Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

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Summary of Herbicide Effects to Wildlife 

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U.S. Fish and Wildlife Service 

Prepared by: Shawna L. Bautista, Wildlife Biologist, 

Invasive Plant EIS 

US Forest Service, Region 6 Regional Office, Portland, OR 

February 2005 
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

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Summary of Herbicide Effects to Wildlife ................................................... 1 

Citation Method Used in This Document................................................................................. 1 

Herbicides Analyzed................................................................................................................. 1 

Terms and acronyms used in this document............................................................................. 2 

Inerts, Adjuvants and Impurities............................................................................................... 4 

Effects of Impurities ................................................................................................................. 9 

Metabolites.............................................................................................................................. 10 

Toxicity Data and Exposure Analysis..................................................................... 12 

The Use of Surrogate Species................................................................................... 12 

Doses and Responses................................................................................................. 13 

Factors that Influence Exposure and Dose............................................................. 13 

Body Weight............................................................................................................ 13 

Metabolic Rate........................................................................................................ 14 

Oral Routes............................................................................................................. 14 

Dermal Route.......................................................................................................... 15 

Summary of Exposure Scenarios............................................................................. 15 

Acute Exposures........................................................................................................ 16 

Chronic Exposures.................................................................................................... 16 

Herbicide Effects on Amphibians........................................................................................... 28 

Dicamba ...................................................................................................................... 28 

Glyphosate .................................................................................................................. 29 

Sulfometuron methyl .................................................................................................. 30 

Triclopyr ..................................................................................................................... 30 

Herbicide Effects on Invertebrates.......................................................................... 31 

Likelihood these exposures and effects will actually occur.................................................... 34 

Chlorsulfuron .............................................................................................................. 35 

Clopyralid ................................................................................................................... 35 

Dicamba ...................................................................................................................... 35 

Glyphosate .................................................................................................................. 35 

Imazapyr ..................................................................................................................... 36 

Metsulfuron methyl..................................................................................................... 36 

Picloram...................................................................................................................... 37 

Triclopyr ..................................................................................................................... 37 

CHLORSULFURON...................................................................................................... 38 

Small Insectivorous Mammal ......................................................................................... 51 

Clopyralid / Highest Application Rate.................................................................. 115 

Dicamba / Highest Application Rate .................................................................... 117 

Glyphosate / Highest Application Rate................................................................. 119 

Imazapic / Typical Application Rate .................................................................... 120 

Metsulfuron methyl / Typical Application Rate ................................................... 124 

Picloram / Typical Application Rate..................................................................... 126 

Sethoxydim/ Highest Application Rate ................................................................ 129 

Sulfometuron methyl / Typical Application Rate................................................. 130 

Sulfometuron methyl / Highest Application Rate................................................. 131 
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

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Summary of Herbicide Effects to Wildlife 

This document is a summary of toxicity information presented in Forest Service Risk 

Assessments (SERA 1998, 2001, 2003) and some public literature. I summarized 

information found in the human health and ecological risk assessment sections of the risk 

assessments, and obtained literature published in peer-reviewed journals, from authors, and 

on the internet. I conducted the literature search primarily to verify figures in the risk 

assessments, or to find specific values - it was not a comprehensive search. Syracuse 

Environmental Research Associates (SERA) conducted very comprehensive searches of the 

literature when preparing the risk assessments, and also evaluated the research papers for 

quality of methods and analysis used. 

Citation Method Used in This Document 

Because a large number of risk assessments produced by SERA are the basis for this 

document, many of them were produced in the same year, and the inherent difficulty in 

accurately tracking citations designated by year and lower case letter (e.g. 2003a, 2003b, 

etc.), I have resorted to a different citation convention. For risk assessments produced by 

SERA, the author and year is followed by the chemical name analyzed in the cited risk 

assessment. For example, information taken from the glyphosate risk assessment produced 

by SERA in 2003 is cited as: (SERA 2003 Glyphosate). Hopefully, this will avoid 

confusion when the inevitable rearranging of information takes place during editing. 

Information in this report is taken from risk assessments produced by SERA unless 

otherwise noted.

Herbicides Analyzed 

The herbicides included in this summary are those being analyzed in the Region 6 Invasive 

Plant Environmental Impact Statement (EIS) (Table 1). These herbicides or formulations are 

registered for use in forestry applications, right-of-ways, or rangelands and are appropriate 

for use against invasive plant species in Region 6 of the USDA Forest Service. The mention 

of trade names or commercial products does not constitute endorsement or recommendation 

for use.

Table 1. Herbicides analyzed and some representative formulation names. 

Chemical Name Trade Name 

Chlorsulfuron Telar, Glean, Corsair 

Clopyralid Transline, Stinger 

Dicamba Banvel, Vanquish 

Glyphosate RoundUp, Rodeo, Accord 

Imazapic Plateau 

Imazapyr Arsenal, Chopper, Stalker 

Metsulfuron methyl Escort 

Picloram Tordon 

Sethoxydim Poast 

Sulfometuron methyl Oust 

Triclopyr Garlon, Pathfinder, Remedy 

2,4-D Weedone, Weedar, Savage 

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It is not feasible to evaluate specific effects to specific wildlife species at a regional scale. 

The effects of herbicide use must be evaluated at the site-specific scale before any projects 

involving herbicide use are authorized. However, it is useful to understand the general and 

relative risks that proposed herbicides pose to wildlife in the planning area. 

The following discussion will provide information on all herbicides considered in the USDA 

Forest Service, Pacific Northwest Region, Invasive Plant EIS. Refer to the following text 

box for terms and concepts about potential effects of herbicides. 

Terms and acronyms used in this document. 

Allometric = pertaining to allometry, the study and measure of growth. In toxicology, the 

study of the relationship of body size to various processes that may impact how chemicals 

affect the organism or how the chemicals are transported within the organism. 

bioconcentration = the net accumulation of a substance by an aquatic organism as a result of 

uptake directly from aqueous solution (i.e. water with other stuff mixed in). 

bioaccumulation = the net accumulation of a substance by an organism as a result of uptake 

directly from all environmental sources and from all routes of exposure (primarily from food 

or water that is ingested). 

dose = the actual quantity of a chemical administered to, or absorbed by, an organism. 

gavage = a method of dose administration; the substance is placed directly in the stomach.. 

exposure = the amount of chemical in contact with an animal. 

LD50 (lethal dose50) - The dose of a chemical calculated to cause death in 50% of a defined 

experimental animal population over a specified observation period. The observation period 

is typically 14 days. 

LOAEL = Lowest-observed-adverse-effect level; lowest exposure associated with an 

adverse effect. 

NOEL = No-observed-effect level; no effects attributable to treatment. 

NOAEL =No-observed-adverse-effect level: An exposure level at which there are no 

statistically or biologically significant increases in the frequency or severity of adverse 

effects between the exposed population and its appropriate control; some effects may be 

produced at this level, but they are not considered as adverse, or as precursors to adverse 

effects. In an experiment with several NOAELs, the regulatory focus is primarily on the 

highest one, leading to the common usage of the term NOAEL as the highest exposure 

without adverse effects. 

NOEC = No-observed-effect concentration; synonymous with NOEL. 

Surfactant = surface acting agent; any substance that when dissolved in water or an aqueous 

solution reduces its surface tension or the interfacial tension between it and another liquid. 

Surrogate = a substitute; lab animals are substituted for humans or other wildlife in toxicity 

testing. 

Toxicity index = in this document, it is the dose of herbicide used to determine the potential 

for an adverse effect to wildlife. It is the lowest dose reported to cause the most sensitive 

effect in the most sensitive species tested, and is usually a reported NOAEL for a sub-lethal 

effect, but may be an LD50 (or a portion thereof) when data is lacking. 

a.e. = acid equivalent 

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a.i. = active ingredient 

kg = kilogram, equivalent to 1000 grams or 2.2 pounds 

g = gram, equivalent to 1000 milligrams or about 0.035 ounce (28 g = 1 ounce) 

mg = milligram; 0.001 gram. 

mg/L = milligrams per liter; equivalent to ppm. 

mg/kg = milligrams per kilogram; equivalent to ppm. 

ppm = part(s) per million; equivalent to mg/L and mg/kg. 

ppb = part(s) per billion 

Herbicides have the potential to adversely affect the environment. The U.S. Environmental 

Protection Agency (EPA) must register all herbicides prior to their sale, distribution, or use in 

the United States. In order to register herbicides for outdoor use, the EPA requires the 

manufacturers to conduct a safety evaluation on wildlife including toxicity testing on 

representative species of birds, mammals, freshwater fish, aquatic invertebrates, and 

terrestrial and aquatic plants. An ecological risk assessment uses the data collected to 

evaluate the likelihood that adverse ecological effects may occur as a result of herbicide use. 

The Forest Service conducts its own risk assessments, focusing specifically on the type of 

herbicide uses in forestry applications. The Forest Service contracts with SERA to conduct 

human health and ecological risk assessments for herbicides that may be proposed for use on 

National Forest System lands. The information contained in this EIS relies on these risk 

assessments. All toxicity data, exposure scenarios, and assessments of risk are based upon 

information in the SERA risk assessments unless otherwise noted. Typical application rates 

of herbicides and nonylphenol polyethoxylate (NPE) surfactant used in this analysis can be 

found in Table 2. 

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Table 2. Herbicide and nonylphenol polyethoxylate application rates used to treat 

invasive plants. Included are the incidental rates of application of the impurity 

hexachlorobenzene. 

Herbicide Typical 

Application Rate 

lb ai/ac* 

Lowest 

Application Rate 

lb ai/ac 

Highest 

Application Rate 

lb ai/ac 

Chlorsulfuron 0.056 0.0059 0.25 

Clopyralid 0.35 0.1 0.5 

Dicamba 0.3 0.25 2 

Glyphosate 2 0.5 7 

Imazapic 0.13 0.031 0.19 

Imazapyr 0.45 0.03 1.25 

Metsulfuron Methyl 0.03 0.013 0.15 

Picloram 0.35 0.13 1.0 

Sethoxydim 0.3 0.094 0.38 

Sulfometuron Methyl 0.045 0.03 0.38 

Triclopyr 1.0 0.1 10 

2,4-D 1.0 0.5 2.0 

Nonylphenol 

Polyethoxylate 

1.67 0.167 6.68 

Hexachlorobenzene# 0.000004 0.0000024 0.000012 

* pounds of active ingredient per acre

#These application rates reflect the incidental rates of application of the impurity 

hexachlorobenzene. 

