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Internal Memo
Ministry of Health
To:
Sally Gilbert
David Ogilvie
From:
Naty Foronda
Subject:
Review of maximum acceptable value (MAV) for sodium fluoroacetate (1080)
Date:
10 August 2011
For Your:
ACTION (X)
DECISION ( X)
INFORMATION (X)
1982
The Environmental Risk Management Authority’s (now the Environmental Protection Agency)
decision on reassessment of 1080 was finalised in August 2007. Dr Michael Ta
ACT ylor made a
submission during the reassessment process and one of the items raised was the forthcoming
review of the provisional MAV in the Drinking water Standards New Zealand given the more recent
(and the latest) toxicology information on the potential adverse health effects of 1080. The
purpose of this memo is recommend a PMAV including the rationale in the derivation of that value.
A short value is also being proposed.
Principal study and supporting studies
INFORMATION
Eason et al. (2001) conducted a 90 day subchronic study in which three groups of 10 male and 10
females Sprague-Dawley rats, about 6 weeks of age, were dosed with 1080-treated water at 0.025,
0.075, and 0.25 mg kg-1day-1 by oral gavage once daily for 90 days. A group of 10 male and 10
female rats were administered with water only and served as the control group. The control and
0.25 mg/kg/day groups included 10 additional rats of each sex that were treated for 90 days, then
OFFICIAL
maintained without treatment for a further 56-day recovery period.
Findings at necroscopy (date of terminal sa
THE crifice not specified) included severe hypospermia of
the epididymis and severe degeneration of the seminiferous tubules of the testes in male rats
dosed with 0.25 mg kg-1day-1. It was confirmed that recovery from testicular damage did not occur
even after 56 days without treatment. The no-observed-adverse-effect-level (NOAEL
)1 for rats
administered with 1080 via oral gavage for 90 days was 0.075 mg kg-1day-1. The authors also
UNDER
noted increases in heart weight in both male and female Sprague-Dawley rats when compared
with controls. No effects were noted in the lower dose groups. Cardiomyopathy was seen in 50%
(10/20) of males dosed with 1080 at 0.25 mg kg-1day-1 and 5% (1/20) female rat, suggesting a
gender difference. The NOAEL for rats was reported to be 0.075 mg kg-1day-1 by the same
authors.
RELEASED
Dose response modelling of the data for testicular (males) and myocardial toxicity (males and
females) was conducted to derive a benchmark dose for 1080 (Foronda et al. 2007a). A
benchmark dose (BMDL10 is the lower confidence limit of the dose that gives a 10% excess in
abnormal responses above the spontaneous background level) of 0.10 mg/kgbw/day was derived
and used for further quantification in this assessment.
Supporting studies
1 NOAEL is
the highest exposure level at which there are no biologically significant increases in the frequency or
severity of adverse effect between the exposed population and its appropriate control; some effects may be
produced at this level, but they are not considered adverse or precursors of adverse effects (IPCS 2000).
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Effects on testes
Reduction in plasma testosterone concentrations and degeneration of seminiferous tubules were
observed in lizards exposed to repeated sublethal doses equivalent to 100 and 200 mg kg-1 day-1
for 15 days (Twigg et al. 1988). Savarie (1984) also observed that 1080 exposures resulted in
testicular damage and elevated concentrations of citrate after the 15-day exposure period (Twigg
et al. 1986). Degeneration of seminiferous tubules was observed in testes from some of the lizards
treated at a single dose of 100 or 250 mg kg-1. Some lizards received multiple doses of 5 (5x), 20
(5x), or 50 mg kg-1 day-1 (5x) for 15 days. The lowest dose in the study was 5 mg kg-1 which was
20-fold higher than the highest dose used in the pivotal study exhibiting overt signs of testicular
toxicity in rats. Sullivan et al. (1979) considered that the testis was the organ most vulnerable to
1080 poisoning. Overt signs of toxicity were observed in rats weighing 165-180 g after 7 days
exposure to 1080 at concentrations of 6.6 ppm (ingested a daily average of 0.037 mg rat –1 or 0.18
mg kg-1) or 20 ppm (ingested a daily average of 0.14 mg rat –1 or 0.71 mg kg-1). Six rats per group
were euthanised daily during the 7-day treatment and others at 3, 7, 14 and 21 days after the end
1982
of each treatment period. These effects included decreased testicular weight, morphological
damage to the testes, degeneration of seminiferous tubules, and altered spermatogenesis.
Regeneration started to occur on the 7th day of treatment and spermatogenesis was stil abnormal
ACT
by day 21 after treatment. Testicular changes in rats exposed to 2.2 ppm 1080 (ingested a daily
average of 0.016 mg rat –1 or 0.078 mg kg-1) were not as widespread as those exposed at higher
concentrations of 1080 and al testes were histologically normal 7 days after treatment. Because
of the short exposure time, this study is not comparable to the 90-day study of Eason
et al. (2001)
and Eason and Turck (2002) where the rats under study did not recover during the 56-day
recovery period.
Five Sprague-Dawley rats weighing 400-450 g were administered 20 ppm fluoroacetate in drinking
INFORMATION
water for 7 days. There were sharp decreases in sperm counts during treatment, but the sperm
counts of all animals, after treatment, were practically zero in approximately 3 weeks. Sixty-five
days after treatment, partial sperm count recovery was observed in two of these rats. The five
treated rats all showed advanced patchy degeneration changes, primarily sloughing and
aggregation of spermatozoa, which fused to form striking multinucleated forms. Several tubules
also showed an intermediate coagulative necrosis. In a
OFFICIAL ll five rats, both epididymides contained
luminal cellular necrosis (Al-Juburi
et al. 1989). Al-Juburi
et al. (1989) claimed that the rats were
treated with doses of fluoroacetate similar to those used by Sullivan and co-workers (1979) and
THE
that the results were similar. However, direct comparison cannot be made because Al-Juburi
et al. (1989) only provided the concentration of 1080 while the water intake was actually measured by
Sullivan
et al. (1979), which permitted estimates of fluoroacetate ingested by animals.
UNDER
In another study, laboratory rats exposed for a period of approximately four months to 26 ppm of
1080 in drinking water (consumption volumes not specified) showed severe damage of the testes,
characterised by massive disorganisation of the seminiferous tubules, nearly total loss of functional
cells, absence of sperm, and damage to the Sertoli cells (Smith
et al. 1977). Regressive
modifications of the seminiferous tubules were observed by Mazzanti
et al. (1965) in the testes of
albino rats. No NOAEL was established from this older study. The main objective was
ascertaining the presence
RELEASED of fluoride in the skeletal system. This study was written in Italian and
only a very short summary was provided in English, describing only the testicular effects of 1080.
Eisler (1995) noted that sublethal effects of 1080 included testicular damage in rats after exposure
to 0.07-0.71 mg kg-1 drinking water for 7 days. This study demonstrated that testicular effects of
1080 were manifested after a relatively short period of time and consistently at high levels of
exposures.
A dose-response relationship was observed in minks and ferrets after dietary exposure to 1080.
Minks suffered severe impaired reproduction presumed to be due to oligo- or aspermia, or
spermatopathy after dietary exposure to 0.80 ppm of 1080 for two months (Hornshaw
et al. 1986).
Animals were fed with diets containing 0.05, 0.20 or 0.80 ppm of 1080, resulting in estimated
average dose of 0.01, 0.045, and 0.165 mg day-1, respectively based on their daily food
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consumption. No NOEL/NOAEL was reported from this study. In the same study, young ferrets
were exposed to 1.08, 1.94, and 3.50 ppm of 1080, resulting in an estimated average dose of 0.26,
0.40, and 0.60 mg day-1, respectively based on their daily food consumption. Reduction in testes
weights was observed at 1.94 and 3.50 ppm of 1080 (significantly different from control, p0.05).
In comparison, adult ferrets were exposed to 4.76, 8.56, and 15.40 ppm of 1080, resulting in
estimated average doses of 0.66, 0.84, and 0.80 mg day-1, respectively, based on their daily food
consumption. Testes weights, although reduced, were not significantly different from the control.
This il ustrates that young ferrets were more susceptible to the toxic effects of 1080 than adults
with regard to testes weight because their food consumption is almost twice than the adults, i.e.,
cumulative food intake for 4 weeks is 6,937 g vs 3,528 g.
In another study (Shinoda
et al. 2000), single oral doses of 1080, either 0.5 or 1.0 mg kg-1 was
administered for a short period of time. Sprague-Dawley rats showed signs of testicular toxicity
after a single oral dose of 1.0 mg kg-1 and were sacrificed 6 to 72 hours later. Necrosis in
spermatids, probably resulting from rapid and severe adenosine triphosphate (ATP) depletion, and
apoptosis in spermatogonia from gradual and partial ATP depletion, was observed. At
1982a later
stage, it was noted that 1080 inhibited spontaneous spermatogonial apoptosis.
ACT
In an investigation carried out by Wolfe (1988) to evaluate the subchronic toxicity of 1080,
Sprague-Dawley rats were dosed by oral gavage with 0.05, 0.20, and 0.50 mg kg-1day-1 1080 for a
period of 13 weeks. Treatment-related findings included decreased testes/epididymides weights,
testicular changes and immature/abnormal and reduced number of sperms in the epididymal ducts
and epididymides. A NOEL of 0.05 mg kg-1day-1 was reported in this study.
b. Myocardial toxicity
INFORMATION
Rammel (1993) and Eason
et al. (1994b) claimed that cumulative damage to the heart or other
organs from repeated exposure to large sublethal doses of 1080 can occur in sheep (
Ovis aries).
Smaller doses of 1080 given at regular intervals produced cumulative effects (Annison
et al. 1960)
and resulted in myocardial damage in sheep, probably due to increased accumulation of citrate in
the heart. The cumulative effect of 1080 has been noted in other species, such as the rat. This
has been attributed largely to the slowness of the kidn
OFFICIAL ey in clearing fluoroacetate in the body
(Chenoweth 1949). Sheep were affected differently from rats in that further doses following the
initial administration of 1080 proved to be fatal. Rats were able to tolerate non-fatal dose of 1080
THE
for the next 24 to 36 hours fol owing further administration of 1080. There has been little reliable
information on 1080’s action and toxicity in the larger domestic animals (Annison
et al. 1960).
It has been suggested that 1080 was rapidly eliminated in al species tested, hence it is not
cumulative (Rammel 1993), but re
UNDER peated exposure to sublethal doses of 1080 can result in
cumulative damage to the heart or other organs (Peters 1963; Annison
et al. 1960). Inflammation
of the heart occurred in rats exposed to 1080 at dosages of 0.05, 0.20, and 0.50 mg kg-1day-1 for
13 weeks by oral gavage (Wolfe 1988).
