Inputs for the Assessment of the
Cumulative Dietary Exposure to Organophosphorus Pesticides on
Foods
See file ll_C1 .xls
Foods in CSFII 1994-1998 are listed in descending order of per capita
consumption by children
C-2. Summary of PDP Residue Analyses of Organophosphorus
Pesticides on Foods (1994-2004)
See file II C 2.xls
Section II.C.1 & 2 - Page 320 of 522

-------
C-3. A summary of FDA Total Diet Study Analyses for Organophosphorus Pesticides in Meats
(1991-2001)
Table II.C-3.1 A summary of FDA Total Diet Study Analyses for Organophosphorus Pesticides in Meats
(1991-2001).
Food No
Sample Description
Year
Market
Basket
Residue Found
Concentration
(ppm)
017
ham, baked
1991
3
no residue found
0
017
ham, baked
1992
1
no residue found
0
017
ham, baked
1992
2
parathion
0.02
017
ham, baked
1992
2
phosalone
0.06
017
ham, baked
1993
1
no residue found
0
017
ham, baked
1993
2
no residue found
0
017
ham, baked
1993
3
no residue found
0
017
ham, baked
1994
1
no residue found
0
017
ham, baked
1994
2
no residue found
0
017
ham, baked
1994
3
parathion
0.02
017
ham, baked
1994
4
no residue found
0
017
ham, baked
1995
1
no residue found
0
017
ham, baked
1995
2
no residue found
0
017
ham, baked
1995
3
no residue found
0
017
ham, baked
1996
1
no residue found
0
017
ham, baked
1996
2
no residue found
0
017
ham, baked
1996
3
diazinon
0.01
017
ham, baked
1996
3
fenamiphos
0.03
017
ham, baked
1996
3
parathion
0.02
017
ham, baked
1996
4
no residue found
0
017
ham, baked
1997
1
no residue found
0
017
ham, baked
1997
2
no residue found
0
017
ham, baked
1997
3
no residue found
0
Section II.C.3 - Page 321 of 522

-------
Food
017
017
017
017
017
017
017
017
017
017
017
017
017
017
017
017
017
017
017
017
018
018
018
018
018
018
018
018
018
018
/tjk\
Sample Description
Year
Market
Basket
Residue Found
Concentration
(PPm)
ham, baked
1997
no residue found
ham
baked
1998
no residue found
ham
baked
1998
no residue found
ham
baked
1998
no residue found
ham
baked
1998
parathion
0.02
ham
baked
1998
profenofos
0.02
ham
baked
1998
terbufos
0.02
ham
baked
1999
no residue found
ham
baked
1999
no residue found
ham
baked
1999
no residue found
ham
baked
2000
no residue found
ham
baked
2000
no residue found
ham
baked
2000
no residue found
ham
baked
2000
no residue found
ham
baked
2001
no residue found
ham
baked
2001
no residue found
ham
baked
2001
demeton-S sulfone
0.1
ham
baked
2001
fenamiphos sulfoxide
0.04
ham
baked
2001
parathion
0.02
ham, baked
2001
no residue found
pork chop, pan-cooked
1991
no residue found
pork chop, pan-cooked
1992
no residue found
pork chop, pan-cooked
1992
no residue found
pork chop, pan-cooked
1993
no residue found
pork chop, pan-cooked
1993
no residue found
pork chop, pan-cooked
1993
parathion
0.02
pork chop, pan-cooked
1994
chlorpyrifos
0.002
pork chop, pan-cooked
1994
diazinon
0.0008
pork chop, pan-cooked
1994
parathion
0.02
pork chop, pan-cooked
1994
no residue found
Section II.C.3 - Page 322 of 522

-------
Food
018
018
018
018
018
018
018
018
018
018
018
018
018
018
018
018
018
018
018
018
018
018
018
018
018
018
018
018
018
018
/tjk\
Sample Description
Year
Market
Basket
Residue Found
Concentration
(PPm)
pork chop, pan-cooked
1994
no residue found
pork chop
pan-cooked
1994
no residue found
pork chop
pan-cooked
1995
no residue found
pork chop
pan-cooked
1995
no residue found
pork chop
pan-cooked
1995
no residue found
pork chop
pan-cooked
1996
no residue found
pork chop
pan-cooked
1996
diazinon
0.01
pork chop
pan-cooked
1996
parathion
0.02
pork chop
pan-cooked
1996
no residue found
pork chop
pan-cooked
1996
no residue found
pork chop
pan-cooked
1997
no residue found
pork chop
pan-cooked
1997
no residue found
pork chop
pan-cooked
1997
no residue found
pork chop
pan-cooked
1997
no residue found
pork chop
pan-cooked
1998
diazinon
0.01
pork chop
pan-cooked
1998
parathion
0.02
pork chop
pan-cooked
1998
trichlorfon
0.02
pork chop
pan-cooked
1998
no residue found
pork chop
pan-cooked
1998
no residue found
pork chop
pan-cooked
1998
no residue found
pork chop
pan-cooked
1999
no residue found
pork chop
pan-cooked
1999
no residue found
pork chop
pan-cooked
1999
no residue found
pork chop
pan-cooked
2000
no residue found
pork chop
pan-cooked
2000
azinphos-methyl oxygen analog
0.04
pork chop
pan-cooked
2000
diazinon
0.02
pork chop
pan-cooked
2000
fenthion oxygen analog sulfoxide
0.02
pork chop
pan-cooked
2000
naled
0.02
pork chop
pan-cooked
2000
parathion
0.02
pork chop
pan-cooked
2000
no residue found
Section II.C.3 - Page 323 of 522

-------
Food
018
018
018
018
018
018
018
019
019
019
019
019
019
019
019
019
019
019
019
019
019
019
019
019
019
019
019
019
019
019
Sample Description
Year
Market
Basket
Residue Found
pork chop, pan-cooked
2000
no residue found
pork chop, pan-cooked
2001
no residue found
pork chop, pan-cooked
2001
no residue found
pork chop, pan-cooked
2001
no residue found
pork chop, pan-cooked
2001
chlorethoxyfos
pork chop, pan-cooked
2001
diazinon
pork chop, pan-cooked
2001
parathion
pork sausage, pan-cooked
1991
no residue found
pork sausage
pan-cooked
1992
no residue found
pork sausage
pan-cooked
1992
no residue found
pork sausage
pan-cooked
1993
no residue found
pork sausage
pan-cooked
1993
no residue found
pork sausage
pan-cooked
1993
no residue found
pork sausage
pan-cooked
1994
no residue found
pork sausage
pan-cooked
1994
no residue found
pork sausage
pan-cooked
1994
no residue found
pork sausage
pan-cooked
1994
no residue found
pork sausage
pan-cooked
1995
no residue found
pork sausage
pan-cooked
1995
no residue found
pork sausage
pan-cooked
1995
no residue found
pork sausage
pan-cooked
1996
no residue found
pork sausage
pan-cooked
1996
no residue found
pork sausage
pan-cooked
1996
no residue found
pork sausage
pan-cooked
1996
no residue found
pork sausage
pan-cooked
1997
no residue found
pork sausage
pan-cooked
1997
diazinon
pork sausage
pan-cooked
1997
ethion
pork sausage
pan-cooked
1997
methamidophos
pork sausage
pan-cooked
1997
parathion
pork sausage
pan-cooked
1997
ethion
Section II.C.3 - Page 324 of 522

-------
fQ\
iW
Food No
Sample Description
Year
Market
Basket
Residue Found
Concentration
(PPm)
019
pork sausage, pan-cooked
1997
3
phosalone
0.003
019
pork sausage, pan-cooked
1997
4
no residue found
0
019
pork sausage, pan-cooked
1998
1
no residue found
0
019
pork sausage, pan-cooked
1998
2
ethion
0.002
019
pork sausage, pan-cooked
1998
3
acephate
0.02
019
pork sausage, pan-cooked
1998
3
diazinon
0.01
019
pork sausage, pan-cooked
1998
3
parathion
0.02
019
pork sausage, pan-cooked
1998
3
phosalone
0.04
019
pork sausage, pan-cooked
1998
4
no residue found
0
019
pork sausage, pan-cooked
1999
1
ethion
0.002
019
pork sausage, pan-cooked
1999
2
no residue found
0
019
pork sausage, pan-cooked
1999
3
no residue found
0
019
pork sausage, pan-cooked
2000
1
no residue found
0
019
pork sausage, pan-cooked
2000
2
ethion
0.003
019
pork sausage, pan-cooked
2000
3
no residue found
0
019
pork sausage, pan-cooked
2000
4
no residue found
0
019
pork sausage, pan-cooked
2001
1
no residue found
0
019
pork sausage, pan-cooked
2001
2
diazinon
0.04
019
pork sausage, pan-cooked
2001
2
fenthion oxygen analog
0.04
019
pork sausage, pan-cooked
2001
2
fenthion sulfone
0.08
019
pork sausage, pan-cooked
2001
2
parathion
0.04
019
pork sausage, pan-cooked
2001
3
no residue found
0
019
pork sausage, pan-cooked
2001
4
no residue found
0
020
pork bacon, pan-cooked
1991
3
no residue found
0
020
pork bacon, pan-cooked
1992
1
no residue found
0
020
pork bacon, pan-cooked
1992
2
no residue found
0
020
pork bacon, pan-cooked
1993
1
parathion
0.02
020
pork bacon, pan-cooked
1993
2
parathion
0.02
020
pork bacon, pan-cooked
1993
3
no residue found
0
020
pork bacon, pan-cooked
1994
1
no residue found
0
Section II.C.3 - Page 325 of 522

-------
Food
020
020
020
020
020
020
020
020
020
020
020
020
020
020
020
020
020
020
020
020
020
020
020
020
020
020
020
020
020
020
/tjk\
Sample Description
Year
Market
Basket
Residue Found
Concentration
(PPm)
pork bacon, pan-cooked
1994
no residue found
pork bacon
pan-cooked
1994
no residue found
pork bacon
pan-cooked
1994
no residue found
pork bacon
pan-cooked
1995
no residue found
pork bacon
pan-cooked
1995
no residue found
pork bacon
pan-cooked
1995
no residue found
pork bacon
pan-cooked
1996
no residue found
pork bacon
pan-cooked
1996
no residue found
pork bacon
pan-cooked
1996
no residue found
pork bacon
pan-cooked
1996
no residue found
pork bacon
pan-cooked
1997
azinphos-ethyl
0.2
pork bacon
pan-cooked
1997
diazinon
0.01
pork bacon
pan-cooked
1997
parathion
0.02
pork bacon
pan-cooked
1997
no residue found
pork bacon
pan-cooked
1997
no residue found
pork bacon
pan-cooked
1997
diazinon
0.01
pork bacon
pan-cooked
1997
parathion
0.02
pork bacon
pan-cooked
1997
trichlorfon
0.02
pork bacon
pan-cooked
1998
no residue found
pork bacon
pan-cooked
1998
no residue found
pork bacon
pan-cooked
1998
no residue found
pork bacon
pan-cooked
1998
no residue found
pork bacon
pan-cooked
1999
no residue found
pork bacon
pan-cooked
1999
no residue found
pork bacon
pan-cooked
1999
no residue found
pork bacon
pan-cooked
2000
no residue found
pork bacon
pan-cooked
2000
no residue found
pork bacon
pan-cooked
2000
no residue found
pork bacon
pan-cooked
2000
chlorpyrifos oxygen analog
0.2
pork bacon
pan-cooked
2000
dimethoate
0.04
Section II.C.3 - Page 326 of 522

-------
Food
020
020
020
020
020
020
021
021
021
021
021
021
021
021
021
021
021
021
021
021
021
021
021
021
021
021
021
021
021
021
/tjk\
Sample Description
Year
Market
Basket
Residue Found
Concentration
(PPm)
pork bacon, pan-cooked
2000
malathion oxygen analog
0.2
pork bacon, pan-cooked
2000
parathion
0.04
pork bacon, pan-cooked
2001
no residue found
pork bacon, pan-cooked
2001
no residue found
pork bacon, pan-cooked
2001
no residue found
pork bacon, pan-cooked
2001
no residue found
pork roast
baked
1991
no residue found
pork roast
baked
1992
no residue found
pork roast
baked
1992
no residue found
pork roast
baked
1993
no residue found
pork roast
baked
1993
no residue found
pork roast
baked
1993
no residue found
pork roast
baked
1994
no residue found
pork roast
baked
1994
no residue found
pork roast
baked
1994
no residue found
pork roast
baked
1994
no residue found
pork roast
baked
1995
ethion oxygen analog
0.02
pork roast
baked
1995
parathion
0.02
pork roast
baked
1995
no residue found
pork roast
baked
1995
no residue found
pork roast
baked
1996
no residue found
pork roast
baked
1996
no residue found
pork roast
baked
1996
no residue found
pork roast
baked
1996
azinphos-methyl
0.2
pork roast
baked
1996
diazinon
0.01
pork roast
baked
1996
parathion
0.02
pork roast
baked
1997
no residue found
pork roast
baked
1997
no residue found
pork roast
baked
1997
no residue found
pork roast
baked
1997
no residue found
Section II.C.3 - Page 327 of 522

-------
Food
021
021
021
021
021
021
021
021
021
021
021
021
021
021
021
021
021
021
021
021
021
021
021
021
022
022
022
022
022
022
/tjk\
Sample Description
Year
Market
Basket
Residue Found
Concentration
(PPm)
pork roast, baked
1998
1
no residue found
pork roast
baked
1998
no residue found
pork roast
baked
1998
diazinon
0.02
pork roast
baked
1998
omethoate
0.04
pork roast
baked
1998
parathion
0.02
pork roast
baked
1998
tribufos
0.02
pork roast
baked
1998
no residue found
pork roast
baked
1999
no residue found
pork roast
baked
1999
no residue found
pork roast
baked
1999
no residue found
pork roast
baked
2000
no residue found
pork roast
baked
2000
no residue found
pork roast
baked
2000
diazinon
0.02
pork roast
baked
2000
fenthion oxygen analog sulfoxide
0.1
pork roast
baked
2000
naled
0.1
pork roast
baked
2000
parathion
0.02
pork roast
baked
2000
no residue found
pork roast
baked
2001
no residue found
pork roast
baked
2001
diazinon
0.02
pork roast
baked
2001
fenthion oxygen analog
0.02
pork roast
baked
2001
fenthion sulfone
0.04
pork roast
baked
2001
parathion
0.02
pork roast
baked
2001
no residue found
pork roast
baked
2001
no residue found
lamb chop, pan-cooked
1991
no residue found
lamb chop, pan-cooked
1992
no residue found
lamb chop, pan-cooked
1992
no residue found
lamb chop, pan-cooked
1993
no residue found
lamb chop, pan-cooked
1993
no residue found
lamb chop, pan-cooked
1993
no residue found
Section II.C.3 - Page 328 of 522

-------
fQ\
iW
Food No
Sample Description
Year
Market
Basket
Residue Found
Concentration
(ppm)
022
lamb chop, pan-cooked
1994
1
chlorpyrifos
0.006
022
lamb chop, pan-cooked
1994
1
diazinon
0.009
022
lamb chop, pan-cooked
1994
1
parathion
0.02
022
lamb chop, pan-cooked
1994
2
no residue found
0
022
lamb chop, pan-cooked
1994
3
diazinon
0.002
022
lamb chop, pan-cooked
1994
4
parathion
0.02
022
lamb chop, pan-cooked
1995
1
no residue found
0
022
lamb chop, pan-cooked
1995
2
no residue found
0
022
lamb chop, pan-cooked
1995
3
no residue found
0
022
lamb chop, pan-cooked
1996
1
no residue found
0
022
lamb chop, pan-cooked
1996
2
no residue found
0
022
lamb chop, pan-cooked
1996
3
no residue found
0
022
lamb chop, pan-cooked
1996
4
no residue found
0
022
lamb chop, pan-cooked
1997
1
no residue found
0
022
lamb chop, pan-cooked
1997
2
no residue found
0
022
lamb chop, pan-cooked
1997
3
diazinon
0.01
022
lamb chop, pan-cooked
1997
3
mevinphos, (e)-
0.01
022
lamb chop, pan-cooked
1997
3
parathion
0.02
022
lamb chop, pan-cooked
1997
4
no residue found
0
022
lamb chop, pan-cooked
1998
1
no residue found
0
022
lamb chop, pan-cooked
1998
2
no residue found
0
022
lamb chop, pan-cooked
1998
3
no residue found
0
022
lamb chop, pan-cooked
1998
4
no residue found
0
022
lamb chop, pan-cooked
1999
1
chlorpyrifos
0.0002
022
lamb chop, pan-cooked
1999
2
diazinon
0.02
022
lamb chop, pan-cooked
1999
2
disulfoton sulfone
0.02
022
lamb chop, pan-cooked
1999
2
ethoprop
0.02
022
lamb chop, pan-cooked
1999
2
parathion
0.02
022
lamb chop, pan-cooked
1999
3
cadusafos
0.02
022
lamb chop, pan-cooked
1999
3
diazinon
0.002
Section II.C.3 - Page 329 of 522

-------
Food
022
022
022
022
022
022
022
022
022
022
029
029
029
029
029
029
029
029
029
029
029
029
029
029
029
029
029
029
029
029
/tjk\
Sample Description
Year
Market
Basket
Residue Found
Concentration
(PPm)
lamb chop, pan-cooked
1999
diazinon
0.02
lamb chop
pan-cooked
1999
parathion
0.02
lamb chop
pan-cooked
2000
no residue found
lamb chop
pan-cooked
2000
no residue found
lamb chop
pan-cooked
2000
no residue found
lamb chop
pan-cooked
2000
no residue found
lamb chop
pan-cooked
2001
no residue found
lamb chop
pan-cooked
2001
no residue found
lamb chop
pan-cooked
2001
no residue found
lamb chop
pan-cooked
2001
no residue found
bologna
iced
1991
no residue found
bologna
iced
1992
no residue found
bologna
iced
1992
no residue found
bologna
iced
1993
no residue found
bologna
iced
1993
no residue found
bologna
iced
1993
no residue found
bologna
iced
1994
no residue found
bologna
iced
1994
no residue found
bologna
iced
1994
no residue found
bologna
iced
1994
no residue found
bologna
iced
1995
no residue found
bologna
iced
1995
no residue found
bologna
iced
1995
no residue found
bologna
iced
1996
no residue found
bologna
iced
1996
no residue found
bologna
iced
1996
diazinon
0.01
bologna
iced
1996
fenamiphos
0.03
bologna
iced
1996
parathion
0.02
bologna
iced
1996
no residue found
bologna
iced
1997
no residue found
Section II.C.3 - Page 330 of 522

-------
Food
029
029
029
029
029
029
029
029
029
029
029
029
029
029
029
029
029
029
029
029
029
029
029
029
030
030
030
030
030
030
/tjk\
Sample Description
Year
Market
Basket
Residue Found
Concentration
(PPm)
bologna, sliced
1997
no residue found
bologna
iced
1997
no residue found
bologna
iced
1997
no residue found
bologna
iced
1998
diazinon
0.01
bologna
iced
1998
DDVP
0.02
bologna
iced
1998
parathion
0.02
bologna
iced
1998
no residue found
bologna
iced
1998
no residue found
bologna
iced
1998
no residue found
bologna
iced
1999
no residue found
bologna
iced
1999
no residue found
bologna
iced
1999
no residue found
bologna
iced
2000
no residue found
bologna
iced
2000
azinphos-methyl oxygen analog
0.08
bologna
iced
2000
diazinon
0.04
bologna
iced
2000
fenthion oxygen analog sulfoxide
0.04
bologna
iced
2000
naled
0.04
bologna
iced
2000
parathion
0.04
bologna
iced
2000
no residue found
bologna
iced
2000
no residue found
bologna
iced
2001
no residue found
bologna
iced
2001
no residue found
bologna
iced
2001
no residue found
bologna, sliced
2001
no residue found
salami, sliced
1991
no residue found
salami, sliced
1992
no residue found
salami, sliced
1992
no residue found
salami, sliced
1993
no residue found
salami, sliced
1993
no residue found
salami, sliced
1993
no residue found
Section II.C.3 - Page 331 of 522

-------
Food
030
030
030
030
030
030
030
030
030
030
030
030
030
030
030
030
030
030
030
030
030
030
030
030
030
030
030
030
030
030
/tjk\
Sample Description
Year
Market
Basket
Residue Found
Concentration
(PPm)
salami
sliced
1994
1
no residue found
salami
iced
1994
no residue found
salami
iced
1994
no residue found
salami
iced
1994
no residue found
salami
iced
1995
no residue found
salami
iced
1995
no residue found
salami
iced
1995
no residue found
salami
iced
1996
no residue found
salami
iced
1996
diazinon
0.01
salami
iced
1996
parathion
0.02
salami
iced
1996
no residue found
salami
iced
1996
no residue found
salami
iced
1997
no residue found
salami
iced
1997
diazinon
0.01
salami
iced
1997
methamidophos
0.02
salami
iced
1997
parathion
0.02
salami
iced
1997
no residue found
salami
iced
1997
no residue found
salami
iced
1998
no residue found
salami
iced
1998
no residue found
salami
iced
1998
no residue found
salami
iced
1998
no residue found
salami
iced
1999
no residue found
salami
iced
1999
no residue found
salami
iced
1999
no residue found
salami
iced
2000
no residue found
salami
iced
2000
azinphos-methyl oxygen analog
0.04
salami
iced
2000
diazinon
0.02
salami
salami
iced
iced
2000
2000
fenthion oxygen analog sulfoxide
naled
0.02
0.02
Section II.C.3 - Page 332 of 522

-------
Food
030
030
030
030
030
030
030
030
030
030
238
238
238
238
238
238
238
238
238
238
238
238
238
238
238
238
238
238
238
238
/tjk\
Sample Description
Year
Market
Basket
Residue Found
Concentration
(PPm)
salami, sliced
2000
parathion
0.02
salami
sliced
2000
no residue found
salami
sliced
2000
chlorpyrifos oxygen analog
0.1
salami
sliced
2000
dimethoate
0.02
salami
sliced
2000
malathion oxygen analog
0.1
salami
sliced
2000
parathion
0.02
salami
sliced
2001
no residue found
salami
sliced
2001
no residue found
salami
sliced
2001
no residue found
salami, sliced
2001
no residue found
veal cutlet, pan-cooked
1991
no residue found
vea
cut
pan-cooked
1992
no residue found
vea
cut
pan-cooked
1992
no residue found
vea
cut
pan-cooked
1993
parathion
0.02
vea
cut
pan-cooked
1993
no residue found
vea
cut
pan-cooked
1993
parathion
0.02
vea
cut
pan-cooked
1994
parathion
0.02
vea
cut
pan-cooked
1994
no residue found
vea
cut
pan-cooked
1994
malathion
0.001
vea
cut
pan-cooked
1994
no residue found
vea
cut
pan-cooked
1995
no residue found
vea
cut
pan-cooked
1995
no residue found
vea
cut
pan-cooked
1995
no residue found
vea
cut
pan-cooked
1996
no residue found
vea
cut
pan-cooked
1996
no residue found
vea
cut
pan-cooked
1996
no residue found
vea
cut
pan-cooked
1996
azinphos-methyl
0.2
vea
cut
pan-cooked
1996
diazinon
0.01
vea
cut
pan-cooked
1996
parathion
0.02
vea
cut
pan-cooked
1997
no residue found
Section II.C.3 - Page 333 of 522

-------
Food
238
238
238
238
238
238
238
238
238
238
238
238
238
238
238
238
238
238
238
238
238
238
239
239
239
239
239
239
239
239
/tjk\
Sample Description
Year
Market
Basket
Residue Found
Concentration
(PPm)
veal cutle
pan-cooked
1997
no residue found
vea
cut
pan-cooked
1997
no residue found
vea
cut
pan-cooked
1997
no residue found
vea
cut
pan-cooked
1998
no residue found
vea
cut
pan-cooked
1998
no residue found
vea
cut
pan-cooked
1998
no residue found
vea
cut
pan-cooked
1998
parathion
0.02
vea
cut
pan-cooked
1998
profenofos
0.02
vea
cut
pan-cooked
1998
terbufos
0.02
vea
cut
pan-cooked
1999
no residue found
vea
cut
pan-cooked
1999
no residue found
vea
cut
pan-cooked
1999
no residue found
vea
cut
pan-cooked
2000
no residue found
vea
cut
pan-cooked
2000
no residue found
vea
cut
pan-cooked
2000
no residue found
vea
cut
pan-cooked
2000
no residue found
vea
cut
pan-cooked
2001
no residue found
vea
cut
pan-cooked
2001
no residue found
vea
cut
pan-cooked
2001
demeton-S sulfone
0.1
vea
cut
pan-cooked
2001
fenamiphos sulfoxide
0.04
vea
cut
pan-cooked
2001
parathion
0.02
veal cutlet, pan-cooked
2001
no residue found
ham luncheon meat, sliced
1991
no residue found
ham luncheon meat, sliced
1992
no residue found
ham luncheon meat, sliced
1992
parathion
0.02
ham luncheon meat, sliced
1992
phosalone
0.06
ham luncheon meat, sliced
1993
no residue found
ham luncheon meat, sliced
1993
no residue found
ham luncheon meat, sliced
1993
no residue found
ham luncheon meat, sliced
1994
no residue found
Section II.C.3 - Page 334 of 522

-------
fQ\
iW
Food No
Sample Description
Year
Market
Basket
Residue Found
Concentration
(ppm)
239
ham luncheon meat, sliced
1994
2
no residue found
0
239
ham luncheon meat, sliced
1994
3
parathion
0.02
239
ham luncheon meat, sliced
1994
4
no residue found
0
239
ham luncheon meat, sliced
1995
1
ethion oxygen analog
0.02
239
ham luncheon meat, sliced
1995
1
parathion
0.02
239
ham luncheon meat, sliced
1995
2
diazinon
0.01
239
ham luncheon meat, sliced
1995
2
parathion
0.02
239
ham luncheon meat, sliced
1995
3
no residue found
0
239
ham luncheon meat, sliced
1996
1
no residue found
0
239
ham luncheon meat, sliced
1996
2
no residue found
0
239
ham luncheon meat, sliced
1996
3
no residue found
0
239
ham luncheon meat, sliced
1996
4
no residue found
0
239
ham luncheon meat, sliced
1997
1
no residue found
0
239
ham luncheon meat, sliced
1997
2
no residue found
0
239
ham luncheon meat, sliced
1997
3
no residue found
0
239
ham luncheon meat, sliced
1997
4
no residue found
0
239
ham luncheon meat, sliced
1998
1
diazinon
0.01
239
ham luncheon meat, sliced
1998
1
DDVP
0.02
239
ham luncheon meat, sliced
1998
1
parathion
0.02
239
ham luncheon meat, sliced
1998
2
no residue found
0
239
ham luncheon meat, sliced
1998
3
no residue found
0
239
ham luncheon meat, sliced
1998
4
no residue found
0
239
ham luncheon meat, sliced
1999
1
no residue found
0
239
ham luncheon meat, sliced
1999
2
no residue found
0
239
ham luncheon meat, sliced
1999
3
no residue found
0
239
ham luncheon meat, sliced
2000
1
no residue found
0
239
ham luncheon meat, sliced
2000
2
no residue found
0
239
ham luncheon meat, sliced
2000
3
no residue found
0
239
ham luncheon meat, sliced
2000
4
no residue found
0
239
ham luncheon meat, sliced
2001
1
no residue found
0

Section II.C.3 - Page 335 of 522

-------
* ~ v*
rv *
Food No
Sample Description
Year
Market
Basket
Residue Found
Concentration
(ppm)
239
ham luncheon meat, sliced
2001
2
diazinon
0.02
239
ham luncheon meat, sliced
2001
2
fenthion oxygen analog
0.02
239
ham luncheon meat, sliced
2001
2
fenthion sulfone
0.04
239
ham luncheon meat, sliced
2001
2
parathion
0.02
239
ham luncheon meat, sliced
2001
3
no residue found
0
239
ham luncheon meat, sliced
2001
4
no residue found
0
Section II.C.3 - Page 336 of 522

-------
i jQu'i
C-4. Permissible Crop Translations for Pesticide Monitoring Data Table
Table II.C-4.1 Permissible Crop Translations for Pesticide Monitoring Data24.
Commodity Analyzed
Commodity translated to...
Comments
Potato
Subgroup 1-C