Source: USDA Forest Service 2003, SERA 1998, 2001, 2003 

Herbicides are not pure compounds and they contain the active ingredient, impurities, 

adjuvants, inert ingredients, and may also contain surfactants. The effects of inert 

ingredients, adjuvants, impurities and surfactants to wildlife are discussed first, followed by a 

discussion of the effects of the active ingredients. 

Inerts, Adjuvants and Impurities 

Inert compounds are those that are intentionally added to a formulation, but have no 

herbicidal activity and do not affect the herbicidal activity. Inerts are added to the 

formulation to facilitate its handling, stability, or mixing. Impurities are inadvertent 

contaminants in the herbicide, usually present as a result of the manufacturing process. 

Adjuvants are compounds added to the formulation to improve its performance. They can 

either enhance the activity of an herbicide’s active ingredient (activator adjuvant) or offset 

any problems associated with its application (special purpose or utility modifiers). 

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Surfactants are one type of adjuvant that makes the herbicide more effective by increasing 

absorption into the plant, for example.

Inerts and adjuvants, including surfactants, are not under the same registration guidelines as 

are pesticides. The EPA classifies these compounds into four lists based on the available 

toxicity information. List 1 contains “inerts of toxicological concern”; List 2 contains 

“potentially toxic inerts, high priority for testing”; List 3 contains “inerts of unknown 

toxicity”; and List 4 contains “minimal risk inerts” or “inerts for which EPA has sufficient 

information to conclude that their current use patterns will not adversely affect public health 

or the environment.” If the compounds are not classified as toxic, then all information on 

them is considered proprietary and the manufacturer need not disclose their identity. 

Therefore, inerts and adjuvants generally do not have the same amount of research conducted 

on their effects, compared to active ingredients. 

Inert Ingredient Effects

There is very little data regarding the effects to most wildlife species from inert ingredients 

contained in the 12 herbicides considered in this EIS. None of the inert ingredients included 

on EPA’s List 2, 3, or 4 need to be disclosed on the herbicide label, despite evidence that 

some compounds on these lists may cause adverse effects to laboratory animals and humans 

(Anonymous 1999; Cox 1999; Knight 1997; Knight and Cox 1998; Marquardt et al. 1998). 

EPA’s own website (http://www.epa.gov/opprd001/inerts/) states, “Since neither federal law 

nor the regulations define the term "inert" on the basis of toxicity, hazard or risk to humans, 

non-target species, or the environment, it should not be assumed that all inert ingredients are 

non-toxic.” Northwest Coalition for Alternatives to Pesticides (NCAP) obtained the identity 

of many inert ingredients through a Freedom of Information Act request; the list of inerts 

they obtained can be found at http://www.pesticide.org/FOIA/

Many of the inert ingredients are proprietary in nature and have not been tested on laboratory 

or wildlife species. SERA obtained clearance to access confidential business information 

(i.e. the identity of proprietary ingredients) and used this information in the preparation of the 

risk assessment. However, toxicity data to support any assessment of hazard or risk are 

usually very poor, even when the identity of the inert is known. 

Chlorsulfuron – The identity of inerts used in chlorsulfuron are confidential, but SERA 

reviewed them for preparation of the risk assessment (SERA 2003 Chlorsulfuron). EPA has 

not classified any of the inerts as toxic. These inert ingredients do not affect the assessment 

of risk 

Clopyralid – Identified inerts include monoethanolamine and isopropyl alcohol, both 

approved food additives. These inert ingredients do not impact the assessment of risk 

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Dicamba – The identity of inerts used in Banvel® and Vanquish® are confidential, but 

SERA reviewed them for preparation of the risk assessment (SERA, 2003-Dicamba). EPA 

has not classified any of the inerts as toxic. A comparison of toxicity data on Banvel® with 

corresponding data on dicamba indicates that there are no substantial differences in terms of 

acute lethal potency (see SERA, 2003-Dicamba, p. 3-12). However, Banvel® causes severe 

skin irritation while the DMA salt of dicamba (the active ingredient in Banvel®) does not 
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(Budai et al., 1997; Kuhn, 1997, 1998 as cited in SERA, 2003-Dicamba). No similar studies 

are available for Vanquish®. But a formulation containing the active ingredient in Vanquish 

(IPA salt of dicamba) was found to have a lower acute lethal potency to bobwhite quail than 

other forms of dicamba (SERA, 2003-Dicamba citing Beavers 1986 and Campbell et al. 

1993). 

Glyphosate – There are at least 35 glyphosate formulations that are registered for forestry 

applications (SERA, 2003-Glyphosate) with a variety of inert ingredients. SERA obtained 

clearance to access confidential business information (i.e. the identity of proprietary 

ingredients) and used this information in the preparation of the risk assessment. Surfactants 

(discussed below) were the only additives identified that impact risk (SERA, 2003-

Glyphosate). 

Imazapic - The identity of inerts used in imazapic formulations are confidential, but SERA 

reviewed them for preparation of the risk assessment (SERA, 2003-Imazapic). EPA has not 

classified any of the inerts as toxic. 

Imazapyr – The identity of inerts used in imazapic formulations are confidential, but SERA 

reviewed them for preparation of the risk assessment (SERA, 2003-Imazapyr). No 

apparently hazardous materials were identified in the review of inerts. The NCAP website 

(http://www.pesticide.org/FOIA/picloram.html) identifies only glacial acetic acid, an 

approved food additive, as an inert ingredient. Isopropanolamine is also present, and it is 

classified as a List 3 inert. 

Metsulfuron methyl - The identity of inerts used in metsulfuron methyl formulations are 

confidential, but SERA reviewed them for preparation of the risk assessment (SERA, 2003-

Metsulfuron methyl). EPA has not classified any of the inerts as toxic. 

Picloram – The formulations Tordon K and Tordon 22K contain the following inerts: 

potassium hydroxide, ethoxylated cetyl ether, alkyl phenol glycol ether, and emulsified 

silicone oil (NCAP website; www.pesticide.org/FOIA/picloram.html). Potassium hydroxide 

is an approved food additive. The other compounds are all on EPA’s List 4B, inerts of 

minimal concern. They may also contain the surfactant polyglycol 26-2, which is on EPA’s 

List 3: Inerts of Unknown Toxicity, discussed in the following section. The toxicity data on 

the formulations encompasses toxic risk from the inerts. Inerts in picloram formulations do 

not appear to pose a unique toxic risk to wildlife (SERA, 2003-Picloram). 

Sethoxydim - The formulation Poast® contains 74 percent petroleum solvent that includes 

naphthalene. The EPA has placed this naphthalene on List 2 (“agents that are potentially 

toxic and a high priority for testing”). Petroleum solvents and naphthalene depress the 

central nervous system and cause other signs of neurotoxicity (SERA, 2001). Poast® has 

also been reported to cause skin and eye irritation. There is no information suggesting that 

the petroleum solvent has a substantial impact on the toxicity of sethoxydim to experimental 

animals, with the important and notable exception of aquatic animals (SERA, 2001). Poast® 

is much more toxic to aquatic species than sethoxydim. 

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Sulfometuron methyl - The identity of inerts used in Oust are confidential, but SERA 

reviewed them for preparation of the risk assessment (SERA, 2003-Sulfometuron). EPA has 
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not classified any of the inerts as toxic. Based on comparison of the toxicities of the active 

ingredient and the formulation, there is no reason to suspect that Oust contains other 

ingredients that substantially affect the potential risk to wildlife. 

Triclopyr - Formulations contain ethanol (Garlon 3A) or kerosene (Garlon 4), which are 

known to be neurotoxic. However, the toxicity of these compounds is less than that of 

triclopyr, so the amount of ethanol and kerosene in these formulations is not toxicologically 

significant (SERA, 2003-Triclopyr) for wildlife. 

2,4-D – There is no discussion of inert ingredients in the SERA risk assessment for 2,4-D. 

Identities of inerts contained in many formulations are available at the NCAP website 

(www.pesticide.org/FOIA/24d.html). Most inert ingredients identified are on EPA’s List 3 

or List 4 for inert ingredients and not identified as toxic. However, several formulations 

contain inerts that are on EPA’s List 2; Potentially Toxic Inerts, High Priority for Testing. 

List 2 inerts in some 2,4-D formulations include: 

• Antifoam 1400 (CAS # 1330-20-7) 

• Xylene (CAS # 1330-20-7) 

• Diethanolamine (CAS # 111-42-2) 

• Petroleum solvent (CAS # 64742-94-5) 

• Hydrogenated aliphatic solvent (CAS # 64742-47-8) 

• Butoxyethanol (CAS # 11-76-2) 

The amount of inert ingredients in the formulations is generally not known, so exposure and 

dose estimates cannot be calculated. Use of formulations containing toxic inert ingredients 

may increase the risk of toxic effects to wildlife above that, or in addition to, the risk 

discussed for the active ingredient. 

Surfactant Effects 

Surfactants, or surface-acting agents, facilitate and enhance the absorbing, emulsifying, 

dispersing, spreading, sticking, wetting, or penetrating properties of herbicides. There is a 

fair amount of research on the effects of surfactants to terrestrial and aquatic organisms 

because they are widely used in detergents, cosmetics, shampoos and other products designed 

for human exposure. 

The following information is taken from “Analysis of Issues Surrounding the Use of Spray 

Adjuvants With Herbicides” (USDA FS, 2002) and “Human and Ecological Risk Assessment 

of Nonylphenol Polyethoxylate-based (NPE) Surfactants in Forest Service Herbicide 

Applications” (USDA FS, 2003). Refer to these documents for more complete discussions. 

Some glyphosate formulations contain polyethoxylated tallow amine (POEA) surfactant, 

which is substantially more toxic to aquatic species than glyphosate or other surfactants that 

may be used with glyphosate (SERA, 2003-Glyphosate, p. 4-14). In the SERA risk 

assessment, the toxicity of glyphosate is characterized based on the use of a surfactant, 

either in the formulation or added as an adjuvant in a tank mixture (SERA, 2003-

Glyphosate, p. 4-14). 

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Polyglycol 26-2, used in picloram, will impact mitochondrial function in vitro, but 

information is insufficient to evaluate risks to wildlife in vivo from field applications at 

plausible levels of exposure (SERA, 2003-Picloram). 