Merino sheep treated with a single high dose of 0.5-1.0 mg kg-1 bw 1080 dosed by stomach tube
on Lucerne hay exhibited myocardial lesions which were sometimes inconspicuous. Multifocal
RELEASED
areas of necrosis in various stages of development were observed in animals subacutely and
chronically treated (over 167 days in one sheep) at a lower dose range of 0.05-0.1 mg kg-1day-1
(Schultz
et al. 1982). This latter experiment was conducted at various duration of exposures, e.g.,
41, 66, 33 days.
The citrate content of hearts of rats injected intraperitoneally with 20 mg kg-1 bw was examined,
and citrate accumulation was observed in 1080-poisoned tissues (Wil iamson
et al. 1964). The
1080 treatment was given 30 minutes before the hearts were removed. The results suggested that
although the initial effect of fluoroacetate is to give rise to fluorocitrate and disrupt the TCA cycle,
the secondary inhibition of phosphofructokinase by the accumulated citrate was lethal. This was
due to the cell’s deprivation of pyruvate which would eventually overcome aconitase inhibition
(Williamson
et al. 1964).
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Acute multifocal injury to the myocardium, after 1080 doses as low as 0.11 mg
kg-1day-1 for 3-7 days, was observed in several research studies carried out in Australia (Eason
et
al. 1994b). Whittem and Murray (1963) demonstrated mild but characteristic cardiac
histopathology in sheep dosed with 0.055 mg kg-1day-1 of fluoroacetate by stomach tube, and
typical cardiac histopathology at 0.11 mg kg-1
day-1. However, the duration of this study was not specified. The same authors compared the
poisoning arising from the gidea plant (
Acacia georginae) and potassium fluoroacetate poisoning in
sheep. One group of sheep was fed with powdered gidea and another with purified potassium
fluoroacetate at similar dose rates, i.e., 0.22 mg potassium fluoroacetate kg-1 day-1 equivalent to
7.3 g powdered gidea leaf kg-1 day-1. This comparison was made based on the assumption that all
organical y bound fluorine in gidea was as toxic as potassium fluoroacetate, for an unspecified
period of exposure. Because palatability became a problem, sheep were fed by stomach tube with
either a watery suspension or various extracts of finely hammer-milled gidea leaves. Similar
symptoms, such as sudden collapse, spasmodic breathing, and typical cardiac histopathology,
such as acute myocardial damage were observed in animals fed gidea which suggeste
1982 d that
fluoroacetate in gidea was as toxic as potassium fluoroacetate. In the same study, similar acute
myocardial lesions were found in the hearts of sheep and guinea pigs treated with potassium
ACT
fluoroacetate. Whittem and Murray (1963) suggested that the most susceptible target organ is the
myocardium as revealed by the pathologic lesions.
Peters
et al. (1972) and Savarie (1984) suggested that fluorocitrate was present in smaller
amounts than fluoroacetate and it was not as toxic as fluoroacetate after oral ingestion or
parenteral administration. These authors further concluded that the decreased fluorocitrate toxicity
was apparently due to its larger molecular size, which would not be so readily absorbed through
tissues. The toxic principle in gidea was identified as the fluoroacetate ion by conversion to the
INFORMATION
butyl ester and the use of gas chromatography. Infra-red absorption spectra confirmed the
identification of fluoroacetate (Oelrichs and McEwan 1961).
Uncertainty Factors
An uncertainty factor of 3000 was used: 10 to account for
OFFICIAL interspecies extrapolation, 10 for
differences in human sensitivity, 10 for use of a subchronic study for a chronic RfD derivation, and
3 for the lack of reproductive/developmental studies and toxicity studies in a second species.
THE
Tolerable Daily Intake (TDI)
It is proposed that the BMDL10 0.10 mg/kg/day be used in deriving the TDI rather than the NOAEL
UNDER
as the BMD approach uses all of the experimental data to fit one or more dose response curves
(Foronda et al 2007a). The TDI therefore equates to 0.10 mg/kg/day/3000 = 0.00003 mg/kg/day
(0.03 µg/kg/day).
Oral TDI
Critical Effect
Experimental
UF MF
RfD
RELEASED
Doses*
Cardiomyopathy in females and males; altered spermatogenesis,
BMDL10: 0.10
3000 1 3E-5
severe degeneration of seminiferous tubules of the testes in males mg/kg/day
mg/kg/day
90 day Rat Oral Study (gavage)
LOAEL: 0.25
mg/kg/day
Eason et al. (2001)
The US EPA has derived the following reference dose (RfD)
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Oral RfD *
Critical Effect
Experimental
UF MF
RfD
Doses*
Increased heart weight in females and males; decreased testis
NOAEL: 0.05
3000 1 2E-5
weight and altered spermatogenesis in males
mg/kg/day
mg/kg/day
13-Week Rat Oral Study (gavage)
LOAEL: 0.20
mg/kg/day
U.S. EPA, 1988
* RfD, ADE, ADI have similar meaning and intent as the TDI.
EPA’s (formerly ERMANZ) derivation of Acceptable Daily Exposure (ADE)*
1982
The chronic exposure threshold was the Acceptable Daily Exposure of 0.02 μg/kg bw/day. This
value was used to derive separate potential daily exposures (PDE) for different routes:
ACT
PDEfood = 0.006 μg/kg bw/day
PDEwater = 0.01 μg/kg bw/day
PDEinhalation = 0.002 μg/kg bw/day
PDEdermal = 0.002 μg/kg bw/day
EPA has not derived an “official” TEL for 1080 yet. The hazardous Substances (Sodium
INFORMATION
Fluoroacetate) Transfer Notice 2005 established a TELwater of 3.5 μg/l. This was based on the
PMAV established by the Ministry, rather on the derivation of an ADE and PDEwater. The EPA
proposes that this value is retained pending revision of the PMAV by the Ministry.
Recommendations
OFFICIAL
1) Provisional MAV
THE
The BMDL computed for male cardiomyopathy (0.10 mg/kg body weight/day) and for testicular
effects (0.11 mg/kg body weight/day) were chosen as these effects were considered to be the most
sensitive end points (Foronda et al. 2007b). The proposed PMAV was calculated as follows:
UNDER
PMAV = (BMDL10/UF) * body wt* proportion of total intake)/(daily intake of DW)
0.10 mg/kg/3000 x 70 kg x 0.5/2L =
= 0.00058 mg/L (rounded to 0.0006 mg/L)
Where: RELEASED
BMDL10 = 0.10 mg/kg
Average quantity of water consumed by an adult = 2 L per day
Average weight of adult = 70 kg
Proportion of total intake allocated to drinking-water = 0.8
Uncertainty factor = 3000 (10 for intraspecies variation, 10 for interspecies variation, 10 for use of
a subchronic study for a chronic TDI derivation, and 3 for incompleteness of database)
2)
Short-term PMAV
Since it is recognised that there is a chance that members of the public might be exposed to high
concentrations of 1080 over a short period without the chronic PMAV being exceeded, setting an
ARfD appears to be appropriate. Solecki et al (2005) developed a list of possible relevant end
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points that are relevant in setting ARfD, such as for instance developmental effects, eg
malformations and other effects on the offspring. ARfD values that were derived from embryo/feto
toxicity in rats or rabbits are considered appropriate to sufficiently protect women of childbearing
age including the developing organism. However, knowledge on the mode of action of an acute
exposure during a sensitive window of fetal development and of the postnatal consequences of
fetal observations is currently very limited.
While an ARfD based on developmental (embryo/foetal) effects would be appropriate for women of
child-bearing age, it is recognised that the same value may be overly conservative with respect to
other subgroups in the population. Depending on the type of effect seen and the species
evaluated, the use of an ARfD based on a developmental effect, e.g., skeletal or soft tissue
malformations, could be inappropriate for children aged 1 to 6 years; as they are unlikely to be at
risk for the developmental toxicity observed. In this situation, separate model ing with respect to
acute dietary intake of residues can be performed taking into account age-specific acute
consumption data. Alternatively, it might be necessary to address higher sensitivity of children to
other forms of acute toxicity by testing during early life-stages.
1982
The WHO Guidelines (2011) say: "Cyanide is rapidly detoxified, and exposure spread throughout the
day will further reduce the potential for effects.
This health-based value would be suitable for use
ACT
for a limited period of up to 5 days, which is the longest period likely to be required under the
circumstances of such an emergency. However, it is probable that, in most circumstances, this
value will be highly conservative for short-term exposure."
A developmental toxicity study (Eason et al. 1999) in pregnant Sprage-Dawley rats were oral y
given a single daily dose of 1080 solution at 0, 0.1, 0.33 or 0.75 mg/kg/day (26 female rats in each
group) from day 6 through to day 17 of gestation and euthanised on day 20. Skeletal abnormalities
were found in fetuses exposed at 0.33 and 0.75 mg/kg/day groups. The abnorm
INFORMATION alities included
abnormal development of the forelimbs, characterised by bent scapula, humerus and radius or
ulna, and observed in 24%, 12% and 8% litters respectively. These changes were treatment-
related, and were classified as irreversible alterations of skeletal development (malformations). At
0.33 and 0.75 mg/kg/day, bent ribs were observed in 20% and 52% of litters respectively.
Unossified sternebrae were also observed in 72% of litters at 0.75 mg/kg/day. Bent or wavy ribs
OFFICIAL
and unossified sternebrae were classified as variations rather than malformations because these
effects were considered to be reversible. No clinical symptoms of maternal toxicity were observed
at any dose. Decreased maternal and foeta
THE l body weight was observed at the highest dose tested
of 0.75 mg/kg/day. No external or visceral soft tissue abnormalities were observed in fetuses at
any dose. The no-observed –effect level (NOEL) for maternal toxicity was 0 .33 mg/kgbw/day and
a NOAEL of 0.1 mg/kgbw/day based on irreversible skeletal malformations were reported.
UNDER
In a developmental pilot study (Eason et al. 1999) in five rats per treatment group dosed oral y with
1080 solution at 0, 0.05, 0.1, 0.5, or 1.0 mg/kgbw/day, maternal toxicity (weight loss and 60%
mortality) and decreased litter size were observed at 1.0 mg/kgbw/day. There were no effects on
uterine parameters (gravid uterine weight, number of implantations, resorptions and live and dead
fetuses) at all dose levels. The NOEL was 0.5 mg/kgbw/day based on gross pathological
examination of the female rats (the fetuses were not examined).
RELEASED
An ARfD of 0.0003 mg/kg bw was estimated on the basis of a NOAEL of 0.1 mg/kg bw per day for
teratogenicity in developmental toxicity study in rats and using an uncertainty factor of 300.
For the purposes of setting a short term PMAV, a TDI was derived using
Acute PMAV
The derivation of acute PMAV is done in the normal manner and allocating 100% of the ARfD to
drinking water. Derivation was calculated as follows:
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PMAVacute = (NOAEL /UF) * body wt* proportion of total intake)/(daily intake of DW)
= (0.10/300)* 70 *1)/2
= 0.035 mg/L
where:
NOAEL = 0.10 mg/kg
Average quantity of water consumed by an adult = 2 L per day
Average weight of adult = 70 kg
Proportion of total intake allocated to drinking-water = 1
Uncertainty factor = 300 (10 for intraspecies variation, 10 for interspecies variation, and 3 for
incompleteness of database)
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ACT
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INFORMATION
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INFORMATION
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THE
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Biochemical and Biophysical Research Communication 17: 696-702.