Carrot
Subgroup 1-A or 1-C

Head Lettuce
Cabbage, Chinese cabbage napa (tight headed
varieties), Brussels sprouts, radicchio
All have a head morphology best represented by lettuce. All are in Subgroup
5A except radicchio (4-A).
Broccoli
Cauliflower, Chinese broccoli, Chinese cabbage
bok choy, Chinese mustard, kohlrabi
Broccoli better represents these heading, thickly stemmed and/or more
branching cole crops than spinach does.
Spinach
Subgroup 4-A, Subgroup 5-B and Subgroup 4-B
(except celery and fennel unless a strong case can
be made)
Celery and fennel typically are excluded since residues may be higher in these
crops due to the whorled, overlapping petioles which may retain spray residues.
Green Bean
Subgroups 6-A and 6-B

Soybean
Subgroup 6-C

Tomato or bell pepper
Group 8
All are fruiting vegetables.
Cucumber
Subgroup 9-B
All are cucurbit vegetables; residues in melon and pumpkin expected to be
lower because of removal of rind.
Cantaloupe or Winter squash
Subgroup 9-A and pumpkin
Orange
Group 10
Fruit will be peeled before analysis by PDP.
Apple or Pear
Group 11
All are pome fruits.
Peach
Group 12, except cherries (sweet and tart)
All are stone fruits.
Grape
Kiwifruit
Based on similar cultural practices.
Wheat
Group 15, except corn, rice, or wild rice
All are small grain crops or closely related thereto.
Milk
Meat
Metabolism study must indicate that residues in meat, fat, and meat-by-products
will likely be equal to or lower than residues in milk. If dermal use is allowed on
beef cattle, then it must be permitted and used on dairy cattle as well.
24 Extracted from OPP/HED SOP 99.3
Section II.C.4 - Page 337 of 522

-------
C-5. Processing Factors Used in Estimating Residues of OP Pesticides in Food Commodities
See file ll_C_5.xls
C-6. Translation of Residue Source Data to CSFII Food Forms
See file ll_C_6.xls
C-7. Summary of Residue Distribution Inputs to DEEM-FCID for Cumulative OP Exposure Assessment
See file ll_C_7.xls
C-8. Analysis of Chemicals and Foods in the Upper Portion of OP Cumulative Exposure Distribution for
Children 3-5 Years Old
See file ll_C_8.xls
C-9. Co-Occurrence of Organophosphorus Pesticides on PDP Samples, 1994-2004
See file II.C 9.xls
Section II.C. 5, 6, 7, 8, & 9 - Page 338 of 522

-------
D-1. Supplemental Distributions of Exposure Data Incorporated in the
Residential Assessment
Study Summary
MRID 410547-05 (Exposures of Applicators to Propoxur during
Residential Application of an Aerosol Spray Containing 1%
Propoxur): Applicators in the study each applied one 16-ounce
aerosol can in each of the 15 residences situated in Vero Beach,
Florida. The entire contents were applied to each house. The
volunteers sprayed to cracks, crevices along baseboards and other
woodwork, under sinks and behind appliances. The majority of the
exposure was to the hands, neck and head (~85%).
Unit Exposure Data
Table II.D-1.1 Dermal Unit Exposure Data (MRID 41054705) Used for Indoor
Aerosol Applicator Scenarios)
Dermal Unit
Exposure Values
(mg/oz ai handled)
	5A	
	5^3	
	7	
	3A	
	2_3	
	3	
	7J	
	2_5	
	3A	
	0J)	
	3J3	
0.98
	27	
0.85
0.85
Section II.D.1 - Page 339 of 522

-------
Table II.D-1.2 Inhalation Unit Exposure Data (MRID 41054705 Used for
Indoor Aerosol Applicator Scenarios)
Inhalation Unit
Exposure Values
(mg/oz ai handled)
0.33
0.043
0.51	
0.38
0.49
0.48
0.42
0.35
0.56
0.16
0.25
0.22
0.25
	0J	
0.14
Statistical Analysis Details
Distributional parameters were estimated for the dermal unit exposure
(Table II.D. 1 1) and inhalation unit exposure (Table II.D. 1 2) values for
pressurized can sprayer applications of propoxur. Both unit exposure
values are expressed in terms of milligrams per ounce of active
ingredient applied. The dermal and inhalation unit exposure values
were assumed to be lognormally distributed (i.e. fitted with a lognormal
distribution). For these datasets, the shape (a) and scale (P)
lognormal parameters were estimated by calculating the mean and
standard deviation of the natural logarithms (base e) of the dermal and
inhalation unit exposure values, respectively. Parametric estimates of
the arithmetic mean (jx) and standard deviation (a) of the lognormal
distribution were then calculated based on the shape and scale
parameter estimates. The formulae used to calculate the mean and
standard deviation are given below
ji = exp(a + ^p2)
a = fi^/exp(p2) -1
Shapiro-Wilk (S-W) normality test statistics were used to assess the
lognormal assumption implicit in the parametric calculations of the mean
and standard deviation. The means, standard deviations, and p-values of
Section II.D.1 - Page 340 of 522

-------
the S-W statistics are provided in Table II.D. 1 3. A small p-value indicates
that logarithms of the dermal and inhalation unit exposure values are not
normally distributed, or equivalently, that the dermal and inhalation unit
exposure values are not lognormally distributed. For both the dermal and
inhalation pressurized can datasets, the S-W p-values are greater than
0.05.
Table II.D-1.3 Lognormal Distributions of Dermal and Inhalation Unit
Exposure Values Used for Indoor Aerosol Applicator Scenarios)
Application
Method
Exposure
Route
Deposition (mg/cm^) and
Air Concentration (mg/m3)
Distributions
Shapiro-Wilk
p-value
Handheld
Aerosol Spray
Can
Dermal
LN(10.03, 12.84)
0.069
Inhalation
LN(0.34, 0.27)
0.063
NOTES:
LN(|a, ct) represents a lognormal distribution with mean=|a and standard deviations.
Additionally, probability plots were used to qualitatively assess the
appropriateness of the lognormal assumptions. Generally a probability
plot displays the actual values of a dataset (represented as points) and
their expected values (represented as a line) for the specified distribution.
The closer the actual values are to their expected values (i.e. the more the
actual values approximate a straight line), the more likely the dataset is of
the specified distribution. The probability plots for the dermal and
inhalation unit exposure datasets are provided in Figures II.D. 1 1 and 2.
The probability plots indicate that both datasets are reasonably
approximated by lognormal distributions.
Section II.D.1 - Page 341 of 522

-------
Figure II.D-1.1 Dermal Unit Exposure Probability Plot
2.5-
.01 .05.10 .25 .50
.99
2-
1.5-
0.5-
0-
-0.5-
3
2
1
0
1
2
3
Normal Quantile Plot
Figure II.D-1.2 Inhalation Unit Exposure Probability Plot
0-
.01 .05.10 .25 .50
.99
-0.5-
-1.5-
-2-
-2.5-
-3-
-3.5-
3
2
1
0
1
2
3
Normal Quantile Plot
Section II.D.1 - Page 342 of 522

-------
E-1. OP Cumulative Exposure in Drinking Water: The Effects of Water
Chlorination on Organophosphate (OP) Pesticides (Phase I)
This report is an addendum to the 2002 OP CRA drinking water
appendix II.E.4 - Effects of Drinking Water Treatment on Organophosphate
Pesticides. Phase I of this study evaluated the potential of ten OP pesticides
to form oxons as a result oxidation during drinking water treatment
processes. Phase II of the study evaluated the potential of the sulfone and
sulfoxide transformation products of disulfoton, phorate, and terbufos to
form oxons.
The studies were conducted by the USEPA Office of Pesticide
Program (OPP) Biological and Economic Analysis Division (BEAD)
laboratories and have been reviewed by the USEPA Office of Research and
Development (ORD). The results support the oxon characterization in the
drinking water exposure assessment for the 2006 OP CRA.
1. Executive Summary - Phase I
Ten organophosphate (OP) pesticides [phorate, disulfoton, terbufos,
methidathion, bensulide, chlorethoxyfos, phosmet, methyl parathion,
phostebupirim, and temephos] were evaluated for their potential to undergo
oxidation to their respective oxons in laboratory water simulating the
chlorination process in drinking water facilities over a 72 hour exposure
period. Samples were collected after 0, 1, 4, 24, and 72 hours of
chlorination and analyzed by both gas chromatography-mass selective
detection (GC-MSD) and liquid chromatography-tandem mass spectrometry
(LC/MS/MS) to determine the presence of the pesticides and their oxons.
The results show that only two of the ten OP pesticides [methidathion
and methyl parathion] are stable in buffered water (without chlorination) over
the 72 hour exposure period. The eight remaining OP pesticides [phorate,
disulfoton, terbufos, bensulide, chlorethyoxyfos, phostebupirim, phosmet,
and temephos] were unstable and degraded in the buffered water over the
72 hour exposure period.
The results also show that in chlorinated water, three of the ten OP
pesticides [phorate, disulfoton, and terbufos] did not undergo oxidation to
their oxons under the experiment conditions. Phosmet oxon was initially
formed; however, it degraded and was not detected after 24 hours. Five of
the remaining six OP pesticides [methidathion, bensulide, chlorethyoxyfos,
methyl parathion, and phostebupirim] formed stable oxons over the 72
exposure period. The oxon of the last remaining OP pesticide, temephos, is
not commercially available and its presence could not be confirmed under
Section II.E. 1 - Page 343 of 522

-------
the experimental conditions. However, a full scan spectrum of the oxidation
products from an exploratory LC/MS study revealed the presence of a
compound with the same molecular ion profile as would be expected for the
temephos oxon. Table II.E-1.1 summarizes the results of the experiment.
able II.E-1.1 Results for parameters examined in study.
OP Pesticide
Stability in
water over 72
hours (no
chlorination)
Oxon formation
after 1 hour
(upon
chlorination)
Oxon
stability
after 72
hours
Phorate
Poor
No
-
Disulfoton
Poor
No
-
Terbufos
Poor
No
-
Methidathion
Good
Yes
Good
Bensulide
Poor
Yes
Good
Chlorethoxyfos
Poor
Yes
Good
Methyl parathion
Good
Yes
Good
Phosmet
Poor
Yes
Poor
Phostebupirim
Poor
Yes
Good
Temephos
Poor
Possible
(not confirmed)
n/a
In accordance with the Quality Assurance Project Plan (QAPP) for
study, there were two elements necessary for the strict qualitative
interpretation whether the ten OP pesticides underwent oxidative
desulfonation during a 72 hour contact time in chlorinated laboratory water.
This conclusion would be reached if the oxons are detected at any
quantifiable level in either replication in the chlorinated laboratory water
treatments at any sampling time and the OP pesticides are stable in non-
chlorinated laboratory water. Only methidathion and methyl parathion met
those criteria.
2. Introduction
The application of pesticides in arable lands has resulted in the
contamination of natural waters such as surface water and groundwater.
The initial contamination at the application sites has spread via surface
runoff to nearby lakes, rivers, and streams and through subsurface
transport to aquifers. The contaminated surface waters and ground waters
are eventually used as source or raw waters in some community drinking
water systems. After subjecting the raw water to different treatment
processes in the water purification facilities, the concentrations of the
pesticides may change or remain essentially the same in the treated or
final drinking water. Studies conducted by scientists at EPA's ORD in
Cincinnati (Miltner et al, 1989) indicate that conventional treatment
(coagulation/clarification, filtration, softening, recarbonation, and
chlorination) are generally not effective in removing certain pesticides from
Section II.E. 1 - Page 344 of 522

-------
raw water. However, other pesticides are unstable in the presence of
chemical disinfectant such as chlorine.
Previous studies in Japan (Magara et al, 1994) and United States
(Tierney et al, 2001; Duirk and Collette, 2006) indicate that certain
organophosphate pesticides can be transformed to their oxons during
chemical disinfection by chlorine compounds. This chemical
transformation process is shown in Figure III.E-1.1.
Figure II.E-1.1 Oxidative Desulfonation Reaction of an
Organophosphate Pesticide in Chlorinated Water.
This transformation is a concern because chlorination is the most
commonly used disinfection technique in many US drinking water
treatment plants and the product oxons are generally considered to be
more toxic than the parent compounds.
The Food Quality Protection Act of 1996 (FQPA) requires that all
chemical pesticide residues in or on food be examined for any possible
adverse health effects through exposure. Drinking water is one of the
pathways for dietary exposure. Three organophosphate pesticides
(diazinon, chlorpyrifos, and malathion) have been examined and have
been found to transform during chlorination into their associated oxons.
However, a number of other organophosphate pesticides have little or no
data on their potential for transformation during these conditions.
Consequently, data and additional information are needed on the probable
oxidation of these organophosphate pesticides and the relative stability of
oxons in chlorinated water. The ten organophosphate pesticides and their
degradation products considered in this study are listed in Table II.E-1. 2.
o
Section II.E. 1 - Page 345 of 522

-------
Table II.E-1.2 Selected Organophosphate Pesticides from the Cumulative
OP Assessment without Water Treatment Data on Chlorination Effects on
Oxon Formation
OP Parent
OP Degradation Products
Phorate
phorate oxon
phorate sulfoxide
phorate sulfone
phorate sulfoxide oxon
phorate sulfone oxon
Disulfoton
disulfoton oxon
disulfoton sulfoxide
disulfoton sulfone
disulfoton sulfoxide oxon
disulfoton sulfone oxon
Terbufos
terbufos oxon
terbufos sulfoxide
terbufos sulfone
terbufos sulfoxide oxon
terbufos sulfone oxon
Methidathion
methidathion oxon
Bensulide
bensulide oxon
Chlorethoxyfos
chlorethoxyfos oxon
Methyl parathion
methyl paraoxon
Phosmet
phosmet oxon
Phostebupirim
phostebupirim oxon
Temephos
Temephos oxon (not available)
The objective of this study was to provide a qualitative screening
level assessment on the potential for oxon formation in chlorinated
laboratory water and the stability of the selected organophosphate
pesticides in both un-chlorinated and chlorinated water and the stability of
their respective oxons in the chlorinated laboratory water. There are
approximately twenty organophosphate pesticides considered in the
cumulative OP risk assessment. The ten selected pesticides being tested
in this study consisted of the pesticides, which are capable of forming
oxons, have outdoor use patterns, and have no chlorination water
treatment data available. These data will be used in the revised
cumulative OP risk assessment to characterize the potential for human
exposure to oxons in treated water.
Section II.E. 1 - Page 346 of 522

-------
3. Project Description
The project description is listed in the study protocol in Appendix 1
(Section 7). A brief summary description follows:
For each of the ten OP pesticides to be tested, the experimental
design consisted of:
-	One replicate OP control [test water + OP pesticide, without chlorine]
-	One replicate chlorine control [test water + chlorine]
-	Two replicates of treatment [OP pesticide + test water + chlorine]
-	One buffered water sample spiked with the ten pesticides and nine
oxons at a concentration of % of the spiking concentration (50 ppb) at
each sampling time.
Chlorination experiments were conducted in Fisher Environmental
Grade reagent water to eliminate chlorine demand considerations. Similar
testing conditions using laboratory waters are recommended as screening
level testing for CCL water treatment studies and pesticide treatment
studies at ORD. The chlorine dose in the laboratory water was equivalent
to the recommended maximum disinfectant residual (RMDL) of 4 mg/L
free chlorine concentration ± 10%. The pH of the Fisher reagent water
was adjusted to pH 8 to represent typical water treatment conditions. The
experiment was conducted for 72 hours with sampling times immediately
prior to chlorination (~2 minutes after pesticide dosing), 1 hour, 4 hours,
24 hours, and 72 hours post chlorination. The 24 and 72 hour sampling
times were selected to represent the treatment system water residence
and/or distribution transport times of approximately 24 hr or longer. The
pesticide concentration in the experiment was 100 ppb or below the
solubility limit of the pesticide whichever is lower. The experiments were
conducted using a mixture of the OP pesticides delivered to the system
with low co-solvent concentrations or in the absence of co-solvents. The
chlorine demand from co-solvents and degradation processes was
determined by measuring free chlorine at each sampling interval.
Section II.E. 1 - Page 347 of 522

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i
4. Method and Materials
Fisher Scientific Certified Environmental Grade water was used as
the test water. Water quality parameters of the test water were:
Water samples were labeled clearly, and included date, time, and
name of the preparer(s). To preserve the integrity of the data, all samples
were stored at ~ 4°C until extraction to minimize the physicochemical
changes in the samples. If sample extraction into a solvent was
necessary, extracts were stored below 0°C and also analyzed as soon as
possible. All samples used and generated during the study were properly
disposed of.
Quality assurance samples consisted of:
1)	reagent water blank - analysis of reagent water (one time only);
2)	method blank - analysis of buffered reagent water plus chlorine;
(time 1 hr);
3)	non-chlorinated degradation check - analysis of buffered reagent
water plus OPs; (time 0, 1, 4, 24, and 72 hrs);
4)	matrix water blank - analysis of buffered reagent water (time 0);
5)	matrix water spike - analysis of buffered reagent water plus 50
ppb of the OP parent(s) plus 50 ppb oxon(s) (one spike per analytical
sample set).
These measures were classified as critical measurements and were
prepared and analyzed with each group of samples to monitor laboratory
contamination and method performance. Addition of surrogate
compounds to environmental samples was also recommended to measure
the efficiency of the method. The surrogate compounds was not normally
found in the environment and was selected such that the interference with
elution of target analytes and the effect from sample matrix were minimal.
a. Analytical Procedures
The analytical procedures used were able to accurately identify and
measure the presence of the target analytes in the samples.
Identification and quantitation of residues were by gas
Test
Color
Residue after Evaporation
Fluorescence (as quinine)
Resistivity
Total Organic Carbon
Value
<	5
<	1
<	100
> 18
<20
Unit
APHA
ppm
ppt
MQ
ppb
Section II.E. 1 - Page 348 of 522

-------
chromatography-mass selective detection (GC/MSD) and/or liquid
chromatography/tandem mass spectrometry (LC/MS/MS) techniques.
A calibration curve was constructed with mixtures(s) of pure
standards (target analytes) with the spiking level and method detection
limit as the bounding concentrations. Complete initial calibration
curves were prepared monthly, and the individual calibration standards
verified each day of operation.
In some cases, the analytical procedures were not completely
developed to allow for complete quantification of the parent OP and its
degradation products. Nevertheless, the analytical method was
capable of providing clear separation of known pesticide residues on
chromatograms to allow for residue identification.
b. Test Protocol
These studies were conducted at the OPP/BEAD/ACB Fort Meade
and OPP/BEAD/ECB Stennis Space Center laboratories. A complete
description of testing protocol can be found in the Appendix 1 (Section
7).
The control treatments were used to assess whether the OP
pesticide undergoes oxidation in non-chlorinated laboratory water and
to assess whether OP pesticide or its degradation products were in the
chlorinated water without pesticide dosing. Because the experimental
design had minimal replication and the analytical methods were not
fully vetted for all the OP pesticides and their oxon degradation
products, there was strict qualitative interpretation (i.e. presence or
absence of oxon) on whether OP pesticides underwent oxidative
desulfonation during a 72 hour contact time in chlorinated laboratory
water. This deduction was reached if oxons were detected at any
quantifiable level in either replication in the chlorinated laboratory water
treatments at any sampling time and the OP pesticide was stable in
non-chlorinated laboratory water. Additionally, the detection of oxons
in chlorinated water at the 24 hour or 72 hour sampling times will
suggest the oxon was stable enough in chlorinated water to have the
potential for dietary exposure through drinking water
The primary focuses of these studies were the OP parent
pesticides and their associated oxons, degradation products. Later
studies will address the measurements of the sulfone, sulfoxide,
sulfone oxon, and sulfoxide oxon degradation products for selected OP
pesticides. Method detection and reporting limits will be reported in
revisions to this QAPP once the analytical methods have been
assessed.
Section II.E. 1 - Page 349 of 522

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. Assessment and Oversight
A QA/QC laboratory audit was performed at the conclusion of the
water chlorination studies with OP pesticides and their oxon
degradation products. Subsequently, QA/QC audits will be performed
at the conclusion of the water chlorination studies with certain OP
pesticides and their sulfone, sulfoxide, sulfone oxon, and sulfoxide
oxon.
Results
. The Formation of Oxons from Ten OP Pesticides in Water
Ten organophosphate (OP) pesticides [phorate, disulfoton,
terbufos, methidathion, bensulide, chlorethoxyfos, phosmet, methyl
parathion, phostebupirim, and temephos] were evaluated for their
potential to undergo oxidation to their respective oxons in laboratory
water simulating the chlorination process in drinking water facilities. In
these studies, the OP pesticides were dissolved into pH 8.0 buffered
water and then chlorinated with a sodium hypochlorite solution. Over a
72 hour exposure period, water samples were collected, extracted
whenever applicable, and analyzed by both gas chromatography-mass
selective detection (GC-MSD) and liquid chromatography-tandem
mass spectrometry (LC/MS/MS) to determine the presence of the
pesticides and their oxons. The results are presented in Appendix 2
(Section 8) for both the GS-MSD and LC/MS/MS studies.
The results of both studies (GC-MSD & LC/MS/MS) showed that
three of the ten OP pesticides (phorate, disulfoton, and terbufos) did
not undergo oxidation into their oxons under the experiment conditions.
Phosmet oxon was initially formed; however, it degraded and was not
detected after 24 hours. Five of the remaining six OP pesticides
[methidathion, bensulide, chlorethyoxyfos, methyl parathion, and
phosetebuprim] formed stable oxons over the 72 exposure period. The
oxon of the last remaining OP pesticide, temephos, is not commercially
available and its presence could not be confirmed under the
experimental conditions. However, a full scan spectrum of the
oxidation products in an exploratory LC/MS study revealed the
presence of a compound with the same molecular ion profile as would
be expected for the temephos oxon. This exploratory study was
conducted at a concentration of 5 ppm of temephos in chlorinated
laboratory water. The detected compound increased in concentration
during a 24 hour exposure period, simultaneously, with the decrease of
the parent OP temephos. The lack of an authentic standard of the
temephos oxon limits the complete confirmation of this oxon.
Section II.E. 1 - Page 350 of 522

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The analytical methods of GC-MSD and LC/MS/MS were
complimentary to each other in the detection of all 10 OP pesticide
parents and their oxons. The current GC/MSD conditions were not
suitable for the detection of bensulide, while the LC/MS/MS conditions
were not suitable for the detection of methyl parathion and
chlorethoxyfos. However, their oxons were detectable under both
method conditions.
b.	The Stability of Ten OP Pesticides in Water
Ten organophosphate (OP) pesticides [phorate, disulfoton,
terbufos, methidathion, bensulide, chlorethyoxyfos, phosmet, methyl
parathion, phosetebuprim, and temephos] were evaluated in buffered
laboratory water to act as a control to the separate studies of the
pesticides in the buffered water during the chlorination process. In
these studies the OP pesticides were dissolved into a pH 8.0 buffered
water. Over a 72 hour exposure period, water samples were collected,
extracted, and analyzed by both gas chromatography-mass selective
detection (GC-MSD) and liquid chromatography-tandem mass
spectrometry (LC/MS/MS) to determine the presence of the pesticides
and their oxons without chlorination. The results are presented in
Appendix 2 (Section 8) for both the GS-MSD and LC/MS/MS studies.
The results demonstrated that two of the ten OP pesticides
[methidathion and methyl parathion], are stable in the buffered water
without chlorination over the 72 hour exposure period. The eight
remaining OP pesticides [phorate, disulfoton, terbufos, bensulide,
chlorethyoxyfos, phosetebuprim, phosmet, and temephos] were
unstable and degraded in the buffered water over the 72 hour
exposure period.
c.	The Stability of Free Chlorine Concentrations in Water
The concentration of chlorine as free chlorine was evaluated in
buffered laboratory water to act as a control to the separate studies of
the pesticides in the buffered water during the chlorination process. In
these studies chlorine as free chlorine was added to a pH 8.0 buffered
water. Over a 72 hour exposure period, water samples were collected
and analyzed to determine the stable concentration of this form of
chlorine. In both studies the concentration of free chlorine remained
stable within 10% of the initial concentration and neither the OP
pesticides nor their oxons were detected at any time during the 72 hour
exposure period.
Section II.E. 1 - Page 351 of 522

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d. The Stability of 10 OP Pesticides and Their Oxons as Laboratory
Control Spike Samples
Ten organophosphate (OP) pesticides [phorate, disulfoton,
terbufos, methidathion, bensulide, chlorethyoxyfos, phosmet, methyl
parathion, phosetebuprim, and temephos] and their nine available
oxons [temephos oxon is not available] were spiked into pH 8.0
buffered laboratory water to act as laboratory control spike samples.
These samples were used to assess the detection of these compounds
at the time of analysis. The water samples were collected, spiked,
extracted whenever applicable, and analyzed by both gas
chromatography-mass selective detection (GC-MSD) and liquid
chromatography-tandem mass spectrometry (LC/MS/MS) to determine
the concentration of the pesticides and their oxons. The results are
presented in Appendix 2 (Section 8) for both the GS-MSD and
LC/MS/MS studies.
The results demonstrated that these pesticides, with the exception
of methyl parathion and methidathion, were unstable and degrade in
the buffered water if they were allowed to remain for any prolonged
period prior to extraction and/or analysis. In the LC/MS/MS studies the
laboratory control spike samples remained in the buffered water until
analyzed. That time period could be as much as 4 hours. This resulted
in varying degrees of degradation of the pesticides. In the GC-MSD
studies the laboratory control spike samples were extracted at different
time periods. For the D = 0 sample period the water sample was
extracted within 1 hour, D = 4 sample period within 24 hours, and D =
72 within 1 minute. The results demonstrated that the longer the time
between collections and extraction the less stable were the pesticides
in water.
On the other hand, all nine oxons were stable in the buffered water
prior to analysis in both of the studies.
6. Summary
There were two elements necessary to the strict qualitative
interpretation whether these ten OP pesticides underwent oxidative
desulfonation during a 72 hour contact time in chlorinated laboratory
water. This conclusion could be reached if:
1) The oxons are detected at any quantifiable level in either replication in
the chlorinated laboratory water treatments at any sampling time
o There were six quantifiable oxons detected in the chlorinated
laboratory water within the seventy two hour exposure period
Section II.E. 1 - Page 352 of 522

-------
[methidathion oxon, methyl paraoxon, phosmet oxon, bensulide
oxon, phostebupirim oxon, and chlorethoxyfos oxon],
o There was mass spectral evidence of the possible formation of a
seventh oxon [temephos oxon]. However, there is, at present, no
authentic temephos oxon standard to positively confirm this result
and
2)	The OP pesticides are stable in non-chlorinated laboratory water,
o There were only two OP pesticides that were stable in the
unchlorinated laboratory water [methidathion and methyl parathion],
3)	Additionally, the detection of oxons in chlorinated water at the 24 hour
or 72 hour sampling times would suggest the oxon is stable enough in
chlorinated water to have the potential for dietary exposure through
drinking water.
o Both of these oxons [methidathion oxon and methyl paraoxon] were
stable at both the 24 hour and 72 hour sampling times.
Only methidathion and methyl parathion meet the criteria as
established in the QAPP to conclude that they underwent oxidative
desulfonation.
7. References
Duirk, S. Collette, T. 2006. Degradation of Chlorpyrifos in Aqueous
Solutions: Pathways, Kinetics, and Modeling. Environ. Sci. Technol. 40:
546-551.
Magara, Y. et al. 1994. Degradation of pesticides by chlorination during
water purification. Water Sci. Technol. 30(7): 119-128.
Miltner, R.J., D.B. Baker, T.F. Speth, and C.A. Fronk.1989. Treatment of
seasonal Pesticides in Surface waters. Jour. Amer. Water Works Assoc.
81: 43-52.
Tierney, D.P. et al., 2001. Chlorine degradation of six organophosphorus
insecticides and four oxons in a drinking water matrix. Syngenta Crop
Protection Center, Greensboro, NC.
* ~ v.
v ' * ^
Section II.E. 1 - Page 353 of 522

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8. Appendix 1: Procedures for the Preliminary Laboratory Study
on the Effects of Chlorinated Water on OP Pesticides
This appendix was prepared by the Water Treatment Effects
Workgroup, Environmental Fate and Effects Division of the USEPA Office of
Pesticide Programs on April 24, 2006.
a. Introduction
Previous studies in Japan (Magara et al, 1994) and United States
(Tierney et al, 2001) indicate that certain organophosphate pesticides can
be transformed during disinfection by chlorine compounds to oxons. This
chemical transformation process is shown in Figure II.E-1.2.
Figure II.E-1.2 Oxidative Desulfonation Reaction of an Organophosphate
Pesticide in Chlorinated Water.
This transformation is a concern because chlorination is widely used
in many drinking water treatment plants and the product oxons are
generally considered to be more toxic than the parent compounds.
Consequently, data and additional information are needed on the probable
oxidation of selected organophosphate pesticides and the relative stability
of oxons in chlorinated water. The organophosphate pesticides and their
degradation products considered in this testing protocol are listed in Table
o
II.E-1.3.
Section II.E. 1 - Page 354 of 522