The primary active ingredient in many of the non-ionic surfactants used by the Forest Service 

is a component known as nonylphenol polyethoxylate (NPE). NPE is found in these 

commercial surfactants at rates varying from 20 to 80 percent. NPE is formed through the 

combination of ethylene oxide with nonylphenol (NP), and may contain small amounts of unreacted NP. The properties of the particular NPE depend upon the number of ethoxylate 

groups that are attached to the NP. The most common NPE used in surfactants with 

pesticides is a mixture that has, as a majority, 8-10 ethoxylate groups attached, and can be 

abbreviated NP9E. NP is a material recognized as hazardous by the U.S. EPA (currently on 

U.S. EPA’s inerts List 1). Both NP and NPE exhibit estrogen-like properties, although they 

are much weaker than the natural estrogen, estradiol. 

Potential effects of NPE were analyzed using exposure scenarios to quantitatively estimate 

the dose of NPE that birds and mammals may receive if they consumed contaminated 

vegetation or prey, or if a small mammal was directly sprayed. Each estimated dose was 

compared to toxicity levels reported from laboratory data and summarized in USDA FS 

2003. Data is lacking on the toxic effects of NP or NPE to birds, with only the median lethal 

dose (LD50) identified in the literature. Risk to birds is therefore evaluated using the toxicity 

values from mammals, which introduces additional uncertainty into the conclusions 

regarding birds. Data for terrestrial invertebrates is lacking or insufficient, so risks cannot be 

adequately characterized. 

NP and NPE are weakly estrogenic in aquatic and terrestrial organisms (1000 to 100,000 

times weaker than natural estrogen). NP and NPE are not toxic to soil microbes. NP is 

highly toxic to many aquatic organisms at low concentrations (currently on U.S. EPA’s Inert 

List 1). 

The use of NPE-based surfactants in any of the 12 herbicides considered in this EIS could 

result in toxic effects to some mammals and birds at typical and high application rates 

(project file worksheets; USDA, FS 2003). The exposure scenarios and calculated doses 

used in the analysis represent worst-case scenarios and are not entirely plausible. At the 

typical application rate, adverse effects could occur to small mammals that may be directly 

sprayed, large mammals and large birds consuming contaminated vegetation, and small 

mammals and small birds consuming contaminated insects. At the highest application rate, 

adverse effects could occur to small mammals that may be directly sprayed, large or small 

mammals and large birds consuming contaminated vegetation, small mammals and small 

birds consuming contaminated insects, and a predatory bird consuming a small mammal that 

has been directly sprayed. No chronic exposures result in plausible risk to mammals or 

birds. 

8

NP and NPE have been studied for effects to aquatic organisms. NP is more toxic than 

NP9E, by one to three orders of magnitude (USDA FS, 2003). The toxicities of the 

intermediate breakdown products, NPEC and others, are intermediate between NP and NPE. 

In the aquatic environment, the breakdown products NP1EC and NP2EC are likely to be 
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present also. These two metabolites are known to affect vitellogenin (a precursor for egg 

yolk) production in male fish, but NP, which is a more potent estrogenic compound, did not 

cause vitellogenin increases in male Xenopus laevis, or leopard frogs (Selcer et al., 2001; 

cited in USDA FS, 2003). 

Mann and Bidwell (2000, 2001) tested several Australian frogs and Xenopus for effects to 

NP8E. They found that Xenopus was the most sensitive to toxic effects, with an LC50 of 3.9 

ppm (3.9 mg/L). Similar to studies with herbicides, the LC50 values for the frogs are 

comparable to those for fish (USDA FS, 2003). NP8E inhibited growth at concentrations as 

low as 1 ppm (Mann and Bidwell, 2000, 2001). Mild narcosis of tadpoles can occur at EC50

values as low as 2.3 ppm, and reduced dissolved oxygen content in the water lowered the 

EC50 values by about half as compared to normal oxygen levels. The tadpoles recovered 

from the narcosis. Malformations in Xenopus occurred at EC50 values between 2.8 and 4.6 

mg/L. 

NP may cause tail resorption with a 14-day NOEC of 25 ppb for Xenopus laevis (Fort and 

Stover, 1997; cited in USDA FS, 2003). NP also increased the percentage of female Xenopus

developing from tadpoles exposed to 22 ppb for 12 weeks, but did not produce this effect at 

2.2 ppb. 

During operational use of NPE surfactant, ambient levels of NP9E (including a small 

percentage of NP, NP1EC, and NP2EC) could average 12.5 ppb (range 3.1 to 31.2 ppb). The 

duration of these exposures from Forest Service use would generally be much shorter than 

those used in laboratory experiments, due to transport by flowing streams, dilution, and 

environmental degradation. These levels are not likely to adversely affect amphibians found 

in the Pacific Northwest for normal operations. However, overspray or accidental spills 

could produce concentrations of NP9E that could adversely affect amphibians, particularly in 

small stagnant ponds. 

Effects of Impurities 

All herbicides likely contain impurities as a result of the synthesis or production process. 

The toxic effects of impurities are addressed in toxicity tests using the technical grade 

product, which would contain the impurities. 

Hexachlorobenzene is an impurity in the technical grade products of clopyralid and picloram. 

Hexachlorobenzene is a ubiquitous and persistent chemical in the environment, as it is used 

or present in a wide variety of manufacturing processes. It has been shown to cause tumors 

in mice, rats and hamsters, and EPA has classified it as a probable human carcinogen (SERA, 

2003-Picloram). The amount of hexachlorobenzene released into the environment from 

Forest Service use of picloram and clopyralid is inconsequential in comparison to existing 

background levels and the annual release from manufacturing processes (SERA, 2003-

Picloram, pp. 3-25). The use of picloram and clopyralid in remote forest locations could 

constitute the primary source of localized contamination however. The projected amounts of 

hexachlorobenzene released during invasive plant treatments is calculated to be well below 

the level that poses a risk to cancer in mammals. 

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POEA surfactant used in Roundup and Roundup Pro contain 1,4-dioxane as an impurity, 

which has been classified by EPA as a probable human carcinogen. Based on current 

toxicity data and an analysis by Borrecco and Neisess (1991), the potential effects of 1,4-

dioxane are encompassed by the available toxicity data on the Roundup formulation (SERA, 

2003-Glyphosate). Borrecco and Neisess (1991) also demonstrated that the upper limit of 

risk of cancer from this impurity was less than one in a million. 

Triclopyr contains an impurity, 2- butoxyethanol (aka EGBE), that is a major industrial 

chemical used in a wide variety of industrial and commercial applications. It is known to 

cause fragile red blood cells in rodents (Borrecco and Neisess 1991). EGBE has been 

classified as moderately toxic by EPA. Borrecco and Neisess (1991) found that potential 

doses of EGBE to mammals were less than 0.001 of the lowest LD50 and did not substantially 

increase risk over the risk identified for triclopyr, even under worst case scenarios. Data on 

toxicity of EGBE to birds was lacking, but the authors conclude that comparative sensitivities 

between birds and mammals, and the extremely low doses indicated a low risk to birds. 

Metabolites 

Similar to impurities, the potential health effects of herbicide metabolites are often accounted 

for in the available toxicity studies, assuming that the toxicological effects of metabolism 

within the test animal species would be similar to those in other animals. The potential toxic 

effects of environmental metabolites (those formed as a result of processes outside of the 

body) may not be accounted for by laboratory toxicity studies. 

TCP (3,5,6-trichloro-2-pyridinol) is an environmental metabolite of triclopyr. In mammals, 

TCP has about the same toxicity as triclopyr. No quantitative estimate of exposure to 

mammals or birds was calculated in the SERA risk assessment, due to the lack of appropriate 

data. However, since TCP is as toxic as triclopyr, the risk characterization for triclopyr could 

be applied to TCP. 

Site-specific analysis is necessary to further evaluate the risk of toxic effects from TCP. 

Endocrine disruption 

Recent information has highlighted the potential for certain synthetic and natural chemicals 

to affect endocrine glands, hormones, and hormone receptors (endocrine system). The 

endocrine system helps control metabolism, body composition, growth and development, 

reproduction, and many other physiological regulators. An endocrine disrupter is a substance 

that may exert effects to the body by affecting the availability of a hormone to its target 

tissue(s) and/or affecting the response of target tissues to the hormone (SERA, 2002). 

Estrogen is a prominent hormone in animal systems and substances that mimic estrogen or 

stimulate similar responses in target tissues are referred to as “estrogenic.” 

10

Scientists have expressed concern regarding estrogenic effects of synthetic chemicals since 

before the 1970’s. The EPA (1997) reports effects of endocrine disruption in animals that 

“include abnormal thyroid function and development in fish and birds; decreased fertility in 

shellfish, fish, birds, and mammals; decreased hatching success in fish, birds, and reptiles; 

demasculinization and feminization of fish, birds, reptiles, and mammals; defeminization and 
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masculinization of gastropods, fish, and birds; decreased offspring survival; and alteration of 

immune and behavioral function in birds and mammals.” 

Some of the more noted endocrine glands include gonads, adrenal, pancreas, thyroid and 

pituitary. Alteration in endocrine function may affect reproductive output (i.e. feminization, 

masculization), and therefore, could affect population numbers of affected species. 

Many of the known endocrine disrupting contaminants have been banned or are regulated 

(e.g. DDT/DDE, PCB, TCDD). Some endocrine disrupting compounds are persistent and are 

still found within the living tissue of wildlife; their decomposition half-life is lengthy, and 

they are bioaccumulatory and present at high background levels. A local example is the high 

level of DDT/DDE and PCB that are found within peregrine falcons in the Pacific Northwest 

(Pagel, unpub. data). Research has suggested that embryonic exposure to endocrine 

disrupters may cause permanent health effects to adult animals. Some of these effects may 

include altered blood hormone levels, reduced fecundity, reproductive behavioral alterations, 

reduced immune function, masculization and feminization, undescended testicles, increased 

cancer rates, altered bone density and structure, and malformed fallopian female reproductive 

tract (Kubiak et al., 1989; Colborn and Clement, 1992; White et al., 1994; Fry, 1995; 

LeBlanc, 1995). Examples of wildlife species that have been adversely affected by 

endocrine disrupters include wood ducks in Arkansas, wasting and embryonic deformities of 

Great Lakes piscivorous birds, reproductive abnormalities of snapping turtles, gulls, trout and 

salmonids, alligators, mink, and Florida panther (Bishop et al. 1991, Colborn, 1991; 

Facemire et al., 1995; Fox et al., 1978, 1981, 1991 (a, b); Fry and Toone, 1981; Fry et al., 

1987; Giesyet et al., 1994; Gilbertson et al., 1991; Guillette et al., 1994, 1995; Kubiak et al., 

1989; Mac and Edsall, 1991, 1993; Leatherland, 1993; Peakall and Fox, 1987; White and 

Hoffman, 1995; and Wren, 1991). 