Wolfe, G.W. (1988). “Subchronic toxicity study in rats with sodium fluoroacetate”. Hazleton
Laboratories America, Inc. Contract Report HLA Study No. 2399-118 (unpublished). 91 pp.
U.S. EPA. 1988. Subchronic Toxicity Study in Rats with Sodium Fluoroacetate. HLA study No.
2399-118. Office of Solid Waste and Emergency Response, Washington, DC.
1982
ACT
INFORMATION
OFFICIAL
THE
UNDER
RELEASED
9
Document 2
Pesticides (15 of them) in the 2008 DWSNZ with a PMAV set by the MoH
Prepared by David Ogilvie, 3 Dec 2018
Azinphos methyl – no longer on ACVM Register
A tolerable daily intake approach was used by the MoH for the derivation of the provisional MAV
for azinphos methyl in drinking-water, as follows:
0.125 mg/kg body weight per day x 70 kg x 0.1 = 0.00438 mg/L (rounded to 0.004 mg/L)
2 L x 100
where:
• No-Observable-Adverse-Effect Level = 0.125 mg/kg body weight per day
• Average weight of adult = 70 kg
• Average quantity of water consumed by an adult = 2 L per day
• Proportion of tolerable daily intake allocated to drinking-water = 10%
1982
• Uncertainty factor = 100.
ACT
Bromacil – still on ACVM Register
The MAV is provisional because it was developed by the MoH in-house rather than by WHO. A
tolerable daily intake approach has been used for the derivation of the MAV for bromacil in drinking-
water, as follows:
10 mg/kg body weight per day x 70 kg x 0.1 = 0.35 mg/L (rounded to 0.4 mg/L)
2 L x 100
INFORMATION
where:
• No-Observable-Adverse-Effect Level = 10 mg/kg body weight per day
• Average weight of adult = 70 kg
• Average quantity of water consumed by an adult = 2 L per day
• Proportion of tolerable daily intake allocated to drinking
OFFICIAL -water = 10%
• Uncertainty factor = 100.
THE
Diuron - still on ACVM Register
A tolerable daily intake approach has been used by the MoH for the derivation of the PMAV for
diuron in drinking-water, as follows:
UNDER
0.625 mg/kg body weight per day x 70 kg x 0.1 = 0.02 mg/L
2 L x 100
where:
-
No-Observable-Adverse-Effect Level = 0.625 mg/kg body weight per day
-
Average weight of a
RELEASED dult = 70 kg
-
Average quantity of water consumed by an adult = 2 L per day
-
Proportion of tolerable daily intake allocated to drinking-water = 10%
-
Uncertainty factor = 100.
Document 2
Hexazinone - still on ACVM Register
A tolerable daily intake approach was used by the MoH to derive the provisional MAV for hexazinone
in drinking-water, as follows:
10 mg/kg body weight per day x 70 kg x 0.1 = 0.35 mg/L, rounded to 0.4 mg/L
2 L x 100
where:
-
No-Observable-Adverse-Effect Level = 10 mg/kg body weight per day.
-
Average weight of adult = 70 kg
-
Average quantity of water consumed by an adult = 2 L per day
-
Proportion of tolerable daily intake allocated to drinking-water = 10%
-
Uncertainty factor = 100.
1982
Metalaxyl - still on ACVM Register
A tolerable daily intake approach was used by the MoH for the derivation of the provisional MAV
for metalaxyl in drinking-water, as follows:
ACT
3 mg/kg body weight per day x 70 kg x 0.1 = 0.105 mg/L (rounded to 0.1 mg/L)
2 L x 100
where:
-
No-Observable-Adverse-Effect Level = 3 mg/kg body weight per day.
-
Average weight of adult = 70 kg
-
Average quantity of water consumed by an adult = 2 L per day
INFORMATION
-
Proportion of tolerable daily intake allocated to drinking-water = 10%
-
Uncertainty factor = 100.
Metribuzin - still on ACVM Register
OFFICIAL
A tolerable daily intake approach was used by the MoH for the derivation of the provisional MAV
for metribuzin in drinking-water, as follows:
THE
2 mg/kg body weight per day x 70 kg x 0.1 = 0.07 mg/L
2 L x 100
where:
UNDER
-
No-Observable-Adverse-Effect Level = 2 mg/kg body weight per day
-
Average weight of adult = 70 kg
-
Average quantity of water consumed by an adult = 2 L per day
-
Proportion of tolerable daily intake allocated to drinking-water = 10%
-
Uncertainty factor = 100.
RELEASED
Document 2
Oryzalin - still on ACVM Register
A tolerable daily intake approach was used by the MoH for the derivation of the provisional MAV
for oryzalin in drinking-water, as follows:
12 mg/kg body weight per day x 70 kg x 0.1 = 0.4 mg/L
2 L x 100
where:
-
No-Observable-Adverse-Effect Level = 12 mg/kg body weight per day
-
Average weight of adult = 70 kg
-
Average quantity of water consumed by an adult = 2 L per day
-
Proportion of tolerable daily intake allocated to drinking-water = 10%
-
Uncertainty factor = 100.
1982
Oxadiazon - still on ACVM Register
A tolerable daily intake approach was used by the MoH for the derivation of the PMAV for oxadiazon
in drinking-water, as follows:
ACT
5 mg/kg body weight per day x 70 kg x 0.1 = 0.175 mg/L (rounded to 0.2 mg/L)
2 L x 100
where:
-
No-Observable-Adverse-Effect Level = 5 mg/kg body weight per day
-
Average weight of adult = 70 kg
-
Average quantity of water consumed by an adult = 2 L per day
INFORMATION
-
Proportion of tolerable daily intake allocated to drinking-water = 10%
-
Uncertainty factor = 100.
Picloram - still on ACVM Register
OFFICIAL
A tolerable daily intake approach was used by the MoH for the derivation of the provisional MAV
for picloram in drinking-water, as follows:
THE
0.07 mg/kg body weight per day x 70 kg x 0.1 = 0.245 mg/L (rounded to 0.2 mg/L)
2 L
where:
UNDER
-
Tolerable Daily Intake = 0.07 mg/kg body weight per day
-
Average weight of adult = 70 kg
-
Average quantity of water consumed by an adult = 2 L per day
-
Proportion of tolerable daily intake allocated to drinking-water = 10%.
RELEASED
Document 2
Pirimiphos methyl - still on ACVM Register
The provisional MAV for pirimiphos methyl was calculated by the New Zealand Ministry of Health
as follows:
0.03 mg/kg x 70 kg x 0.1 = 0.105 mg/L (rounded to 0.1 mg/L)
2 L
where:
-
Acceptable daily intake = 0.03 mg/kg body weight
-
Average weight of adult = 70 kg
-
Proportion of acceptable daily intake allocated to drinking-water = 0.1
-
Average quantity of water consumed by an adult = 2 L/day.
Pirimisulfuron methyl - still on ACVM Register
1982
A tolerable daily intake approach was used by the MoH for the derivation of the provisional MAV
for pirimisulfuron methyl in drinking-water, as follows: (also called primisulfuron methyl)
ACT
0.25 mg/kg body weight per day x 70 kg x 0.1 = 0.9 mg/L
2 L
Where:
-
No-Observable-Adverse-Effect Level = 0.25 mg/kg body weight per day
-
Average weight of adult = 70 kg
-
Average quantity of water consumed by an adult = 2 L per day
-
Proportion of tolerable daily intake allocated to drinking-water = 10%.
INFORMATION
Terbacil - still on ACVM Register
The provisional MAV for terbacil in drinking-water was derived by the MoH as follows:
1.25 mg/kg body weight per day x 70 kg x 0.1 = 0.0
OFFICIAL 44 mg/L (rounded to 0.04 mg/L)
2 L x 100
where:
THE
-
No-observable-adverse-effect level = 1.25 mg/kg-day based on the absence of increase in
thyroid/body weight ratio, a slight increase in liver weights, and an elevated alkaline phosphatase
level, in a 2-year dog feeding study
-
Average weight of an adult = 70 kg
UNDER
-
Proportion of tolerable daily intake allocated to drinking-water = 0.1
-
Average quantity of water consumed by an adult per day = 2 L
-
Uncertainty factor = 100.
RELEASED
Document 2
Thiabendazole - still on ACVM Register
A tolerable daily intake approach was used by the MoH for the derivation of the provisional MAV
for thiabendazole in drinking-water, as follows:
3 mg/kg body weight per day x 70 kg x 0.1 = 0.35 mg/L (rounded to 0.4 mg/L)
2 L x 30
where:
-
No-Observable-Adverse-Effect Level = 3 mg/kg body weight per day
-
Average weight of adult = 70 kg
-
Average quantity of water consumed by an adult = 2 L per day
-
Proportion of tolerable daily intake allocated to drinking-water = 10%
-
Uncertainty factor = 30.
1982
Triclopyr - still on ACVM Register
The provisional MAV for triclopyr in drinking-water was derived by the MoH using a tolerable daily
intake approach as follows:
ACT
3 mg/kg body weight/day x 70 kg x 0.1 = 0.105 mg/L (rounded to 0.1 mg/L)
2 L/day x 100
where:
-
No-observable-adverse-effect level = 3 mg/kg body weight per day from a two year feeding
study in rats
-
Average weight of adult = 70 kg
INFORMATION
-
Average quantity of water consumed by an adult = 2 L per day
-
Proportion of tolerable daily intake allocated to drinking-water = 0.1
-
Uncertainty factor = 100 (for intra and inter-species variation)
OFFICIAL
1080 - still on ACVM Register
The provisional MAV for 1080 was calculated by the New Zealand Ministry of Health using an
THE
NOAEL derived from a Department of Conservation teratology study of rats (Eason, 1999) as
follows:
0.1 mg/kg x 70 kg x 0.5 = 0.0035 mg/L
2 L x 500
UNDER
where:
-
No-Observable-Effect Level = 0.1 mg/kg body weight per day
-
Average weight of adult = 70 kg
-
Average quantity of water consumed by an adult = 2 L per day
-
Proportion of lowest lethal dose allocated to drinking-water = 0.5
-
Uncertainty factor = 500 (10 for intraspecies variation, 10 for interspecies variation, 5 for
RELEASED
the inadequacy of the studies and database).
Document 3
1982
Volume 3
ACT
Datasheets –
Chemical and INFORMATION
physical
OFFICIAL
determinands
THE
UNDER
Part 2.3: Pesticides
2019 RELEASED
Released 2019
health.govt.nz
Document 3
2.3 Pesticides
Introductory notes
1.