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Table II.E-1.1 Selected Organophosphate Pesticides from the Cumulative
OP Assessment without Water Treatment Data on Chlorination Effects on
Oxon Formation
OP Parent
OP Degradation Products
Phorate
phorate oxon

phorate sulfoxide

phorate sulfone

phorate sulfoxide oxon

phorate sulfone oxon
Disulfoton
disulfoton oxon

disulfoton sulfoxide

disulfoton sulfone

disulfoton sulfoxide oxon

disulfoton sulfone oxon
Terbufos
terbufos oxon

terbufos sulfoxide

terbufos sulfone

terbufos sulfoxide oxon

terbufos sulfone oxon
Methidathion
methidathion oxon
Bensulide
bensulide oxon
Chlorethoxyfos
chlorethoxyfos oxon
Methyl parathion
methyl paraoxon
Phosmet
phosmet oxon
Phostebupirim
phostebupirim oxon
Temephos
temephos oxon (not available)
Chlorination experiments will be conducted in Fisher certified
environmental grade test water. Although the experiments will be
conducted in environmental grade water, water pH (pH=8) will be altered
to represent water treatment plant conditions. The chlorine dose in the
laboratory water will be equivalent to the recommended maximum
disinfectant residual (RMDL) of 4 mg/L free chlorine. Because the
laboratory water will have extremely low chlorine demand, the free
chlorine concentration and total chlorine concentration should be similar.
The pH of the laboratory water will be adjusted to pH 8 to represent typical
water treatment conditions. The experiment will be conducted for 72
hours with sampling times immediately prior to chlorination and 1 hour, 4
hours, 24 hours, and 72 hours post chlorination. The 24 and 72 hour
sampling times were selected to represent the treatment system water
residence and/or distribution transport times of approximately 24 hr or
longer. The pesticide concentration in the experiment will be 100 ug/L or
below the solubility limit of the pesticide whichever is lower. The
experiments will be conducted using a mixture of the OP pesticides. The
experiments will be conducted with low co-solvent concentrations or in the
absence of co-solvents. The chlorine demand from co-solvents and
Section II.E. 1 - Page 355 of 522

-------
degradation processes will be determined by measuring free chlorine at
each sampling interval.
The experimental plan will consist of a series of preliminary studies
and final studies. These studies will be conducted by EPA personnel at
the Biological and Economic Analysis Division Fort Meade Analytical
Laboratory and Stennis Space Center Environmental Chemistry
Laboratory. The chlorination study protocol and QAPP will be reviewed by
Richard Miltner, P.E. from the ORD/NRMRL/Water Supply and Water
Resources Division/ Treatment Technology Evaluation Branch.
Final chlorination studies for selected OP pesticides will be
conducted once analytical methods are developed with reliable
identification of the OP pesticide and their oxon degradation products in
chlorinated test water. These studies will be conducted using a factorial
experimental design [5 sampling times x 2 replicates pesticide(s),
chlorination treatments x 1 pesticide(s), non-chlorinated water treatment
(control) + 1 chlorinated water (control) + 1-3 buffered water spiked with a
intermediate level of parent(s) and oxon(s)].
b. Objectives
The objective is to qualitatively determine oxon formation and stability
in chlorinated, laboratory water for selected OP pesticides. These data
will be used in the revised cumulative OP risk assessment to characterize
the potential for human exposure to oxons in treated water.
c.	Glassware, Pipets, and other containers
Glassware, pipettes, and other devices used in the study should be
chlorine-demand free. Soak dark or amber incubation bottles in detergent
(Fisher FL-70, 4%, Fair Lawn, NJ or comparable) overnight, rinse four
times with hot tap water, and then two times with distilled and deionized
water. Place in 10 - 20 mg/L chlorine solution for 24 hr. After rinsing four
times with distilled and deionized water and one to two times with
laboratory clean water, dry in 1400 C oven overnight. Clean pipettes may
need to be stored in ~ 50 mg/L CI2 solution and rinsed three times with
dosing solution before use. Store in same chlorine solution after use.
d.	Materials
The following solutions will be prepared for this study:
(1) pH 6.7 borate buffer: 1.0 M boric acid [ACS grade] and 0.11 M
NaOH (ACS grade) prepared in boiled laboratory reagent water;
Section II.E. 1 - Page 356 of 522

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(2)	pH 8 borate buffer: 1.0 M boric acid (ACS grade) and 0.26 M NaOH
(ACS grade) prepared in boiled laboratory reagent water;
(3)	Chlorine solution (1000 - 3000 mg/L CI2 ): Dilute reagent-grade
stock solution of sodium hypochlorite (5 -13%) with laboratory
reagent water. Check the exact concentration using Standard
Methods (1998) or a commercial chlorine measurement kit that can
detect down to 0.1 mg/L CI2.
(4)	pH 8 hypochlorite-buffer solution: Add about 4-5 volume of
chlorine solution (~ pH 11) to one volume of pH 6.7 borate buffer.
The resulting solution gives a pH 8. About a 20% decrease in
chlorine strength is expected. About 2.5 ml_ of this combined
dosing hypochlorite-buffer solution can be added to a 1-L test water
(<0.5% water sample volume change)
e.Test	Waters
Fisher Environmental Grade water will be used in the water
chlorination studies. Laboratory reagent water will be used for cleaning
and reagent preparation.
f.	Chlorine Residuals Measurement
Free chlorine residuals will be measured using a Hach pocket
colorimeter analysis system and Hach Methods 8021 for free chlorine in
water. This DPD method is equivalent to USEPA Method 330.5 for
wastewater. It can measure free chlorine at reasonable detection limits (at
least 0.1 mg/L free chlorine).
g.	Preliminary and Final Study
Preliminary studies with one replication will be conducted to provide
sufficient experience in measuring analytes in chlorinated water as well as
an exercise in sequencing/timing the laboratory operations for the
chlorination experiments. Once the preliminary studies have been
conducted, final water chlorination studies will be done using two
replicates for the test water. Appropriate OP pesticide and chlorine
residual controls will be prepared and monitored during the chlorination
tests.
h.	Chlorine Dosing Study
Before the chlorination experiments are started, the chlorine demand
of the test waters has to be established to determine the dose of chlorine
solution that provides the target 4.0 ± 0.4 mg/L free chlorine residual.
Chlorine demand of the Fisher environmental grade water will be
determined. Chlorine demand is operationally defined as chlorine dose
Section II.E. 1 - Page 357 of 522

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(applied free chlorine) - free remaining chlorine residual under a specified
contact or incubation period, pH and temperature. For the preliminary
study, only one replicate is desirable. The unchlorinated Fisher
Environmental Grade water can be used for this purpose, but it must
include appropriate concentrations of co-solvents that will be used to
introduce OP pesticides into solution as well as similar reaction vessels
used in the experiment.
(1)	Add 2 ml pH 8 borate buffer to 1 L (or proportional volumes) of
unchlorinated Fisher Environmental Grade water.
(2)	Check the pH. If necessary, adjust to pH 8 with dilute H2S04 or
dilute NaOH.
(3)	Fill each incubation bottle (300 - 500 ml) three quarters full with the
unchlorinated Fisher Environmental Grade water. Two bottles will
be needed. Addition of co-solvent, in the appropriate concentration
as would be employed in (I) below, may be necessary to mimic co-
solvent additions through pesticide dosing procedures. The doses
should be set up in duplicate to determine if the initial dosing at 4
mg/L will result in a > 1 mg/L free chlorine residual after 24 hours in
the Fisher Environmental Grade water containing the co-solvents.
Initial dose of 4.0 mg/L free chlorine is appropriate.
(4)	Add pH 8 hypochlorite-buffer solution through a pipette held just
above water surface. Dose the appropriate volume of
hydrochlorite-buffer solution to give the required dose in full bottles.
(5)	Cap the bottle and invert twice.
(6)	Fill to top of bottle with pH 8 borate buffered unchlorinated Fisher
Environmental Grade water and cap head space-free.
(7)	Invert 10 times
(8)	Incubate for 24 hr in the dark at room temperature.
(9)	After incubation, measure the free chlorine residual, pH, and
temperature. (Note: Addition of hypochlorite-buffer solution should
be sequenced and timed to provide allowance for measurement of
free chlorine residual and pH for each test water)
(10)	The initial chlorine dose that yields an initial free chlorine residual of
4.0 ± 0.4 mg/L Cb and a > 1.0 ± 0.4 mg/L at 24 hours will be
selected and used in the chlorination and product stability
assessment discussed below.
i. Chlorination and Product (Oxon) Stability Experiments
The study will be conducted in 4L low density polyethylene reaction
vessels that can be covered with black plastic to simulate dark condition.
For this final study , the chlorination experiment at pH=8 should be done in
duplicate, along with one replicate OP control [test water + OP pesticides,
without chlorine], one replicate chlorine control [test water + chlorine], and
one buffered water control [test water for spiking with immediate
Section II.E. 1 - Page 358 of 522

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concentrations of OPs and oxons] indicated as A1, A2, B, C, and D
solutions in Table II.E-4, respectively.
i.	For Treatment A:
(1)	Put 2L of unchlorinated Fisher Environmental Grade water and
add 4 ml of pH 8 borate buffer in a dark, 4L polyethylene reaction
vessel. This will require five 4L vessels.
(2)	Measure pH and adjust, if necessary, to pH 8 with dilute H2S04
or dilute NaOH.
(3)	Dose with OP pesticide(s) to achieve a concentration of 100
pg/L or below the water solubility limit, whichever is lower.
(4)	Collect the unchlorinated, pesticide spiked OP sample.
(5)	Add pH 8 hypochlorite-buffer solution to give an initial free
chlorine residual of 4.0 ± 0.4 mg/L CI2 and a subsequent free chlorine
residual of > 1.0 ± 0.4 mg/L at 24 hours. Dose the appropriate volume
of hypochlorite-buffer solution to give the required dose in the 2L
sample. The time of chlorination is T = 0.
(6)	Prior to taking water samples, stir solution with the aid of
magnetic stirring bar for two minutes.
(7)	Take samples at the time intervals for analysis summarized in
Table 2:
OP pesticide - 0 (prechlorination), 1 hr, 4 hr, 24 hr, 72 hr
Transformation products (oxon, sulfoxide, sulfone, sulfone oxon,
sulfoxide oxon) - 0 (prechlorination), 1 hr, 4hr, 24 hr, 72 hr
(8)	The samples are immediately withdrawn from the reaction
vessel and then quenched stoichiometrically with sodium thiosulfate
(with slight excess) based on the free chlorine residual [1.25 mg per
100 ml aliquot]. The samples should be stored in the dark at 0 - 4°C, if
they cannot be analyzed right away.
(9)	Separate samples will be taken to measure the free chlorine
residual, pH, and temperature.
(10)	Analyze the quenched samples for the parent compound,
primary product (oxon) by appropriate analytical method (GC/MS or
LC/MS/MS). Other transformation products will be identified, when
possible, and described as tentatively identified compounds.
ii.	For Treatment B:
(1)	Put 2L of unchlorinated Fisher Environmental Grade water
and add 4 ml of pH 8 borate buffer in a dark, 4L polyethylene
reaction vessel.
(2)	Measure pH and adjust, if necessary, to pH 8 with dilute
H2S04 or dilute NaOH.
Dose with OP pesticide(s) to achieve a concentration of 100
pg/L or below the water solubility limit, whichever is lower.
Section II.E. 1 - Page 359 of 522

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(3)	At approximately the same time as the collection of the
chlorinated samples in Treatment A, collect the unchlorinated,
pesticide spiked OP samples at 0, 1, 4, 24 and 72 hours. The
samples should be stored in the dark at 0 - 4°C, if they cannot be
analyzed right away.
(4)	Separate samples will be taken to measure the pH and
temperature.
(5)	Analyze the samples for the parent compound, primary
product (oxon) by appropriate analytical method (GC/MS or
LC/MS/MS). Other transformation products will be identified, when
possible, and described as tentatively identified compounds.
. For Treatment C:
(1)	Put 2L of unchlorinated Fisher Environmental Grade water
and add 4 ml of pH 8 borate buffer in a dark, 5L polyethylene
reaction vessel.
(2)	Measure pH and adjust, if necessary, to pH 8 with dilute
H2S04 or dilute NaOH.
(3)	Add pH 8 hypochlorite-buffer solution to give an initial free
chlorine residual of 4.0 ± 0.4 mg/L CI2 and a subsequent free
chlorine residual of > 1.0 ± 0.4 mg/L at 24 hours. Dose the
appropriate volume of hypochlorite-buffer solution to give the
required dose in the 2L sample.
(4)	Prior to taking water samples, stir solution with the aid of
magnetic stirring bar for two minutes.
(5)	Collect a sample after about 1 hour for OP pesticides and for
oxons.
(6)	The sample is withdrawn from the reaction vessel and then
quenched with the selected reducing agent (with slight excess)
based on the free chlorine residual [1.25 mg per 100 ml aliquot].
The aliquots should be stored in the dark at 0 - 4° C, if they cannot
be analyzed right away.
(7)	A separate sample will be taken to measure the free chlorine
residual, pH, and temperature at 1 hour.
(8)	Analyze the sample for the parent compound, primary
product (oxon) by appropriate analytical method (GC/MS or
LC/MS/MS). Other transformation products will be identified, when
possible, and described as tentatively identified compounds.
Section II.E. 1 - Page 360 of 522

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iv. For Treatment D:
(1) Put 2L of unchlorinated Fisher Environmental Grade water
and add 4 ml of pH 8 borate buffer in a dark, 5L polyethylene
reaction vessel.
(2) Measure pH and adjust, if necessary, to pH 8 with dilute
H2S04 or dilute NaOH.
(3) Collect 100 ml samples of the unchlorinated, buffered water
at each sampling interval of 0, 1, 4, 24, and 72 hours.
(4) These samples will be spiked with the OP pesticide(s) and
oxon(s) at a spiking level of 50 ppb, as necessary.
(6) The samples will be stored for possible analysis with sample
set batches. The samples should be stored in the dark at 0-4° C, if
they cannot be analyzed right away.
(7) A separate sample is taken to measure the pH and
temperature.
(8) Analyze the samples for the parent compound, primary
product (oxon) by appropriate analytical method (GC/MS or
LC/MS/MS). Other transformation products will be identified, when
possible, and described as tentatively identified compounds.
Table II.E-1.2 Proposed Sampling and Analysis Regime
Treatment Condition
(Treated Water Samples
and Controls: OP
pesticide)
Sampling Times
A1 A2
OP OP
Cl2 ci2
h2o h2o
Pre-
chlorination
Postchlorination
0
1 hr
4 hrs
24 hrs
72 hrs
OP
OP
OP
OP
OP
Oxon1
Oxon
Oxon
Oxon
Oxon

CI
CI
CI
CI
B
OP
H20
OP
OP
OP
OP
OP
Oxon
Oxon
Oxon
Oxon
Oxon
C
CI2
H20

Oxon

-------
j. Data Reduction and Reporting
Report detections of parent OP and its degradation products.
Calculate concentrations, when possible, of OP pesticides and their
stability products. Report identities and structural formulas of
transformation products.
k. Interpretation of Results
The interpretation of study results will be dependent on the
detection of oxon degradation products in the chlorinated test water
treatments. The control treatments will be used to assess whether the
OP pesticide undergoes oxidation in non-chlorinated test water and to
assess whether OP pesticide or its degradation products are in the
chlorinated water without pesticide dosing. Because the experimental
design has minimal replication and the analytical methods are not fully
vetted for all the OP pesticides and their oxon degradation products,
there will be strict qualitative interpretation on whether OP pesticides
undergo oxidative desulfonation during a 72 hour contact time in
chlorinated laboratory water.
This deduction will be reached if oxons are detected in either
replication in the chlorinated laboratory water treatments at any sampling
time and the OP pesticide is stable in non-chlorinated laboratory water.
Additionally, the detection of oxons in chlorinated water at the 24 hour or
72 hour sampling times will suggest the oxon is stable enough in
chlorinated water to have the potential for dietary exposure through
drinking water.
I. References
Magara, Y. et al., 1994. Degradation of pesticides by chlorination during
water purification. Water Sci. Technol. 30(7): 119-128.
Tierney, D.P. et al., 2001. Chlorine degradation of six organophosphorus
insecticides and four oxons in a drinking water matrix. Syngenta Crop
Protection Center, Greensboro, NC.
Summers, R.C., et al., 1996. Assessing DBP yield: uniform formation
conditions. J. Amer. Water Works Assoc. 88(6): 80-93.
Section II.E. 1 - Page 362 of 522

-------
9. Appendix 2: Results of Analyses of OP Pesticides and Oxons
in the Water Chlorination Studies
Table II.E-1.3 Results of the GC-MSD Analyses of OP Pesticides and Oxons
in the Water Chlorination Studies - ECB


Parent OP
Oxon

Time,



D-



D-
OP
hrs
A1
A2
B
spike2
A1
A2
B
spike2
Methidathion
0
106
64
107
51
ND
ND
ND
48

1
ND
ND
110
NA
90
98
ND
NA

4
ND
ND
109
47
81
97
ND
47

24
ND
ND
103
NA
72
77
ND
NA

72
ND
ND
101
59
66
67
ND
59
Methyl
0
95
94
96
47
ND
ND
ND
48
parathion
1
12
ND
89
NA
90
69
ND
NA

4
ND
ND
98
46
72
85
ND
47

24
ND
ND
83
NA
66
70
ND
NA

72
ND
ND
88
53
68
66
ND
59
Phosmet
0
80
81
81
20
ND
ND
ND
20

1
ND
ND
103
NA
57
69
ND
NA

4
ND
ND
17
2
7
9
ND
2

24
ND
ND
ND
NA
ND
ND
ND
NA

72
ND
ND
ND
49
ND
ND
ND
43
Phorate
0
62
61
62
38
ND
ND
ND
38

1
ND
ND
68
NA
ND
ND
ND
NA

4
ND
ND
52
25
ND
ND
ND
32

24
ND
ND
17
NA
ND
ND
ND
NA

72
ND
ND
11
45
ND
ND
ND
45
Bensulide1
0
NA
NA
NA
NA
NA
NA
NA
NA

1
NA
NA
NA
NA
NA
NA
NA
NA

4
NA
NA
NA
NA
NA
NA
NA
NA

24
NA
NA
NA
NA
NA
NA
NA
NA

72
NA
NA
NA
NA
NA
NA
NA
NA
Chlorethoxy-
0
41
43
41
29
ND
ND
ND
39
fos
1
12
12
42
NA
26
30
ND
NA

4
ND
ND
32
26
41
55
ND
38

24
ND
ND
3
NA
26
30
ND
NA

72
ND
ND
ND
51
23
23
ND
54
Disulfoton
0
64
64
64
36
ND
ND
ND
40

1
ND
ND
68
NA
ND
ND
ND
NA

4
ND
ND
56
34
ND
ND
ND
37

24
ND
ND
24
NA
ND
ND
ND
NA

72
ND
ND
16
45
ND
ND
ND
48
Terbufos
0
63
63
65
39
ND
ND
ND
38

1
ND
ND
64
NA
ND
ND
ND
NA
Section II.E. 1 - Page 363 of 522

-------


Parent OP
Oxon

Time,



D-



D-
OP
hrs
A1
A2
B
spike2
A1
A2
B
spike2

4
ND
ND
46
34
ND
ND
ND
31

24
ND
ND
9
NA
ND
ND
ND
NA

72
ND
ND
ND
49
ND
ND
ND
46
Phostebupirim
0
79
79
78
41
ND
ND
ND
44

1
2
2
71
NA
44
43
ND
NA

4
ND
ND
65
42
42
50
ND
43

24
ND
ND
30
NA
44
43
ND
NA

72
ND
ND
14
51
47
50
ND
52
Temephos3
0
93
94
94
50
NA
NA
NA
NA

1
ND
ND
121
NA
NA3
NA
NA
NA

4
ND
ND
93
41
NA
NA
NA
NA

24
ND
ND
43
NA
NA
NA
NA
NA

72
ND
ND
11
50
NA
NA
NA
NA
Bensulide is not suitable for the current GC-MSD conditions
2 Only the D-Spike Samples at 0, 4, and 72 hours were analyzed.
3Temephos oxon standard is not available.
Table II.E-1.4 Results of the LC/MS/MS Analyses of OP Pesticides and
Oxons in the Water Chlorination Studies - ACB


Parent OP
Oxon
OP
Time,
hrs
A1
A2
B
D-
spike1
A1
A2
B
D-
spike1
Methidathion
0
67
64
72
39
ND
ND
ND
44

1
ND
ND
73
44
80
81
ND
48

4
ND
ND
73
45
87
81
ND
50

24
ND
ND
74
47
80
76
ND
51

72
ND
ND
77
NA
58
50
ND
NA
Methyl
0
NA
NA
NA
NA
ND
ND
ND
52
parathion2
1
NA
NA
NA
NA
58
46
ND
53

4
NA
NA
NA
NA
79
72
ND
55

24
NA
NA
NA
NA
81
72
ND
58

72
NA
NA
NA
NA
78
75
ND
NA
Phosmet3
0
NA
NA
NA
NA
NA
NA
NA
NA

1
NA
NA
NA
NA
NA
NA
NA
NA

4
NA
NA
NA
NA
NA
NA
NA
NA

24
NA
NA
NA
NA
NA
NA
NA
NA

72
NA
NA
NA
NA
NA
NA
NA
NA
Phorate
0
22
23
26
18
ND
ND
ND
45

1
ND
ND
24
19
ND
ND
ND
43

4
ND
ND
20
18
ND
ND
ND
45

24
ND
ND
11
22
ND
ND
ND
50

72
ND
ND
8
NA
ND
ND
ND
NA
Section II.E. 1 - Page 364 of 522

-------


Parent OP
Oxon

Time,



D-



D-
OP
hrs
A1
A2
B
spike1
A1
A2
B
spike1
Bensulide'
0
15
15
18
14
ND
ND
ND
43

1
2
2
21
15
58
57
ND
44

4
2
3
16
14
57
52
ND
46

24
ND
ND
15
15
55
49
ND
48

72
ND
ND
17
NA
60
56
ND
NA
Chlorethoxy-
0
NA
NA
NA
NA
ND
ND
ND
40
fos2
1
NA
NA
NA
NA
17
15
ND
38

4
NA
NA
NA
NA
25
23
ND
38

24
NA
NA
NA
NA
24
20
ND
40

72
NA
NA
NA
NA
17
13
ND
NA
Disulfoton
0
ND
ND
ND
10
ND
ND
ND
49

1
ND
ND
ND
9
ND
ND
ND
47

4
ND
ND
ND
10
ND
ND
ND
50

24
ND
ND
ND
11
ND
ND
ND
51

72
ND
ND
ND
NA
ND
ND
ND
NA
Terbufos
0
11
11
13
11
ND
ND
ND
33

1
ND
ND
12
11
ND
ND
ND
30

4
ND
ND
8
11
ND
ND
ND
32

24
ND
ND
3
12
ND
ND
ND
39

72
ND
ND
6
NA
ND
ND
ND
NA
Phostebupirim
0
19
19
23
18
ND
ND
ND
48

1
2
3
22
17
49
ND
ND
48

4
1
1
14
18
55
51
ND
48

24
ND
ND
8
18
59
54
ND
51

72
ND
ND
10
NA
56
52
ND
NA
Temephos4
0
55
54
67
10
NA4
NA
NA
NA

1
3
3
46
9
NA
NA
NA
NA

4
3
3
49
9
NA
NA
NA
NA

24
ND
ND
40
10
NA
NA
NA
NA

72
ND
ND
NA
NA
NA
NA
NA
NA
Sample D-spike 72 hrwas not included
2	Methyl parathion and chloroethoxyfos are not suitable for the current LC/MS conditions
3	only traces remained after 24 hr.
4Temephos oxon standard is not available.
Section II.E. 1 - Page 365 of 522

-------
E-2. OP Cumulative Exposure in Drinking Water: The Effects of Water
Chlorination on Three Specific Organophosphate (OP) Pesticides
(Phase II)
This report is an addendum to the 2002 OP CRA drinking water
appendix III.E.4 - Effects of Drinking Water Treatment on
Organophosphate Pesticides. Phase I of this study evaluated the potential
of ten OP pesticides to form oxons as a result oxidation during drinking
water treatment processes. Phase II of the study evaluated the potential of
the sulfone and sulfoxide transformation products of disulfoton, phorate,
and terbufos to form oxons.
The studies were conducted by the USEPA Office of Pesticide
Program (OPP) Biological and Economic Analysis Division (BEAD)
laboratories and have been reviewed by the USEPA Office of Research
and Development (ORD). The results support the oxon characterization in
the drinking water exposure assessment for the 2006 OP CRA.
1. Executive Summary - Phase II
Three organophosphate (OP) pesticides [phorate, disulfoton, terbufos]
were evaluated for their potential to undergo oxidation to their respective
oxidative products [oxons, sulfoxides, sulfoxide oxons, sulfones, and sulfone
oxons] in laboratory water simulating the chlorination process in drinking
water facilities over a 72 hour exposure period. Samples were collected
after 0, 0.25, 4, 24, and 72 hours of chlorination and analyzed by both gas
chromatography-mass selective detection (GC-MSD) and liquid
chromatography-tandem mass spectrometry (LC/MS/MS) to determine the
presence of the pesticides and their oxidative products. The data obtained
supplement previous data obtained on a more extensive group of
organophosphate pesticides (Phase I).
The results of the Phase II Experiment confirm the results of the Phase
I Experiment in that these three OP pesticides [phorate, disulfoton, terbufos]
are unstable and degraded in unchlorinated buffered laboratory water over
the 72 hour exposure period. In addition, as in the Phase I experiments,
phorate, disulfoton, and terbufos did not undergo oxidation to their oxons
upon chlorination under the experiment conditions.
However, in the current experiment, it was determined that two of the
OP pesticides [phorate and disulfoton] underwent oxidation to other
oxidation products [sulfone oxons]. The phorate sulfone oxon was detected
at the 4 and 24 sampling times at trace concentrations (detection limit) and
was not detected at the 72 hours. The disulfoton sulfone oxon was detected
at the 0.25 hour sampling time in significant concentrations which increased
at 4 hours, and then gradually decreased during the 72 hour exposure
Section II.E.2 - Page 366 of 522

-------
period. This oxidative product was present at both the 24 and 72 hour
sampling times.
In the first four hours of the experiment, significant amounts of the
sulfoxide oxons of the three OP pesticides were detected; however, they
were not stable for more than 4 hours, which suggests that the sulfoxide
oxons are one of the intermediate oxidation products to the sulfone oxons.
Re-examination of the gas chromatographic/mass spectrometric
chromatograms (GC-MSD) of the Phase I Experiment reveals the presence
of these same oxidative products at approximately the same exposure
periods and further confirms the findings of the Phase II Experiment.
Table II.E-2.1 Results for pesticides and oxidation products examined in
study.
OP
Parent OP
Sulfoxide Oxon
Sulfone Oxon
Pesticide
Stability
Oxon

Forma-
Stability
Forma-
Stabili

in water
formation
Oxon
tion
after 72
tion
ty

over 72
after 1 hr
stability
after 1
hrs
after 1
after

hrs (no
(upon
after 72
hr

hr
72 hrs

chlorin-
chlorin-
hrs





ation)
ation)





Phorate
Poor
None
-
Yes
No
Yes
No
Disulfoton
Poor
None
-
Yes
No
Yes
Yes
Terbufos
Poor
None
-
Yes
No
No
-
In accordance with the Quality Assurance Project Plan (QAPP) for this
phase of the study, there were two elements necessary for the strict
qualitative interpretation whether the three OP pesticides underwent
oxidative desulfonation during a 72 hour contact time in chlorinated
laboratory water. This conclusion would be reached if the oxidative products
are detected at any quantifiable level in either replication in the chlorinated
laboratory water treatments at any sampling time and the OP pesticides are
stable in non-chlorinated laboratory water. Because none of the parent OPs
were stable in non-chlorinated water, none of the three pesticides met those
criteria.
2. Introduction
The application of pesticides in arable lands has resulted in the
contamination of natural waters such as surface water and groundwater.
The initial contamination at the application sites has spread via surface
runoff to nearby lakes, rivers, and streams and through subsurface
transport to aquifers. The contaminated surface waters and ground waters
are eventually used as source or raw waters in some community drinking
water systems. After subjecting the raw water to different treatment
processes in the water purification facilities, the concentrations of the
Section II.E.2 - Page 367 of 522