Of the chemicals analyzed in this DEIS, 2,4-D and NPE surfactants have been identified as 

potentially having estrogenic effects (USGS, 1998; Bakke, 2003). Triclopyr and glyphosate 

have been evaluated for endocrine disrupting effects, and the weight of evidence indicates 

that these herbicides cause no specific toxic effects on endocrine function (SERA, 2002). 

One study on glyphosate, Yousef et al. (1995), indicated that there may be some concerns 

with glyphosate, but the study was poorly conducted and results are not reliable. 

Sulfometuron methyl can cause malformations in amphibians (SERA, 2003-Sulfometuron), 

but whether the malformations are caused by endocrine disruption, cellular toxicity, or other 

pathway has not been reported. 

Synergistic Effects 

Certain chemicals may cause synergistic effects in the presence of other chemicals: that is, 

the total effect of two chemicals may be greater than that suggested by the sum of the effects 

from the individual components (USEPA, 2000). However, information regarding the 

existence or potential for synergistic effects from the herbicides discussed in this document is 

very limited. 

11

Some of the herbicides analyzed in this document (e.g. 2,4-D and picloram) have been 

investigated for possible synergistic effects but the study designs were insufficient for the 

assessment of toxicologic interactions (SERA, 2003-Picloram; p. 3-35) However, data on 

this potential effect is incomplete and not likely to be obtained in the foreseeable future: the 
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

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sheer number of potential combinations of contaminants, environmental stressors, and 

wildlife species make it unfeasible to investigate thoroughly. 

USEPA (2000) did state that for exposures at low doses, with low risk for each component in 

the chemical mixture, that the likelihood of significant interaction (e.g. synergistic effects) is 

usually considered to be low. Likewise, a report by ATSDR (2004) cited several studies 

using rats that found no synergistic effects for mixtures of four, eight and nine chemicals at 

low (sub-toxic) doses. But statistically significant interactions (both syntergistic and 

antagonistic) have been noted in some studies. Unfortunately, even with excellent data, the 

uncertainties and complexities of chemical interactions create substantial uncertainty in the 

risk characterization for chemical mixtures (ATSDR, 2004; USEPA, 2000). 

Effects of Active Ingredients and Surrogate Species

Generally, active ingredients have been tested on only a limited number of species and 

mostly under laboratory conditions. While laboratory experiments can be used to determine 

acute toxicity and effects to reproduction, cancer rates, birth defect rates, and other effects 

that must be considered, laboratory experiments do not account for wildlife in their natural 

environments. This leads to uncertainty in the risk assessment analysis. Environmental 

stressors can increase the adverse effects of contaminants, but the degree to which these 

effects may occur for various herbicides is largely unknown. Adverse affects to wildlife 

health such as lethargy, weight loss, nausea, and fluid loss due to diarrhea or vomiting, can 

affect their ability to compete for food, locate and/or capture food, avoid or fight off 

predators, or reproduce. The following analysis relies on these types of effects, when 

sufficient data exists, rather than lethal doses, to determine the potential for doses to cause an 

“adverse effect” to wildlife. 

FS/SERA risk assessments and published literature are the primary sources of information 

used to evaluate effects of herbicides to wildlife. First, we discuss field studies found in the 

published literature regarding potential effects of herbicide use to wildlife. Then, qualitative 

and quantitative information from the FS/SERA risk assessments and published literature 

regarding effects of active ingredients are discussed. 

Toxicity Data and Exposure Analysis 

The FS/SERA risk assessments present the toxicity data from studies conducted to meet EPA 

registration requirements and from published literature. In addition, exposure of various 

animals to herbicide is quantitatively estimated to characterize risk from the use of each 

herbicide. 

The Use of Surrogate Species

Most toxicity testing utilizes surrogate species. Surrogate species serve as a substitute for the 

species of interest, because all species of interest could not be tested. Surrogate species are 

typically organisms that are easily tested using standardized methods, are readily available, 

and inexpensive. Rare species are not tested and the physiological requirements for some 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

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organisms prohibit their use in toxicity testing because these requirements cannot be met 

within the test system. Even when desired species are available (e.g. salmon), researchers 

may choose a surrogate, like zebrafish (Danio rerio)(aka zebra danio), because test results 

are more easily discerned with the surrogate, and reproductive capacity allows testing of 

large numbers of individuals, among other reasons (Scholz, unpublished. proposal, 2003). 

However, caution should to be taken when addressing ecological risk and the use of 

surrogates when analyzing those ecological risks. Some herbicides demonstrate more 

variation than others in effects among different species, and very limited numbers of species 

have been tested. 

Because of the variation of responses among species, and the uncertainty with regard to how 

accurately a surrogate species may represent other wildlife, the FS/SERA risk assessments 

use the most sensitive endpoint from the most sensitive species tested as the toxicity index 

for terrestrial wildlife. This does not alleviate concerns over interspecies variations in 

response, however. 

Doses and Responses

The likelihood that an animal will experience adverse effects from an herbicide depends on: 

(1) the inherent toxicity of the chemical, (2) the amount of chemical to which an animal is 

exposed, (3) the amount of chemical actually received by the animal (dose), and (4) the 

inherent sensitivity of the animal to the chemical. 

The toxicity of the chemical is measured by laboratory tests required by EPA. The amount 

of chemical to which an animal may be exposed is influenced by several factors, discussed 

below. When an animal is exposed to a chemical, only a portion of the chemical applied or 

ingested is actually absorbed or taken in by the animal (the dose). Various absorption rates 

for wildlife are not available, so some scenarios use the same value for exposure and dose. 

Also, different species have different susceptibilities to various chemicals. This is discussed 

more in the section on surrogates. 

Factors that Influence Exposure and Dose 

The exposure of an animal to an herbicide is greatly influenced by relationships between 

body size and several physiological, metabolic, and pharmacological processes (allometry). 

For example, allometric relationship dictates that animals of smaller size have a larger 

amount of surface area for their mass than larger animals. This relationship greatly 

influences basic physiological properties, such as food consumption and thermoregulation. 

Some of the allometric factors that influence exposure to herbicides are detailed below. 

Body Weight 

Several parameters used to estimate herbicide contact are reported on a “per body weight” 

basis, expressed in grams (g) or kilograms (kg). For example, both food and water ingestion 

rates are reported on a per body weight basis (such as gram of fresh food or water per gram 

of fresh body weight per day). Body weights, in units of mass, are reported as fresh weight 

that might be obtained by weighing a live animal in the field. Also, body weight data are 

used in empirical models to calculate some parameters, such as surface area, when there no 

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specific measurements are available. Calculations of “potential dose to animal” use body 

weight of animals. 

Metabolic Rate 

Metabolic rate is not directly calculated in this document, or in the FS/SERA risk 

assessments, but reported values for various species are used to calculate food consumption 

requirements. It is reported on the basis of kilocalories per day for units of body weight 

(kcal/kg/day). Metabolic rate is closely related to body size, with smaller animals generally 

having higher metabolic rates than larger animals. 

Contact Rate 

Exposure involves direct contact with the herbicide, and wildlife may be exposed to 

herbicides by ingesting the chemical (oral) or by external contact (dermal). Oral exposures 

may occur from eating contaminated vegetation or prey, drinking contaminated water, or by 

grooming activities. Dermal exposures may occur from direct spray, or contact with 

contaminated vegetation or water. These contact routes are influenced by allometric 

relationships, as well as habitat preferences and feeding behaviors. 

Oral Routes

Food ingestion: Small animals generally have higher caloric requirements than large 

animals, so a small animal ingests a greater amount of food per unit body weight compared 

to large animals. A 20g mouse, for example, will generally consume an amount of food 

equal to about 15 percent of its body weight every day, depending on calorie content of the 

diet. A value of 3.6 g of food consumed per day for a 20g mouse is used in the FS/SERA 

risk assessments for calculating exposure from contaminated food. This is equivalent to 18 

percent of the body weight and is generated from general allometric relationships for food 

consumption in rodents (US EPA/ORD, 1993, p. 3-6, as cited in SERA, 2003-Glyphosate). 

This value may underestimate exposure to small mammals that consume primarily 

vegetation, rather than seeds (SERA, 2003a). Food consumption is calculated from caloric 

requirements for different sized animals for the various exposure scenarios in the FS/SERA 

risk assessments. 

Dietary composition: Dietary composition is an important consideration in exposure 

assessments because different foods have varying herbicide residues. Grasses may have 

substantially higher residues than fruits or other vegetation (Kenaga, 1973; Fletcher et al. 

1994; Pfleeger et al., 1996). The FS/SERA risk assessments use data from Siltanen et al. 

(1981) for concentrations on fruit. Also, small insects may contain higher residues than large 

insects, based on empirical relationships (Pfleeger et al., 1996). Some herbicides have the 

potential to bioaccumulate in fish; therefore fish-eating birds may be exposed. Caloric 

content of various foods, with caloric requirements of animals, is used to estimate daily 

amount of food consumed based on data from US EPA/ORD 1993 (as cited in SERA, 2003-

Glyphosate). In the FS/SERA risk assessments, exposure scenarios use a large herbivore 

consuming 100 percent grass diet, a large bird consuming grass, a small bird consuming 

small insects, and a predatory bird consuming contaminated fish (SERA, 2003-Glyphosate, 

p. 4-14 to 4-15). 

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Water ingestion: There are well-established relationships between body weight and water 

consumption across a wide range of mammalian species. Mice, weighing about 20 g (0.02 

kg) consume about 0.005 L of water/day (i.e. 0.25 L/kg/day). These values are used in the 

exposure scenarios for small mammals. Since the body size to volume relationship dictates 

that smaller animals will receive larger doses for a given exposure, consumption of 

contaminated water is not calculated for larger animals. Water ingestion is obviously 

influenced by environmental factors, such as heat and availability. But estimates for the 

variability in water consumption are not available for wildlife. 