Pesticides can have more than one common name, trade name and chemical
name. The CAS Registry Number (Chemical Abstracts Systematic names) is a
single identifier aimed to remove any ambiguity arising from the various
nomenclatures. An internet site for finding pesticide names for a CAS number is
http://www.alanwood.net/pesticides/index_rn2_frame.html. Or to find a CAS
number for a pesticide:
1982
http://www.alanwood.net/pesticides/index_cn_frame.html.
2.
The Drinking-water Standards for New Zealand (DWSNZ) define a MAV as the
ACT
concentration of a determinand, below which the presence of the determinand
does not result in any significant risk to a consumer over a lifetime of
consumption. For carcinogenic chemicals, the MAVs set in the DWSNZ general y
represent a risk of one additional incidence of cancer per 100,000 people
ingesting the water at the concentration of the MAV for a lifetime of 70 years.
The World Health Organization (WHO) states that a drinking-water guideline
value (equivalent to our MAVs) normal y represents the concentration o
INFORMATION f a
constituent that does not result in any significant risk to health over a lifetime of
consumption.
3.
USEPA
OFFICIAL
(a)
MCL: Some datasheets include the USEPA’s MCL. Title 40, Protection of
Environment, Chapter I: Environmental Protection Agency, Part 141,
THE
National Primary Drinking Water Regulations, § 141.1 40 CFR Ch. I (7–1–02
edition) defines MCL (maximum contaminant level) as the maximum
permissible level of a contaminant in water which is delivered to any user
of a public water system.
UNDER
(b)
RfD: Some datasheets also include the reference dose (usual y meaning
the chronic reference dose) or RfD, which the USEPA defines as “an
estimate (with uncertainty spanning perhaps an order of magnitude) of a
daily oral exposure to the human population (including sensitive
subgroups) that is likely to be without an appreciable risk of deleterious
RELEASED
effects during a lifetime”.
An ARfD or acute reference dose, is defined as the maximum quantity of
an agricultural or veterinary chemical that can safely be consumed as a
single, isolated, event. Note that the 2001 JMPR defined the acute
reference dose as “The acute RfD of a chemical is an estimate of the
amount of a substance in food and/or drinking-water, normal y expressed
on a body-weight basis, that can be ingested in a period of 24 hours or
less without appreciable health risk to the consumer on the basis of al
known facts at the time of the evaluation”.
ii
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Document 3
(c)
HHBPs: The USEPA maintains a table of Human Health Benchmarks for
Pesticides that includes RfDs and ARfDs for (currently) 363 pesticides. The
HHBPs were original y developed in 2012. The table includes a column for
“acute or one-day HHBPs”, another for “chronic or lifetime (non-cancer)
HHBPs”, and one for “carcinogenic HHBPs”. HHBPs are the concentrations
in water at or below which adverse health effects are not anticipated from
one-day or lifetime exposures. HHBPs are derived for the most sensitive
population group. Details can be accessed at
http://www.epa.gov/sites/production/files/2015-10/documents/hh-
benchmarks-techdoc.pdf or
http://iaspub.epa.gov/apex/pesticides/f?p=HHBP:home.
The acute HHBP = [aRfD (mg/kg bw/day) x BW (kg) x 1,000 (µg/mg)] /
[Drinking Water Intake (L/day)] where BW = 10 kg for children and 66 kg
1982
for females 13–49 years and Drinking Water Intake = 1 L/day for children
and 2 L/day for females 13–49 years. In essence, these can be considered
ACT
to be one day MAVs.
The chronic HHBP = [cRfD (mg/kg bw/day) x BW (kg) x 1,000 (µg/mg) x
0.2 RSC] / [Drinking Water Intake (L/day)] where BW = 70 kg for general
population and 66 kg for females 13–49 years and Drinking Water Intake =
2 L/day for general population as well as for females 13–49 years and RSC
= Relative Source Contribution assumed as 20 percent. This calculation is
basical y the same as that used by the WHO in deriving their guideline
INFORMATION
values, and hence our MAVs.
The formula for deriving carcinogenic HHBP = [10–6 or 10–4/Drinking
Water Unit Risk (ppb-1), where Drinking Water Unit Risk (ppb-1) = [CSF
(per mg/kg/day) x 2(L/day)]/[70 kg x1000 (µg/mg)].
OFFICIAL
Because pesticides should only be found rarely in New Zealand waters, and
for short periods, the acute one day HHBP (where available) has been
THE
included in the datasheets.
(d)
DWEL: The USEPA also uses the concept of Drinking Water Equivalent
Level or DWEL, which is defined as “a lifetime exposure concentration
protective of ad
UNDER verse, non-cancer health effects, that assumes al of the
exposure to a contaminant is from drinking water”. The DWEL is calculated
by multiplying the oral chronic RfD (mg/kg/d) by 70 (kg body weight)
divided by 2 (L/day consumption).
The USEPA review their MCLs, DWELs and RfDs regularly. The 2012 values
can be found at:
RELEASED
http://water.epa.gov/action/advisories/drinking/upload/dwstandards
2012.pdf.
(e)
Carcinogenicity: The USEPA classification of carcinogenicity as at
24 September 2008, has been included where available. See latest list at
http://envirocancer.cornell.edu/turf/chemseval.pdf. This also explains
their classification groups.
GUIDELINES FOR DRINKING-WATER QUALITY MANAGEMENT FOR NEW ZEALAND:
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VOLUME 3 DATASHEETS – CHEMICAL AND PHYSICAL DETERMINANDS: PART 2.3 PESTICIDES
Document 3
4.
The Australian guideline values for pesticides are not always based on health
issues. For pesticides that are not approved for use in water or in water
catchments, the guideline value is often set at or about the analytical limit of
determination. Where a pesticide is approved for use in water or in water
catchments, the guideline value is set at a level consistent with good
management practice and which would not result in any significant risk to health
of the consumer over a lifetime of consumption. These datasheets only include
their health based guideline values, see
http://www.nhmrc.gov.au.
5.
The Australian Government’s Department of Health and Ageing, Office of
Chemical Safety and Environmental Health has a document that lists the
Acceptable Daily Intakes (ADIs)* for Agricultural and Veterinary Chemicals, where
“the acceptable daily intake (ADI) for humans is considered to be a level of intake
1982
of a chemical that can be ingested daily over an entire lifetime without any
appreciable risk to health. It is calculated by dividing the overal NOEL from the
animal studies by a safety factor. The magnitude of the safety factor is selected
ACT
to account for uncertainties in extrapolation of animal data to humans, variation
between humans, the completeness of the toxicological data base and the
nature of the potential adverse effects”. Their ADIs (which are updated regularly)
appear in these datasheets. See
http://www.health.gov.au/internet/main/publishing.nsf/Content/ocs-adi-
list.htm. They also publish Acute Reference Doses for Agricultural and Veterinary
Chemicals (cal ed the ARfD List), see
INFORMATION
http://www.health.gov.au/internet/main/publishing.nsf/content/ocs-arfd-
list.htm.
Note: The acceptable daily intake (ADI) is similar in definition and intent to terms
such as reference dose (RfD), reference concentration (RfC) and tolerable daily
intake (TDI). They are an estimate of the daily exp
OFFICIAL osure to humans that is likely
to be without appreciable risk of deleterious effects during a lifetime of
continuous exposure. The derivati
THE on of a TDI involves identifying the critical
effect(s), and selecting the pivotal study, the point of departure, and appropriate
uncertainty factors (UFs).
6.
A MAV had been developed for most of the early pesticides because of their
UNDER
usual y general and high level of toxicity and/or persistence. Many of these
products now have restricted use in New Zealand or have been withdrawn.
Despite this, most of these MAVs have been retained because traces of some of
these older pesticides can stil be found in the soil or possibly groundwater.
Most pesticides included in this section of the datasheets do not have a MAV but
RELEASED
are registered for agricultural use in New Zealand and appear on the NZFSA’s
complete database of Agricultural Compounds and Veterinary Medicines (ACVM)
as at 2009 (see
https://eatsafe.nzfsa.govt.nz/web/public/acvm-register and
select entire register). Many of these are fairly new products with a much more
specific application, are usual y a lot less persistent, and are mostly used at a
much lower dose. Many of these are yet to be evaluated in the WHO
Guidelines
for Drinking-water Quality.
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VOLUME 3 DATASHEETS – CHEMICAL AND PHYSICAL DETERMINANDS: PART 2.3 PESTICIDES
Document 3
7.
The WHO has developed a classification of pesticides by hazard, where:
• Class IA is extremely hazardous
• Class IB is highly hazardous
• Class II is moderately hazardous
• Class III is slightly hazardous
See The WHO Recommended Classification of Pesticides by Hazard.
http://www.who.int/ipcs/publications/pesticides_hazard/en/.
8.
Pesticides can participate in a number of transformation processes resulting in a
large number of degradation products. The AWWA Research Foundation
produced in 2008 “
Pesticide Degradates of Concern to the Drinking Water
Community”: 143 pages. See
1982
http://www.waterrf.org/PublicReportLibrary/2938.pdf.
They report that 92 pesticide degradates have been detected in the environment
ACT
with 29 detected in groundwater and 27 detected in surface waters. Degradates
of alachlor, acetochlor, atrazine, cyanazine, dichloropropene, dicamba and
2,4-D were likely to be the greatest concern to water supplies in the USA,
whereas in the UK they were cyanazine, isoproturon and flufenacet. All are used
in New Zealand.
9.
DWI (2010) published a 478-page report “A Desk Study on Pesticide Metabolites,
Degradation and Reaction Products to Inform the Inspectorate’s P
INFORMATION osition on
Monitoring Requirements”, DWI Project: 70/2/232. See
http://dwi.defra.gov.uk/research/completed-research/2000todate.htm.
10. “Review of Trends in Agricultural Pesticide Use in New Zealand” (1999) MAF
Policy Technical Paper 99/11 (
www.maf.gov
OFFICIAL
t.nz/mafnet/rural-nz/sustainable-
resource-use/resource-management/pesticide-use-
trends/PesticideTrends.pdf)
THE discusses how pesticides were used in New
Zealand up to 1998.
11. IUPAC (2003) Technical Report: “Significance of impurities in the safety
evaluation of crop protection products”, includes:
UNDER
There may be substantial differences in the chemical composition of
technical-grade products of the same active ingredient manufactured
under different conditions, from different raw materials, or by different
routes of synthesis. Resulting differences in impurity content may
significantly affect the toxicological properties of pesticide products.
RELEASED
See
Pure Appl Chem 75(7) 2003, pp 937–73, for details of the more significant
impurities. Available at:
http://old.iupac.org/publications/pac/2003/pdf/7507x0937.pdf.
12. Dow Chemical Company maintains a “Product Safety Assessment Finder” on their
website:
http://www.dow.com/productsafety/assess/finder.htm.
GUIDELINES FOR DRINKING-WATER QUALITY MANAGEMENT FOR NEW ZEALAND:
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13. ESR coordinates a survey of pesticides in groundwater throughout New Zealand.