-------
pesticides may change or remain essentially the same in the treated or
final drinking water. Studies conducted by scientists at EPA's ORD in
Cincinnati (Miltner et al, 1989) indicate that conventional treatment
(coagulation/clarification, filtration, softening, recarbonation, and
chlorination) are generally not effective in removing certain pesticides from
raw water. However, other pesticides are unstable in the presence of
chemical disinfectant such as chlorine.
Previous studies in Japan (Magara et al, 1994) and United States
(Tierney et al, 2001; Duirk and Collette, 2006) indicate that certain
organophosphate pesticides can be transformed to their oxons during
chemical disinfection by chlorine compounds. This chemical
transformation process is shown in Figure II.E.2 1.
Figure II.E-2.1 Oxidative Desulfonation Reaction of an Organophosphate
Pesticide in Chlorinated Water.
This transformation is a concern because chlorination is the most
commonly used disinfection technique in many US drinking water
treatment plants and the product oxons are generally considered to be
more toxic than the parent compounds.
The Food Quality Protection Act of 1996 (FQPA) requires that all
chemical pesticide residues in or on food be examined for any possible
adverse health effects through exposure. Drinking water is one of the
pathways for dietary exposure. Five organophosphate pesticides
(diazinon, chlorpyrifos, methidathion, methyl parathion, and malathion)
have been examined and have been found to transform during
chlorination into their associated oxons. Three specific organophosphate
pesticides [phorate, disulfoton, and terbufos] have other known oxidative
products [sulfoxides, sulfoxide oxons, sulfones, and sulfone oxons] for
which there is little or no data on their potential for oxidative transformation
during these conditions. Consequently, data and additional information are
needed on the probable oxidation of these organophosphate pesticides
and the relative stability of oxidative products in chlorinated water. The
three organophosphate pesticides and their degradation products
considered in this study are listed in Table II.E-2.2.
o
Section II.E.2 - Page 368 of 522

-------
Table II.E-2.2 Selected Organophosphate Pesticides from the Cumulative
OP Assessment without Water Treatment Data on Chlorination Effects on
Oxon Formation
OP Parent
OP Degradation Products
Phorate
phorate oxon
phorate sulfoxide
phorate sulfone
phorate sulfoxide oxon
phorate sulfone oxon
Disulfoton
disulfoton oxon
disulfoton sulfoxide
disulfoton sulfone
disulfoton sulfoxide oxon
disulfoton sulfone oxon
Terbufos
terbufos oxon
terbufos sulfoxide
terbufos sulfone
terbufos sulfoxide oxon
terbufos sulfone oxon
The objective of this study is to provide a qualitative screening level
assessment on the potential for oxidation product formations in chlorinated
laboratory water and the stability of the selected organophosphate
pesticides in both un-chlorinated and chlorinated water and the stability of
their respective oxidation products in the chlorinated laboratory water.
There were approximately twenty organophosphate pesticides considered
in the cumulative OP risk assessment. The three selected pesticides
being tested in this study consist of the pesticides, which are capable of
forming multiple oxidation products, have outdoor use patterns, and have
no chlorination water treatment data available. These data will be used in
the revised cumulative OP risk assessment to characterize the potential
for human exposure to oxons in treated water.
3. Project Description
The project description is listed in the study protocol in Appendix 1
(Section 7). A brief summary description follows:
For each of the ten OP pesticides to be tested, the experimental
design consisted of:
-	One replicate OP control [test water + OP pesticide, without chlorine]
-	One replicate chlorine control [test water + chlorine]
-	Two replicates of treatment [OP pesticide + test water + chlorine]
-	One buffered water sample spiked with the ten pesticides and nine
oxons at a concentration of % of the spiking concentration (50 ppb) at
each sampling time.
Section II.E.2 - Page 369 of 522

-------
Chlorination experiments will be conducted in Fisher Environmental
Grade reagent water to eliminate chlorine demand considerations. Similar
testing conditions using laboratory waters are recommended as screening
level testing for CCL water treatment studies and pesticide treatment
studies at ORD. The chlorine dose in the laboratory water will be
equivalent to the recommended maximum disinfectant residual (RMDL) of
4 mg/L free chlorine concentration ± 10%. The pH of the Fisher reagent
water will be adjusted to pH 8 to represent typical water treatment
conditions. The experiment will be conducted for 72 hours with sampling
times immediately prior to chlorination (~2 minutes before pesticide
dosing), 0.25 hour, 4 hours, 24 hours, and 72 hours post chlorination. The
24 and 72 hour sampling times were selected to represent the treatment
system water residence and/or distribution transport times of
approximately 24 hr or longer. The pesticide concentration in the
experiment will be 100 ppb or below the solubility limit of the pesticide
whichever is lower. The experiments will be conducted using a mixture of
the OP pesticides delivered to the system with low co-solvent
concentrations or in the absence of co-solvents. The chlorine demand
from co-solvents and degradation processes will be determined by
measuring free chlorine at each sampling interval.
4. Method and Materials
Fisher Scientific Certified Environmental Grade water was used as
the test water. Water quality parameters of the test water were:
Test
Value
Unit
Color
< 5
APHA
Residue after Evaporation
< 1
ppm
Fluorescence (as quinine)
< 100
ppt
Resistivity
> 18
MQ
Total Organic Carbon
<20
ppb
Water samples must be labeled clearly, and should include date,
time, and name of the preparer(s). To preserve the integrity of the data,
all samples must be stored at ~ 4°C until extraction to minimize the
physicochemical changes in the samples. If sample extraction into a
solvent is necessary, extracts must be stored below 0°C and also
analyzed as soon as possible. All samples used and generated during the
study should be properly disposed of.
Quality assurance samples shall consist of:
1)	reagent water blank - analysis of reagent water (one time only);
2)	method blank - analysis of buffered reagent water plus chlorine;
[Carboy C, Table 1]; (time 0.25 hr);
Section II.E.2 - Page 370 of 522

-------
3)	non-chlorinated degradation check - analysis of buffered reagent
water plus OPs [Carboy B, Table 2]; (time 0, 0.25, 4, 24, and 72 hrs);
4)	matrix water blank - analysis of buffered reagent water (time 0);
5)	matrix water spike - analysis of buffered reagent water plus 50
ppb of the OP parent(s) plus 50 ppb oxon(s) (one spike per analytical
sample set).
These measures are classified as critical measurements and should
be prepared and analyzed with each group of samples to monitor
laboratory contamination and method performance. Addition of surrogate
compounds to environmental samples is also recommended to measure
the efficiency of the method. The surrogate compounds should not be
normally found in the environment and should be selected such that the
interference with elution of target analytes and the effect from sample
matrix are minimal.
a.	Analytical Procedures
The analytical procedures used should be able to accurately
identify and measure the presence of the target analytes in the
samples. Identification and quantitation of residues will be by gas
chromatography-mass selective detection (GC/MSD) and/or liquid
chromatography/tandem mass spectrometry (LC/MS/MS) techniques.
A calibration curve will be constructed with mixtures(s) of pure
standards (target analytes) at concentrations that range from twice the
spiking level to the method detection limit. Complete initial calibration
curves shall be prepared monthly, and the individual calibration
standards verified each day of operation.
In some cases, the analytical procedures may not be completely
developed to allow for complete quantification of the parent OP and its
degradation products. Nevertheless, the analytical method should be
capable of providing clear separation of known pesticide residues on
chromatograms to allow for residue identification.
b.	Test Protocol
These studies will be conducted at the OPP/BEAD/ACB Fort
Meade and OPP/BEAD/ECB Stennis Space Center laboratories. A
complete description of testing protocol can be found in the Appendix 1
(Section 7). Final studies will not be conducted for compounds unless
the analytical method has been shown to be capable of detecting of
the parent compounds and their oxons in chlorinated water during the
preliminary testing stage.
Section II.E.2 - Page 371 of 522

-------
The control treatments will be used to assess whether the OP
pesticide undergoes oxidation in non-chlorinated laboratory water and
to assess whether OP pesticide or its oxidation products are in the
chlorinated water without pesticide dosing. Because the experimental
design has minimal replication and the analytical methods are not fully
vetted for all the OP pesticides and their oxidation products, there will
be strict qualitative interpretation (i.e. presence or absence of oxidation
product) on whether OP pesticides [phorate, disulfoton, and terbufos]
undergo oxidative desulfonation during a 72 hour contact time in
chlorinated laboratory water. This deduction will be reached if their
oxidation products [sulfoxides and sulfones and their associated
sulfoxide and sulfone oxons] are detected at any quantifiable level in
either replication in the chlorinated laboratory water treatments at any
sampling time and the OP pesticide is stable in non-chlorinated
laboratory water. Additionally, the detection of oxidation products in
chlorinated water at the 24 hour or 72 hour sampling times will suggest
the oxidation product is stable enough in chlorinated water to have the
potential for dietary exposure through drinking water.
c. Assessment and Oversight
A QA/QC laboratory audit will be performed at the conclusion of the
water chlorination studies with OP pesticides and their sulfone,
sulfoxide, sulfone oxon, and sulfoxide oxon.
Results
a. The Formation of Oxidation Products from the Three OP
Pesticides in Chlorinated Water
Three organophosphate (OP) pesticides [phorate, disulfoton,
terbufos] were evaluated for their potential to undergo oxidation to their
respective oxidation products in laboratory water simulating the
chlorination process in drinking water facilities. In these studies, the
OP pesticides were dissolved into pH 8.0 buffered water and then
chlorinated with a sodium hypochlorite solution. Over a 72 hour
exposure period, water samples were collected, processed, and
analyzed by both gas chromatography-mass selective detection (GC-
MSD) and liquid chromatography-tandem mass spectrometry
(LC/MS/MS) to determine the presence of the pesticides and their
oxons. The results are presented in Appendix 2 for both the GS-MSD
and LC/MS/MS studies.
The results of both studies (GC-MSD & LC/MS/MS) showed that
the three OP pesticides (phorate, disulfoton, and terbufos) did not
undergo oxidation into their oxons under the experiment conditions.
Section II.E.2 - Page 372 of 522

-------
Two of the twelve remaining oxidation products [phorate sulfone oxon
and disulfoton sulfone oxon] formed stable compounds over the 24
exposure period, but only the disulfoton sulfone oxon was present at
72 hours. The phorate sulfone oxon was present at trace concentration
at the minimum detection limit; the disulfoton sulfone oxon was present
at higher concentrations. In the first four hours of the experiment,
phorate sulfoxide oxon, disulfoton sulfoxide oxon, and terbufos
sulfoxide oxon were detected; however, they were unstable and
disulfoton sulfoxide oxon was not detected at the 4 hour exposure time
and phorate sulfoxide oxon and terbufos sulfoxide oxon were not
detected at the 24 hour exposure time.
A re-examination of the full scan of the gas chromatographic/mass
spectrometric (GC-MSD) chromatograms from the Phase I Experiment
confirmed these findings.
The analytical methods of GC-MSD and LC/MS/MS were
complimentary in the detection of the three OP pesticide parents and
the majority of their oxidation products. The current GC/MSD
conditions were not suitable for the detection of phorate sulfoxide,
phorate sulfoxide oxon, terbufos sulfoxide, and terbufos sulfoxide
oxon; however, the LC/MS/MS conditions were suitable for all 18
compounds in the study.
b. The Stability of Three OP Pesticides in Unchlorinated Water
The three organophosphate (OP) pesticides [phorate, disulfoton,
terbufos] were evaluated in buffered laboratory water to act as a
control to the separate studies of the pesticides in the buffered water
during the chlorination process. In these studies the OP pesticides
were dissolved into a pH 8.0 buffered water. Over a 72 hour exposure
period, water samples were collected, processed, and analyzed by
both gas chromatography-mass selective detection (GC-MSD) and
liquid chromatography-tandem mass spectrometry (LC/MS/MS) to
determine the presence of the pesticides and their oxons without
chlorination. The results are presented in Appendix 2 for both the GS-
MSD and LC/MS/MS studies.
The results demonstrated and confirm that the three OP pesticides
[phorate, disulfoton, and terbufos] are unstable and degrade in the
buffered water without chlorination over the 72 hour exposure period.
Trace concentrations of disulfoton sulfoxide were detected at the
minimum detection limit.
Section II.E.2 - Page 373 of 522

-------
A re-examination of the full scan of the gas chromatographic/mass
spectrometry (GC-MSD) chromatograms from the Phase I Experiment
confirmed these findings.
c.	The Stability of Free Chlorine Concentrations in Water
The concentration of chlorine as free chlorine was evaluated in
buffered laboratory water to act as a control to the separate studies of
the pesticides in the buffered water during the chlorination process. In
these studies chlorine as free chlorine was added to a pH 8.0 buffered
water. Over a 72 hour exposure period, water samples were collected
and analyzed to determine the stable concentration of this form of
chlorine. In both studies the concentration of free chlorine remained
stable within 25% of the initial concentration and neither the OP
pesticides nor their oxidation products were detected at any time
during the 72 hour exposure period.
d.	The Stability of the Three OP Pesticides and Their Oxidation
Products as Laboratory Control Spike Samples
Three organophosphate (OP) pesticides [phorate, disulfoton,
terbufos] and their fifteen available oxidation products (Table 1) were
spiked into pH 8.0 buffered laboratory water to act as laboratory control
spike samples. These samples were used to assess the method
performance of the course of the study. The water samples were
collected, spiked, processed, and analyzed by both gas
chromatography-mass selective detection (GC-MSD) and liquid
chromatography-tandem mass spectrometry (LC/MS/MS) to determine
the concentration of the pesticides and their oxidation products. The
results are presented in Appendix 2 for both the GS-MSD and
LC/MS/MS studies.
6. Summary
There were two elements necessary to the strict qualitative
interpretation whether these three OP pesticides underwent oxidative
desulfonation during a 72 hour contact time in chlorinated laboratory
water. This conclusion could be reached if:
1) The oxidation products of the three OP pesticides are detected at
any quantifiable level in either replication in the chlorinated laboratory
water treatments at any sampling time.
o There were five quantifiable oxidation products detected in the
chlorinated laboratory water during the seventy two hour exposure
period [phorate sulfoxide oxon, phorate sulfone oxon, disulfoton
Section II.E.2 - Page 374 of 522

-------
sulfoxide oxon, disulfoton sulfone oxon, and terbufos sulfoxide
oxon],
and
2)	The OP pesticides are stable in non-chlorinated laboratory water,
o All three OP pesticides were unstable and degraded in the
unchlorinated laboratory water.
3)	Additionally, there were detection of oxidation products in
chlorinated water at the 24 hour or 72 hour sampling times would
suggest the oxidation product is stable enough in chlorinated water
to have the potential for dietary exposure through drinking water.
o One of the oxidation products [phorate sulfone oxon] was stable at
trace levels at the 24 hour sampling time and one of the oxidation
products [disulfoton sulfone oxon] was stable at both the 24 and 72
hour sampling times.
None of the three parent OP pesticides meet the criteria as
established in the QAPP to conclude that they underwent oxidative
desulfonation into their respective oxons. However, it should be noted that
two of the parents [phorate and disulfoton] underwent oxidative
desulfonation to phorate sulfone oxon and disulfoton sulfone oxon.
7. References
Duirk, S. Collette, T. 2006. Degradation of Chlorpyrifos in Aqueous
Solutions: Pathways, Kinetics, and Modeling. Environ. Sci. Technol. 40:
546-551.
Magara, Y. et al. 1994. Degradation of pesticides by chlorination during
water purification. Water Sci. Technol. 30(7): 119-128.
Miltner, R.J., D.B. Baker, T.F. Speth, and C.A. Fronk.1989. Treatment of
seasonal Pesticides in Surface waters. Jour. Amer. Water Works Assoc.
81: 43-52.
Tierney, D.P. et al., 2001. Chlorine degradation of six organophosphorus
insecticides and four oxons in a drinking water matrix. Syngenta Crop
Protection Center, Greensboro, NC.
USEPA, Laboratory Study on the Effects of Chlorinated Water on OP
Pesticides, Quality Assurance Project Plan, OPP/EFED/WTEWG, April 24,
2006.
Section II.E.2 - Page 375 of 522

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USEPA, Laboratory Study on the Effects of Chlorinated Water on OP
Pesticides, Final Report, OPP/EFED/WTEWG, May 15, 2006.
8. Appendix 1: Procedures for the Preliminary Laboratory Study
on the Effects of Chlorinated Water on OP Pesticides, Phase II
This appendix was prepared by the Water Treatment Effects
Workgroup, Environmental Fate and Effects Division of the USEPA Office
of Pesticide Programs on June 8, 2006.
a. Introduction
Previous studies in Japan (Magara et al, 1994) and United States
(Tierney et al, 2001) indicate that certain organophosphate pesticides
can be transformed during disinfection by chlorine compounds to
oxons. This chemical transformation process is shown in Figure II.E.2
2.
Figure II.E-2.2 Oxidative Desulfonation Reaction of an
Organophosphate Pesticide in Chlorinated Water.
This transformation is a concern because chlorination is widely
used in many drinking water treatment plants and the product oxons
are generally considered to be more toxic than the parent compounds.
Consequently, data and additional information are needed on the
probable oxidation of selected organophosphate pesticides and the
relative stability of oxons in chlorinated water. In the Laboratory Study
on the Effects of Chlorinated Water on OP Pesticides, Phase I, ten
organophosphate (OP) pesticides were examined and it was
determined that five OP pesticides [methidathion, bensulide,
chlorethyoxyfos, methyl parathion, and phostebupirim] formed stable
oxons in chlorinated water. However, three of those pesticides
[phorate, disulfoton, and terbufos] have additional oxidation products
[sulfoxides, sulfoxide oxons, sulfones, and sulfone oxons] that can be
formed. The organophosphate pesticides and their oxidation products
considered in this testing protocol are listed in Table II.E.2 3.
o
Section II.E.2 - Page 376 of 522

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Table II.E-2.3 Selected Organophosphate Pesticides from the Cumulative
OP Assessment without Water Treatment Data on Chlorination Effects on
Oxon Formation
OP Parent
OP Degradation Products
Phorate
phorate oxon
phorate sulfoxide
phorate sulfone
phorate sulfoxide oxon
phorate sulfone oxon
Disulfoton
disulfoton oxon
disulfoton sulfoxide
disulfoton sulfone
disulfoton sulfoxide oxon
disulfoton sulfone oxon
Terbufos
terbufos oxon
terbufos sulfoxide
terbufos sulfone
terbufos sulfoxide oxon
terbufos sulfone oxon
Chlorination experiments will be conducted in Fisher certified
environmental grade test water. Although the experiments will be
conducted in environmental grade water, water pH (pH=8) will be
altered to represent water treatment plant conditions. The chlorine
dose in the laboratory water will be equivalent to the recommended
maximum disinfectant residual (RMDL) of 4 mg/L free chlorine.
Because the laboratory water will have extremely low chlorine demand,
the free chlorine concentration and total chlorine concentration should
be similar. The pH of the laboratory water will be adjusted to pH 8 to
represent typical water treatment conditions. The experiment will be
conducted for 72 hours with sampling times immediately prior to
chlorination and 0.25 hour, 4 hours, 24 hours, and 72 hours post
chlorination. The 24 and 72 hour sampling times were selected to
represent the treatment system water residence and/or distribution
transport times of approximately 24 hr or longer. The pesticide
concentration in the experiment will be 100 Dg/L or below the solubility
limit of the pesticide whichever is lower. The experiments will be
conducted using a mixture of the OP pesticides. The experiments will
be conducted with low co-solvent concentrations or in the absence of
co-solvents. The chlorine demand from co-solvents and degradation
processes will be determined by measuring free chlorine at each
sampling interval.
The experimental plan will consist of a series of preliminary
studies and final studies. These studies will be conducted by EPA
personnel at the Biological and Economic Analysis Division Fort
Meade Analytical Laboratory and Stennis Space Center Environmental
Section II.E.2 - Page 377 of 522

-------
Chemistry Laboratory. The chlorination study protocol and QAPP will
be reviewed by Richard Miltner, P.E. from the ORD/NRMRL/Water
Supply and Water Resources Division/ Treatment Technology
Evaluation Branch.
Final chlorination studies for selected OP pesticides will be
conducted once analytical methods are developed with reliable
identification of the OP pesticide and their oxon degradation products
in chlorinated test water. These studies will be conducted using a
factorial experimental design [5 sampling times x 2 replicates
pesticide(s), chlorination treatments x 1 pesticide(s), non-chlorinated
water treatment (control) + 1 chlorinated water (control) + 1-3 buffered
water spiked with a intermediate level of parent(s) and oxon(s)].
b.	Objectives
The objective is to qualitatively determine oxon formation and
stability in chlorinated, laboratory water for selected OP pesticides.
These data will be used in the revised cumulative OP risk assessment
to characterize the potential for human exposure to oxons in treated
water.
c.	Glassware, Pipets, and other containers
Glassware, pipettes, and other devices used in the study should
be chlorine-demand free. Soak dark or amber incubation bottles in
detergent (Fisher FL-70, 4%, Fair Lawn, NJ or comparable) overnight,
rinse four times with hot tap water, and then two times with distilled
and deionized water. Place in 10 - 20 mg/L chlorine solution for 24 hr.
After rinsing four times with distilled and deionized water and one to
two times with laboratory clean water, dry in 1400 C oven overnight.
Clean pipettes may need to be stored in ~ 50 mg/L CI2 solution and
rinsed three times with dosing solution before use. Store in same
chlorine solution after use.
d.	Materials
The following solutions will be prepared for this study:
(5)	pH 6.7 borate buffer: 1.0 M boric acid [ACS grade] and 0.11 M NaOH
(ACS grade) prepared in boiled laboratory reagent water;
(6)	pH 8 borate buffer: 1.0 M boric acid (ACS grade) and 0.26 M NaOH
(ACS grade) prepared in boiled laboratory reagent water;
(7)	Chlorine solution (1000 - 3000 mg/L CI2 ): Dilute reagent-grade stock
solution of sodium hypochlorite (5 -13%) with laboratory reagent
water. Check the exact concentration using Standard Methods (1998)
Section II.E.2 - Page 378 of 522

-------
or a commercial chlorine measurement kit that can detect down to
0.1 mg/L CI2.
(8) pH 8 hypochlorite-buffer solution: Add about 4-5 volume of chlorine
solution (~ pH 11) to one volume of pH 6.7 borate buffer. The
resulting solution gives a pH 8. About a 20% decrease in chlorine
strength is expected. About 2.5 ml_ of this combined dosing
hypochlorite-buffer solution can be added to a 1-L test water (<0.5%
water sample volume change)
e.	Test Waters
Fisher Environmental Grade water will be used in the water
chlorination studies. Laboratory reagent water will be used for
cleaning and reagent preparation.
f.	Chlorine Residuals Measurement
Free chlorine residuals will be measured using a Hach pocket
colorimeter analysis system and Hach Methods 8021 for free chlorine in
water. This DPD method is equivalent to USEPA Method 330.5 for
wastewater. It can measure free chlorine at reasonable detection limits
(at least 0.1 mg/L free chlorine).
g.	Preliminary and Final Study
Preliminary studies with one replication will be conducted to
provide sufficient experience in measuring analytes in chlorinated
water as well as an exercise in sequencing/timing the laboratory
operations for the chlorination experiments. Once the preliminary
studies have been conducted, final water chlorination studies will be
done using two replicates for the test water. Appropriate OP pesticide
and chlorine residual controls will be prepared and monitored during
the chlorination tests.
h.	Chlorine Dosing Study
Before the chlorination experiments are started, the chlorine
demand of the test waters has to be established to determine the dose
of chlorine solution that provides the target 4.0 ± 0.4 mg/L free chlorine
residual. Chlorine demand of the Fisher environmental grade water
will be determined. Chlorine demand is operationally defined as
chlorine dose (applied free chlorine) - free remaining chlorine residual
under a specified contact or incubation period, pH and temperature.
For the preliminary study, only one replicate is desirable. The
unchlorinated Fisher Environmental Grade water can be used for this
purpose, but it must include appropriate concentrations of co-solvents
Section II.E.2 - Page 379 of 522

-------
that will be used to introduce OP pesticides into solution as well as
similar reaction vessels used in the experiment.
1.	Add 2 ml pH 8 borate buffer to 1 L (or proportional
volumes) of unchlorinated Fisher Environmental Grade
water.
2.	Check the pH. If necessary, adjust to pH 8 with dilute H2S04
or dilute NaOH.
3.	Fill each incubation bottle (300 - 500 ml) three quarters full
with the unchlorinated Fisher Environmental Grade water.
Two bottles will be needed. Addition of co-solvent, in the
appropriate concentration as would be employed in (I)
below, may be necessary to mimic co-solvent additions
through pesticide dosing procedures. The doses should be
set up in duplicate to determine if the initial dosing at 4 mg/L
will result in a > 1 mg/L free chlorine residual after 24 hours
in the Fisher Environmental Grade water containing the co-
solvents. Initial dose of 4.0 mg/L free chlorine is appropriate.
4.	Add pH 8 hypochlorite-buffer solution through a pipette held
just above water surface. Dose the appropriate volume of
hydrochlorite-buffer solution to give the required dose in full
bottles.
5.	Cap the bottle and invert twice.
6.	Fill to top of bottle with pH 8 borate buffered unchlorinated
Fisher Environmental Grade water and cap head space-free.
7.	Invert 10 times
8.	Incubate for 24 hr in the dark at room temperature.
9.	After incubation, measure the free chlorine residual, pH, and
temperature. (Note: Addition of hypochlorite-buffer solution
should be sequenced and timed to provide allowance for
measurement of free chlorine residual and pH for each test
water)
10.	The initial chlorine dose that yields an initial free chlorine
residual of 4.0 ± 0.4 mg/L Cb and a > 1.0 ± 0.4 mg/L at 24
hours will be selected and used in the chlorination and
product stability assessment discussed below.
i. Chlorination and Product (Oxon) Stability Experiments
The study will be conducted in 4L low density polyethylene reaction
vessels that can be covered with black plastic to simulate dark condition.
For this final study , the chlorination experiment at pH=8 should be done
in duplicate, along with one replicate OP control [test water + OP
pesticides, without chlorine], one replicate chlorine control [test water +
chlorine], and one buffered water control [test water for spiking with
Section II.E.2 - Page 380 of 522

-------
immediate concentrations of OPs and oxons] indicated as A1, A2, B, C,
and D solutions in Table II.E-4, respectively.
i. For Treatment A:
(1)	Put 2L of unchlorinated Fisher Environmental Grade water and
add 4 ml of pH 8 borate buffer in a dark, 4L polyethylene reaction
vessel. This will require five 4L vessels.
(2)	Measure pH and adjust, if necessary, to pH 8 with dilute
H2S04 or dilute NaOH.
(3)	Dose with OP pesticide(s) to achieve a concentration of 100
pg/L or below the water solubility limit, whichever is lower.
(4)	Collect the unchlorinated, pesticide spiked OP sample.
(5)	Add pH 8 hypochlorite-buffer solution to give an initial free
chlorine residual of 4.0 ± 0.4 mg/L CI2 and a subsequent free
chlorine residual of > 1.0 ± 0.4 mg/L at 24 hours. Dose the
appropriate volume of hypochlorite-buffer solution to give the
required dose in the 2L sample. The time of chlorination is T = 0.
(6)	Prior to taking water samples, stir solution with the aid of
magnetic stirring bar for two minutes.
(7)	Take samples at the time intervals for analysis summarized in
Table 2:
OP pesticide - 0 (prechlorination), 1 hr, 4 hr, 24 hr, 72 hr
Transformation products (oxon, sulfoxide, sulfone, sulfone oxon,
sulfoxide oxon) - 0 (prechlorination), 1 hr, 4hr, 24 hr, 72 hr
(8)	The samples are immediately withdrawn from the reaction
vessel and then quenched stoichiometrically with sodium thiosulfate
(with slight excess) based on the free chlorine residual [1.25 mg per
100 ml aliquot]. The samples should be stored in the dark at 0 - 4°C,
if they cannot be analyzed right away.
(9)	Separate samples will be taken to measure the free chlorine
residual, pH, and temperature.
(10)	Analyze the quenched samples for the parent compound,
primary product (oxon) by appropriate analytical method (GC/MS or
LC/MS/MS). Other transformation products will be identified, when
possible, and described as tentatively identified compounds.
ii. For Treatment B:
(1)	Put 2L of unchlorinated Fisher Environmental Grade water
and add 4 ml of pH 8 borate buffer in a dark, 4L polyethylene
reaction vessel.
(2)	Measure pH and adjust, if necessary, to pH 8 with dilute
H2S04 or dilute NaOH.
Dose with OP pesticide(s) to achieve a concentration of 100
pg/L or below the water solubility limit, whichever is lower.
Section II.E.2 - Page 381 of 522