Grooming: Birds and mammals may spend a great deal of time grooming fur or feathers. If 

the animal has been exposed to herbicide, some chemical may be absorbed through the 

grooming process. However, a study by Gaines (1969, as cited in SERA, 2001) suggests that 

grooming is not significant in the toxic response of small mammals. At any rate, the doses 

received from grooming would be less than those received through contaminated food or 

direct spray, given the assumptions in the exposure scenarios. See dermal exposure route 

information below. 

Dermal Route

Dermal contact can occur from direct spray or contact with contaminated vegetation or water. 

Since only a small portion of an applied herbicide would be available as dislodgeable residue 

on vegetation, or in a water body where it was diluted, dermal exposure is modeled only for 

direct spray scenarios in FS/SERA risk assessments. The extent of dermal contact for an 

animal depends on the application rate of the herbicide, the surface area of the animal, and 

the rate of absorption. Since a larger proportion of a small animal’s body would be involved, 

relative to larger animals, direct spray scenarios are only conducted for a small mammal and 

a honeybee in FS/SERA risk assessment (SERA, 2001). Skin, fur and feathers provide some 

protection from chemicals, and not all of the chemical on an animal will be absorbed. 

Amphibians may be an exception, since their skin may be much more permeable than the 

skin of a mammal or bird. In this document, we assume that the skin affords no protection at 

all (e.g., 100 percent absorption). Scenarios with a different assumption regarding absorption 

may be found in the various FS/SERA risk assessments. The approach taken here (100 

percent absorption) may account for multiple absorption pathways, such as dermal absorption 

plus that from grooming or preening. However, there is no quantitative data available 

regarding this assumption. The actual dose received after dermal exposure is also influenced 

by the specific herbicide considered since different herbicides have different dermal 

absorption rates and properties (SERA, 2001, section 3.9). 

Summary of Exposure Scenarios 

An exposure scenario was developed, and a quantitative estimate of dose received by the 

animal type in the scenario was calculated when enough data was available (SERA, 2001). 

While it is possible to model exposure in a very large number of non-target animals, highly 

species-specific exposure assessments are of little use in the absence of species specific doseresponse data (SERA, 2001). The exposure assessment should not be more complicated than 

the dose-response assessment. Therefore, exposure scenarios used in this document are 

calculated when dose-response data for specific herbicides indicate that one group and/or size 

of animal may be more sensitive than others. For example, if data indicates that larger 

mammals may be more sensitive than smaller mammals, separate exposure scenarios have 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

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been developed for each. In the absence of such data, only exposures for small mammals 

may be calculated because they would receive the highest dose per kg body weight. 

The exposure scenarios that are used in the Ecological Risk Assessments (SERA, 2001) 

and/or for this EIS (project file worksheets) are as follows: 

Acute Exposures 

20 g mammal: A mouse-sized mammal is directly sprayed over 50 percent of body surface 

area and 100 percent absorption occurs over one day. A “mouse” consumes contaminated 

vegetation, daily food consumption equal to 18 percent of body weight (a value between seed 

diet and vegetation diet needs), and one day’s diet is 100 percent contaminated. A “mouse” 

consumes contaminated insects, daily food consumption equals 50 percent of body weight, 

and one day’s diet is 100 percent contaminated. A “mouse” consumes contaminated water 

(volume water consumed is based on allometric relationship) after spill of 200 gallons into a 

small pond (with no dissipation or degradation of the herbicide). 

5 kg mammal: A fox-sized animal consumes small mammal prey that has been contaminated 

by direct spray. Daily food consumption equals 8 percent of body weight. 

70 kg mammal: A deer-sized animal consumes contaminated grass (grass has higher 

herbicide residues), daily food consumption is 14.16 kg/day (equal to 20 percent of body 

weight), and one day’s diet is 100 percent contaminated. 

4 kg bird: A goose-sized bird consumes contaminated grass and one day’s diet is 100 percent 

contaminated. 

10 g bird: A small, passerine-sized bird consumes contaminated small insects and one day’s 

diet is 100 percent contaminated. 

Predatory bird: A bird-of-prey consumes fish that has been contaminated by an accidental 

spill of 200 gal into a small pond. Assumptions used include no dissipation of herbicide, 

bioconcentration is equilibrium with water, contaminant level in whole fish is used, and 

upper estimate assumes 15 percent of body weight eaten/day. A spotted-owl sized bird 

consumes small mammal prey that has been contaminated by direct spray. 

Terrestrial invertebrate: A honeybee (0.093g) is directly sprayed and 100 percent absorption 

occurs over one day. 

Chronic Exposures 

20 g mammal: A mouse-sized mammal consumes contaminated vegetation for 90 days 

(upper estimate assumes 20 percent of diet is contaminated), and the herbicide dissipates over 

time. A “mouse” consumes contaminated ambient water for an extended period. 

70 kg mammal: A deer-sized mammal consumes contaminated grass for 90 days (upper 

estimate assumes 100 percent of diet is contaminated), and the herbicide dissipates over time. 

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4kg bird: A goose-sized bird consumes contaminated grass for 90 days (upper estimate 

assumes 100 percent of diet is contaminated), and herbicide dissipates over time. 

Predatory bird: A bird-of-prey consumes fish from contaminated water over a lifetime. 

Assumptions used include dissipation and degradation of herbicide is considered, 

bioconcentration is equilibrium with water, contaminant level in whole fish is used, and 

upper estimate assumes 15 percent of body weight eaten/day. 

No data are available to estimate chronic exposures from contaminated insects or mammal 

prey, so risk from chronic exposure is estimated using the acute dose compared to the chronic 

toxicity index. 

In this document, only the highest ranges of exposure assumptions are included, although a 

more complete range of possible values is included in the SERA risk assessments. For 

example, for a given herbicide, residues of the herbicide on vegetation that are reported in the 

literature will vary between studies and by vegetation type. A range of residue rates is used 

in the SERA risk assessment worksheets, but only the highest reported rates are used in the 

data reported here. Only the highest values are used here to reduce length and complexity of 

this document and also to present a reasonable “worst-case” exposure analysis. 

Estimated doses from the above exposure scenarios are compared to toxicity levels from 

laboratory research. The lowest reported dose that caused the most sensitive effect in the 

most sensitive species is used in this analysis to indicate the potential for an adverse effect 

when that dose is exceeded. These doses are referred to as “toxicity indices” in this 

document, and NOAEL’s are used whenever possible. If available data have not identified a 

NOAEL, then an LD50 or other level may be used. Table 3 lists the toxicity indices for 

mammals and Table 4 lists the toxicity indices for birds. 

Following the tables are summaries of herbicide effects to birds and mammals, reptiles, 

amphibians, and terrestrial invertebrates based on the results of the analysis and information 

in the literature. The likelihood that potential adverse effects would occur is then discussed 

followed by a brief summary of some of the available field studies. The document concludes 

with detailed descriptions of the exposure scenario results for each scenario and herbicide. 

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Table 3. Toxicity indices for mammals used in the effects analysis. Indices represent 

the most sensitive endpoint from the most sensitive species for which adequate data 

are available.

Herbicide Duration Endpoint Dose Species Effect Noted at 

LOAEL 

Chlorsulfuron Acute NOAEL 75 mg/kg Rabbit Decreased weight 

gain at 200 mg/kg 

Chronic NOAEL 5 mg/kg/day Rat Weight changes at 25 

mg/kg/day 

Clopyralid Acute NOAEL 75 mg/kg Rat Decreased weight 

gain at 250 mg/kg 

Chronic NOAEL 15 mg/kg/day Rat Thickening of gastric 

epithelium at 150 

mg/kg/day 

Dicamba Acute – 

larger 

mammal 

NOAEL 3 mg/kg Rabbit Weight loss, increased 

post-implant losses, 

decreased number of 

live young at 10 mg/kg 

Acute – 

smaller 

mammal 

NOAEL1 30 mg/kg Rat Neurotoxic effects 

(e.g. impaired gait) at 

300 mg/kg 

Chronic – 

all sizes 

NOAEL 3 mg/kg/day Rabbit Weight loss, increased 

post-implant losses, 

decreased number of 

live young at 10 mg/kg 

Glyphosate Acute NOAEL 175 mg/kg Rabbit Diarrhea at 350 mg/kg 

Chronic NOAEL 175 mg/kg/day Rabbit Diarrhea at 350 mg/kg 

Imazapic Acute NOAEL 350 mg/kg Rabbit Decreased body 

weight at 500 mg/kg 

Chronic NOAEL2 45 mg/kg Dog Microscopic muscle 

effects at 137 mg/kg 

Imazapyr Acute NOAEL 250 mg/kg Dog No effects at highest 

doses tested 

Chronic NOAEL 250 mg/kg/day Dog No effects at highest 

doses tested 

Metsulfuron 

methyl 

Acute NOAEL3 25 mg/kg Rat Decreased weight 

gain at 500 mg/kg 

Chronic NOAEL 25 mg/kg/day Rat Decreased weight 

gain at 125 mg/kg 

Picloram Acute NOAEL 34 mg/kg Rabbit Decreased weight 

gain at 172 mg/kg 

Chronic NOAEL 7 mg/kg Dog Increased liver weight 

at 35 mg/kg4

Sethoxydim Acute NOAEL 160 mg/kg5 Rabbit Reduced number of 

viable fetuses, some 

dam mortality at 480 

mg/kg 

Chronic NOAEL 9 mg/kg/day Dog Mild anemia at 18 

mg/kg/day 

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Table 3. Toxicity indices for mammals used in the effects analysis. Indices represent 

the most sensitive endpoint from the most sensitive species for which adequate data 

are available.

Herbicide Duration Endpoint Dose Species Effect Noted at 

LOAEL 

Sulfometuron 

methyl 

Acute NOAEL 87 mg/kg Rat Decreased body 

weight at 433 mg/kg 

Chronic NOAEL 2 mg/kg/day Rat Effects on blood and 

bile ducts at 20 

mg/kg/day 

Triclopyr6 Acute NOAEL 100 mg/kg Rat Malformed fetuses at 

300 mg/kg 

Chronic7 NOAEL 0.5 mg/kg/day Dog Effect on kidney at 2.5 

mg/kg/day 

2,4-D Acute “nonlethal” 10 mg/kg Rat & 

Dog 

Effects on kidney, 

blood, and liver 

Chronic NOAEL 1 mg/kg/day Rat & 

Dog 

Effects on kidney, 

blood, and liver at 5 

mg/kg/day 

NPE 

Surfactants 

Acute NOAEL 10 mg/kg Rat Slight reduction of 

polysaccharides in 

liver at 50 mg/kg/day 

Chronic NOAEL 10 mg/kg/day Rat Increased weights of 

liver, kidneys, ovaries, 

and decreased live 

pups at 50 mg/kg/day 

1 Small animals are less susceptible than larger animals. NOAEL estimated from LOAEL of 300 

mg/kg/day for neurotoxic effects, using safety factor of 10 to extrapolate from a LOAEL to a NOAEL. 