The survey has been completed every four years since 1990 with 2014 being the
seventh. The report for the 2014 survey covers 165 groundwaters; pesticides
were detected in 28 wells (17 percent), with 10 of these having two or more
pesticides. Seven pesticides were detected in one well and 21 different pesticides
were detected. Herbicides were the most frequently detected group with four
insecticides and two fungicides also detected. There were 31 detections
(61 percent) of triazine herbicides with terbuthylazine being the most frequently
detected (16 detections). There were four pesticide detections exceeding
0.001 mg/L. One sample exceeded the MAV: dieldrin was detected at
0.000043 mg/L, slightly in excess of the MAV of 0.00004 mg/L. The next highest
detection relative to the MAV was terbuthylazine at 17 percent of the MAV with
the remainder of detections being less than 5 percent of the MAV. For details, 1982
see: Humphries B, Close M (2015)
National Survey of Pesticides in Groundwater
2014, Client Report No CSC 15003, 33 pp.
http://www.marlborough.govt.nz/Environment/Groundwater/~/media/F
ACT
ile
s/MDC/Home/Environment/Groundwater/2015%20Reports/National_Surve
y_of_Pesticides_in_Groundwater_Report_final.pdf.
14. The most commonly used pesticides in New Zealand up to 2004 (excluding
domestic) appear in the fol owing table. Source: Manktelow et al 2005, Trends in
Pesticide Use in New Zealand 2004: Report to the Ministry for the Environment,
Project SMF4193 – modified – copied from “Literature Review of Organic
INFORMATION
Chemicals of Emerging Environmental Concern in Use in Auckland”, Auckland
Regional Council, Technical Report No. 028, December 2008, 193 pp.
http://www.arc.govt.nz/albany/fms/main/Documents/Plans/Technical%20p
ublications/Technical%20reports/1-50/TR2008-028%20-
%20Literature%20Review%20of%20Organic%20Chemicals%20of%20Emergi
OFFICIAL
ng%20Environmental%20Concern%20in%20Use%20in%20Auckland.pdf.
The table does not include minera
THE l oils (ca. 25 t/y). A number of other pesticides
are used in domestic, roadside and specialty applications, including pyrethroids,
neonicotinoids, and anticoagulant rodenticides. Some of these, while used in
much lower volumes, are likely to be more hazardous to the environment.
UNDER
RELEASED
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Document 3
Chemical compound
Active ingredient
Percentage
Mode of action
type (FAO category)
of sales
phenoxy hormones
MCPA, 2,4-D, mecoprop, MCPB
25 percent
synthetic auxin
(herbicides)
dithiocarbamates
mancozeb, metiram, thiram,
11 percent
lipid synthesis inhibitors
ziram
(fungicides)
phosphonyls
glyphosate, glufosinate-
8.4 percent
amino acid inhibitor
ammonium
(herbicides)
triazines
terbuthylazine, hexazinone,
7.6 percent
photosynthesis
atrazine, simazine, propazine
inhibitors (herbicides)
plant growth regulators hydrogen cyanamide,
6.9 percent
growth inhibitors/
1982
ammonium thiosulphate,
retardants (herbicides)
chlomequat-chloride,
mepiquat-chloride
ACT
inorganics
copper compounds, sulphur
6.9 percent
mostly fungicides
compounds, phosphorous acid
organophosphates
diazinon, methamidophos,
3.6 percent
neurotoxic (insecticides)
chlorpyrifos, fenamiphos,
pirimiphos-methyl, phorate
chloroacetanilides
acetochlor, alachlor,
3.0 percent
seedling shoot
INFORMATION
propachlor
inhibitors (herbicides)
other fungicides
captan, chlorothalonil,
2.4 percent
fungicides
metalaxyl-m, tolylfluanid
urea derivatives
isoproturon, linuron
2.0 percent
photosynthesis
OFFICIAL
inhibitors (herbicides)
other hormone types
triclopyr, pichloram
1.3 percent
synthetic auxin
THE
(herbicides)
dinitroanilines
trifluralin
0.4 percent
–
N-methyl carbamate
aldicarb, carbaryl, carbofuran,
0.4 percent
inhibition of the
UNDER
insecticides
formetanate HCl, methiocarb,
acetylcholinesterase
methomyl, oxamyl, pirimicarb,
enzyme
propoxur and thiodicarb
15. Some physical data have been included for some pesticides. The fol owing
discussion has mostly been taken from
RELEASED
http://npic.orst.edu/ingred/ppdmove.htm and
http://pubs.usgs.gov/circ/2005/1291/ (accessed 2013).
The soil half-life is a measure of the persistence of a pesticide in soil. Pesticides
can be categorised on the basis of their half-life as non-persistent, degrading to
half the original concentration in less than 30 days; moderately persistent,
degrading to half the original concentration in 30 to 100 days; or persistent,
taking longer than 100 days to degrade to half the original concentration.
A ”typical soil half-life” value is an approximation and may vary greatly because
persistence is sensitive to variations in site, soil, and climate.
GUIDELINES FOR DRINKING-WATER QUALITY MANAGEMENT FOR NEW ZEALAND:
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Note: The United Nations Environment Programme (UNEP), Secretariat of the
Stockholm Convention on Persistent Organic Pol utants, as amended in 2009,
Annex D (b) Persistence:
(i)
evidence that the half-life of the chemical in water is greater than two
months, or that its half-life in soil is greater than six months, or that its
half-life in sediment is greater than six months; or
(i )
evidence that the chemical is otherwise sufficiently persistent to justify its
consideration within the scope of this convention.
This definition is consistent with the European Union definition for a very
persistent pesticide of a half-life in soil of greater than six months (Regulation EC
No 1107/2009 concerning the placing of plant protection products on the
market).
1982
Two of the parameters used most often to describe the partitioning of a
compound among environmental media are (1) the Henry’s Law constant (KH),
ACT
which describes partitioning between air and water, and (2) the soil organic
carbon-water partition coefficient (Koc), which describes partitioning between
water and the organic matter in soil or sediment.
A pesticide with a high KH is volatile and thus, primarily tends to reside in and be
transported by air. As a result, such compounds are rarely retained for long in
streams or soil, but if they reach groundwater, they may remain for substantial
periods of time because there is comparatively little exposure to the atmosphere.
INFORMATION
The sorption coefficient (Koc) describes the tendency of a pesticide to bind to
soil particles. Sorption retards movement, and may also increase persistence
because the pesticide is protected from degradation. The higher the Koc, the
greater the sorption potential, ie, the lower the mobility. Koc is derived from
laboratory data. Many soil and pesticide factors m
OFFICIAL ay influence the actual
sorption of a pesticide to soil. Because they associate more strongly with organic
matter than with water, pesticides with high Koc values are sometimes referred
THE
to as hydrophobic. Compounds with low Koc values (which therefore tend to
favour water over organic matter) are described as hydrophilic. As a result of
their affinity for organic matter, the more persistent hydrophobic pesticides are
likely to accumulate not only in soils and sediments, but also in fish, birds,
UNDER
mammals, and other biota. Pesticides with high Koc values are typical y not very
water soluble and wil preferential y adhere to soils rather than be dissolved in
water. This means that pesticides in this class are unlikely to be carried offsite in
run-off as dissolved substances; instead, they are transported on sediment
particles. For example DDT with a Koc of 100,000 adheres strongly to soil.
Diazinon has a
RELEASED Koc of 1,580 and is readily transported as the free substance
dissolved in water. The California Department of Pesticide Regulation has
determined that pesticides with a Koc less than 1,900 have potential to
contaminate groundwater.
The GUS or Groundwater Ubiquity Score is an empirical y derived value that
relates pesticide persistence (half-life) and sorption in soil (sorption coefficient,
Koc). The GUS may be used to rank pesticides for their potential to move toward
groundwater. The pesticide movement rating is derived from the GUS. GUS =
log10 (half-life) x [4 – log10 (Koc)]. Movement ratings range from extremely low
to very high. Pesticides with a GUS less than 0.1 are considered to have an
extremely low potential to move toward groundwater. Values of 1.0–2.0 are low,
viii
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Document 3
2.0–3.0 are moderate, 3.0–4.0 are high, and values greater than 4.0 have a very
high potential to move toward groundwater.
16.
Threshold values indicating potential for groundwater contamination by
pesticides: The USEPA developed the fol owing values in 1986 (taken from
http://psep.cce.cornell.edu/facts-slides-self/facts/pest-gr-gud-grw89.aspx):
Chemical or physical property
Threshold value
Water solubility
greater than 30 mg/L
Henry’s Law constant
less than 10-2 atm/m3 mol
Kd
less than 5, usual y less than 1 or 2
Koc
less than 300 to 500
1982
Hydrolysis half-life
more than 25 weeks
Photolysis half-life
more than 1 week
ACT
Field dissipation half-life
more than 3 weeks
The likelihood of a pesticide to volatilise is a function of both its vapour pressure
and its solubility. This function is expressed by Henry’s Law constant.
(Unfortunately there are many different ways to express Henry’s Law constant,
and many different units are used.)
Kd = the concentration of chemical adsorbed divided by the concen
INFORMATION tration of
chemical dissolved. The major drawback of using Kd to predict leaching of
pesticides is that it is highly dependent on soil characteristics. Organic matter is
the most important soil constituent determining pesticide retention. It therefore
is useful to adjust the Kd value by the percent organic carbon in the soil. This
OFFICIAL
yields another adsorption coefficient, Koc, which is relatively independent of soil
type. Koc = Kd divided by the percent organic carbon in the soil.
THE
17. An excellent primer on toxicology has been prepared by the Australian Pesticides
and Veterinary Medicines Authority (APVMA). See
http://apvma.gov.au/node/1036.
UNDER
18. Neonicotinoids (or neonics) are a class of neuro-active insecticides chemical y
similar to nicotine. These compounds account for about 25 percent of the
current (2013) global insecticide market. The neonicotinoids include (on ACVM
Register as at October 2013):
acetamiprid (yes)
clothianidin (yes)
RELEASED
dinotefuran (no)
imidacloprid (yes)
nitenpyram (yes)
nithiazine (no)
thiacloprid (yes)
thiamethoxam (yes)
GUIDELINES FOR DRINKING-WATER QUALITY MANAGEMENT FOR NEW ZEALAND:
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On 24 May 2013, the European Commission imposed a number of use restrictions
on neonicotinoid insecticides, which are suspected to be a contributing factor of
bee colony col apse disorder. The European Commission has adopted a proposal
(Regulation (EU) No 485/2013) to restrict the use of three pesticides belonging to
the neonicotinoids family (clothianidin, imidacloprid and thiametoxam) for a
period of two years from December 2013. See:
http://ec.europa.eu/food/animal/liveanimals/bees/neonicotinoids_en.htm.
Clothianidin is a primary metabolite of thiamethoxam. The chloronicotinyl
insecticides (thiamethoxam, clothianidin, imidacloprid) are more toxic than the
cyano substituted (thiacloprid, acetamiprid). See also: FERA (2013) Neonicotinoid
Pesticides and Bees, The Food and Environment Research Agency (UK), 133 pp.
http://www.fera.defra.gov.uk/scienceResearch/scienceCapabilities/chemical
sEnvironment/documents/syngentaNeonicotinoidReportJan13.pdf.