-------
(3)	At approximately the same time as the collection of the
chlorinated samples in Treatment A, collect the unchlorinated,
pesticide spiked OP samples at 0, 1, 4, 24 and 72 hours. The
samples should be stored in the dark at 0 - 4°C, if they cannot be
analyzed right away.
(4)	Separate samples will be taken to measure the pH and
temperature.
(5)	Analyze the samples for the parent compound, primary
product (oxon) by appropriate analytical method (GC/MS or
LC/MS/MS). Other transformation products will be identified, when
possible, and described as tentatively identified compounds.
iii.	For Treatment C:
(1)	Put 2L of unchlorinated Fisher Environmental Grade water
and add 4 ml of pH 8 borate buffer in a dark, 5L polyethylene
reaction vessel.
(2)	Measure pH and adjust, if necessary, to pH 8 with dilute
H2SO4 or dilute NaOH.
(3)	Add pH 8 hypochlorite-buffer solution to give an initial free
chlorine residual of 4.0 ± 0.4 mg/L CI2 and a subsequent free
chlorine residual of > 1.0 ± 0.4 mg/L at 24 hours. Dose the
appropriate volume of hypochlorite-buffer solution to give the
required dose in the 2L sample.
(4)	Prior to taking water samples, stir solution with the aid of
magnetic stirring bar for two minutes.
(5)	Collect a sample after about 1 hour for OP pesticides and for
oxons.
(6)	The sample is withdrawn from the reaction vessel and then
quenched with the selected reducing agent (with slight excess)
based on the free chlorine residual [1.25 mg per 100 ml aliquot].
The aliquots should be stored in the dark at 0 - 4° C, if they cannot
be analyzed right away.
(7)	A separate sample will be taken to measure the free chlorine
residual, pH, and temperature at 1 hour.
(8)	Analyze the sample for the parent compound, primary
product (oxon) by appropriate analytical method (GC/MS or
LC/MS/MS). Other transformation products will be identified, when
possible, and described as tentatively identified compounds.
iv.	For Treatment D:
(1) Put 2L of unchlorinated Fisher Environmental Grade water
and add 4 ml of pH 8 borate buffer in a dark, 5L polyethylene
reaction vessel.
Section II.E.2 - Page 382 of 522

-------
(2) Measure pH and adjust, if necessary, to pH 8 with dilute
H2S04 or dilute NaOH.
(3) Collect 100 ml samples of the unchlorinated, buffered water
at each sampling interval of 0, 1, 4, 24, and 72 hours.
(4) These samples will be spiked with the OP pesticide(s) and
oxon(s) at a spiking level of 50 ppb, as necessary.
(6) The samples will be stored for possible analysis with sample
set batches. The samples should be stored in the dark at 0-4° C, if
they cannot be analyzed right away.
(7) A separate sample is taken to measure the pH and
temperature.
(8) Analyze the samples for the parent compound, primary
product (oxon) by appropriate analytical method (GC/MS or
LC/MS/MS). Other transformation products will be identified, when
possible, and described as tentatively identified compounds.
Table II.E-2.4 Proposed Sampling and Analysis Regime
Treatment Condition
(Treated Water Samples
and Controls: OP
pesticide)
Sampling Times
A1 A2
OP OP
Cl2 Cl2
h2o h2o
Pre-
chlorination
Postchlorination
0
1 hr
4 hrs
24 hrs
72 hrs
OP
OP
OP
OP
OP
Oxon1
Oxon
Oxon
Oxon
Oxon

CI
CI
CI
CI
B
OP
H20
OP
OP
OP
OP
OP
Oxon
Oxon
Oxon
Oxon
Oxon
C
CI2
H20

Oxon

D
H20
Spiked OP
Spiked
OP
Spiked
OP
Spiked
OP
Spiked
OP
Spiked Oxon
Spiked
Oxon
Spiked
Oxon
Spiked
Oxon
Spiked
Oxon
1- Sulfone, sulfoxide, sulfone oxon, and sulfoxide oxon will be analyzed if appropriate for the test
pesticide. This assumes analytical methods and analytical standards are available for the various
degradation products.
j. Data Reduction and Reporting
Report detections of parent OP and its degradation products.
Calculate concentrations, when possible, of OP pesticides and their
stability products. Report identities and structural formulas of
transformation products.
Section II.E.2 - Page 383 of 522

-------
k. Interpretation of Results
The interpretation of study results will be dependent on the
detection of oxidation products in the chlorinated test water treatments.
The control treatments will be used to assess whether the OP pesticide
undergoes oxidation in non-chlorinated laboratory water and to assess
whether OP pesticide or its oxidation products are in the chlorinated
water without pesticide dosing. Because the experimental design has
minimal replication and the analytical methods are not fully vetted for
all the OP pesticides and their oxidation products, there will be strict
qualitative interpretation (i.e. presence or absence of oxidation
products) on whether OP pesticides [phorate, disulfoton, and terbufos]
undergo oxidative desulfonation during a 72 hour contact time in
chlorinated laboratory water. This deduction will be reached if their
oxidation products [sulfoxides and sulfones and their associated
sulfoxide and sulfone oxons] are detected at any quantifiable level in
either replication in the chlorinated laboratory water treatments at any
sampling time and the OP pesticide is stable in non-chlorinated
laboratory water. Additionally, the detection of oxidation products in
chlorinated water at the 24 hour or 72 hour sampling times will suggest
the oxidation product is stable enough in chlorinated water to have the
potential for dietary exposure through drinking water
I. References
Magara, Y. et al., 1994. Degradation of pesticides by chlorination during
water purification. Water Sci. Technol. 30(7): 119-128.
Tierney, D.P. et al., 2001. Chlorine degradation of six organophosphorus
insecticides and four oxons in a drinking water matrix. Syngenta Crop
Protection Center, Greensboro, NC.
Summers, R.C., et al., 1996. Assessing DBP yield: uniform formation
conditions. J. Amer. Water Works Assoc. 88(6): 80-93.
USEPA, Laboratory Study on the Effects of Chlorinated Water on OP
Pesticides, Quality Assurance Project Plan, OPP/EFED/WTEWG, April
24, 2006.
USEPA, Laboratory Study on the Effects of Chlorinated Water on OP
Pesticides, Final Report, OPP/EFED/WTEWG, May 15, 2006.
Section II.E.2 - Page 384 of 522

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9. Appendix 2: Results for the Laboratory Study on the Effects of
Chlorinated Water on OP Pesticides, Phase II
Table II.E-2.5 Results of the LC/MS/MS Analyses of the OP Pesticides Terbufos, Phorate
and Disulfoton and Degradation in Chlorinated and Unchlorinated Water	
Sample
Sample
Time
parent
oxon
Sulfox-
ide
sulfone
oxon
sulfox-
ide
oxon
sulfone
MDL

5
5
10
25
4
4
Terbufos
A1
0
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
15 min
N.D.
N.D.
N.D.
N.D.
35
N.D.
4 h
N.D.
N.D.
N.D.
N.D.
4
N.D.
24 h
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
72 h
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
A2
0
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
15 min
N.D.
N.D.
N.D.
N.D.
31
N.D.
4 h
N.D.
N.D.
N.D.
N.D.
5
N.D.
24 h
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
72 h
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
B
0
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
15 min
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
4 h
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
24 h
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
72 h
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
C

N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
D
0
N.A.
N.A.
N.A.
N.A.
N.A.
N.A.
15 min
N.D.
41
37
42
52
55
4 h
N.D.
34
32
41
49
54
24 h
N.D.
34
33
47
50
48
72 h
N.D.
38
34
39
51
53
Phorate
A1
0
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
15 min
N.D.
N.D.
N.D.
N.D.
73
N.D.
4 h
N.D.
N.D.
N.D.
N.D.
35
5
24 h
N.D.
N.D.
N.D.
N.D.
N.D.
8
72 h
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
A2
0
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
15 min
N.D.
N.D.
N.D.
N.D.
82
N.D.
4 h
N.D.
N.D.
N.D.
N.D.
47
4
24 h
N.D.
N.D.
N.D.
N.D.
N.D.
6
72 h
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
B
0
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
15 min
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
4 h
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
Section II.E.2 - Page 385 of 522

-------
Sample
Sample
Time
parent
oxon
Sulfox-
ide
sulfone
oxon
sulfox-
ide
oxon
sulfone
MDL

5
5
10
25
4
4

24 h
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
72 h
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
C

N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
D
0
N.A.
N.A.
N.A.
N.A.
N.A.
N.A.
15 min
N.D.
45
69
33
49
50
4 h
N.D.
41
56
35
44
42
24 h
N.D.
42
56
37
49
45
72 h
N.D.
47
83
39
53
47
Disul
foton
A1
0
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
15 min
N.D.
N.D.
N.D.
N.D.
54
21
4 h
N.D.
N.D.
N.D.
N.D.
N.D.
54
24 h
N.D.
N.D.
N.D.
N.D.
N.D.
47
72 h
N.D.
N.D.
N.D.
N.D.
N.D.
26
A2
0
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
15 min
N.D.
N.D.
N.D.
N.D.
51
24
4 h
N.D.
N.D.
N.D.
N.D.
N.D.
54
24 h
N.D.
N.D.
N.D.
N.D.
N.D.
41
72 h
N.D.
N.D.
N.D.
N.D.
N.D.
23
B
0
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
15 min
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
4 h
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
24 h
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
72 h
N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
C

N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
D
0
N.A.
N.A.
N.A.
N.A.
N.A.
N.A.
15 min
N.D.
42
40
42
51
65
4 h
N.D.
40
45
41
54
54
24 h
N.D.
40
37
39
49
50
72 h
N.D.
38
40
40
53
55

Section II.E.2 - Page 386 of 522

-------
Table II.E-2.6 Results of the ECB GC-MSD Analyses of the OP Pesticides Terbufos,
Phorate and Disulfoton and Degradation in Chlorinated and Unchlorinated Water
Sample
Sample
Time
parent
oxon
Sulfox-
ide
sulfone
oxon
sulfox-
ide
oxon
sulfone
Terbufos
MDL

1
3

1

1
A1
0
51
N.D.

N.D.

N.D.
15 min
N.D.
N.D.

N.D.

N.D.
4 h
N.D.
N.D.

N.D.

N.D.
24 h
N.D.
N.D.

N.D.

N.D.
72 h
N.D.
N.D.

N.D.

N.D.
A2
0
59
N.D.

N.D.

N.D.
15 min
N.D.
N.D.

N.D.

N.D.
4 h
N.D.
N.D.

N.D.

N.D.
24 h
N.D.
N.D.

N.D.

N.D.
72 h
N.D.
N.D.

N.D.

N.D.
B
0
N.A.
N.A.

N.A.

N.A.
15 min
73
N.D.

N.D.

N.D.
4 h
23
N.D.

N.D.

N.D.
24 h
7
N.D.

N.D.

N.D.
72 h
2
N.D.

N.D.

N.D.
C

N.D.
N.D.

N.D.

N.D.
D
0
N.A.
N.A.

N.A.

N.A.
15 min
N.A.
N.A.

N.A.

N.A.
4 h
29
36

47

52
24 h
44
52

56

59
72 h
33
35

48

42
Phorate
MDL

1
3

1

2
A1
0
56
N.D.

N.D.

N.D.
15 min
N.D.
N.D.

N.D.

N.D.
4 h
N.D.
N.D.

N.D.

4
24 h
N.D.
N.D.

N.D.

2
72 h
N.D.
N.D.

N.D.

N.D.
A2
0
63
N.D.

N.D.

N.D.
15 min
N.D.
N.D.

N.D.

N.D.
4 h
N.D.
N.D.

N.D.

4
24 h
N.D.
N.D.

N.D.

2
72 h
N.D.
N.D.

N.D.

N.D.
B
0
N.A.
N.A.

N.A.

N.A.
15 min
78
N.D.

N.D.

N.D.
4 h
29
N.D.

N.D.

N.D.
24 h
14
N.D.

N.D.

N.D.
72 h
8
N.D.

N.D.

N.D.
C

N.D.
N.D.

N.D.

N.D.
Section II.E.2 - Page 387 of 522

-------
Sample
Sample
Time
parent
oxon
Sulfox-
ide
sulfone
oxon
sulfox-
ide
oxon
sulfone
D
0
N.A.
N.A.

N.A.

N.A.

15 min
N.A.
N.A.

N.A.

N.A.

4 h
27
31

47

46

24 h
43
48

57

50

72 h
35
32

49

42
Disul
foton
MDL

1
1
1
3
3
3
A1
0
58
N.D.
3
N.D.
5
N.D.

15 min
N.D.
N.D.
N.D.
N.D.
N.D.
36

4 h
N.D.
N.D.
N.D.
N.D.
N.D.
38

24 h
N.D.
N.D.
N.D.
N.D.
N.D.
22

72 h
N.D.
N.D.
N.D.
N.D.
N.D.
14
A2
0
66
N.D.
4
N.D.
3
N.D.

15 min
N.D.
N.D.
N.D.
N.D.
15
36

4 h
N.D.
N.D.
N.D.
N.D.
N.D.
29

24 h
N.D.
N.D.
N.D.
N.D.
N.D.
20

72 h
N.D.
N.D.
N.D.
N.D.
N.D.
17
B
0
N.A.
N.A.
N.A.
N.A.
N.A.
N.A.

15 min
77
N.D.
3
N.D.
4
N.D.

4 h
33
N.D.
3
N.D.
N.D.
N.D.

24 h
2
N.D.
2
N.D.
N.D.
N.D.

72 h
3
N.D.
3
N.D.
N.D.
N.D.
C

N.D.
N.D.
N.D.
N.D.
N.D.
N.D.
D
0
N.A.
N.A.
N.A.
N.A.
N.A.
N.A.

15 min
N.A.
N.A.
N.A.
N.A.
N.A.
N.A.

4 h
31
31
43
47
28
58

24 h
44
44
46
52
25
60

72 h
36
35
46
35
23
49

Section II.E.2 - Page 388 of 522

-------
~
E-3. Water Outputs - Region A
See file Water Outputs - Region A.xls
E-4. Water Outputs - Region B
See file Water Outputs - Region B.xls
E-5. Water Outputs - Region C
See file Water Outputs - Region C.xls
E-6. Water Outputs - Region D
See file Water Outputs - Region D.xls
E-7. Water Outputs - Region E
See file Water Outputs - Region E.xls
E-8. Water Outputs - Region F
See file Water Outputs - Region F.xls
E-9. Water Outputs - Region G
See file Water Outputs - Region G.xls
•1, ,
-------
G-1. Sensitivity Analysis: Cancellation of Azinphos-Methyl Group 3 Uses
A. Background
The food component of the Organophosphorus Cumulative Risk
Assessment (OP CRA) is to a large extent based on pesticide residue
information collected by USDA's Pesticide Data Program (PDP) from
1994 to 2004. The PDP sampling design and procedures provide OPP
with a nationally representative sample of selected food commodities
available to the US population in grocery stores.
Inherent in the use of such monitoring data that has been collected
over an extended length of time is the concern that any changes in
pesticide use patterns will not be reflected in the data. The OPs in
particular have undergone sizable changes in use patterns as a result
of the individual chemical decisions. In cases for which legal
agreements have been signed or voluntary cancellations implemented,
the uses have been removed from the assessment.
The OP CRA Update 2006 has incorporated the phase-out of
domestic uses that was recently proposed by the Agency concerning
the remaining (Group 3) uses of azinphos-methyl (AZM). Specifically,
all domestic uses for AZM on almonds, Brussels sprouts, pistachios,
walnuts, apples, blueberries, cherries, parsley, and pears are to be
phased out effective in 2007 or 2010. This information was
incorporated into this Update by removing from the food assessment
all AZM residues on these crops which are domestically-grown25;
residues on imported crops were not changed. All other uses of this
pesticide have already been voluntarily cancelled by the manufacturer.
These mitigation actions for AZM were proposed due primarily to
issues associated with worker exposure, and not dietary exposure.
Thus, dietary risk and exposure estimates presented in OP CRA
Update 2006 are not expected to differ significantly from those that do
not incorporate these 2007 and 2010 AZM proposed use cancellations.
The purpose of this sensitivity analysis is to determine the extent to
which the inclusion of domestic AZM residues on Group 3 crops affect
the exposure and risk estimates presented in Chapter I.C.
25As part of its standard sampling procedure, USDA PDP collects detailed information for each of
the hundreds of samples collected each year. An essential component of this detailed sampling
information is the origin of sample. Specifically whether the food commodity was grown
domestically or imported.
Section II.G.1 - Page 390 of 522
-------
B. Approach
In the food component of the OP CRA Update 2006, PDP analytical
samples of AZM residues identified as domestic in origin were
completely removed from the assessment. As a sensitivity analysis
and to ensure that risks prior to any use cancellations are not above
the Agency's level of concern, OPP has performed a parallel exposure
analysis in which AZM Group 3 domestic uses are retained.
PDP samples of domestic origin that were analyzed for residues of
AZM (or its metabolite) were included in this sensitivity analyses for
any commodities that are used by OPP to represent pesticide residues
in almonds, Brussels sprouts, pistachios, walnuts, apples, blueberries,
cherries, parsley, and pears26. All other residue and consumption
information from the food component of the OP CRA Updated 2006
remained unchanged for this sensitivity analysis (see Chapter I.C for
details). Resulting exposure and risk estimates under this scenario
would be expected to be more typical of the near term (e.g., through
2007 and 2010) before the AZM Group 3 cancellation becomes
effective.
C. Results
In Chapter I.C, the margins of exposure (MOEs) at 95th, 99th, and
99.9th percentiles of exposure are reported for the 21-day exposure
period for various age groups, the mostly highly exposed of which
were children 1-2 and 3-5 years old. Briefly, the MOEs for the 21-day
assessment are above or very close to the target of 100 at the 99.9th
percentile of exposure for all age groups; the MOEs for the 95th and
99th percentiles of exposure are well above 100.
Table II.G-4.1 provides a comparison of MOEs at 99.9th percentiles
of exposure from the 21-day food assessment presented in Chapter
I.C and the 21-day food assessment described in this Appendix.
Tables II.G-4.2 and II.G-4.3 provide similar comparisons of the MOEs
at the 99th and 95th percentiles of exposure. Although only two most
highly exposed age groups are presented in these Tables, the MOEs
for the all other age groups exceed the target MOE of 100 at the
percentiles presented.
26 For detailed information regarding crops and foods to which PDP commodities are translated
see Appendices II.C.4 and II.C.6.
Section II.G.1 - Page 391 of 522
-------
Table II.G-1.1 Cumulative Food Assessment MOEs at the 99.9th Percentile
Exposure.

Single Day MOE
without AZM
Group 3 Uses
Single Day MOE
with AZM Group 3
Uses
Children 1-2 yrs
110
110
Children 3-5 yrs
99
98
Table II.G-1.2 Cumulative Food Assessment MOEs at the 99th Percentile.

Single Day MOE
without AZM
Group 3 Uses
Single Day MOE
with AZM Group 3
Uses
Children 1-2 yrs
250
240
Children 3-5 yrs
300
290
Table II.G-1.3 Cumulative Food Assessment MOEs at the 95th Percentile of
Exposure.

Single Day MOE
without AZM
Group 3 Uses
Single Day MOE
with AZM Group 3
Uses
Children 1-2 yrs
550
520
Children 3-5 yrs
670
620
D. Conclusions
When these Group 3 AZM uses are included in this alternative
assessment (i.e, incorporated back into the exposure and risk
calculations), MOEs at the 99.9th percentile of exposure remain virtually
unchanged for children 1-2 and change from 99 to 98 for children 3-5.
Thus, the AZM use cancellations that have been proposed to take effect in
2007 to 2010 do not significantly impact the dietary exposure and risk
estimates presented in the OP CRA Update 2006.
Section II.G.1 - Page 392 of 522
-------
G- 2. Characterization of Potential Oxon Formation and Exposure in
Drinking Water
A number of OP pesticides have the potential to convert to more toxic
oxon transformation products as a result of chlorination/oxidation during
standard drinking water treatment. Additional studies conducted since 2002
confirm the potential for OP pesticides to form stable oxon transformation
products as a result of chlorination. Less data are available characterizing
the potency of most oxons For those oxons with insufficient toxicity
information, EPA used high end adjustment factors of 10X and 100X to
account for the potential increased potency of the oxon relative to the
parent. With protective assumptions (100% conversion from the parent to
the oxon, instantaneous transformation to oxon with no degradation), EPA
estimated that the oxons would not appreciably change the cumulative OP
distributions with a 10X or, in most scenarios, with the 100X oxon
adjustment factor. As described in detail below, the exception is for Region
C (Southwest / Central Valley, CA, exposure scenario) where the 100X
oxon adjustment factor increased estimated peak cumulative concentrations
by as much as 35-50X, largely due to methidathion. Overall, EPA's
continues to conclude that risk from drinking water exposure to OPs is
below the level of concern for the cumulative risk assessment. As
described below, the increase in peak cumulative concentrations for
methidathion are believed to result from compounding high end
assumptions on the potency and the exposure to the oxon. This
compounding decreases the confidence surrounding the risk estimates.
This appendix characterizes the degree of confidence and uncertainty
in regarding oxon formation and decline and oxon toxicity and identifies
additional information needed to quantify the potential impacts of oxon
formation on the OP cumulative exposure in drinking water.
1. Screening Level Approach: Potential for Oxon Formation as a
Result of Drinking Water Treatment
For the OP pesticides, information on the potential to form oxons as
a result of chlorination and on differential toxicities between parent and
oxon are not sufficient to make quantitative adjustments to the cumulative
exposure estimates. The Agency has used a screening level approach to
evaluate the potential contribution of potential oxon exposure in drinking
water to the cumulative risk of the OPs. The purpose of this analysis was
1) to consider the degree to which exposure to the oxons
from drinking water may qualitatively change the
Agency's conclusion that the risk from drinking water
Section II. G.2 - Page 393 of 522
-------
exposure to OPs is below the level of concern and
2) to determine whether additional information may be
needed concerning oxon toxicity, extent and rate of oxon
formation as a result of standard drinking water treatment,
and/or the rate of breakdown of the oxons after formation in
order to better refine and quantify risk to the oxons.
Based on published literature, registrant-submitted studies, US
EPA laboratory studies (summarized in Appendices II.E. 1 and II.E.2), and
monitoring data (most notably a 1999-2000 USGS reservoir monitoring
study; see Bloomquist et al, 2001), EPA has identified ten OP pesticides
with the potential to form stable oxons as a result of chlorination: azinphos
methyl, bensulide, chlorethoxyphos, chlorpyrifos, diazinon, dimethoate,
disulfoton sulfone, malathion, methidathion, methyl parathion, and
phostebuipirim. The supporting evidence is summarized in Table I.E-2 of
the drinking water exposure section (I.E) and in Appendices II.E-1 and
II.E.2. The studies summarized in Table I.E-2 are only designed to
determine whether oxons form as a result of chlorination and whether they
are stable for at least 72 hours after formation. More extensive studies
would be required to determine the rates of formation and decline of oxons
in treated water.
2. Estimating the Impacts of Potential Oxon Formation on OP
Cumulative Distributions in Drinking Water
In estimating potential oxon impacts, the Agency assumed that any
transformation as a result of chlorination results in complete conversion to
the oxon and that the resulting oxon would be stable for at least 72 hours,
sufficient time to move through the distribution system. The resulting
estimates of oxon residues in drinking water represent an upper bound of
the potential oxon levels that may actually occur in drinking water. As
mentioned earlier, the studies referenced in Table I.E-2 were not designed
to determine definitively what percentage of the parent OP might convert
to the oxon. While this percentage is likely to vary depending on treatment
conditions, anything less than 100% conversion will result in lower oxon
levels than estimated. Similarly, the Agency's assumption that the oxons
remain stable after they are formed is an upper bound estimate of the
extent that the oxons degrade at any appreciable rate between the time
they are formed to when they are distributed at the tap.
EPA had sufficient data to estimate oxon adjustment factors that
reflect the greater toxicity of the oxon for three OP pesticides - dimethoate
(3X), chlorpyrifos (10X) and methyl parathion (10X). For the remaining OP
pesticides which form oxons, insufficient data exists to determine a
potential oxon adjustment factor. For these pesticides, the Agency used
Section II. G.2 - Page 394 of 522
-------
oxon adjustment factors of 10X and 100X to consider upper bound
estimates of potential oxon potentcy. These adjustment factors were
applied to the pesticide concentrations in water.
As noted in the drinking water exposure section (I.E), the exposure
scenario for Region A (Florida) had the highest estimated peak
concentrations of any of the regional scenarios. Because none of the OP
residues driving exposure in this region formed oxons, this regional
distribution served as a reference point to compare the impact of oxon
formation on drinking water exposures in other regions.
While the 10X oxon adjustment factor resulted in increases in
estimated peak concentrations ranging from less than 25% to 3-5X
(Region C), all of the regional distributions remained well below that of
Region A (Figure II.G.2 1) and thus below the level of concern for the
cumulative risk assessment. Peak concentrations from the Region A
scenario (dark blue line in the figure) is at least 6X to more than an order
of magnitude greater than those from any other region.
Figure II.G-2.1 Frequency distribution of each of the regional OP cumulative
drinking water exposures, including oxon adjustment factors (10X).
¦ RegA-Oxon(10x def.)
-RegB-Oxon (10x def.)
RegC-Oxon(10x def.)
RegD-Oxon(10x def.)
-RegE-Oxon(10x def.)
RegF-Oxon(10x def.)
-RegG-Oxon(10x def.)
Percentile
When the 100X oxon adjustment factor is applied, peak
concentrations in Regions B, C, E, F, and G shifted upwards in relation to
that of Region A but remained below the below the level of concern for the
Section II. G.2 - Page 395 of 522
-------
cumulative risk assessment. The noted exception is for the cumulative
distribution for Region C which increased by 30 to 50X, surpassing the
distribution of Region A (Figure II.G.2 2), primarily due to the oxon of
methidathion. This resulted in estimated MOEs for drinking water
exposure ranging from 16 to 99 for the first third of the year for children 1
to 2 years of age at the 99.9th percentile (21-day rolling average) (Figure
II.G.2 3).
Figure II.G-2.2 Frequency distribution of each of the regional OP cumulative
drinking water exposures, including oxon adjustment factors (100X).
RegA-Oxon(100x def.)
RegB-Oxon(100x def.)
RegC-Oxon(100x def.)
RegD-Oxon(100x def.)
RegE-Oxon(100x def.)
RegF-Oxon(100x def.)
RegG-Oxon(100x def.)
3.5E-02
o 3.0E-02
re 2.5E-02
£
|> 2.0E-02
O 1.5E-02
5.0E-03
Percentile
0.0E+00 -f-
85
Section II. G.2 - Page 396 of 522
-------
Figure II.G-2.3 Margins of Exposure (MOE) for Cumulative OP Residues
from Multiple Routes of Exposure in Region C for Children 1-2 Years Old at
the 99.9th Percentile of Exposure.
21 Day Rolling Average REGION C assuming 100X oxon for CHILDREN 1-2 with AZM in for
Group 3 and using the FOOD version 20
Julian Days
¦7'7^tt^^t'?OT-CMn^lfl(DNCOO)0'-CMPl'7lfl(DNCOO)Oi-(N|CO'7IO(£)
i-CMCO*3-lOtOI^COi-i-i-i-i-i-i-i-i-i-CMCMCMCMCMCMCMCMCMCMCOCOCOCOCOCOCO
100000 J

Food MOE —Drinking Water MOE —Total MOE — Inhalation MOE —Dermal MOE —Oral (non-dietary) MOE |
3. Characterizing Oxon Exposure in Region C
The exposure scenario for Region C includes a number of oxon
formers with peak concentrations within two orders of magnitude of the
cumulative peaks (chlorpyrifos, diazinon, dimethoate, methidathion,
methyl parathion). With no oxon adjustments taken into account, the major
OP pesticides contributing to the cumulative OP residues are
methamidiphos, methidathion, and phorate (including the sulfone and
sulfoxide residues). Figure II.G.2 4 provides a representative illustration of
the relative contributions of OP residues to the cumulative exposure
across 4 years (of a 35-year simulation). Of the major contributors, only
methidathion has the potential to form an oxon as a result of chlorination.
Section II. G.2 - Page 397 of 522
-------
Figure II.G-2.4 Contributions of individual OP pesticides to the RPF-
adjusted cumulative load for Region C (CA Central Valley) with no oxon
adjustment factor.
* ~ v.
¦ ¦¦/
O"
o
tn
o
.c
a
o
¦g
E
ro
o
E
O)
E
o
o
1.6E-03
1.4E-03
1.2E-03
1.0E-03
8.0E-04
6.0E-U4
4.0E-04
2.0E-04