Identical to observed NOAEL for neurotoxicity in rabbits (Hoberman 1992). 

2 Imazapic – NOAEL calculated from a LOAEL of 137 mg/kg/day and application of a safety factor of 3 to 

extrapolate from a LOAEL to a NOAEL. 

3 The acute NOAEL of 24 mg/kg is very close to the chronic NOAEL, so chronic value is used for acute 

exposures as well. 

4 USEPA/OPP 1998 

5 Source of the value used by EPA (180 mg/kg) is not well documented, so the lower value of 160 mg/kg 

from a rabbit study is used as the toxicity index for this analysis (BASF 1980, MRID 00045864 cited in 

SERA, 2003-Triclopyr). 

6 Triclopyr BEE and TEA have equal toxicities to mammals (SERA, 2003a). 

7 Value taken from Quast et al. 1976 as cited in SERA Triclopyr 2003. This represents an extremely 

conservative approach, explained in more detail in the write up on triclopyr later in this document. 

Source: SERA 1998, 2001, 2003, 2004 and USDA FS 2003.

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Table 4. Toxicity indices for birds used in the effects analysis. Indices represent 

the most sensitive endpoint from the most sensitive species for which adequate 

data are available.

Herbicide Duration Endpoint Dose Species Effects Noted at 

LOAEL 

Chlorsulfuron Acute NOAEL 1686 mg/kg Quail No significant effects at 

highest dose 

Chronic NOAEL 140 

mg/kg/day 

Quail No significant effects at 

highest dose 

Clopyralid Acute NOAEL 670 mg/kg Mallard & 

Quail 

No signs of toxicity 

reported, LOAEL not 

determined 

Chronic1 NOAEL 15 

mg/kg/day 

Rat Thickening of gastric 

epithelium at 150 

mg/kg/day 

Dicamba Acute NOAEL 13.6 mg/kg Quail Neurotoxic effects at 27 

mg/kg/day 

Chronic NOAEL 13.6 

mg/kg/day2

Quail Neurotoxic effects at 27 

mg/kg/day 

Glyphosate Acute NOAEL 562 mg/kg Mallard & 

Quail 

No effects at highest 

dose 

Chronic NOAEL 100 mg/kg Mallard & 

Quail 

No effects on 

reproduction at highest 

dose 

Imazapic Acute NOAEL 1100 mg/kg Quail No effects at highest 

dose 

Chronic NOAEL 113 

mg/kg/day 

Quail Decreased weight gain 

in chicks at 170 

mg/kg/day 

Imazapyr Acute NOAEL 674 mg/kg Quail No effects at highest 

dose 

Chronic NOAEL 200 

mg/kg/day 

Mallard & 

Quail 

No effects at highest 

dose 

Metsulfuron 

methyl 

Acute NOAEL 1043 mg/kg Quail No significant effects at 

highest dose 

Chronic NOAEL 120 

mg/kg/day 

Mallard & 

Quail 

No significant effects at 

highest dose 

Picloram Acute NOAEL 1500 mg/kg Chicken 

& 

pheasant 

No effect to 

reproduction. LOAEL 

not reported 

Chronic3 NOAEL 7 mg/kg/day Dog Increased liver weight 

at 35 mg/kg/day 

Sethoxydim Acute NOAEL >500 mg/kg Mallard & 

Quail 

No or low mortality at 

highest doses tested. 

LOAEL not available. 

Chronic LOAEL4 10 

mg/kg/day 

Mallard Decreased number of 

normal hatchlings at 10 

mg/kg/day 

Sulfometuron Acute NOAEL 312 mg/kg Mallard Decreased weight gain 

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Table 4. Toxicity indices for birds used in the effects analysis. Indices represent 

the most sensitive endpoint from the most sensitive species for which adequate 

data are available.

Herbicide Duration Endpoint Dose Species Effects Noted at 

LOAEL 

methyl at 625 mg/kg/day 

Chronic5 NOAEL 2 mg/kg/day Rat Effects on blood and 

bile ducts at 20 

mg/kg/day 

Triclopyr 

BEE6

Acute LD50 388 mg/kg Quail 50% mortality at 388 

mg/kg 

Chronic NOAEL 10 

mg/kg/day 

Mallard & 

quail 

Decreased survival of 

offspring, reduced 

eggshell thickness at 

20 mg/kg/day 

Triclopyr 

TEA 

Acute LD50 535 mg/kg Quail 50% mortality at 535 

mg/kg 

Chronic NOAEL 10 

mg/kg/day 

Mallard & 

Quail 

Decreased survival of 

offspring, reduced 

eggshell thickness at 

20 mg/kg/day 

2,4-D Acute LD50 562 mg/kg7 Mallard & 

Quail 

50% mortality at 562 

mg/kg 

Chronic7 NOAEL 1 mg/kg/day Rat & 

dog 

Effects on kidney, 

blood, and liver at 5 

mg/kg/day 

NPE 

Surfactants9

Acute NOAEL 10 mg/kg Rat Slight reduction of 

polysaccharides in liver 

at 50 mg/kg/day 

Chronic NOAEL 10 

mg/kg/day 

Rat Increased weights of 

liver, kidneys, ovaries, 

and decreased live 

pups at 50 mg/kg/day 

1 Chronic toxicity studies in birds are not available, so the value from mammal studies is used. 

2 Higher reported NOAEL for chronic dietary exposure is 92 mg/kg/day, with no signs of neurotoxicity. 

The lower value from acute exposures is used in FS/SERA risk assessment for chronic exposures as a 

more protective toxicity index. 

3 Chronic toxicity studies in birds are not available, so the value from mammal studies is used. 

4 Based on one study in which a NOAEL was not determined, so the LOAEL is used. 

5 Birds may be somewhat less sensitive than mammals, but data are limited, so the lower value from 

mammal studies is used. 

6 Unlike in mammals, the toxicities of triclopyr BEE and triclopyr TEA are different for birds, so the 

indices of the two forms of triclopyr are presented separately 

7 Weed Science Society of America 2002. 

8 No chronic toxicity data for birds is available; so the mammal chronic value is used. Acute toxicity of 

2,4-D to mammals is somewhat lower than it is for birds. 

9 Data on birds is not available in published literature. This information from an unpublished study 

referred to in USDA FS 2003. Since information is lacking, this value is used for illustrative purposes 

only and no attempt is made to quantify risk to birds from NPE surfactants. 

Source: SERA 1998, 2001, 2003, 2004; USDA FS 2003; and Weed Science Society of America 2002.

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Summary of Herbicide Effects to Birds and Mammals

The data available for mammals are derived from numerous studies conducted to meet 

registration requirements, and primarily on laboratory animals that serve as surrogates. Data 

for mammals are available for more types of toxicity tests and often on a wider variety of 

species than are available for birds. 

Availability of information on the direct toxicological effects of the 12 herbicides on wild 

mammals varies by herbicide. Glyphosate and 2,4-D have been widely studied, including 

field applications. Little or no data on wildlife may exist for other herbicides. Herbicides 

have been tested on only a limited number of species under conditions that may not wellrepresent populations of free-ranging animals (SERA 1998, 2001, 2003). 

Toxicity data available for birds are derived from studies conducted to meet registration 

requirements, and primarily on domestic birds that serve as surrogates. There are typically 

fewer types of toxicity studies conducted on birds using a more restricted variety of species 

than are conducted for mammals. Almost all laboratory data is collected on mallards and 

northern bobwhite. How the sensitivities of different bird species to herbicides may vary 

from that reported for mallard and bobwhite is not known. 

Tables 5 and 6 summarize the results of exposure scenarios for the 12 herbicides and NPE 

surfactants considered in this analysis. Chlorsulfuron, imazapic, imazapyr, and metsulfuron 

methyl do not appear to pose any plausible risk to terrestrial wildlife or bees at either the 

typical or highest application rates. When an herbicide does pose plausible risk, it is 

consistently insectivorous and grass-eating animals that are most likely to receive doses 

above the toxicity index. Direct spray of mammals is a concern only for 2,4-D, and NPE 

surfactants at the typical application rate, and additionally, dicamba at the highest application 

rate. Fish-eating birds do not receive a dose above the toxicity index for any herbicide or 

application rate. Consumption of contaminated water, even as the result of an accidental 

spill, results in doses well below the toxicity index for all herbicides. For the herbicides 

considered in this analysis, birds are less sensitive than mammals to acute exposures. 

Chronic toxicity data on birds is often limited. 

Dicamba, triclopyr, and 2,4-D have the highest potential to adversely affect wildlife. 

Dicamba has a relatively low acute toxicity to adult animals, in terms of direct lethal doses, 

but adverse effects on reproduction and nervous systems occur at much lower doses. 

Dicamba shows a consistent pattern of increased toxicity to larger sized animals, across 

several species and animal types (i.e. birds and mammals). Dicamba exposures exceed the 

toxicity indices for five scenarios at the typical application rate, and nine scenarios at the 

highest application rate. 

22

Triclopyr TEA and BEE are somewhat more toxic to birds than triclopyr acid. The toxicities 

of these compounds to mammals show no remarkable differences. Triclopyr can be acutely 

lethal only at very high doses. However, indications of adverse effects to the kidney can 

occur at very low doses, at least in dogs. These adverse effects are indicated by increases in 

blood urea nitrogen and creatinine in dogs, but no histopathological changes to the kidneys 
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

were found. Triclopyr exposures exceed the toxicity indices for eight scenarios at the typical 

application rate, and 12 scenarios at the highest application rate. 