1982
19. Drinking water standards in England and Wales are now set out in European and
ACT
UK legislation. They are cal ed Prescribed Concentrations or Values (PCVs) and
many are different from WHO’s Guideline Values. See: DWI (2010) The Water
Supply (Water Quality) Regulations 2010,
Water, England and Wales 994 (W.99):
42 pp.
http://dwi.defra.gov.uk/stakeholders/legislation/wsr2010wales.pdf.
20. Many vertebrate toxic agents (VTAs) are used in New Zealand. Datasheets have
been prepared for brodifacoum, bromadiolone, chloralose, 3-chloro-p-toluidine
hydrochloride, cholecalciferol, coumatetralyl, difethialone, diphacinine,
INFORMATION
flocoumafen, norbormide, PAPP, phosphine, pindone, strychnine and 1080.
21.
Triazole derivatives: These are general y considered to comprise triazole alanine
(TA), 1,2,4-triazole (1,2,4-T), triazole acetic acid (TAA) and triazole lactic acid
(TLA). They are common metabolites of the triazo
OFFICIAL le-containing fungicides which
includes the fol owing 18 triazole active fungicides:
bromuconazole, cyproconazo
THE le, difenoconazole, epoxiconazole,
fenbuconazole, fluquinconazole, flusilazole, flutriafol, ipconazole,
metconazole, myclobutanil, paclobutrazol, penconazole, propiconazole,
prothioconazole, tebuconazole, tetraconazole, triticonazole.
UNDER
Others that are sometimes mentioned are azaconazole, hexaconazole,
triadimefon, triadimenol and uniconazole.
An abbreviated datasheet for the triazoles has been included. For further detail,
refer to the individual fungicide datasheets.
RELEASED
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Document 3
Contents
The datasheet for
Bacillus thuringiensis israelensis is included in the Bacteria
datasheets. Abamectin and streptomyces – see actinomycetes (bacteria section) for
brief discussion.
If a pesticide does not appear in the contents list, do ‘a find’: for example, a pesticide
frequently cal ed dacthal or DCPA appears here as chlorthal-dimethyl.
1982
Abamectin, avermectin
1
Acephate
6
ACT
Acetochlor
10
Acibenzolar
15
Alachlor
19
Aldicarb
26
Aldrin/dieldrin
33
INFORMATION
Allethrin
42
Ametoctradin
46
Ametryn
49
OFFICIAL
Aminoethoxyvinylglycine
52
1-Aminomethanamide dihydrogen tetraoxosulphate
55
THE
Aminopyralid
57
Amitraz
60
Amitrole
UNDER
63
Asulam
67
Atrazine
71
Azaconazole
84
Azinphos methy
RELEASED
l
86
Azocyclotin
93
Azoxystrobin
96
Benalaxyl
100
Bendiocarb
103
Benomyl and carbendazim
106
Bentazone
111
Benzalkonium chloride
120
GUIDELINES FOR DRINKING-WATER QUALITY MANAGEMENT FOR NEW ZEALAND:
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Benzovindiflupyr
123
Benzyladenine
126
Bifenthrin
129
Bitertanol
134
Bixafen
137
Boscalid
140
Brodifacoum
143
Bromacil
147
Bromadiolone
153 1982
Bromopropylate
156
Bromoxynil
158
ACT
Bupirimate
162
Buprofezin
164
Captan
168
Carbaryl
173
Carbofuran
INFORMATION
179
Carbosulfan
187
Carboxin
190
Carfentrazone-ethyl
193
OFFICIAL
Chloralose
197
Chlorantraniliprole
THE
200
Chlordane
204
Chlordecone
211
UNDER
Chlorethephon
214
Chlorfenvinphos
217
Chloridazon
220
Chlorimuron
223
RELEASED
Chlormequat chloride
226
Chlorobenzilate
229
3-chloro-p-toluidine hydrochloride
232
Chlorothalonil
235
Chlorotoluron
244
Chlorpropham
248
Chlorpyriphos
253
Chlorsulfuron
261
xii
GUIDELINES FOR DRINKING-WATER QUALITY MANAGEMENT FOR NEW ZEALAND:
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Document 3
Chlorthal-dimethyl
264
Chlorthiamid
269
Cholecalciferol
271
Clethodim
274
Clodinafop-propargyl
278
Clofentezine
281
Clomazone
284
Clopyralid
287
Cloquintocet mexyl
291
1982
Clothianidin
293
Coumaphos
29
ACT
7
Coumatetralyl
300
Cyanazine
302
Cyantraniliprole
309
Cyazofamid
313
Cyflufenamid
INFORMATION
316
Cyfluthrin
319
Cyhalothrin
324
Cymoxanil
329
OFFICIAL
Cypermethrin
332
Cyproconazole
THE
340
Cyprodinil
344
Cyromazine
348
UNDER
2,4-D
353
Dalapon
363
Daminozide
367
Dazomet
370
RELEASED
2,4-DB
373
DDT and its derivatives
378
Deltamethrin
390
Desmedipham
394
Diazinon
397
1,2-dibromo-3-chloropropane
404
1,2-dibromoethane
409
Dicamba
415
GUIDELINES FOR DRINKING-WATER QUALITY MANAGEMENT FOR NEW ZEALAND:
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VOLUME 3 DATASHEETS – CHEMICAL AND PHYSICAL DETERMINANDS: PART 2.3 PESTICIDES
Document 3
Dichlobenil
421
Dichlofenthion
425
Dichlofluanid
427
3,4-Dichloroaniline and 3,5-Dichloroaniline
431
4,5-dichloro-2-octyl-3(2h)-isothiazolone
436
Dichlorophen
441
1,2-dichloropropane
443
1,3-dichloropropane
450
1,3-dichloropropene
453 1982
Dichlorprop
460
Dichlorvos
466
ACT
Dicloran
472
Dicofol
476
Dicyclanil
482
Didecyl dimethyl ammonium bromide
484
Difenoconazole
INFORMATION
488
Difethialone
492
Diflubenzuron
495
Diflufenican
501
OFFICIAL
Diiodomethylsulfonyl toluene
503
Dimethenamid
THE
506
Dimethoate
510
Dimethomorph
518
UNDER
Dinoseb
521
Diphacinone
525
Diquat
528
Dithianon
537
RELEASED
Diuron
540
Dodine
547
Emamectin benzoate
550
Endosulfan
555
Endothal
564
Endrin
569
Epoxiconazole
574
Esfenvalerate
577
xiv
GUIDELINES FOR DRINKING-WATER QUALITY MANAGEMENT FOR NEW ZEALAND:
VOLUME 3 DATASHEETS – MICRO-ORGANISMS: PART 1.1 BACTERIA
Document 3
Ethanedinitrile
582
Ethion
585
Ethofumesate
588
Ethylene thiourea
591
Etofenprox
595
Etoxazole
598
Etridiazole
602
Famphur
605
Fenamidone
607
1982
Fenamiphos
610
Fenarimol
61
ACT
5
Fenbuconazole
618
Fenbutatin oxide
622
Fenhexamid
625
Fenitrothion
628
Fenoprop
INFORMATION
633
Fenoxaprop-p-ethyl
638
Fenoxycarb
642
Fenpiclonil
645
OFFICIAL
Fenpropidin
648
Fenpropimorph
THE
651
Fenpyrazamine
654
Fenpyroximate
657
UNDER
Fenthion
661
Fipronil
665
Flamprop-isopropyl
669
Flazasulfuron
672
RELEASED
Flocoumafen
675
Flonicamid
678
Florasulam
681
Fluazifop-p-butyl
684
Fluazinam
688
Fludioxonil
691
Flufenacet
695
Flumethrin
698
GUIDELINES FOR DRINKING-WATER QUALITY MANAGEMENT FOR NEW ZEALAND:
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VOLUME 3 DATASHEETS – CHEMICAL AND PHYSICAL DETERMINANDS: PART 2.3 PESTICIDES
Document 3
Flumetsulam
701
Flumioxazin
703
Fluopicolide
707
Fluopyram
711
Fluoxastrobin
714
Flupropanate-sodium
717
Fluquinconazole
720
Fluroxypyr
723
Flusilazole
726 1982
Flusulfamide
729
Fluthiacet-methyl
731
ACT
Flutriafol
734
Fluxapyroxad
738
Folpet
742
Foramsulfuron
746
Forchlorfenuron
INFORMATION
749
Formetanate
752
Formothion
755
Fosetyl aluminium
758
OFFICIAL
Fuberidazole
763
Furalaxyl
THE
766
Furathiocarb
768
Gibberellic acid
770
UNDER
Glufosinate-ammonium
773
Glyphosate
778
Guazatine
788
Halauxifen-methyl
791
RELEASED
Halosulfuron-methyl
794
Haloxyfop
797
Heptachlor and Heptachlor epoxide
801
Hexachlorobenzene
808
Hexachlorocyclohexane
815
Hexaconazole
820
Hexazinone
823
Hexythiazox
830
xvi
GUIDELINES FOR DRINKING-WATER QUALITY MANAGEMENT FOR NEW ZEALAND:
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Document 3
Hydramethylnon
834
Hydrogen cyanamide
837
8-Hydroxyquinoline
840
Imazalil
844
Imazapyr
847
Imazethapyr
851
Imidacloprid
854
Indaziflam
858
Indolebutyric acid
861
1982
Indoxacarb
863
Iodocarb
86
ACT
6
Iodomethane
869
Iodosulfuron-methyl-sodium
872
Ioxynil
875
Ipconazole
877
Iprodione
INFORMATION
881
Iprovalicarb
887
Irgarol
890
Isazofos
893
OFFICIAL
Isoproturon
895
Isopyrazam
THE
899
Isoxaben
903
Kasumin
906
UNDER
Kresoxim-methyl
908
Lindane
911
Linuron
919
Lufenuron
924
RELEASED
Malathion
927
Maleic hydrazide
935
Mancozeb
939
Mandipropamid
944
Marbofloxacin
947
MCPA
949
MCPB
956
Mecoprop
961
GUIDELINES FOR DRINKING-WATER QUALITY MANAGEMENT FOR NEW ZEALAND:
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Document 3
Mefenpyr
967
Mepiquat chloride
970
Mesosulfuron-methyl
973
Mesotrione
975
Metalaxyl
978
Metaldehyde
984
Metamitron
988
Metam sodium
991
Methabenzthiazuron
995 1982
Methamidophos
997
Methiocarb
1002
ACT
Methomyl
1006
Methoprene
1012
Methoxychlor
1016
Methoxyfenozide
1021
1-Methylcyclopropene
1
INFORMATION
025
Methylene bisthiocyanate
1028
Methyl isothiocyanate
1031
Methyl parathion
1034
OFFICIAL
Metiram
1041
Metofluthrin
THE
1045
Metolachlor
1048
Metrafenone
1056
UNDER
Metribuzin
1059
Metsulfuron
1067
Milbemectin
1072
Mirex
1075
RELEASED
Molinate
1079
Monocrotophos
1084
Myclobutanil
1087
Naphthenates
1091
1-Naphthylacetic acid
1094
Neem oil
1098
Nicarbazin
1102
Niclosamide
1106
xviii GUIDELINES FOR DRINKING-WATER QUALITY MANAGEMENT FOR NEW ZEALAND:
VOLUME 3 DATASHEETS – MICRO-ORGANISMS: PART 1.1 BACTERIA
Document 3
Nicosulfuron
1109
Nitenpyram
1112
Norbormide
1114
Norflurazon
1116
Novaluron
1120
Octhilinone
1124
N-octyl bicycloheptene dicarboximide
1127
Oryzalin
1129
Oxadiazon
1134
1982
Oxamyl
1138
Oxathiapiprolin
114
ACT
3
Oxine-Copper
1146
Oxyfluorfen
1149
Paclobutrazol
1152
PAPP, para-aminopropiophenone
1155
Paraquat
INFORMATION
1159
Parathion
1164
Penconazole
1170
Pencycuron
1173
OFFICIAL
Pendimethalin
1176
Pentachlorophenol
THE
1182
Penthiopyrad
1192
Permethrin
1195
UNDER
Phenmedipham
1204
d-Phenothrin
1207
Phenylphenol
1210
Phorate
1215
RELEASED
Phosphine
1220
Phoxim
1223