¦	Methidathion
¦	Methamidiphos
~	Phorate
~	Dimethoate
~	Disulfoton
~	Diazinon
~	Other OPs




























0.0E+00
(M CM CM CM CM CN CO co (otococo^r^rtt
CD CD CD CD CD CO CD CD CDCDCDCOCDCDCDCD
0)0)0)0) 0)0)0)0)0)0)0)0)0)0)0)0)
LO LO
CD CD
O) O)
CD CD
CD CD
O) O)
CD CD
CD CD
O) O)
CO LO h- O)
Date
When thelOOX oxon adjustment factor is used, methidathion
becomes the dominant contributor to the OP cumulative exposure (Figure
II.G.2 5). Note that the scale of the graph increases by 30X between the
two figures. The phorate peak shown in 1962 (Figure II.G.2 4), which
remains unchanged because no oxons are formed, is dwarfed in Figure
II.G.2 5 while the methidathion peaks increase with the oxon adjustment
factor.
Section II. G.2 - Page 398 of 522
-------
Figure II.G-2.5 Contributions of individual OP pesticides to the RPF-
adjusted cumulative load for Region C (CA Central Valley) with a default
100X oxon adjustment factor.
5.0E-02
¦	Methidathion (100x)
¦	Methamidiphos
~	Phorate
~	Dimethoate (3x)
¦	Disulfoton
~	Diazinon (100x)
~	Other OPs
4.5E-02
4.0E-02
3.5E-02
Q.
3.0E-02
2.5E-02
2.0E-02
J? 1.5E-02
1.0E-02
5.0E-03
0.0E+00
Date
4. Characterizing the Risk to Methidathion Oxon
The Agency has taken a screening approach to evaluating the
impact of direct exposure to oxons derived from drinking water processing
chlorination. This approach included high end assumptions for conversion
from the parent to the oxon, stability of the oxon, and the toxicity of oxon
degradate. These assumptions used in combination result in exaggerated
risk to the oxon. Even with these high end assumptions, the risk from the
oxons are below the level for the majority of scenarios, including all
scenarios which used the 10X toxicity adjustment factor. The noted
exception was for methidathion oxon in Region C when using the 100X
toxicity adjustment factor.
Methidathion was included in the 2006 USEPA BEAD study
(Appendix II.E.1). Although the studies were not designed to make
quantitative estimates of oxon formation and decline, it does provide an
indication of the relative degree of oxon formation and stability.
Methidathion was stable in buffered, nonchlorinated water. In other word,
there is potential for it to persist in the water as it goes through the
treatment plant. Methidathion converted fairly rapidly under chlorination -
90-98% conversion to the oxon within 1 hr. These data suggest that the
assumption that 100% of the parent compound converts to the oxon is not
unreasonable. After 72 hr, two-thirds of the oxon was still detected,
Section II. G.2 - Page 399 of 522
-------
suggesting that methidation-oxon is fairly stable within the perspective of a
DW treatment distribution system.
Monitoring data on methidathion is scarce, particularly in
methidathion use areas. While methidathian was not included in the
USGS NAWQA study, a study conducted by California DPR and USGS
found methidathion detections from dormant spray to orchards in 18% of
water samples monitored (see Water Appendix III.E 2 from the 2002 OP
CRA). The modeled exposure for methidation has a maximum of 0.15 ppb
and a 99th percentile concentration of 0.06 ppb. These concentrations are
comparable to maximum reported detections from available monitoring
studies. Information from the USEPA BEAD study combined with the
monitoring studies suggests that actual estimates of DW exposure for
methidathion and its oxon are reasonable approximations of the potential
concentrations in Region C where methidathion is used on orchard crops.
The relative potency of methidathion oxon compared to the parent
compound for brain ChE inhibition s unknown but is expected to be lower
than the 100X toxicity adjustment factor. For dimethoate, methyl
parathion, and chlorpyrifos where there is sufficient information to
evaluate relative potency for brain ChE inhibition, the oxon is less than
10X more potent compared to the parent for brain ChE inhibition.
Theoretically, if the oxon were up to 100X more potent than the parent,
then the oxon would be almost 20X more potent than dicrotophos which is
the most potent OP pesticide and which does not require activation to the
oxon but instead is active as the parent compound. Although not
impossible, it is unlikely that methidathion oxon is actually 100X more
potent that the parent. Moreover, there are no available data comparing
the relative sensitivity of juvenile and adult animals (ie, a comparative ChE
study) for methidathion. As such, the full 10X FQPA factor has been
retained for methidathion. Overall, the Agency believes that the
uncertainties associated with the toxicity of the oxon are key in the
characterization of the risk to methidathion oxon in drinking water. The
Agency also believes that risks reported here are exaggerated and the
actual risk is significantly lower. To confim this, the Agency will be issuing
a data call-in notice for a 28-day repeated-dose toxicity study with
methidathion oxon.
Section II. G.2 - Page 400 of 522
-------

i

G-3. Characterization of OP Cumulative Residues in Drinking Water:
Region A
EPA estimated distributions of individual and cumulative OP pesticide
residues in drinking water in high potential exposure areas across different
regions of the country. In the south Florida scenario, which represents the
few surface water sources of drinking water in Region A, estimated
concentrations of total phorate residues (parent plus sulfoxide and sulfone
transformation products) reached as high as 1 to 11 ug/l (ppb) for periods of
short duration (days). The transformation products form in the environment
and, based on available literature, are expected to be equal in toxicity to
phorate. These phorate peaks drove the OP cumulative exposure estimates
for drinking water in this region, resulting in MOEs ranging from 79 to 94 for
Children 1-2 year old at the 99.9th percentile of exposure on days 229 to
244.
The drinking water exposure estimated for this region is likely an
overestimate because laboratory studies indicate that phorate and its
sulfoxide and sulfone transformation products are likely to break down
rapidly (on the order of minutes to hours) during the chlorination process of
drinking water treatment (see Appendices II.E. 1 and II.E.2) In addition, the
estimated concentrations of total phorate residues are likely to be
overestimates for the following reasons:
Peak concentrations assume that phorate applications on
sugarcane occur on the same day. Because of the estimated
acreage being treated, phorate applications are likely to be
spread out over time. Thus, the peak concentrations are likely to
be lower than estimated.
The estimated phorate concentrations better reflect
concentrations in drainage canals and water retention structures.
Reductions in concentrations are likely to occur with holding time
(phorate residues degrade with half-lives on the order of days in
aquatic environments) and with dilution as the drainage waters
flow into larger water bodies used for drinking water supplies.
While these factors cannot be quantified, qualitatively they indicate that
concentrations of total phorate residues in drinking water will be
substantially lower than estimated for this region. This appendix
characterizes the estimated total phorate concentrations for those high-
exposure drinking water sources in south Florida and documents the lines of
evidence indicating that actual OP levels in drinking water will be lower than
estimated.
Section II.G.3 - Page 401 of 522
-------
1. Estimated Exposures for Drinking Water in Region A
Of the OP pesticides used in the south Florida region, phorate had
the highest estimated concentrations (Table II.G.3 2). The phorate
residues in Table II.G.3 1 reflect a combination of the parent phorate and
the sulfoxide and sulfone transformation products.
Table II.G-3.1 Estimated percentile concentrations of individual OP
pesticides in the south Florida surface water exposure scenarios (not
adjusted for relative potency).	
Chemical
Crop/Use
Percentile concentration in ug/l (ppb)
Max 99in 95in 90in 80in
Region A (Florida): South FL
Acephate
Peppers
7.6E-02
6.8E-03
8.5E-04
2.8E-04
8.7E-05
Chlorpyrifos
Corn, citrus
2.0E-01
9.6E-02
4.9E-02
3.3E-02
2.1E-02
Diazinon
Lettuce, tomato
2.9E-02
1.5E-02
8.8E-03
6.1E-03
3.9E-03
Ethoprop
Sugarcane
1.5E+00
5.1E-01
2.5E-01
1.7E-01
9.8E-02
Methamid-
ophos
Acephate
degradate, tomato
9.3E-03
1.7E-03
2.6E-04
8.4E-05
1.6E-05
Phorate (1)
Corn, sugarcane
1.1E+01
7.2E-01
1.8E-02
1.1E-04
5.4E-09
(1) Estimated concentrations for phorate reflect combined residues of the parent and its
sulfoxide and sulfone transformation products.
The temporal and spatial extent of potential high OP exposure is
limited to a relatively short duration in the fall, associated with phorate and
ethoprop applications to sugarcane. Figure II.G.3 1 shows the distribution
of combined OP concentrations (in methamidophos equivalents) over 35
years of simulated weather patterns. Generally one to two brief peaks (few
days in duration) occur within a short time span every year. The
magnitude of the peaks varies, depending on the timing of the runoff
events after application and on the magnitude of runoff. The estimated
peaks assume that the applications occur on the same day every year.
Year-to-year peaks are likely to vary in timing because the actual dates of
application may vary within an optimal window of application from year to
year. Thus, the spread in yearly peaks may be broader than shown in the
figure.
Section II.G.3 - Page 402 of 522
-------
Figure II.G-3.1 Estimated OP Cumulative Concentrations (in
Methamidophos Equivalents) Reflecting 35 Years of Weather Data.
>
"5
c*
0)

o
.c
Q.
O
¦a
E
re
.c
0>
E
c
0)
o
c
o
o
5.0E-02
4.5E-02
4.0E-02
3.5E-02
3.0E-02
2.5E-02
2.0E-02
1.5E-02
1.0E-02
5.0E-03
L
0.0E+00 -I—*—¦t ¦- Y —*-i ¦—Y ¦- 1—¦¦i ¦¦ ¦!
J-49 J-51 J-53 J-55 J-57 J-59 J-61 J-63 J-65 J-67 J-69 J-71 J-73 J-75 J-77 J-79 J-81 J-83
Date
When the drinking water exposure estimates are folded into the
cumulative exposure assessment, the estimated peak concentrations for
drinking water result in MOEs ranging from 79 to 94 for children from 1-2
years in age at the 99.9th percentile (Figure II.G-3.2). The brief period of
high exposure (days 229 through 244) coincide with the expected period
of peak exposure based on an early September application of phorate on
sugarcane and sweet corn and of ethoprop on sugarcane.
Section II.G.3 - Page 403 of 522
-------
Figure II.G-3.2 Margins of Exposure (MOE) for Cumulative OP Residues
Region A (Florida) for Children 1-2 Years Old at the 99.9th Percentile of
Exposure.
OP CRA Children 1-2 REGION A Surface Water (NO OXON) 6-5-06 DDVP 21 Days;
MOEs at the 99.9th Percentile
Julian Days
* ^ 0? tS» # & 4> ^	^	^ ^ ^
8
100
®
CL
O)
O)
O)
®
-C
1000
W
LD
O
10000
100000
Food MOE —Drinking Water MOE
Total MOE — Inhalation MOE
Dermal MOE
Oral (non-dietary) MOE
2. Principal Contributors to the OP Cumulative Drinking Water
Exposure in Region A
A CEC analysis of the 99.8th to 100th percentile of exposure to
children (age 1-2 years) shows that the contributing drinking water
exposures at this high end of exposure predominantly come from two
drinking water years - 1977 (50% of exposures) and 1966 (20% of
exposures) (Table II.G-3.2). This coincides with the two highest peak
concentrations estimated for the region (Figure II.G.3 1). The estimated
exposures do not represent historic exposure levels, but only the
probability of exposure based on variability in weather patterns. However,
the analysis indicates that the highest drinking water exposures are not
driven solely by the highest water concentrations in those exposure years
(Table II.G-3.2).
Section II.G.3 - Page 404 of 522
-------
Table II.G-3.2 Exposure analysis for Children 1-2 Years Old For Region A
m	
Demogra
phics
Exposure (mg/ kg-Bod
y Wt /da)
Water
PID-
HH#
Indiv
Itera-
tion
Sex
Age
Body wt
(kq)
Total
Dietary
Water
Cone,
(mg/l)
Year
10154
49603
2
7
F
1Y
10.5
0.0011957
0.0000062
0.0011894
0.0125
1977
20523
52340
2
6
F
2Y
13.2
0.0023352
0.0000447
0.0022905
0.0302
1977
9745
42121
3
8
M
2Y
15.9
0.0013612
0.0012711
0.0000900
0.00143
1979
20068
47302
1
8
F
1Y
10.0
0.0014643
0.0000159
0.0014484
0.0145
1966
8842
28601
1
5
F
1Y
9.5
0.0010625
0.0001106
0.0009519
0.00904
1966
19253
34813
1
1
M
2Y
11.8
0.0010390
0.0006013
0.0004376
0.00516
1979
8162
25601

1
F
1Y
12.3
0.0017498
0.0017483
0.0000015
1.84E-05
1965
18787
28857
1
4
F
2Y
12.3
0.0010176
0.0000572
0.0009603
0.0118
1977
6334
16123
1
3
M
1Y
10.9
0.0010806
0.0001243
0.0009563
0.0104
1977
18015
24339
1
2
M
1Y
13.6
0.0012331
0.0010390
0.0001940
0.00264
1952
6212
15150
1
4
F
1Y
15.0
0.0013518
0.0001001
0.0012517
0.0188
1977
16390
16808
1
6
M
1Y
11.4
0.0017784
0.0000445
0.0017339
0.0198
1977
5230
52024
1
3
F
2Y
13.6
0.0014841
0.0000356
0.0014485
0.0197
1977
14272
35208
1
6
M
2Y
9.5
0.0017544
0.0002197
0.0015347
0.0146
1977
5209
52015
2
8
F
1Y
9.5
0.0011210
0.0001125
0.0010085
0.00958
1977
13763
28721
2
9
M
2Y
10.0
0.0009571
0.0001491
0.0008079
0.00808
1977
4933
48010
2
6
F
1Y
11.4
0.0016704
0.0000564
0.0016140
0.0184
1966
12492
21720
1
10
M
1Y
12.3
0.0009911
0.0001691
0.0008221
0.0101
1966
4878
46511
1
2
F
2Y
13.2
0.0011330
0.0001690
0.0009640
0.0127
1977
11652
17244
1
8
F
1Y
14.5
0.0016687
0.0014836
0.0001851
0.00268
1951
4619
42505
3
3
M
2Y
12.7
0.0013135
0.0012202
0.0000933
0.00118
1952
10231
51115
8
6
F
2Y
13.6
0.0013701
0.0000125
0.0013576
0.0185
1977
3607
28010
3
1
M
1Y
10.0
0.0010041
0.0000574
0.0009468
0.00947
1966
Section II.G.3 - Page 405 of 522
-------
PID-
HH#
19271
35305
3401
27034
18015
24339
2280
21515
14272
35208
1361
17013
12629
22731
1215
16502
11552
16751
1148
16008
19098
31824
1148
16008
14131
32216
1110
15546
20108
47804
753
14009
12467
21706
16398
16813
101
10512
(1)

S,

Demographics
Exposure (mg/ kg-Bodv Wt /da)
Water
Indiv
Itera-
tion
Sex
Age
Body wt
(kg)
Total
Dietary
Water
Cone.
(mg/l)
Year
1Y
9.5
0.0016609
0.0000355
0.0016254
0.0154
1977
M
2Y
10.9
0.0012668
0.0010322
0.0002346
0.00256
1952
M
1Y
13.6
0.0011644
0.0011456
0.0000187
0.000254
1959
1Y
9.5
0.0009687
0.0001143
0.0008545
0.00812
1977
M
2Y
9.5
0.0012525
0.0010988
0.0001537
0.00146
1969
M
2Y
20.5
0.0010669
0.0000757
0.0009911
0.0203
1977
M
1Y
11.4
0.0010534
0.0003172
0.0007362
0.00839
1966
1Y
11.4
0.0010485
0.0000754
0.0009732
0.0111
1966
M
2Y
15.9
0.0016186
0.0000886
0.0015300
0.0243
1977
M
2Y
12.3
0.0009942
0.0009483
0.0000460
0.000566
1955
1Y
10.9
0.0011833
0.0000285
0.0011548
0.0126
1977
M
2Y
12.3
0.0016165
0.0004836
0.0011328
0.0139
1966
2Y
12.7
0.0009783
0.0003152
0.0006631
0.00842
1977
1Y
10.5
0.0010144
0.0000318
0.0009826
0.0103
1977
10
1Y
15.9
0.0011481
0.0011221
0.0000260
0.000413
1953
2Y
11.4
0.0013223
0.0001919
0.0011304
0.0129
1966
M
2Y
16.!
0.0009591
0.0000395
0.0009196
0.0154
1977
1Y
10.9
0.0013047
0.0012731
0.0000316
0.000344
1983
1Y
10.0
0.0014294
0.0000200
0.0014093
0.0141
1977
CALENDEX-FCID CEC Records File for CHILDREN 1-2 WATER CONSUMPTION35
CSFII 1994-98
Analysis Date 07-24-2006/16:05:12/8
Exposure analysis for 3 combined weeks: starting week 35 (of 52)
Exposure amounts adjusted for body weight
Dietary Residue file: C:\Calendexfiles\work\OPCRA\final\23July\water_OPCRA20.R98 Last saved: 7/23/2006
9:40:05 AM
Dietary Adjustment factor #2 used.
Dietary Matching File not used.
No non-dietary (residential) analysis
PRZM-EXAMS file: C:\Calendexfiles\work\OPCRA\final\water\OPCRA_RegA_NoOxon 6-5-06.PE1 Last saved:
Section II.G.3 - Page 406 of 522
-------
Demographics
Exposure (mg/ kg-Body Wt /da)
Water
PID-
Indiv
Itera- Sex
Age
Body wt
Total
Dietary
Water
Cone.
Year
HH#

tion |

(kq)



(mg/l)

6/14/2006 2:21:06 PM
PE Analysis applied to Direct Water
PE Analysis applied to Indirect Water
NOEL Oral = 0.08 mg/kg-BodyWt/day
Lower and upper boundary percentiles entered as 99.800 100.000
Lower and upper exposure boundaries computed as: 0.000955 0.002335
Number of records in this file = 42
The cumulative peak for drinking water is driven largely by phorate
and its sulfoxide and sulfone residues, which form in the environment.
Figure II.G-3.3 shows the tail of the estimated OP cumulative distribution
in drinking water sources, along with the component OP residues
contributing to the cumulative exposure (all concentrations are in
methamidophos equivalents). While both phorate and ethoprop are
applied to sugarcane at the same time and can occur together in water,
the cumulative OP concentrations (shown as a dark blue line in Figure
II.G-3.3) are driven largely by phorate residues (shown as a light blue
line). This reflects differences in the amounts of pesticide applied, fate and
transport properties, as well as relative potency differences, between
phorate residues and ethoprop. Further, the analysis indicates that the
estimated cumulative OP residues in the upper tail of the distribution are
driven largely by phorate use on sugarcane (shown as the green line in
Figure II.G-3.3).
Section II.G.3 - Page 407 of 522
-------
Figure II.G-3.3 Upper Percentiles of Frequency Distribution of Cumulative
OP Concentrations (in Methamidophos Equivalents) With Component OP
Residues.
5.0E-02
4.5E-02
4.0E-02
3.5E-02
3.0E-02
2.5E-02
2.0E-02
1.5E-02
1.0E-02
5.0E-03
0.0E+00
97.0%
—	Cumulative
Phorate - total
—	Phorate - Sugarcane
—	Ethoprop
—	Chlorpyrifos
Diazinon
—	Acephate
—	Methamidophos







/
J


97.5%
98.0%
98.5%
Percentile
99.0%
99.5%
100.0%
3. Characterization of Phorate Concentrations in Drinking Water
a. Fate and Transport Modeling of Total Phorate Residues
Because evidence from literature studies indicate that the
sulfoxide and sulfone transformation products of phorate are expected
to be similar in toxicity to the parent compound, EPA simulated the fate
and transport of the combined toxic residues. Degradation (hydrolysis,
aerobic soil and aquatic metabolism) were calculated based on total
(phorate + sulfoxide + sulfone) residues. In the field, the individual
components will degrade at different rates. Phorate breaks down
relatively quickly in water (aerobic aquatic metabolism half-life of <2
days). The sulfoxide has a half-life of 9 days and the sulfone 21 days.
The half-life for the combined residues was ~50 days. This combined
half-life appears to be skewed by the tail of the degradation profile,
which is not well represented by a first-order degradation model. Thus,
the phorate residues are likely to decline more rapidly than estimated
by the half-life rate used in the exposure assessment.
Section II.G.3 - Page 408 of 522
-------
EPA used the sorption coefficient of the most mobile of the
three chemicals (KoC of 91 for phorate sulfoxide). While this provides a
protective exposure estimate, it will also lead to overestimates to the
extent that the other components are less mobile.
b.	Total Phorate Load in Water
The majority of OP and phorate use in the south Florida
exposure scenario is on sugarcane. While only a relatively small
fraction of the sugarcane acreage was treated with OP pesticides (10%
of acres treated with phorate; 6% with ethoprop), this still accounts for
a relatively large acreage compared to other uses in the area. The
estimated 43,000 acres of sugarcane treated with phorate is still
greater than the total combined acreage of the other OP use crops.
The drinking water exposure assessment assumes that the entire crop
area is treated at the same time. While this assumption is not
unreasonable for smaller watersheds supplying small community water
systems, it is less probable that all 43,000 acres of sugarcane will be
treated at the same time.
As applications are spread out over time, the total phorate load
carried to water as a result of any single runoff event will be less than
estimated assuming the entire application occurs in the same day.
Since the phorate residues are not expected to be persistent in water,
degradation between runoff events not only spreads out the estimated
peak concentrations, but should reduce the total load moving through
the drinking water system at any time.
The Agency does not have any information that would allow it to
quantifiably adjust the distribution and timing of application of phorate
across the extent of treated sugarcane acreage in Florida. Thus, while
we can qualitatively characterize the impact of spreading out the
application, we cannot quantify it at this time.
c.	Nature of Drinking Water Supply
Only a small number of surface water sources of drinking water
occur in south Florida. Sugarcane is grown south of Lake Okeechobee
in the Everglades Agricultural Area (EAA), and to the east into Palm
Beach County. Three community water systems (CWS) draw from the
southern end of Lake Okeechobee, and the city of West Palm Beach
draws water from Clear Lake, which is fed in part by drainage water
from the EAA. The agricultural areas in south Florida include extensive
drainage canals and water retention structures. Thus, the drinking
water exposure scenario for Region A better represents water being
held in canals or retention bodies than in reservoirs that directly supply
Section II.G.3 - Page 409 of 522
-------
the community water systems. Drainage canals from sugarcane fields
are not used directly for drinking water, but water from drainage canals
eventually feed water bodies used in southern Florida for drinking
water supply.
Because the phorate residues degrade in water, any increase in
holding time in retention structures or travel time in canals will result in
some degradation and a lowering of residues in water. Additional
dilution will occur where the drainage water flows into larger water
bodies used for water supply. While the potential dilution effect is
accounted for to a large extent by the percent crop area adjustment
applied for this region, the decline in residues with travel time has not
been taken into account.
d. Drinking Water Treatment Effects
Although the drinking water treatment studies documented in
Appendices II.E. 1 and II.E.2 (EPA, 2006a and 2006b) were designed
only to determine the potential for oxon formation as a result of
chlorination, they also indicate that the phorate residues (parent plus
transformation products) are not likely to be stable as a result of
chlorination. Phorate concentrations dropped to non-detectable levels
within 1 hour of chlorination in benchtop jar tests (Appendices II.E. 1
and II.E.2). Similarly, concentrations of phorate sulfoxide and sulfone
also dropped to non-detectable levels shortly after chlorination. While
phorate sulfoxide oxon was briefly detected in the lab studies, the oxon
was not stable.
Thus, the overall phorate levels in drinking water in south
Florida are likely to be much lower than estimated here.
Section II.G.3 - Page 410 of 522
-------
G-4. Sensitivity Analysis: Acute Hazard Endpoints Compared to Single
Day Food Estimates.
1.	Background
The food component of the Organophosphorus Cumulative Risk
Assessment (OP CRA) Update 2006 presented both single-day and 21-
day exposure estimates for various age groups based on toxicity values
derived from 21-day and longer (steady state) animal toxicity studies. As
explained more fully in Chapter I.G, the Agency believes that the 21-day
rolling average analysis better represents the cumulative risk to the OPs.
The Agency further believes that the single day values compared with
relative potency factors (RPFs) and points of departure (PoDs) derived
from animal data representing steady state brain cholinesterase
inhibition provide high end estimates using compounding conservative
assumptions.
Although the Agency's OP CRA uses steady state brain
cholinesterase data to extrapolate risk from 21-day rolling average
exposure profiles, the Agency is concerned with the potential for peak
exposures to OPs. Single chemical aggregate risk assessments include
thorough analysis of acute exposure to individual OPs. The CRA is
designed to evaluate the combined risk to many OPs. The Agency has
conducted a sensitivity analysis where cumulative risks from single day
food exposures were calculated using RPFs and PoD derived from acute
toxicity studies in rat. The purpose of this analysis was:
1)	to better understand the relationship between the results
reported for the single-day and 21-day rolling average analyses
compared with the steady state hazard data and;
2)	to ensure that the CRA was protective of potential peak
exposures to multiple OPs in food.
2.	Approach
The following analysis is meant only as a sensitivity analysis and is
not intended to replace the results presented in I.C and I.G for the 21-day
rolling average analysis. The Agency only collected acute toxicity
information for those OPs that most significantly contribute to food
exposure for children 1-2 and 3-5 years old. Data from comparative
cholinesterase studies where juvenile (post-natal day 11) or adult rats
were exposed to an oral single dose were preferred when available.
Section II.G.4 - Page 411 of 522
-------
Similar to that described in I.B for data from repeated dosing
comparative cholinesterase studies, the OPCum Risk program was used
to derive the estimates provided in II.G-4.1. In cases where the adult and
pup data were adequately modeled with OPCum Risk, the adult BMD was
used to derive the acute RPF with pup data used to derive the FQPA
safety factor for acute dosing. This approach is similar to that used for the
steady state, repeated dosing studies in I.B.
For four OPs, the pup data were adequately modeled with the
OPCum Risk but the adult data were not. For these four, the pup data
were used directly to estimate the acute RPF. It is preferred to derive
RPFs from a uniform sex and life stage but for purposes of this sensitivity
analysis, this is a reasonable approach.
BMD modeling was not attempted for some OPs, instead the acute
value was estimated from either a NOAEL or LOAEL or an extrapolation
between the NOAEL and LOAEL. For all other OPs not identified as
contributors to the cumulative food exposure assessment, the toxicity
information used in this acute analysis was the same as that reported for
the steady state, repeated exposures. As such, the current analysis
provides an upper bound on potential acute cumulative risks to the OPs.
Acute RPFs were calculated using methamidophos as the index
chemical. RPFs were estimated based on the ratios of BMD10 or other
endpoint as appropriate. The acute PoD was based on the
methamidophos BMDL10 of 0.22 mg/kg from acute brain cholinesterase
inhibition in adult female rat.
These acute endpoints were incorporated into a single-day food
assessment. The same sources of consumption information and residue
data that were used in the single-day and 21-day food assessments
discussed in Section I.C were included in this sensitivity analysis.
Specifically dietary consumption information from USDA's Continuing
Survey of Food Intake by Individuals (1994-1996/1998) and data on OP
residues found in food from USDA's Pesticide Data Program (1994-2004)
were used to assess the single-day food exposure.
Section II.G.4 - Page 412 of 522
-------
~



Table II.G-4.1 Summary Table of Acute Endpoints from Adult or Juvenile
Rats from Single Dosing Studies for Some OPs.
OP
Acute
endpoint
(mg/kg)
Source
FQPA
SF
Acute RPF
(methamidophos
equivalents)
•Azinphos methyl
0.44
BMD10 for female pups (see below)
1
0.59
•
JChlorpyrifos
•
1.1
Estimated from Zheng et al (2000) in
neonates
1
0.24
•Malathion
•
52.5
BMD10 for female pups from Reiss (2006)
1
0.0050
•
jMethyl parathion
0.15
BMD10 for female pups (see below)
1
1.73
JAcephate
0.29
BMD10 for female adult rats (see below)
1
0.90
jDiazinon
0.63
BMD10 for female adult rats (see below)
2
0.41
•
•
•
•Dimethoate
•
•
•
2.19
BMD10 for female adult rats (see below).
Other BMD estimates from same study can
be found in USEPA, 2004.
1
0.12
iDisulfoton
0.138
BMD10 for female adult rats (see below)
1
1.88
iMethamidophos
•
0.26
BMD10 for female adult rats (see below)
2
1.00
•
•Omethoate
•
0.18
BMD10 for female adult rats from TXR No.
0052940, April 11,2005
1
1.44
•ODM
•
0.5
estimated from MRID 43929901
10
0.52
•
•Phosmet
•
9
estimated from MRID 44673301
10
0.029
•
JP ho rate
0.75
estimated from MRID 44719901
10
0.35
w
JMethidathion
1
LOAEL from MRID 43145901, 43145902
10
0.26
IChlorpyrifos methyl
16.2
steady state BMD10
10
0.016
3. Results
In Chapter I.C, the margins of exposure (MOEs) at 95th, 99th, and
99.9th percentiles of exposure are reported for the 21-day and single-day
food assessments based on steady state endpoints. These MOEs were
reported for various age groups, the mostly highly exposed of which were
children 1-2 and 3-5 years old. Briefly, the MOEs for the 21-day
assessment are above or very close to the target of 100 at the 99.9th
percentile of exposure for all age groups; the MOEs for the 95th and 99th
percentiles of exposure are well above 100.
Section II.G.4 - Page 413 of 522
-------
In the single day analyses (using steady state RPFs and PoDs), at the
95th and 99th percentiles of exposure the MOEs for all age groups are
above 100. However for the single-day analyses (using steady state
RPFs and PoDs), the MOEs at the 99.9th percentile of exposure do not
reach the target value of 100 for any of the age groups. More specifically,
the MOEs at the 99.9th percentile of exposure for children 1-2 and
children 3-5 years old are 31 and 35, respectively. MOEs of 100 were
reached at approximately the 99.3rd and 99.5th percentile of exposure for
children 1-2 and 3-5 years old, respectively (see Chapter I.C for detailed
reporting of the MOEs).
When the RPFs based on single-day acute endpoints are
incorporated into the single-day exposure food assessment, the MOEs at
the 99.9th percentile exceeded the target of 100 for all age groups except
children 1-2 and 3-5 years old. The MOEs for these two most highly
exposed age groups reached the target of 100 at approximately the 99.7th
and 99.8th percentiles of exposure, respectively. It is important to note
that for most OPs, the steady state RPFs are included in this sensitivity
analysis. In the event that acute toxicity information were used for more
OPs in this analysis, the MOEs would increase as would the percentile at
which the MOEs reach 100.
Table II.G.4 2-4 provides a comparison of MOEs at 99.9th percentiles
of exposure from the 21-day and single-day food assessments presented
in Chapter I.C and the single-day food assessment described in this
Appendix. Tables II.G.4 3 and II.G.4 4 provide similar comparisons of the
MOEs at the 99th and 95th percentiles of exposure. Although three age
groups are presented in these Tables, the MOEs for the all other age
groups exceed the target MOE of 100 at the percentiles presented.
Section II.G.4 - Page 414 of 522
-------
Table II.G-4.2 Cumulative Food Assessment MOEs at the 99.9th Percentile
Exposure.