2,4-D also has a relatively low acute toxicity to mammals in terms of direct lethal doses, but 

signs of adverse effects to the nervous system or internal organs may occur at very low 

doses. 2,4-D shows a consistent pattern of increased toxicity to larger sized animals. Birds 

appear somewhat less sensitive than mammals to acute toxic effects. The toxicity indices for 

2,4-D in the risk assessment (SERA, 1998) are inconsistent with the most sensitive effects 

reported for mammals (SERA, 1998, p. 3-52). Relying on the most sensitive effects 

reported, 2,4-D use may produce exposures that can have adverse effects to terrestrial 

wildlife in 15 scenarios at the typical application rate, and 16 scenarios at the highest 

application rate. 

Glyphosate, applied at the typical application rate has little potential to adversely affect birds 

or mammals. An exception might be insectivorous birds that experience chronic exposures. 

There are no data available on the persistence or degradation of glyphosate residue on 

insects, so the acute dose is compared to the chronic toxicity index. This is an extremely 

protective approach and may greatly overestimate risk. However, it is worth noting so that 

appropriate protective measures may be taken when using glyphosate in the habitat of 

insectivorous birds. At the highest application rate, glyphosate has the potential to adversely 

affect large grass-eating mammals, and insectivorous birds and mammals in acute and 

chronic exposures. Additionally, grass-eating birds may be adversely affected in a chronic 

exposure. In total, glyphosate exposures exceed the toxicity indices for one scenario at the 

typical application rate, and eight exposures at the highest application rate. 

Clopyralid, applied at the typical application rate has little potential to adversely affect birds 

or mammals, except for insectivorous birds and mammals. There are no data available on the 

persistence or degradation of clopyralid residue on insects, so the acute dose is compared to 

the chronic toxicity index. This is an extremely protective approach and may greatly 

overestimate risk. However, it is worth noting so that appropriate protective measures may 

be taken when using clopyralid in the habitat of insectivorous birds and mammals. At the 

highest application rate, clopyralid may adversely affect grass-eating birds, insectivorous 

birds and mammals and predatory birds eating small mammal prey for chronic exposures. 

The same qualification for chronic exposure to insectivorous animals applies to predatory 

birds, in that the acute dose is compared to the chronic toxicity index. No acute exposures 

exceed the toxicity indices. In total, clopyralid exposures exceed the toxicity indices for one 

exposure at the typical application rate, and four at the highest application rate. 

The actual likelihood of exposing specific bird or mammal species depends on the 

application method, size of treatment area, habitat treated, and season of application, and 

must be analyzed at the site-specific level. 

23
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DRAFT 

Table 5. Exposure scenario results from FS/SERA risk assessments for mammals, 

birds, and honeybees using the typical application rate and upper residue rates. 

Symbol meanings are as follows: 

-- Exposure scenario results in a dose below the toxicity index. 

1 Exposure scenario results in a dose that exceeds the toxicity index.

Animal/ 

Scenario 

Chlorsulfuron Clopyralid Dicamba Glyphosate Imazapic Imazapyr Metsulfuron methyl Picloram Sethoxydim Sulfometuron methyl Tirclopyr 2,4-D NPE Surfactant 

ACUTE 

EXPOSURES 

Direct spray, bee -- -- -- -- -- -- -- -- -- -- -- 1

Direct spray, sm. 

mammal -- -- --* -- -- -- -- -- -- -- -- 1 1

Consume 

contaminated 

vegetation 

small mammal -- -- -- -- -- -- -- -- -- -- -- 1 -- 

large mammal -- -- 1 -- -- -- -- -- -- -- -- 1 1

large bird -- -- 1 -- -- -- -- -- -- -- 1 1 1

Consume 

contam. water 

Spill, sm. 

mammal -- -- -- -- -- -- -- -- -- -- -- 1 -- 

Consume 

contam. insects 

small mammal -- -- -- -- -- -- -- -- -- -- -- 1 1

small bird -- -- 1 -- -- -- -- -- -- -- 1 1 1

Consume 

contam. prey 

carnivore (sm. 

mammal) -- -- -- -- -- -- -- -- -- -- -- 1 -- 

predatory bird 

(sm. mammal) -- -- -- -- -- -- -- -- -- -- -- -- -- 

predatory bird 

(fish) -- -- -- -- -- -- -- -- -- -- -- -- -- 

CHRONIC 

EXPOSURES 

24
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Table 5. Exposure scenario results from FS/SERA risk assessments for mammals, 

birds, and honeybees using the typical application rate and upper residue rates. 

Symbol meanings are as follows: 

-- Exposure scenario results in a dose below the toxicity index. 

1 Exposure scenario results in a dose that exceeds the toxicity index.

Animal/ 

Scenario 

Chlorsulfuron Clopyralid Dicamba Glyphosate Imazapic Imazapyr Metsulfuron methyl Picloram Sethoxydim Sulfometuron methyl Tirclopyr 2,4-D NPE Surfactant 

Consume 

contam. veg. 

small mammal, 

on site -- -- -- -- -- -- -- -- -- -- -- 1 -- 

lg. mammal, on 

site -- -- -- -- -- -- -- -- -- -- 1 1 -- 

lg. bird, on site -- -- -- -- -- -- -- -- -- -- 1 1

Consume 

contam. water 

small mammal -- -- -- -- -- -- -- -- -- -- -- -- -- 

Consume 

contam. 

insects# 

small mammal -- 1 1 -- -- -- -- 1 1 1 1 1 1

small bird -- 1 1 1 -- -- -- 1 1 1 1 1 1

Consume 

contam. prey 

carnivore (sm. 

mammal)# -- -- -- -- -- -- -- -- -- -- 1 1 -- 

predatory bird 

(sm. mammal)# -- -- -- -- -- -- -- -- -- -- -- 1 -- 

predatory bird 

(fish) -- -- -- -- -- -- -- -- -- -- -- -- -- 

*Includes scenario for direct spray of a rabbit-sized mammal. 

# Data is lacking regarding chronic exposures, so effects are assumed by comparing acute dose vs. chronic 

NOAEL, which will likely over-estimate actual risk. 

25
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Table 6. Exposure scenario results from FS/SERA risk assessments for mammals, birds, and honeybees 

using the highest application rate and upper residue rates. 

Symbol meanings are as follows: 

-- Exposure scenario results in a dose below the toxicity index. 

♦ Exposure scenario results in a dose that exceeds the toxicity index. 

Animal/Scenario 

Chlorsulfuron Clopyralid Dicamba Glyphosate Imazapic Imazapyr Metsulfuron methyl Picloram Sethoxydim Sulfometuron methyl Triclopyr 2,4-D NPE Surfactant 

ACUTE 

EXPOSURES 

Direct spray, bee -- -- -- ♦ -- -- -- -- -- -- ♦ ♦

Direct spray, sm. 

mammal -- -- ♦* -- -- -- -- -- -- -- -- ♦ ♦

Consume 

contaminated 

vegetation 

small mammal -- -- -- -- -- -- -- -- -- -- -- ♦ ♦

large mammal -- -- ♦ ♦ -- -- -- -- -- -- ♦ ♦ ♦

large bird -- -- ♦ -- -- -- -- -- -- -- ♦ ♦ ♦

Consume 

contam. water 

Spill, sm. 

mammal -- -- -- -- -- -- -- -- -- -- -- ♦ -- 

Consume 

contam. insects 

small mammal -- -- ♦ ♦ -- -- -- ♦ -- -- ♦ ♦ ♦

small bird -- -- ♦ ♦ -- -- -- -- -- -- ♦ ♦ ♦

Consume 

contam. prey 

carnivore (sm. 

mammal) -- -- -- -- -- -- -- -- -- -- -- ♦ -- 

predatory bird 

(sm. mammal) -- -- -- -- -- -- -- -- -- -- -- -- ♦

predatory bird 

(fish) -- -- -- -- -- -- -- -- -- -- -- -- -- 

CHRONIC 

EXPOSURES 

Consume 

contam. veg. 

small mammal, -- -- -- -- -- -- -- -- -- -- -- ♦ -- 

26
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Table 6. Exposure scenario results from FS/SERA risk assessments for mammals, birds, and honeybees 

using the highest application rate and upper residue rates. 

Symbol meanings are as follows: 

-- Exposure scenario results in a dose below the toxicity index. 

♦ Exposure scenario results in a dose that exceeds the toxicity index. 

Animal/Scenario 

Chlorsulfuron Clopyralid Dicamba Glyphosate Imazapic Imazapyr Metsulfuron methyl Picloram Sethoxydim Sulfometuron methyl Triclopyr 2,4-D NPE Surfactant 

on site 

lg. mammal, on 

site -- -- ♦ -- -- -- -- -- -- ♦ ♦ ♦ -- 

lg. bird, on site -- ♦ ♦ ♦ -- -- -- -- ♦ ♦ ♦ ♦

Consume 

contam. water 

small mammal -- -- -- -- -- -- -- -- -- -- -- -- -- 

Consume 

contam. insects# 

small mammal -- ♦ ♦ ♦ -- -- -- ♦ ♦ ♦ ♦ ♦ ♦

small bird -- ♦ ♦ ♦ -- -- -- ♦ ♦ ♦ ♦ ♦ ♦

Consume 

contam. prey 

carnivore (sm. 

mammal)# -- -- -- -- -- -- -- -- -- -- ♦ ♦ ♦

predatory bird 

(sm. mammal)# -- -- -- -- -- -- -- -- ♦ -- ♦ ♦ ♦

predatory bird 

(fish) -- -- -- -- -- -- -- -- -- -- -- -- -- 

* Includes scenario for direct spray of a rabbit-sized mammal. 

# Data is lacking regarding chronic exposures, so effects are assumed by comparing acute dose vs. chronic 

NOAEL, which will likely over-estimate actual risk. 

Herbicide Effects on Reptiles 

There is almost no data available regarding the toxicity of herbicides to reptiles. In a review 

of pesticide effects to reptiles, Pauli and Money (2000) found very few studies, despite 

publications stating the need for such research dating back to Hall (1980). The only 

information available for herbicides included in this EIS is from two reports concerning 2,4-

D. One study investigated the effects of 2,4-D on alligators (Crain et al. 1997, as cited by 

SERA 1998), and Willemsen and Hailey (1989, cited by Pauli and Money 2000) noted 

adverse effects to tortoises in Greece after application of 2,4,5-T and 2,4-D. Pauli and 

Money (2000) concluded, “it is remarkable that no data appear to exist concerning the effects 

on reptiles of field applications of... modern herbicides (e.g., glyphosate, sulfonylureas)...” 