Picloram
1226
Picoxystrobin
1234
Pindone
1237
Pinoxaden
1240
Piperonyl butoxide
1243
Pirimicarb
1246
GUIDELINES FOR DRINKING-WATER QUALITY MANAGEMENT FOR NEW ZEALAND:
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VOLUME 3 DATASHEETS – CHEMICAL AND PHYSICAL DETERMINANDS: PART 2.3 PESTICIDES
Document 3
Pirimiphos methyl
1250
Pirimisulfuron methyl
1258
Polyoxin D
1262
Posaconazole
1264
Prochloraz
1266
Procymidone
1269
Prohexadione-calcium
1274
Prometryn
1277
Propachlor
1280 1982
Propamocarb
1286
Propanil
1290
ACT
Propargite
1296
Propazine
1300
Propetamphos
1307
Propham
1310
Propiconazole
1
INFORMATION
313
Propineb
1319
Propoxur
1324
Propyzamide
1328
OFFICIAL
Proquinazid
1332
Prothioconazole
THE
1335
Prothiofos
1339
Pymetrozine
1341
UNDER
Pyraclostrobin
1345
Pyrazophos
1348
Pyrethrin and Pyrethroids
1351
Pyridate
1356
RELEASED
Pyrimethanil
1360
Pyriproxyfen
1364
Pyroxasulfone
1369
Pyroxsulam
1372
Quinoxyfen
1375
Quintozene
1379
Quizalofop-p-ethyl
1384
Resmethrin
1388
xx
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Document 3
Rotenone
1391
Saflufenacil
1395
Sethoxydim
1399
Simazine
1402
Sodium tetrathiocarbonate
1410
Spinetoram
1414
Spinosad dt
1419
Spiromesifen
1424
Spirotetramat
1427
1982
Spiroxamine
1432
Streptomycin
143
ACT
5
Strychnine
1438
Sulfentrazone
1441
Sulfoxaflor
1444
Sulphaquinoxaline
1447
2,4,5-T
INFORMATION
1450
Tau-fluvalinate
1456
Tebuconazole
1460
Tebufenozide
1464
OFFICIAL
Tebuthiuron
1467
Temephos
THE
1470
Tepraloxydim
1474
Terbacil
1477
UNDER
Terbufos
1482
Terbumeton
1487
Terbuthylazine
1489
Terbutryn
1495
RELEASED
Tetrachlorvinphos
1498
Thiabendazole
1502
Thiacloprid
1507
Thiamethoxam
1511
Thidiazuron
1515
Thifensulfuron-methyl
1518
2-(thiocyanomethylthio) benzothiazole
1521
Thiodicarb
1525
GUIDELINES FOR DRINKING-WATER QUALITY MANAGEMENT FOR NEW ZEALAND:
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Thiophanate-methyl
1529
Thiram
1534
Thymol
1540
Tolclofos-methyl
1543
Toltrazuril
1547
Tolylfluanid
1550
Topramezone
1554
Toxaphene
1557
Tralkoxydim
1562 1982
Triadimefon and Triadimenol
1565
Tri-allate
1571
ACT
Triazole metabolites
1575
Triazophos
1578
Tribenuron
1581
Trichlorfon
1584
Triclopyr
1
INFORMATION
588
Trifloxystrobin
1596
Trifloxysulfuron sodium
1600
Triflumuron
1603
OFFICIAL
Trifluralin
1606
Triforine
THE
1613
Trinexapac-ethyl
1617
Triticonazole
1621
UNDER
Uniconazole
1623
Zinc pyrithione
1626
Zineb
1630
Ziram
1634
RELEASED
1080
1638
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Document 3
1080
CAS No. 62-74-8 for the sodium salt. The IUPAC and CAS name is sodium
fluoroacetate. Also cal ed fluoroacetic acid, sodium monofluoroacetate, sodium
fluorethanoate and 2-fluoroacetic acid. The name of 1080 resulted from an invoice
number at an early research station in the US!
CAS No. 144-49-0 refers to the fluoroacetate ion.
1982
Maximum Acceptable Value (provisional) ACT
Based on health considerations, the concentration of 1080 in drinking-water
should not exceed 0.0035 mg/L. The MAV in the 1995 DWSNZ had been
0.005 mg/L.
1080 is not mentioned in the WHO Guidelines.
INFORMATION
Sources to water
1080 is a highly toxic poison (rodenticide) used for the control of possums, deer, rats
and rabbits. It was introduced increasingly during the 1940s and 1950s as a more
effective and humane alternative to strychnine. It m
OFFICIAL ay enter source waters as a result of
aerial application.
THE
1080 occurs natural y in several plants, such as tea; recent studies at Lincoln University
have detected natural traces of 1080 in puha. It has been found in more than 40 West
Australian plants; possums in New Zealand come from the eastern seaboard of
Australia and are more susceptible to the toxin, unlike their West Australian cousins
UNDER
who are more resilient. It has been used overseas in sewers and ships to control rats.
New Zealand uses approximately 80 percent of the world’s production of
manufactured 1080 amounting to 3.2 tonnes of raw product in the period 1 July 2001
to 30 June 2002. Fol owing a re-assessment by ERMA in August 2007, 1080 continues
to be registered
RELEASED for use in New Zealand; it is a Class B, restricted use poison, and a
license is required for its use.
The Parliamentary Commissioner for the Environment (PCE 2011) reviewed the use of
1080 in New Zealand.
To monitor 1080 operations, more than 500 water samples have been taken in the
target area over the last five years. Less than 2 percent of them (10 samples) have
contained detectable concentrations of 1080. All of these samples were well below the
tolerable exposure limit (TEL) of 3.5 micrograms of 1080 per litre of water
(0.0035 mg/L) set in the reassessment. The highest concentration detected was
0.3 micrograms per litre (0.0003 mg/L) of water. The TEL is set at a level that is
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protective of human health. None of the samples taken from areas in drinking water
catchments have shown any measurable amounts of 1080, ie, <0.0001 mg/L (EPA
2013).
The Environmental Risk Management Authority, now cal ed the Environmental
Protection Agency (EPA), has delegated the function of granting permissions for the
use of selected VTAs to Medical Officers of Health and Health Protection Officers who
are also warranted HSNO enforcement officers and have completed relevant Ministry
of Health courses. In addition to granting permission, the delegation also includes
adding, deleting or otherwise varying any condition on a permission; and/or revoking a
permission. See MoH (2013).
1982
Forms and fate in the environment
ACT
While 1080 is comparatively rapidly eliminated from living animals, it can persist in
carcasses for many months in cool or dry conditions where it wil break down more
slowly and may pose a risk to scavenging dogs. Undigested baits in carcasses remain
toxic for prolonged periods (Eason 2002).
Studies show that 1080 can be metabolised by soil micro-organisms. Sodium
monofluoroacetate derived from baits wil be dispersed by water since it is highly water
INFORMATION
soluble and mobile. If heavy rainfal fol ows the use of 1080 baits, leaching to
unmeasurable concentrations (<0.0001 mg/L) may precede biodegradation. In
comparison to cereal bait, 1080 is retained in carrot baits and wil only slowly leach
from carrots into the soil. In mild weather or warm conditions, such as 11 to 20ºC and
8 to 15 percent moisture, 1080 may be significantly defluorinated in one to two weeks.
OFFICIAL
In less favourable conditions breakdown might take several weeks, and in extreme cold
and drought 1080 residues might persist in baits or in the soil for several months (from
THE
Eason 2002).
1080 can be translocated from water or soil to plants and then defluorinated. It is
absorbed by aquatic organisms but it is not bioaccumulated. NSW Government (2013)
UNDER
reports that fish and some crustaceans (eg, water fleas Daphnia sp.) are relatively
tolerant to 1080, whereas some aquatic insects (eg, mosquito larvae) are susceptible.
Some aquatic plants, such as duckweed (Spirodela oligorrhiza), have been found to be
sensitive.
Water solubility is very high, about 100 percent.
RELEASED
A nationwide water testing programme carried out between 1990 and 2003 showed
that only 5 percent of over 1,450 water samples tested had detectable traces of 1080.
These levels were transient and associated with the visible presence of baits in smal
streams. The 1080 levels ranged from 0.0002 to 0.009 mg/L (Booth et al 1997; Eason
2002; ERMA 2007a).
If released to soil, fluoroacetic acid is expected to have very high mobility based upon
an estimated Koc of 1.4. The pKa of fluoroacetic acid is 2.59, indicating that this
compound wil primarily exist in the dissociated form in the environment and anions
general y do not adsorb more strongly to organic carbon and clay than their neutral
2
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counterparts. Fluoroacetic acid may volatilise from dry soil surfaces based upon its
vapour pressure. Fluoracetic acid has been identified as one which could be removed
by biological sewage treatment provided suitable acclimatisation can be achieved,
suggesting that the compound may be subject to biodegradation in terrestrial or
aquatic systems. If released into water, fluoroacetic acid is not expected to adsorb to
suspended solids and sediment based upon the estimated Koc. The pKa value indicates
fluoroacetic acid wil exist almost entirely in the ionised form at pH values of 5 to 9 and
therefore volatilisation from water surfaces is not expected to be an important fate
process. An estimated BCF of 3 suggests the potential for bioconcentration in aquatic
organisms is low. Hydrolysis is not expected to be an important environmental fate
process since this compound lacks functional groups that hydrolyse under
environmental conditions (EAWAG accessed February 2015).