21-Day Analysis
Based on Steady
State Endpoints
Single-Day Analysis
Based on Steady
State Endpoints
Single-Day Analysis
Based on Single-
Day Endpoints
Children 1-2 yrs
110
30
52
Children 3-5 yrs
99
34
63
Adults 20-49 yrs
280
75
130
Table II.G-4.3 Cumulative Food Assessment MOEs at the 99th Percentile
Exposure.

21-Day Analysis
Based on Steady
State Endpoints
Single-Day Analysis
Based on Steady
State Endpoints
Single-Day Analysis
Based on Single-
Day Endpoints
Children 1-2 yrs
250
130
200
Children 3-5 yrs
300
160
250
Adults 20-49 yrs
610
290
480
Table II.G-4.4 Cumulative Food Assessment MOEs at the 95th Percentile
Exposure.

21-Day Analysis
Based on Steady
State Endpoints
Single-Day Analysis
Based on Steady-
State Endpoints
Single-Day Analysis
Based on Single-
Day Endpoints
Children 1-2 yrs
550
440
610
Children 3-5 yrs
670
510
690
Adults 20-49 yrs
820
990
1400
4. Conclusion
In order to better characterize the single-day food exposure
estimates, the Agency performed a sensitivity analysis that paired single
day-exposure duration with single-day acute endpoints based on brain
cholinesterase data. By incorporating endpoints from toxicity studies with
exposure durations comparable to those being assessed in the food
exposure, the Agency has a better understanding of the extent to which
the use of steady state endpoints in the single-day food assessment
overstates the risks of exposure to OPs. Based on this sensitivity
analysis, the Agency concludes that 1) use of steady state endpoints in
the single-day food assessment overestimates risk by almost 2-fold at the
upper percentiles of exposure and 2) OP CRA was protective of potential
peak exposures to multiple OPs in food.
Section II.G.4 - Page 415 of 522
-------
5. BMD analysis for: Acephate
Acephate:1—D:BRAIN:F:WHOLE
Sun Feb 17 20:03:32 2002
MRID: 4 61518 01Ad Guideline: NONGUIDELINE
Continuous Exponential Model (Decreasing)
Formula: chei = B + (A-B)*exp(-(m*dose)Ag)
Variance Function: power
Highest 2 doses dropped from data set.
The BMD corresponds to a dose that results in a 10% reduction in the
response relative to the control
Summary of Model Fitting Results
AIC	BIC logLik
114.57073 118.77432 -54.28537
Coefficients:
Value Std.Error
A 8.6366705 0.5264088
m 0.3582992 0.0947503
Correlation:
A	m
A 1.0000000 0.7728167
m 0.7728167 1.0000000
Approximate 95% confidence intervals
Coefficients:
lower	est. upper
A 7.6229684 8.6366705 9.785175
m 0.2084456 0.3582992 0.615884
Residual standard error:
lower	est. upper
1.433447 1.806305 2.442940
46151801 Ad 1 D-WHOLE
daW
Cafliniiain- Di.pcirKrtf.Hl MadaI (De= r.E3s.inq'|
Degrees of freedom: 30 total; 28 residual
Goodness of Fit
The chi-squared goodness-of-fit values should be taken as general
indications of fit only. P-values are likely to be inaccurate to some
degree
Pearson Chi-Square Statistic: 0.2075 with 1 degrees of freedom. P =
0. 649
dose n chei Expected sd Exp.SD X2 Resid.
1 0.0 10 8.53 8.636671 0.21 1.821972 -0.1851411
Section II.G.4 - Page 416 of 522
-------
2	0.5 10 7.40 7.220091 1.44 1.529698 0.3719182
3	1.0 10 5.96 6.035858 1.90 1.284309 -0.1867796
BMD Computation
BMD = 0.2941: BMDL = 0.2049
Potency Measures
A unit dose (1 mg/kg) would result in 100*exp(-Potency)% of background
activity
Potency: 0.3583
se: 0.09475
var=seA2: 0.008978
Per cent, of background at unit dose: 70
Per cent, of background at the highest dose: 70
ED50 (95% CI): 1.935 ( 1.152 , 3.248 )
ln(Potency) -1.026
se[log(Potency)]: 0.2644
se[log(Potency)]A2: 0.06993
Section II.G.4 - Page 417 of 522
-------
Acephate:1-D:BRAIN:M:WHOLE
Sun Feb 17 20:05:00 2002
MRID: 4 61518 01Ad Guideline: NONGUIDELINE
Continuous Exponential Model (Decreasing)
Formula: chei = B + (A-B)*exp(-(m*dose)Ag)
Variance Function: power
Highest 2 doses dropped from data set.
The BMD corresponds to a dose that results in a 10% reduction in the
response relative to the control
Summary of Model Fitting Results
AIC	BIC logLik
139.48858 143.69217 -66.74429
Coefficients:
Value Std.Error
A 9.4233756 0.8201802
m 0.4236354 0.1359193
Correlation:
A	m
A 1.0000000 0.7704751
m 0.7704751 1.0000000
Approximate 95% confidence intervals
Coefficients:
lower	est.	upper
A 7.8845617 9.4233756 11.262517
m 0.2195680 0.4236354 0.817364
Residual standard error:
lower	est. upper
2.213380 2.789110 3.772136
46151801 Ad 1 D-WHOLE
~ _
IO -
¦J} -
—
"M -
~ -
o 2 i 0 a 10
daw
CarAiniUirc- Expavrftbl Modal (Docnas-inql
Degrees of freedom: 30 total; 28 residual
Goodness of Fit
The chi-squared goodness-of-fit values should be taken as general
indications of fit only. P-values are likely to be inaccurate to some
degree
Pearson Chi-Square Statistic: 0.415 with 1 degrees of freedom. P =
0.519
dose n chei Expected
1	0.0 10 9.19 9.423376
2	0.5 10 8.01 7.624568
3	1.0 10 6.01 6.169131
sd Exp.SD X2 Resid.
1.04 2.835597 -0.2602621
1.89 2.317218 0.5259940
2.85 1.893605 -0.2657450
BMD Computation
Section II.G.4 - Page 418 of 522
-------
BMD =
0.2487:
BMDL =
0. 1628
Potency Measures
A unit dose (1 mg/kg) would result in 100*exp(-Potency)% of background
activity
Potency: 0.4236
se: 0.1359
var=seA2: 0.01847
Per cent, of background at unit dose: 65
Per cent, of background at the highest dose: 65
ED50 (95% CI): 1.636 ( 0.8724 , 3.069 )
ln(Potency) -0.8589
se[log(Potency)]: 0.3208
se[log(Potency)
Section II.G.4 - Page 419 of 522
-------
Acephate:1—D:BRAIN:F:WHOLE
Sun Feb 17 20:06:14 2002
MRID: 4 61518 01Pup Guideline: NONGUIDELINE
Continuous Exponential Model (Decreasing)
Formula: chei = B + (A-B)*exp(-(m*dose)Ag)
Variance Function: power
The BMD corresponds to a dose that results in a 10^
response relative to the control
reduction in the
Summary of Model Fitting Results
AIC	BIC logLik
91.79047 99.43856 -41.89524
Coefficients:
Value Std.Error
A 4.8229620 0.1653141
B 2.7338332 0.5168364
m 0. 1831715 0. 1177195
Correlation:
A B	m
A 1.0000000 0.5470928	0.6625012
B 0.5470928 1.0000000	0.9503303
m 0.6625012 0.9503303	1.0000000
Approximate 95% confidence intervals
Coefficients:
lower
A 4.50160020 4,
B 1.86895853 2,
est.
8229620 5.
7338332 3.
upper
1672654
9989351
m 0.05027613 0.1831715 0.6673504
Residual standard error:
lower	est.	upper
0.5610703 0.6739836 0.8442186
46151801Pup1 D -WHOLE
4-.
-1	1	r
6 a 10
daw
Cafliniiain- Di.pcirKrtf.Hl Model (Dec reding]
Degrees of freedom: 50 total; 47 residual
Goodness of Fit
The chi-squared goodness-of-fit values should be taken as general
indications of fit only. P-values are likely to be inaccurate to some
degree
Pearson Chi-Square Statistic: 1.695 with 2 degrees of freedom. P =
0.429

dose
n
chei
Expected

sd
Exp.SD
X2 Resid.
1
0.0
10
4 .70
4 . 822962
0
80
0.6680708
-0.58203428
2
0.5
10
4 .86
4.640128
0
86
0.6432862
1. 08085114
3
1.0
10
4 . 39
4 . 473295
0
42
0.6205997
-0.42443042
4
2 . 5
10
4 . 04
4 . 055401
0
45
0.5634268
-0. 08643678
5
10. 0
10
3. 07
3. 068384
0
36
0.4252122
0. 01202137
Section II.G.4 - Page 420 of 522
-------
BMD Computation
BMD = 1.433: BMDL = 0.846
Potency Measures
A unit dose (1 mg/kg) would result in 100*exp(-Potency)% of background
activity
Potency: 0.1832
se: 0.1177
var=seA2: 0.01386
Per cent, of background at unit dose: 83
Per cent, of background at the highest dose: 16
ED50 (95% CI): 3.784 ( 1.074 , 13.34 )
ln(Potency) -1.697
se[log(Potency)]: 0.6427
se[log(Potency)]A2: 0.413
Section II.G.4 - Page 421 of 522
-------
Acephate:1-D:BRAIN:M:WHOLE
Sun Feb 17 20:06:48 2002
MRID: 4 61518 01Pup Guideline: NONGUIDELINE
Continuous Exponential Model (Decreasing)
Formula: chei = B + (A-B)*exp(-(m*dose)Ag)
Variance Function: power
The BMD corresponds to a dose that results in a 10^
response relative to the control
reduction in the
Summary of Model Fitting Results
AIC	BIC logLik
91.73380 99.38189 -41.86690
Coefficients:
Value Std.Error
A 4.8538392 0.1916032
B 2.9464190 0.1488105
m 0.5017972 0.1441051
Correlation:
A B	m
A 1.0000000 0.1359877	0.5910295
B 0.1359877 1.0000000	0.5823909
m 0.5910295 0.5823909	1.0000000
Approximate 95% confidence intervals
Coefficients:
lower
A 4.4832911 4.
B 2.6617570 2.
est.
8538392
9464190
upper
.2550135
.2615241
m 0.2815946 0.5017972 0.8941948
Residual standard error:
lower	est.	upper
0.6092851 0.7319014 0.9167653
46151801Pup1 D -WHOLE
daw
Cafliniiain- Di.pcirKrtf.Hl Model (Dec reding]
Degrees of freedom: 50 total; 47 residual
Goodness of Fit
The chi-squared goodness-of-fit values should be taken as general
indications of fit only. P-values are likely to be inaccurate to some
degree
Pearson Chi-Square Statistic: 3.052 with 2 degrees of freedom. P =
0.217

dose
n
chei
Expected
sd
Exp.SD
X2 Resid.
1
0.0
10
4 . 96
4.853839
0.75
0.7240145
0.4636783
2
0.5
10
4 . 47
4.430585
0.73
0.6536323
0.1906897
3
1.0
10
3. 84
4.101250
0.35
0.6006885
-1.3753328
4
2 . 5
10
3. 64
3.490454
0.53
0.5083676
0.9302434
5
10. 0
10
2 . 93
2.959042
0.47
0.4409028
-0.2082983
Section II.G.4 - Page 422 of 522
-------
BMD Computation
BMD = 0.5852: BMDL = 0.3935
Potency Measures
A unit dose (1 mg/kg) would result in 100*exp(-Potency)% of background
activity
Potency: 0.5018
se: 0.1441
var=seA2: 0.02077
Per cent, of background at unit dose: 61
Per cent, of background at the highest dose: 0.66
ED50 (95% CI): 1.381 ( 0.7868 , 2.425 )
ln(Potency) -0.6896
se[log(Potency)]: 0.2872
se[log(Potency)]A2: 0.08247
Section II.G.4 - Page 423 of 522
-------
6. BMD analysis for: Azinphos methyl
Azinphos-methyl:1-D:BRAIN:F:WHOLE
Tue Jan 25 22:32:28 2005
MRID: 46162101 Guideline: NONGUIDELINE
Continuous Exponential Model (Decreasing)
Formula: chei = B + (A-B)*exp(-(m*dose)Ag)
Variance Function: power
The BMD corresponds to a dose that results in a 10% reduction in the
response relative to the control
Summary of Model Fitting Results
AIC	BIC logLik
67.98541 73.05205 -30.99270
Coefficients:
Value Std.Error
A 6.3561429 0.14634233
m 0.2375225 0. 04047062
Correlation:
A	m
A 1.0000000 0.7634762
m 0.7634762 1.0000000
Approximate 95% confidence intervals
Coefficients:
lower est.	upper
A 6.0666864 6.3561429	6.6594101
m 0.1682302 0.2375225	0.3353557
Residual standard error:
lower	est.	upper
0.4763423 0.5828629 0.7511810
46162101 1 D-WHOLE
IjI' -
-i—

Ijj -



n -



r-j -



~ -



m u iu it m u
dote
Ccrrinucws Erpcnerrid Model {D«screasinq!
Degrees of freedom: 40 total; 38 residual
Goodness of Fit
The chi-squared goodness-of-fit values should be taken as general
indications of fit only. P-values are likely to be inaccurate to some
degree
Pearson Chi-Square Statistic: 4.731 with 2 degrees of freedom. P =
0.0939
dose
1	0. 00
2	0.26
3	0.49
Section II.G.4 - Page 424 of 522
n chei	Expected sd Exp.SD X2 Resid.
10	6.1	6.356143 0.5 0.5947195 -1.3619781
10	6.2	5.975489 0.4 0.5608027 1.2659842
10	5.8	5.657803 0.5 0.5324153 0.8445772
-------
4 1.00 10 4.9 5.012322 0.6 0.4744902 -0.7485759
BMD Computation
BMD = 0.4436: BMDL = 0.3465
Potency Measures
A unit dose (1 mg/kg) would result in 100*exp(-Potency)% of background
activity
Potency: 0.2375
se: 0.04047
var=seA2: 0.001638
Per cent, of background at unit dose: 79
Per cent, of background at the highest dose: 79
ED50 (95% CI): 2.918 ( 2.09 , 4.075 )
ln(Potency) -1.437
se[log(Potency)]: 0.1704
se[log(Potency)]A2: 0.02903
Section II.G.4 - Page 425 of 522
-------
Azinphos-methyl:1-D:BRAIN:M:WHOLE
Tue Jan 25 22:32:43 2005
MRID: 46162101 Guideline: NONGUIDELINE
Continuous Exponential Model (Decreasing)
Formula: chei = B + (A-B)*exp(-(m*dose)Ag)
Variance Function: power
The BMD corresponds to a dose that results in a 10% reduction in the
response relative to the control
Summary of Model Fitting Results
AIC	BIC logLik
81.23741 86.30405 -37.61871
Coefficients:
Value Std.Error
A 6.1740066 0.16787774
m 0.1668837 0.04759997
Correlation:
A	m
A 1.0000000 0.7648504
m 0.7648504 1.0000000
Approximate 95% confidence intervals
Coefficients:
lower	est.	upper
A 5.84334017 6.1740066 6.5233849
m 0.09367979 0.1668837 0.2972911
Residual standard error:
lower	est.	upper
0.5522574 0.6757542 0.8708973
Degrees of freedom: 40 total; 38 residual
Goodness of Fit
The chi-squared goodness-of-fit values should be taken as general
indications of fit only. P-values are likely to be inaccurate to some
degree
Pearson Chi-Square Statistic: 0.3202 with 2 degrees of freedom. P =
0. 852

dose
n
chei
Expected
sd
Exp.SD
X2 Resid.
1
o
o
o
10
6.1
6. 174007
0.5
0.6833425
-0.34247732
2
0.26
10
6.0
5. 911847
0.6
0.6546946
0.42579500
3
0.49
10
5.7
5.689230
0.6
0.6303551
0. 05402769
4
I—1
o
o
10
5.2
5.225050
0.8
0.5795639
-0.13667817
46162101 1 D-WHOLE
uju Qi cu u.b u.a ijq
dose
Ccrrinucufl; Expcnerfld Modd {Oocraasnqj
BMD Computation
Section II.G.4 - Page 426 of 522
-------
BMD = 0.6313: BMDL = 0.4297
Potency Measures
A unit dose (1 mg/kg) would result in 100*exp(-Potency)% of background
activity
Potency: 0.1669
se: 0.047 6
var=seA2: 0.002266
Per cent, of background at unit dose: 85
Per cent, of background at the highest dose: 85
ED50 (95% CI): 4.153 ( 2.375 , 7.264 )
ln(Potency) -1.79
se[log(Potency)]: 0.2852
se[log(Potency)]A2: 0.08136
Section II.G.4 - Page 427 of 522
-------
7. BMD analysis for: Diazinon
DIAZINON:1-D:BRAIN:F:WHOLE
Fri Jan 04 17:10:29 1980
MRID: 4 61663 0 2ACAD11 Guideline: NONGUIDELINE
Continuous Exponential Model (Decreasing)
Formula: chei = B + (A-B)*exp(-(m*dose)Ag)
Variance Function: power
Highest 2 doses dropped from data set.
The BMD corresponds to a dose that results in a 10% reduction in the
response relative to the control
Summary of Model Fitting Results
AIC	BIC logLik
12.023744 15.557906 -3.011872
Coefficients:
Value Std.Error
A 13.2366258 0.07685665
m 0.1662615 0.03335668
Correlation:
A	m
A 1.0000000 0.6319335
m 0.6319335 1.0000000
Approximate 95% confidence intervals
Coefficients:
lower	est.	upper
A 13.0781907 13.2366258 13.3969802
m 0.1096711 0.1662615 0.2520528
Residual standard error:
lower	est.	upper
0.2267656 0.2932080 0.4149923
Degrees of freedom: 24 total; 22 residual
Goodness of Fit
The chi-squared goodness-of-fit values should be taken as general
indications of fit only. P-values are likely to be inaccurate to some
degree
Pearson Chi-Square Statistic: 0.8582 with 1 degrees of freedom. P =
0.354
dose n chei Expected sd Exp.SD X2 Resid.
1	0.00 8 13.3 13.23663 0.2 0.2918109 0.61426556
2	0.03 8 13.1 13.17077 0.2 0.2903590 -0.68935997
46166302ACAD11 1 D - WHOLE
_ K- -
O 'J!'
rN -
~ -
0 30 100 130 200 230 ClOO
daw
CarAiniiaift. Expafwlbl Model f Dcccas-ing'l
Section II.G.4 - Page 428 of 522
-------
3 0.30 8 12.6 12.59260 0.4 0.2776128 0.07541153
BMD Computation
BMD = 0.6337: BMDL = 0.4765
Potency Measures
A unit dose (1 mg/kg) would result in 100*exp(-Potency)% of background
activity
Potency: 0.1663
se: 0.03336
var=seA2: 0.001113
Per cent, of background at unit dose: 85
Per cent, of background at the highest dose: 95
ED50 (95% CI): 4.169 ( 2.814 , 6.177 )
ln(Potency) -1.794
se[log(Potency)]: 0.2006
se[log(Potency)]A2: 0.04025
Section II.G.4 - Page 429 of 522
-------
DIAZ INON:1-D:BRAIN:M:WHOLE
Fri Jan 04 17:10:41 1980
MRID: 4 61663 0 2ACAD11 Guideline: NONGUIDELINE
Continuous Exponential Model (Decreasing)
Formula: chei = B + (A-B)*exp(-(m*dose)Ag)
Variance Function: power
Highest 2 doses dropped from data set.
The BMD corresponds to a dose that results in a 10% reduction in the
response relative to the control
Summary of Model Fitting Results
AIC	BIC logLik
3.077858 6.612020 1.461071
Coefficients:
Value Std.Error
A 12.5768854 0.06336178
m 0.1052754 0.02894230
Correlation:
A	m
A 1.0000000 0.6319335
m 0.6319335 1.0000000
Approximate 95% confidence intervals
Coefficients:
lower est.	upper
A 12.44616514 12.5768854	12.7089785
m 0.05952703 0.1052754	0.1861827
Residual standard error:
lower	est.	upper
0.1878795 0.2429283 0.3438288
46166302ACAD11 1 D - WHOLE
30 110 (J) M a) XO
¦Jaw
Carliniuirc- Expavftbl Model (Docr^s-i^l
Degrees of freedom: 24 total; 22 residual
Goodness of Fit
The chi-squared goodness-of-fit values should be taken as general
indications of fit only. P-values are likely to be inaccurate to some
degree
Pearson Chi-Square Statistic: 4.744 with 1 degrees of freedom. P =
0.0294
dose n chei Expected
1	0.00 8 12.7 12.57689
2	0.03 8 12.4 12.53723
3	0.30 8 12.2 12.18588
sd Exp.SD X2 Resid.
0.3 0.2405733	1.4474623
0.1 0.2398147	-1.6184846
0.2 0.2330941	0.1713184
BMD Computation
Section II.G.4 - Page 430 of 522
-------
BMD =
1. 001:
BMDL =
0.6892
Potency Measures
A unit dose (1 mg/kg) would result in 100*exp(-Potency)% of background
activity
Potency: 0.1053
se: 0.02894
var=seA2: 0.0008377
Per cent, of background at unit dose: 90
Per cent, of background at the highest dose: 97
ED50 (95% CI): 6.584 ( 3.841 , 11.29 )
ln(Potency) -2.251
se[log(Potency)]: 0.2749
se[log(Potency)]A2: 0.07558
Section II.G.4 - Page 431 of 522
-------
DIAZ INON:1-D:BRAIN:F:WHOLE
Fri Jan 04 17:10:54 1980
MRID: 4 61663 02ACPU11 Guideline: NONGUIDELINE
Continuous Exponential Model (Decreasing)
Formula: chei = B + (A-B)*exp(-(m*dose)Ag)
Variance Function: power
Highest 2 doses dropped from data set.
The BMD corresponds to a dose that results in a 10% reduction in the
response relative to the control
Summary of Model Fitting Results
AIC	BIC	logLik
-12.586972 -9.052810 9.293486
Coefficients:
Value Std.Error
A 7.0868338 0.04691799
m 0.3406463 0.03803346
Correlation:
A	m
A 1.0000000 0.6319335	46166302ACPU11 1 D - WHOLE
m 0.6319335 1.0000000
Approximate 95% confidence inte
Coefficients:
lower	est.	upper
A 6.9901967 7.0868338 7.1848067
m 0.2702358 0.3406463 0.4294024
Residual standard error:
lower	est.	upper
0.1380279 0.1784701 0.2525979
rvals
o 20 ao a) ao ico
¦Jaw
Carliniuirc- Expavftbl Model (Docr^s-i^l
Degrees of freedom: 24 total; 22 residual
Goodness of Fit
The chi-squared goodness-of-fit values should be taken as general
indications of fit only. P-values are likely to be inaccurate to some
degree
Pearson Chi-Square Statistic: 0.1007 with 1 degrees of freedom. P =
0.751
dose n chei Expected sd Exp.SD X2 Resid.
1	0.00 8 7.1 7.086834 0.2 0.1781391 0.20904876
2	0.03 8 7.0 7.014779 0.1 0.1763279 -0.23707302
3	0.30 8 6.4	6.398380 0.2 0.1608337 0.02849558
BMD Computation
Section II.G.4 - Page 432 of 522
-------
BMD =
0.3093:
BMDL =
0.2613
Potency Measures
A unit dose (1 mg/kg) would result in 100*exp(-Potency)% of background
activity
Potency: 0.3406
se: 0.03803
var=seA2: 0.001447
Per cent, of background at unit dose: 71
Per cent, of background at the highest dose: 90
ED50 (95% CI): 2.035 ( 1.635 , 2.533 )
ln(Potency) -1.077
se[log(Potency)]: 0.1117
se[log(Potency)]A2: 0.01247
Section II.G.4 - Page 433 of 522
-------
B. BMD analysis for: Dimethoate
DIMETHOATE:1-D:BRAIN:F:WHOLE
Wed Aug 13 20:21:06 2004
MRID: 45529702 Guideline: NONGUIDELINE
Continuous Exponential Model (Decreasing)
Formula: chei = B + (A-B)*exp{-(m*dose)Ag>
Variance Function: power
The BMD corresponds to a dose that results in a 10% reduction in the
response relative to the control
Summary of Model Fitting Results
AIC	BIC logLik
511.0838 515.4810 -252.5419	4SS7970? 1 D - WHOLE
Coefficients:
Value Std.Error
A 1 .400226e+04 1.530550e+02
m 4 . 801487e-02 7.186638e-03
Correlation:
A	m
A 1.0000000 0.5913828
m 0.5913828 1.0000000
Approximate 95% confidence intervals
Coef ficients:
lower	est.	upper
A 1.369314e+04 1.400226e+04 1.431835e+04
m 3.536891e-02 4.801487e-02 6.518233e-02
Residual standard error:
lower	est* upper
563.8050 705.5395 943.0758
Degrees of freedom: 32 total? 30 residual
Goodness of Fit
The chi-squared goodness-of-£it values should be taken as general
indications of fit only. P-values are likely to be inaccurate to some
degree
Pearson Chi-Square Statistic: 2.517 with 2 degrees of freedom. P =
0.284
(
1
1


f
•	1	1	1——i	r
CLQ Q-5 tfl 1J5 20 25 10
dote
Carftnuaufc BrpcrerAal UocW
dose n	chei Expected	sd Exp.SD X2 Resid.
1	0.0	8 14150.00 14002.26 554.8488 698.0731 0.59861865
2	0.1	8 13625.00 13935.19 444.8114 694.7413 -1.26283056
3	0.5 8 13850.00 13670.10 687.1265 681.5724 0.74655058
4	3.0	8 12106.25 12123.84 826.5408 604.7383 -0.08228062
Section II.G.4 - Page 434 of 522
-------
BMD Computation
BMD = 2.194: BMDL = 1.761
Potency Measures
A unit dose (1 irig/kg) would result in 100*exp (-Potency) % of background
activity
Potency: 0.04801
se: 0.007187
var=seA2: 5.165e-05
Per cent, of background at unit dose: 95
Per cent, of background at the highest dose: 87
EDS0 (95% CI): 14.44 ( 10.77 , 19.36 )
In(Potency) -3.036
se[log(Potency)]: 0.1497
se[log(Potency)]A2; 0.0224
Section II.G.4 - Page 435 of 522
-------
DIMETHOATE:1-D:BRAIN:M:WHOLE
Wed Aug 18 20*21*12 2004
MRID: 45529702 Guideline: NONGUIDELINE
Continuous Exponential Model (Decreasing)
Formula: chei = B + (A-B) *exp (-(m*dose) Ag)
Variance Function: power
The BMD corresponds to a dose that results in a 10% reduction in the
response relative to the control
Summary of Model Fitting Results
AIC
515.1097
BIC logLik
519.5069 -254.5549
45529702 1 D WHOLE
Coeff icients:
Value Std.Error
A 1.365711e+04 161.84622769
m 3.9927 5 9e-Q2 0.00778649
Correla tion:
A	m
A 1.0000000 0.5916283
m 0.5916283 1.0000000
Approximate 95% confidence intervals
Coef £ icients:
lower est.	upper
A 1.333055e+04 1.365711e+04	1.399168e+04
m 2.681049e-02 3.992759e-02 5.946226e-02
	1	1	1		1	r
<3X1 CIS 10 TS 20 25 30
dn#o
CcrtruaiB £i|ui»ifat Mate (Dflcr«^srqj
Residual standard error:
lower	est~ upper
595.7456 745.5096 996.5029
Degrees of freedom: 32 total? 30 residual
Goodness of Fit
The chi-squared goodness-of-fit values should be taken as general
indications of fit only. P-values are likely to be inaccurate to some
degree
Pearson Chi-Square Statistic: 0.4635 with 2 degrees of freedom. P =
0.793
dose n
chei Expected
sd Exp.SD X2 Resid.
1	0.0 8 13793.75 13657.11 247.0360 738.2140	0.52351076
2	0.1 8 13543.75 13602.69 802.4238 735.2619	-0.22674697
3	0.5 8 13293.75 13387.17 241.1838 723.5707	-0.36517900
4	3.0 8 12131.25 12115.41 1096.4024 654.5977	0.06846042
Section II.G.4 - Page 436 of 522
-------
BMD Computation
BMD = 2*639: BMDL = 1.998
Potency Measures
A unit dose (1 mg/kg) would result in 100*exp(-Potency)% of background
activity
Potency: 0.03993
s e: 0*007786
var=seA2: 6*063e-05
Per cent* of background at unit dose: 96
Per cent* of background at the highest dose: 89
ED50 (95% CI): 17*36 ( 11*85 , 25,44 )
In(Potency) -3*221
se[log(Potency)]: 0*195
se[log(Potency)]A2: 0*03803
Section II.G.4 - Page 437 of 522
-------
9. BMD analysis for: Disulfoton
DISULFOTON:1-D:BRAIN:F:WHOLE
Fri Jan 04 18:43:46 1980
MRID: 4 65 8 97 0 3ACAD1 Guideline: NONGUIDELINE
Continuous Exponential Model (Decreasing)
Formula: chei = B + (A-B)*exp(-(m*dose)Ag)
Variance Function: power
Highest 1 doses dropped from data set.
The BMD corresponds to a dose that results in a 10% reduction in the
response relative to the control
Summary of Model Fitting Results
AIC	BIC logLik
43.86740 46.53852 -18.93370
Coefficients:
Value Std.Error
A 11.084294 0.2999007
m 0.762279 0.1683987
Correlation:
A	m
A 1.0000000 0.7723353
m 0.7723353 1.0000000
Approximate 95% confidence intervals
Coefficients:
lower	est.	upper
A 10.4664220 11.084294 11.738641
m 0.4772279 0.762279 1.217593
Residual standard error:
lower	est.	upper
0.5830565 0.7828680 1.1914695
46589703ACAD1 1 D - WHOLE
~
s
i
to -


3
'O -



w -
~ -



OJO 0.1 02 0.0 OA 05
daw
CaHiiiHin- Expafwlbl Model f Dcccas-ing'l
Degrees of freedom: 18 total; 16 residual
Goodness of Fit
The chi-squared goodness-of-fit values should be taken as general
indications of fit only. P-values are likely to be inaccurate to some
degree
Pearson Chi-Square Statistic: 6.682 with 1 degrees of freedom. P =
0.00974
dose n chei Expected
1	0.000 6 10.74 11.084294
2	0.125 6 10.71 10.076886
sd Exp.SD X2 Resid.
0.423 0.8038437 -1.049140
0.500 0.7347869 2.110553
Section II.G.4 - Page 438 of 522
-------


7 £
3 0.250 6 8.87 9.161037 0.712 0.6716626 -1.061385
BMD Computation
BMD = 0.1382: BMDL = 0.1014
Potency Measures
A unit dose (1 mg/kg) would result in 100*exp(-Potency)% of background
activity
Potency: 0.7623
se: 0.1684
var=seA2: 0.02836
Per cent, of background at unit dose: 47
Per cent, of background at the highest dose: 83
ED50 (95% CI): 0.9093 ( 0.5897 , 1.402 )
ln(Potency) -0.2714
se[log(Potency)]: 0.2209
se[log(Potency)]A2: 0.0488
Section II.G.4 - Page 439 of 522
-------
DISULFOTON:1-D:BRAIN:M:WHOLE
Fri Jan 04 18:43:53 1980
MRID: 4 65 8 97 0 3ACAD1 Guideline: NONGUIDELINE
Continuous Exponential Model (Decreasing)
Formula: chei = B + (A-B)*exp(-(m*dose)Ag)
Variance Function: power
The BMD corresponds to a dose that results in a 10% reduction in the
response relative to the control
Summary of Model Fitting Results
AIC	BIC logLik
51.32418 54.85835 -22.66209
Coefficients:
Value Std.Error
A 11.9124247 0.24419930
m 0.8093126 0.07207062
Correlation:
A	m
A 1.0000000 0.7614023
m 0.7614023 1.0000000
Approximate 95% confidence intervals
Coefficients:
lower	est. upper
A 11.4166006 11.9124247 12.42978
m 0.6728372 0.8093126 0.97347
Residual standard error:
lower	est.	upper
0.5805750 0.7506838 1.0624814
46589703ACAD1 1 D WHOLE
CO -
iii. -
n	1	1	r
OjO 0.1 02 OJ (U OS
da»
CafUliHiil Dl.pCirKrtf.Hl Model ( DoCi«5-iiH]
Degrees of freedom: 24 total; 22 residual
Goodness of Fit
The chi-squared goodness-of-fit values should be taken as general
indications of fit only. P-values are likely to be inaccurate to some
degree
Pearson Chi-Square Statistic: 3.568 with 2 degrees of freedom. P =
0. 168

dose
n
chei
Expected
sd
Exp.SD
X2 Resid.
1
0. 000
6
11.54
11. 912425
0.300
0.7701785
-1. 1844664
2
0. 125
6
I—1
I—1
o
CO
10.766268
0.323
0.6988619
1. 0996225
3
0.250
6
9. 92
9.730388
0.266
0.6341490
0.7324017
4
0.500
6
7 .81
7.948042
0. 926
0.5221452
-0. 6475853
BMD Computation
Section II.G.4 - Page 440 of 522
-------
BMD =
0.1302:
BMDL =
0. 1136
Potency Measures
A unit dose (1 mg/kg) would result in 100*exp(-Potency)% of background
activity
Potency: 0.8093
se: 0.07207
var=seA2: 0.005194
Per cent, of background at unit dose: 45
Per cent, of background at the highest dose: 67
ED50 (95% CI): 0.8565 ( 0.7193 , 1.02 )
ln(Potency) -0.2116
se[log(Potency)]: 0.08905
se[log(Potency)]A2: 0.00793
Section II.G.4 - Page 441 of 522
-------
DISULFOTON:1-D:BRAIN:F:WHOLE
Fri Jan 04 18:44:04 1980
MRID: 46589704ACPU1 Guideline: NONGUIDELINE
Continuous Exponential Model (Decreasing)
Formula: chei = B + (A-B)*exp(-(m*dose)Ag)
Variance Function: power
The BMD corresponds to a dose that results in a 10% reduction in the
response relative to the control
Summary of Model Fitting Results
AIC	BIC logLik
73.55314 78.61978 -33.77657
Coefficients:
Value Std.Error
A 6.6436319 0.17322549
m 0. 9404764 0.09151811
Correlation:
A	m
A 1.0000000 0.7619614
m 0.7619614 1.0000000
Approximate 95% confidence intervals
Coefficients:
lower	est. upper
A 6.3020495 6.6436319 7.003729
m 0.7723146 0.9404764 1.145253
Residual standard error:
lower	est.	upper
0.5642684 0.6904511 0.8898384
Degrees of freedom: 40 total; 38 residual
Goodness of Fit
The chi-squared goodness-of-fit values should be taken as general
indications of fit only. P-values are likely to be inaccurate to some
degree
Pearson Chi-Square Statistic: 1.927 with 2 degrees of freedom. P =
0.382

dose
n
chei
Expected
sd
Exp.SD
X2 Resid.
1
0. 000
10
6.47
6.643632
0.388
0.7057578
-0.7779896
2
0. 125
10
I—1
CO
5.906771
0.280
0. 6293962
1. 1215727
3
0.250
10
5.23
5.251636
0.508
0.5612968
-0.1218960
4
0.500
10
4 . 12
4.151296
0.732
0.4464055
-0.2216976
46589704ACPU1 1 D - WHOLE
O TTf -
0j0 0.1 02 0J OA OS
da»
CafUiiHiii Di.pcirKrtf.Hl Model ( D TC3L-i nq'|
BMD Computation
Section II.G.4 - Page 442 of 522
-------
BMD = 0.112: BMDL = 0.09657
Potency Measures
A unit dose (1 mg/kg) would result in 100*exp(-Potency)% of background
activity
Potency: 0.94 05
se: 0.09152
var=seA2: 0.008376
Per cent, of background at unit dose: 39
Per cent, of background at the highest dose: 62
ED50 (95% CI): 0.737 ( 0.609 , 0.8919 )
ln(Potency) -0.06137
se[log(Potency)]: 0.09731
se[log(Potency)]A2: 0.009469
Section II.G.4 - Page 443 of 522
-------
DISULFOTON:1-D:BRAIN:M:WHOLE
Fri Jan 04 18:44:12 1980
MRID: 46589704ACPU1 Guideline: NONGUIDELINE
Continuous Exponential Model (Decreasing)
Formula: chei = B + (A-B)*exp(-(m*dose)Ag)
Variance Function: power
The BMD corresponds to a dose that results in a 10% reduction in the
response relative to the control
Summary of Model Fitting Results
AIC	BIC logLik
86.02089 91.08752 -40.01044
Coefficients:
Value Std.Error
A 6.668492 0.2059587
m 1.033329 0.1089400
Correlation:
A	m
A 1.000000 0.760291
m 0.760291 1.000000
Approximate 95% confidence intervals
Coefficients:
lower	est. upper
A 6.2643172 6.668492 7.098744
m 0.8347373 1.033329 1.279168
Residual standard error:
lower	est.	upper
0.6719825 0.8222525 1.0597012
Degrees of freedom: 40 total; 38 residual
Goodness of Fit
The chi-squared goodness-of-fit values should be taken as general
indications of fit only. P-values are likely to be inaccurate to some
degree
Pearson Chi-Square Statistic: 2.08 with 2 degrees of freedom. P =
0.354

dose
n
chei
Expected
sd
Exp.SD
X2 Resid.
1
0. 000
10
6.49
6.668492
0.416
0.8375500
-0.6739183
2
0. 125
10
5. 90
5.860457
0.369
0.7404007
0.1688910
3
0.250
10
5.38
5.150333
0.538
0.6545200
1.1096240
4
0.500
10
3.88
3.977800
0. 859
0.5114876
-0.6046525
46589704ACPU1 1 D - WHOLE

f"--- .
'JJ -

r
	 -
¦l"
o r> -

i
¦M -


~ -
1
i i i i
CIJO 0.1 02 0.3 OA 05
daw
CaHiiiHin- Ex pane fib I Model (De-=rc35-ing'|
BMD Computation
Section II.G.4 - Page 444 of 522
-------
BMD = 0.102: BMDL = 0.08689
Potency Measures
A unit dose (1 mg/kg) would result in 100*exp(-Potency)% of background
activity
Potency: 1.033
se: 0.1089
var=seA2: 0.01187
Per cent, of background at unit dose: 36
Per cent, of background at the highest dose: 60
ED50 (95% CI): 0.6708 ( 0.5456 , 0.8248 )
ln(Potency) 0.03279
se[log(Potency)]: 0.1054
se[log(Potency)]A2: 0.01111
Section II.G.4 - Page 445 of 522
-------
10. BMD analysis for: Methamidophos
Methamidophos:1—D:BRAIN:F:WHOLE
Sun Feb 17 20:34:28 2002
MRID: 4 65 94 0 0 3Ad Guideline: NONGUIDELINE
Continuous Exponential Model (Decreasing)
Formula: chei = B + (A-B)*exp(-(m*dose)Ag)
Variance Function: power
Highest 1 doses dropped from data set.
The BMD corresponds to a dose that results in a 10% reduction in the
response relative to the control
Summary of Model Fitting Results
AIC	BIC logLik
27.83708 30.50820 -10.91854
Coefficients:
Value Std.Error
A 11.7415463 0.19811091
m 0.4025792 0.04353016
Correlation:
A	m
A 1.0000000 0.7750096
m 0.7750096 1.0000000
Approximate 95% confidence intervals
Coefficients:
lower	est.	upper
A 11.3289921 11.7415463 12.1691240
m 0.3201118 0.4025792 0.5062919
Residual standard error:
lower	est.	upper
0.3972568 0.5333953 0.8117898
Degrees of freedom: 18 total; 16 residual
Goodness of Fit
The chi-squared goodness-of-fit values should be taken as general
indications of fit only. P-values are likely to be inaccurate to some
degree
Pearson Chi-Square Statistic: 0.299 with 1 degrees of freedom. P =
0.585
dose n chei Expected sd Exp.SD X2 Resid.
1 0.0 6 11.79 11.741546 0.462 0.5316938 0.2232240
46594Q03Ad 1 D-WHOLE
¦— I.O -
0J0 02 OA 0JG 03 1 JO 12
daw
Cafliniiain- Di.pcirKrtf.Hl Model (Dec reding]
Section II.G.4 - Page 446 of 522
-------
2	0.3 6 10.32 10.405763 0.245 0.4707343 -0.4462707
3	0.6 6 9.26 9.221945 0.606 0.4167640 0.2236627
BMD Computation
BMD = 0.2617: BMDL = 0.2222
Potency Measures
A unit dose (1 mg/kg) would result in 100*exp(-Potency)% of background
activity
Potency: 0.4026
se: 0.04353
var=seA2: 0.001895
Per cent, of background at unit dose: 67
Per cent, of background at the highest dose: 79
ED50 (95% CI): 1.722 ( 1.393 , 2.128 )
ln(Potency) -0.9099
se[log(Potency)]: 0.1081
se[log(Potency)]A2: 0.01169
Section II.G.4 - Page 447 of 522
-------
Methamidophos:1-D:BRAIN:M:WHOLE
Sun Feb 17 20:35:03 2002
MRID: 4 65 94 0 0 3Ad Guideline: NONGUIDELINE
Continuous Exponential Model (Decreasing)
Formula: chei = B + (A-B)*exp(-(m*dose)Ag)
Variance Function: power
The BMD corresponds to a dose that results in a 10% reduction in the
response relative to the control
Summary of Model Fitting Results
AIC	BIC logLik
60.62975 64.16391 -27.31488
Coefficients:
Value Std.Error
A 11.6774231 0.30115998
m 0.3599319 0.03754709
Correlation:
A	m
A 1.000000 0.763505
m 0.763505 1.000000
Approximate 95% confidence intervals
Coefficients:
lower	est.	upper
A 11.0692642 11.6774231 12.3189950
m 0.2899110 0.3599319 0.4468645
Residual standard error:
lower	est.	upper
0.7306618 0.9447461 1.3371477
46594Q03Ad 1 D-WHOLE
CIJO 0 2 OA OJ0 oa 1J0 \2
daH
CafUiiHiii Di.pcirKrtf.Hl Model ( D TC3L-i nq'|
Degrees of freedom: 24 total; 22 residual
Goodness of Fit
The chi-squared goodness-of-fit values should be taken as general
indications of fit only. P-values are likely to be inaccurate to some
degree
Pearson Chi-Square Statistic: 0.5066 with 2 degrees of freedom. P =
0.776
dose n chei Expected
sd
Exp.SD X2 Resid.
1	0.0 6 11.58	11.677423 0.92 0.9520748 -0.25064938
2	0.3 6 10.68	10.482192 0.81 0.8549987 0.56670237
3	0.6 6 9.30 9.409297 0.31 0.7678208 -0.34867669
4	1.2 6 7.59 7.581712 0.94 0.6192252 0.03278316
BMD Computation
Section II.G.4 - Page 448 of 522
-------
BMD =
0.2927:
BMDL =
0.2499
Potency Measures
A unit dose (1 mg/kg) would result in 100*exp(-Potency)% of background
activity
Potency: 0.3599
se: 0.03755
var=seA2: 0.00141
Per cent, of background at unit dose: 70
Per cent, of background at the highest dose: 65
ED50 (95% CI): 1.926 ( 1.57 , 2.363 )
ln(Potency) -1.022
se[log(Potency)]: 0.1043
se[log(Potency)]A2: 0.01088
Section II.G.4 - Page 449 of 522
-------
Methamidophos:1—D:BRAIN:F:WHOLE
Sun Feb 17 20:35:35 2002
MRID: 46594004Pup Guideline: NONGUIDELINE
Continuous Exponential Model (Decreasing)
Formula: chei = B + (A-B)*exp(-(m*dose)Ag)
Variance Function: power
The BMD corresponds to a dose that results in a 10% reduction in the
response relative to the control
Summary of Model Fitting Results
AIC	BIC logLik
41.32496 46.31564 -17.66248
Coefficients:
Value Std.Error
A 6.0844265 0.11060609
m 0. 8573064 0.08206989
Correlation:
A	m
A 1.0000000 0.7565147
m 0.7565147 1.0000000
Approximate 95% confidence intervals
Coefficients:
lower est.	upper
A 5.8643944 6.0844265	6.312714
m 0.7061503 0.8573064	1.040818
Residual standard error:
lower	est.	upper
0.3556643 0.4362566 0.5644058
Degrees of freedom: 39 total; 37 residual
Goodness of Fit
The chi-squared goodness-of-fit values should be taken as general
indications of fit only. P-values are likely to be inaccurate to some
degree
Pearson Chi-Square Statistic: 5.558 with 2 degrees of freedom. P =
0.0621

dose
n
chei
Expected
sd
Exp.SD
X2 Resid.
1
0.0
10
5.88
6.084427
0.299
0.4487305
-1.4406276
2
0.1
10
5.74
5.584539
0.543
0.4134931
1. 1889237
3
0.2
10
5.26
5.125721
0.299
0.3810228
1. 1144414
4
0.4
9
4.22
4.318076
0.289
0.3235313
-0. 9094258
46594004Pup 1 D - WHOLE
o n -
"N -
0j0 0.1 02 OH OA
da»
CafUiiHiii Di.pcirKrtf.Hl Model ( D TC3L-i nq'|
BMD Computation
Section II.G.4 - Page 450 of 522
-------
BMD =
0. 1229:
BMDL =
0.1062
Potency Measures
A unit dose (1 mg/kg) would result in 100*exp(-Potency)% of background
activity
Potency: 0.8573
se: 0.08207
var=seA2: 0.006735
Per cent, of background at unit dose: 42
Per cent, of background at the highest dose: 71
ED50 (95% CI): 0.8085 ( 0.6702 , 0.9754 )
ln(Potency) -0.154
se[log(Potency)]: 0.09573
se[log(Potency)]A2: 0.009164
Section II.G.4 - Page 451 of 522
-------
Methamidophos:1-D:BRAIN:M:WHOLE
Sun Feb 17 20:36:06 2002
MRID: 46594004Pup Guideline: NONGUIDELINE
Continuous Exponential Model (Decreasing)
Formula: chei = B + (A-B)*exp(-(m*dose)Ag)
Variance Function: power
The BMD corresponds to a dose that results in a 10% reduction in the
response relative to the control
Summary of Model Fitting Results
AIC	BIC logLik
15.656566 20.723205 -4.828283
Coefficients:
Value Std.Error
A 5.9354948 0.07809821
m 0.7491898 0.05757268
Correlation:
A	m
A 1.0000000 0.7628871
m 0.7628871 1.0000000
Approximate 95% confidence intervals
Coefficients:
lower	est.	upper
A 5.7794803 5.9354948 6.0957208
m 0.6412533 0.7491898 0.8752943
Residual standard error:
lower	est.	upper
0.2558400 0.3130514 0.4034538
Degrees of freedom: 40 total; 38 residual
Goodness of Fit
The chi-squared goodness-of-fit values should be taken as general
indications of fit only. P-values are likely to be inaccurate to some
degree
Pearson Chi-Square Statistic: 3.792 with 2 degrees of freedom. P =
0. 150

dose
n
chei
Expected
sd
Exp.SD
X2 Resid.
1
o
o
10
(_n
CO
K)
5. 935495
0.293
0.3185202
-1. 146635272
2
0.1
10
5. 65
5.507063
0. 196
0.2959672
1.527220781
3
0.2
10
5. 11
5. 109556
0.409
0.2750110
0. 005110363
4
0.4
10
4 . 37
4.398548
0. 131
0.2374451
-0.380199278
46594004Pup 1 D - WHOLE
l£f _
-
0j0 0.1 02 OH OA
daH
CafUiiHiii Di.pcirKrtf.Hl Model ( D TC3L-i nq'|
BMD Computation
Section II.G.4 - Page 452 of 522
-------
BMD =
0.1406:
BMDL =
0. 1249
Potency Measures
A unit dose (1 mg/kg) would result in 100*exp(-Potency)% of background
activity
Potency: 0.74 92
se: 0.05757
var=seA2: 0.003315
Per cent, of background at unit dose: 47
Per cent, of background at the highest dose: 74
ED50 (95% CI): 0.9252 ( 0.7958 , 1.076 )
ln(Potency) -0.2888
se[log(Potency)]: 0.07685
se[log(Potency)]A2: 0.005905
Section II.G.4 - Page 453 of 522
-------
11. BMD analysis for: Methyl parathion
METHYL PARATHION:1-D:BRAIN:F:WHOLE
Fri Jan 04 14:23:23 1980
MRID: 4 5 64 65 01ACPUllPhase2 Guideline: NONGUIDELINE
Continuous Exponential Model (Decreasing)
Formula: chei = B + (A-B)*exp(-(m*dose)Ag)
Variance Function: power
The BMD corresponds to a dose that results in a 10^
response relative to the control
reduction in the
Summary of Model Fitting Results
AIC	BIC logLik
128.17946 133.24610 -61.08973
Coefficients:
Value Std.Error
A 7.7267980 0.28009260
m 0.7052234 0.07745722
Correlation:
A	m
A 1. 0000000 0. 6121186
m 0.6121186 1. 0000000
Approximate 95% confidence intervals
Coefficients:
lower	est. upper
A 7.1800853 7.7267980 8.315139
m 0.5646286 0.7052234 0.880827
Residual standard error:
lower	est. upper
1.134360 1.388028 1.788860
46646501ACPU11 Phase2 1 D - WHOL

t— i	1	1	1	r
0j0 02 OA OJB OA 1 JO
¦Jaw
rnrt in.kn.p-_ Pj rmncri bl U.-k"LrI ( fI remiml
Degrees of freedom: 40 total; 38 residual
Goodness of Fit
The chi-squared goodness-of-fit values should be taken as general
indications of fit only. P-values are likely to be inaccurate to some
degree
Pearson Chi-Square Statistic: 0.1504 with 3 degrees of freedom. P =
0. 985

dose
n chei
Expected
sd
Exp.SD
X2 Resid.
1
0. 00
8 7 . 66
7 . 726798
0. 199
1.3985679
-0.135090484
2
0. 03
8 7.49
7 . 565042
0.360
1.3695188
-0.154981141
3
0. 11
8 7.30
7.150054
0.426
1.2949706
0.327505621
4
0.30
8 6.25
6.253414
0.427
1.1337783
-0.008516336
Section II.G.4 - Page 454 of 522
-------


7 £
5 1.00 8 3.81 3.817024 1.564 0.6947557 -0.028596565
BMD Computation
BMD = 0.14 94: BMDL = 0.12 65
Potency Measures
A unit dose (1 mg/kg) would result in 100*exp(-Potency)% of background
activity
Potency: 0.7 052
se: 0.07746
var=seA2: 0.006
Per cent, of background at unit dose: 49
Per cent, of background at the highest dose: 49
ED50 (95% CI): 0.9829 ( 0.7925 , 1.219 )
ln(Potency) -0.3492
se[log(Potency)]: 0.1098
se[log(Potency)]A2: 0.01206
Section II.G.4 - Page 455 of 522
-------
METHYL PARATHION:1-D:BRAIN:M:WHOLE
Fri Jan 04 14:23:32 1980
MRID: 4 5 64 65 01ACPUllPhase2 Guideline: NONGUIDELINE
Continuous Exponential Model (Decreasing)
Formula: chei = B + (A-B)*exp(-(m*dose)Ag)
Variance Function: power
The BMD corresponds to a dose that results in a 10^
response relative to the control
reduction in the
Summary of Model Fitting Results
AIC	BIC logLik
102.81324 107.87987 -48.40662
Coefficients:
Value Std.Error
A 7.808377 0.21686653
m 0.963874 0.06213863
Correlation:
A	m
A 1.0000000 0.5990743
m 0.5990743 1.0000000
Approximate 95% confidence intervals
Coefficients:
lower	est. upper
A 7.3814671 7.808377 8.259976
m 0.8459437 0.963874 1.098245
Residual standard error:
lower	est.	upper
0.8454012 1.0344514 1.3331785
45646501ACPU11 Phase2 1 D - WHOL

t——i	1	1	1	r
0.0 02 0.i OJ0 oa 1J0
daH
Ca^LiniHin- E'.MTCf.Hl Model r Dc;rca^ir>3'l
Degrees of freedom: 40 total; 38 residual
Goodness of Fit
The chi-squared goodness-of-fit values should be taken as general
indications of fit only. P-values are likely to be inaccurate to some
degree
Pearson Chi-Square Statistic: 4.648 with 3 degrees of freedom. P =
0. 199

dose n
chei
Expected
sd
Exp.SD
X2 Resid.
1
o
o
o
CO
7 .40
7.808377
0. 189
1. 0752320
-1. 0742457
2
o
o
CO
CO
7 .41
7.585821
0.325
1. 0469749
-0.4749847
3
o
I—1
I—1
CO
7 .18
7.022863
0.284
0. 9752001
0.4557539
4
0.30 8
CO
CO
5.847621
0.514
0. 8238399
1.6561161
5
I—1
o
o
CO
CO
<£>
2.978212
0. 903
0.4425588
-0.5637685
BMD Computation
Section II.G.4 - Page 456 of 522
-------
BMD =
0.1093:
BMDL =
0. 09883
Potency Measures
A unit dose (1 mg/kg) would result in 100*exp(-Potency)% of background
activity
Potency: 0.9639
se: 0.06214
var=seA2: 0.003861
Per cent, of background at unit dose: 38
Per cent, of background at the highest dose: 38
ED50 (95% CI): 0.7191 ( 0.6338 , 0.816 )
ln(Potency) -0.03679
se[log(Potency)]: 0.06447
se[log(Potency)]A2: 0.004156
Section II.G.4 - Page 457 of 522
-------