1982
Typical concentrations in drinking-water ACT
The P2 Chemical Determinand Identification Programme did not find 1080 at
detectable concentrations (limit of detection = 0.0001 mg/L) (ESR 2001).
Removal methods
INFORMATION
No information is available about methods for removing 1080 from water.
Recommended analytical tech
OFFICIAL niques
Referee method
THE
Derivatisation with dicyclohexylcarbodi mide and gas chromatography with electron
capture detection (Ozawa and Tsukioka 1987,
Anal Chem 59: 2914–17).
UNDER
Some alternative methods
No alternative methods have been recommended for 1080 because no methods meet
the required criteria.
RELEASED
Health considerations
Animal studies have shown that 1080 is absorbed rapidly and excreted as unchanged
fluoroacetate and a range of metabolites.
1080 poisoning results from the transformation of fluoroacetate into fluorocitrate
within cell mitochondria. Acute poisoning is characterised by a symptom-free latent
period of half to two hours or longer between ingestion and onset of symptoms
(nausea, vomiting, diarrhoea and hyperactive behaviour leading to convulsions, coma
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and cyanosis). Ventricular fibril ation is noted commonly and is the primary cause of
death. Early symptoms include alteration of heart sounds and premature, weak
contractions.
The LD50 (dose required to kill half a sample human population) is 2.0 mg/kg bw.
Therefore a 70 kg person would need to drink 70,000 litres of water containing
0.002 mg/L of 1080, in one sitting, to absorb a fatal dose. [Note: 0.002 mg/L is half the
MAV, rounded up.] Even al owing a significant safety margin (typical y applied to al ow
for sensitivity in the general population and uncertainty in the toxicological studies), a
safety factor of 1,000 would stil require a person to drink at least 70 litres of water
containing 0.002 mg/L of 1080 before being considered at risk (DoC 2004).
The oral RfD was calculated at 0.00002 mg/kg/d (USEPA 1993) based on increased 1982
heart weight in females and males; decreased testis weight and altered
spermatogenesis in males in a 13-week rat oral study (gavage); NOAEL =
0.05 mg/kg/d.
ACT
Eason and Turck (2002) found from animal toxicology studies commissioned by DoC
and the AHB that 1080 was teratogenic, a male reproductive toxin and a myocardial
toxin in rats.
The No Observable Effect Level (NOEL) for toxicity in rats (0.075 mg/kg-day) indicates
that regular intake of 1080 contaminated water could cause sub-lethal effects. Based
INFORMATION
on this NOEL, a 70 kg person would need to drink 2,680 litres of water containing
0.002 mg/L of 1080 per day, for an extended period of time, for sub-lethal effects to
occur. Allowing a safety margin of 1,000, a person would need to drink their entire
daily intake of two litres a day of water from a contaminated source, for a period of
weeks, to be considered potential y at risk. Similarly, a
OFFICIAL pregnant woman would need to
drink at least three litres a day, al of her daily intake, during the first 90 days of
pregnancy, to receive a daily intake one thousand times less than the NOEL
THE
(0.1 mg/kg-day) for developmental toxicity in rats (Eason and Turck 2002, and
Tremblay et al 2002, in DoC 2004).
Work by Foronda et al (2007) found the BMD10 and BMDL10 for cardiomyopathy and
UNDER
testicular effects were 0.21 mg/kg bw and 0.10 mg/kg bw, respectively. These values
are proposed for use in the eventual determination of the tolerable daily intake (TDI)
for 1080. Based on the best fit of modelled dose–response data, a TDI of 0.03 µg/kg
bw/day was proposed for human health risk assessment of 1080 (Foronda et al 2007a).
Assessment threshold
RELEASED s were established (ERMA 2007a) for acute, subchronic and
chronic exposure to 1080. The acute threshold applied was the estimated minimum
lethal dose (MLD) in humans 0.7 mg/kg bw. The subchronic exposure threshold
established was the acceptable operator exposure (AOEL) of 0.2 μg/kg bw/day
(appropriate only for workers). The Department of Labour’s biological exposure index
for 1080 in urine was used for analysis of some data.
The chronic exposure threshold was the Acceptable Daily Exposure of 0.02 μg/kg
bw/day. This was used to derive separate potential daily exposures (PDE) for different
routes:
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• PDEfood = 0.006 μg/kg bw/day
• PDEwater = 0.01 μg/kg bw/day
• PDEinhalation = 0.002 μg/kg bw/day
• PDEdermal = 0.002 μg/kg bw/day
Derivation of Maximum Acceptable Value
The provisional MAV for 1080 was calculated by the New Zealand Ministry of Health
using an NOAEL derived from a Department of Conservation teratology study of rats
(Eason 1999) as fol ows:
1982
0.1 mg/kg x 70 kg x 0.5 = 0.0035 mg/L
2 L x 500
ACT
where:
• no observable effect level = 0.1 mg/kg body weight per day
• average weight of adult = 70 kg
• average quantity of water consumed by an adult = 2 L per day
• proportion of lowest lethal dose al ocated to drinking-water = 0.5
• uncertainty factor = 500 (10 for intraspecies variation, 10 for interspecies variation,
INFORMATION
5 for the inadequacy of the studies and database).
The MAV in the 1995 DWSNZ had been derived by the MoH as fol ows:
0.5 mg/kg x 70 kg x 0.2 x 2.5 = 0.005 mg/L
OFFICIAL
2 L x 2,000
where:
THE
• lowest lethal dose in humans = 0.5 mg/kg body weight
• average weight of adult = 70 kg
• average quantity of water consumed by an adult = 2 L per day
UNDER
• proportion of lowest lethal dose al ocated to drinking-water = 0.2
• uncertainty factor = 2,000 (10 for intraspecies variation, 2 for interspecies variation,
10 for the inadequacy of the studies and database, 10 for nature and a severity of
effect)
• arbitrary facto
RELEASED r = 2.5 (the determination was done by a very conservative process
which gave a result similar to that found in tea as it is normal y consumed. Tea
leaves are a natural source of 1080. Consequently, the 2.5 factor was applied for
common sense reasons).
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Bibliography
Booth LH, Ogilvie SC, Wright GR, et al. 1997. Water quality monitoring after 1080 pest
control operations.
Water and Wastes in New Zealand 96: 22.
DoC. 2001.
Vertebrate Pesticide Toxicology Manual (Poisons) (2nd edition). Eason CT,
Wickstrom M. Department of Conservation Technical Series 23 [122 pp].
http://www.doc.govt.nz/publications/science-and-technical/products/series/doc-
technical-series/
DoC. 2004.
The Use of 1080 for Pest Control. See section 5.6 [64 pp].
http://www.doc.govt.nz/Documents/conservation/threats-and-impacts/animal-
pests/use-of-1080-04.pdf
1982
DoC. 2009. A re-evaluation of potential rodenticides for aerial control of rodents.
Eason CT, Ogilvie S.
DOC Research & Development Series 312 [34 pp].
ACT
http://www.doc.govt.nz/publications/science-and-technical/products/series/doc-
research-and-development-series/
Eason CT, Gooneratne R, Fitzgerald H, et al. 1994. Persistence of sodium
monofluoroacetate in livestock animals and risk to humans.
Human and Experimental
Toxicology 13(2): 119–22.
Eason CT, et al. 1999. A review of recent regulatory and environmental toxicology
INFORMATION
studies on 1080: results and implications.
New Zealand Journal of Ecology 23(2):
129–37.
Eason CT. 2002.
Technical Review of Sodium Monofluoroacetate (1080) Toxicology.
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http://www.landcareresearch.co.nz/publications/do
OFFICIAL wnloads/AHB_1080_review.p
df
THE
Eason CT, Turck P. 2002. A 90-day toxicological evaluation of compound 1080 (sodium
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Toxicological Sciences 69: 439–47.
EAWAG. Accessed February 2015.
Biocatalysis/Biodegradation Database: Select 1396
compounds.
http://eawag-bbd.e
UNDER thz.ch/index.html
EPA. 2013.
Five-Year Review of the Aerial Use of 1080: 2008 to 2012. Wellington:
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. www.epa.govt.nz. EPA also produces
annual reports on the aerial use of 1080.
ERMA. 2007.
Application for the Reassessment of a Hazardous Substance under Section
RELEASED
63 of the Hazardous Substances and New Organisms Act 1996. Wellington:
Environmental Risk Management Authority. The ful decision [214 pp] is available at:
http://www.ermanz.govt.nz/news-
events/1080/Decision%20_2007.08.10_%20FINAL.pdf
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Evaluation and Review Report: Reassessment of 1080 (HRE05002).
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S
ee: http://www.ermanz.govt.nz/BertDocs/HRE05002-044.pdf Main report
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http://archive.ermanz.govt.nz/news-
events/focus/1080/index.html
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ESR. 2001.
A Report on the Chemical Quality of New Zealand’s Community Drinking
Water Supplies. Client Report FW0120, prepared as part of a Ministry of Health
Contract for Scientific Services [333 pp].
Foronda NM, et al. 2007. A benchmark dose analysis for sodium monofluoroacetate
(1080) using dichotomous toxicity data.
Regulatory Toxicology and Pharmacology 47: 84–9.
Foronda NM, et al. 2007a. The use of myocardial and testicular end points as a basis for
estimating a proposed tolerable daily intake for sodium monofluoroacetate (1080).
Regulatory Toxicology and Pharmacology 47: 29–36.
IPCS. 2001. Sodium fluoroacetate.
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INCHEM.
http://www.inchem.org/pages/pims.html
1982
MoH. 2013.
Issuing Permissions for the Use of Vertebrate Toxic Agents (VTAs): Guidelines
for Public Health Units. Revised 2013. Wellington: Ministry of Health [116 pp].
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Pesticides Used in the Management of Vertebrate Pests in
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in-the-management-of-vertebrate-pests-in-australia-a-review.pdf
Ozawa H, Tsukioka T. 1987. Gas chromatographic determination of sodium
INFORMATION
monofluoroacetate in water by derivatisation with dicyclohexylcardodi mide in water,
Analytical Chemistry 59: 2914–17.
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Evaluating the Use of 1080: Predators, poisons and silent forests. Wellington:
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OFFICIAL
www.pce.parliament.nz
PMEP. 1990. Sodium fluoroacetate (1080) – chemical profile 8/90.
EPA Pesticide
THE
Factsheet 174. Accessed 2011 via PMEP.
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Insecticides. http://pmep.cce.cornell.edu/profiles/index.html
Tremblay LA, Fisher P, Leusch DL. 2002. Evaluation of the potential of sodium
UNDER
monofluoroacetate (1080) and fluorocitrate to bind to mammalian oestrogen receptor.
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Integrated Risk Information System (IRIS).
http://cfpub.epa.gov/ncea/iris/index.cfm?fuseaction=iris.showSubstanceList or
http://www.epa.gov/iris/subst/0469.htm
RELEASED
WHO. 1975. Sodium fluoroacetate.
WHO/FAO Data Sheets on Pesticides 16.
http://www.inchem.org/pages/pds.html
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Document Outline