27
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

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Hall and Henry (1992) stated, “Susceptibility of reptiles to selective pesticides is virtually 

unknown.” 

Hall and Clark (1982) found that the green anole lizard (Anolis carolinenesis) had a similar 

sensitivity as mallards and rats to organophosphates. Conversely, reptiles were reported to 

be more sensitive to some pesticides than birds or mammals (Rudd and Genelly 1956, as 

cited in Hall 1980). Hall (1980) stated that reptiles are apparently less sensitive than fish. 

The FS/SERA risk assessments use amphibians and/or fish as surrogates for reptiles. An 

assumption is made that exposures and doses that are protective of amphibians and fish 

would also be protective of reptiles. Amphibians and fish have very permeable skin, more so 

than reptiles, so they are more likely to absorb contaminants from their environment. And 

their complicated life cycle that includes metamorphosis makes amphibians sensitive 

indicators for environmental effects (Cowman and Mazanti, 2000). However, the lack of 

data from reptiles leads to substantial uncertainty in the risk assessment for reptiles, since the 

response of these animals to doses of herbicide is not known. 

Many reptile species would likely be under some cover during the day, when herbicides may 

be applied. But diurnal reptiles, like lizards, could conceivably be sprayed during 

applications. Nocturnal and diurnal reptiles could be exposed through contact with 

contaminated vegetation and soil or ingestion of contaminated prey. Contaminated water or 

prey could expose aquatic reptiles, but direct spray is not likely. The actual likelihood of 

exposing reptiles depends on the application method, size of treatment area, habitat treated, 

and season of application, and must be analyzed at the site-specific level. 

Herbicide Effects on Amphibians 

Data on toxicity of herbicides to amphibians are limited. Several studies have found that 

amphibians are less sensitive, or about as sensitive, as fish to some herbicides (Berrill et al. 

1994; Berrill et al. 1997; Johnson 1976; Mayer and Ellersieck 1986; Perkins et al. 2000). 

Consequently, separate dose-response assessments from exposure scenarios have not been 

created for amphibians in the FS/SERA risk assessments. Available information on toxicity 

of herbicides to amphibians is summarized below. 

Neither the published literature nor the EPA files include data regarding the toxicity of 

chlorsulfuron, clopyralid, imazapic, imazapyr, metsulfuron methyl, picloram, or sethoxydim 

to amphibian species. However, data for other aquatic species indicate that chlorsufuron, 

clopyralid, imazapic, imazapyr, metsulfuron methyl, and picloram have a very low potential 

to cause any adverse effect in aquatic animals (SERA 2003 Chlorsulfuron; SERA, 2003-

Clopyralid; SERA, 2003-Imazapic; SERA, 2003-Imazapyr; SERA, 2003-Metsulfuron 

methyl; SERA, 2003-Picloram). The formulation Poast is much more toxic to aquatic 

organisms than sethoxydim. However, even considering the higher toxicity of Poast, there is 

no indication that aquatic animals are likely to be exposed to concentrations that would result 

in toxic effects. There is a substantial limitation to this risk characterization in that no 

chronic toxicity studies on aquatic animals are available for either sethoxydim or Poast 

(SERA, 2001 Sethoxydim). 

Dicamba 

28

Johnson (1976) tested the tadpoles of two Australian frog species (Adelotus brevis and 

Limnodynastes peroni) for their responses to dicamba exposure. The 96-hour LC50 was 106 
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

mg/L for L. peroni, and 185 mg/L for A. brevis. The 24-hour LC50 for the two species were 

205 and 220 mg/L, respectively. These values are in the range of those reported for tolerant 

fish species for dicamba exposure (SERA, 2000-Dicamba). Estimated water concentrations 

for dicamba indicate that there is no basis for asserting or predicting that adverse effects to 

aquatic animals are plausible (SERA, 2003-Dicamba). Even the highest water contamination 

rate for an accidental spill is below the LC50 of the most sensitive aquatic animal by a factor 

of 2.5 (SERA, 2003-Dicamba, p. 4-37). 

Glyphosate 

Glyphosate isopropylamine (IPA), RoundUp and POEA surfactant used in RoundUp have 

been specifically tested for ability to cause malformations in the frog embryo teratogenesis 

assay using Xenopus (Perkins et al. 2000). Xenopus is a highly sensitive assay species for 

determining the teratogenicity of chemicals (Mann and Bidwell 2000, Perkins et al. 2000). 

No increases in malformations were noted at levels that were not also lethal to the embryos. 

The RoundUp formulation containing POEA surfactant was 700 times mores toxic than 

glyphosate IPA. POEA surfactant alone was more toxic than the RoundUp formulation. No 

statistically significant increases in abnormalities were seen in any groups exposed to POEA 

at levels that were not also lethal. The 96-hour LC50 for glyphosate IPA was 7297 mg a.e./L, 

and that for RoundUp was 9.3 mg a.e./L. Perkins et al. (2000) calculated that if RoundUp 

was applied at the highest application rate directly to water 15 cm deep (volumn not 

specified), the expected environmental contamination was less than the LC50 and the LC5 by 

a factor of about three. 

A study by Smith (2001) looked at effects to western chorus frog (Pseudacris tiseriata) and 

Plains leopard frog (Rana blairi) from a formulation of glyphosate that contains glyphosate 

IPA and ethoxylated tallowamine surfactant (Kleeraway Grass and Weed Killer RTU 

(Monsanto)). Smith exposed 1-week old tadpoles for 24-hours to the following 

concentrations of Kleeraway: 0.1 (1 part Kleeraway to 9 parts deionized water), 0.1, 0.001, 

and 0.0001. These concentrations are equivalent to 560 mg a.e./L, 56 mg a.e./L, 5.6 mg 

a.e./L, and 0.56 mg a.e./L (SERA, 2003-Glyphosate, p. 4-20). Smith reported some mortality 

at concentrations as low as 0.56 mg a.e./L for both species. Acute exposure to Kleeraway 

had no effect on growth or development of surviving tadpoles. Results found by Smith are 

not consistent with other information on the effects of glyphosate or other formulations to 

amphibians. However, other studies have found that different formulations can have 

different toxicities to frogs (Mann and Bidwell, 1999). Formulations containing surfactant 

are known to have much higher toxicity to amphibians than glyphosate. The Forest Service 

does not use the formulation used in the Smith study. 

Bidwell and Gorrie (1995; cited in SERA 2003 Glyphosate) reported 48-hour LC50 values of 

11.6 mg a.e./L for the Roundup 360 formulation and 121 mg/L for technical grade 

glyphosate using four species of frogs from western Australia. 

At the typical application rate, expected water concentrations for acute and longer-term 

exposures are well below any reported LC50 for amphibians, with the exception of the study 

by Smith (2001) (SERA, 2003-Glyphosate, Worksheet G03). At the highest application rate, 

lethal doses could occur from formulations containing surfactant. 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Sulfometuron methyl 

The effect of sulfometuron methyl to amphibians was investigated in one study using 

Xenopus (Fort 1998; cited in SERA 2003 Sulfometuron methyl). Results of the study found 

that sulfometuron methyl exposure can cause moderately severe malformations in these 

frogs, including miscoiling of the gut, incomplete eye lens formation, abnormal craniofacial 

development, and decreased tail resorption. The concentration that produced these effects 

depended upon the length of exposure, with shorter exposures showing no effect at higher 

concentrations than longer exposures. The author did not sate whether data were reported in 

terms of mg of sulfometuron methyl or mg of Oust. The FS/SERA risk assessment assumes 

that data refer to mg of Oust, to provide the most protection. The NOAEC for malformations 

for 4-hour exposure is 0.38 mg a.i./L, and that for 30-day exposure is 0.0075. However, 

exposure to 0.0075 mg a.i./L for 14 days was identified as the LOAEC for tail resorption rate 

effects. No mortality was observed at concentrations up to 7.5 mg a.i./L. 

Unlike the other FS/SERA risk assessments, a quantitative evaluation of exposure and risk 

from sulfometuron methyl was conducted for amphibians. SERA (2003 Sulfometuron 

methyl) compared estimated water concentrations for acute and chronic exposures to acute 

and chronic NOEC values for frogs, from Fort (1998). The estimated exposure is 0.002 of 

the acute NOEC, and 0.00075 of the chronic NOEC. Therefore, at the typical and highest 

application rates, there is no basis for asserting or predicting that adverse effects to 

amphibians are plausible. There is a substantial reservation in that this conclusion is based 

on data from one species, but other studies have indicated that Xenopus are a sensitive 

indicator for effects to amphibians (Mann and Bidwell 2000, Perkins et al. 2000). 

Triclopyr 

Triclopyr BEE is much more toxic to aquatic species that triclopyr TEA or triclopyr acid 

(SERA 2003 Triclopyr). Triclopyr was specifically tested for ability to cause malformations 

in the frog embryo teratogenesis assay using Xenopus laevis (Perkins et al. 2000). Xenopus is 

a highly sensitive assay species for determining the teratogenicity of chemicals (Mann and 

Bidwell 2000, Perkins et al. 2000). No statistically significant increase in abnormalities were 

seen in any groups exposed to Garlon 3A or Garlon 4 at levels that were not also lethal to the 

embryos. Consistent with results for other aquatic species, Garlon 3A, containing triclopyr 

TEA, was 15 times less toxic than Garlon 4, containing triclopyr BEE. Garlon 4 reduced 

embryo growth at a concentration below the LC50. Perkins et al. (2000) found that the 96-

hour LC50 for Garlon 4 was 10 mg a.e./L, and that for Garlon 3A was 159 mg a.e./L. Perkins 

et al. (2000) calculated that if Garlon 4 was applied at the highest application rate directly to 

water 15 cm deep (volume not specified), the expected environmental contamination was less 

than the LC50 and the LC5 by a factor of about four and three, respectively. 

30

Berrill et al. (1994) conducted toxicity studies on eggs and tadpoles of leopard frog (Rana 

pepiens), green frog (Rana clamitans), and bullfrog (Rana catesbeiana) exposed to technical 

grade triclopyr BEE. The study was conducted in darkness to prevent hydrolysis of triclopyr 

BEE to tricolopyr acid. Exposure of eggs to concentrations up to 4.6 ppm triclopyr a.e. for 

48 hours caused no effect on hatching success, timing, malformations or subsequent 

avoidance behavior of tadpoles hatched from exposed eggs (Berrill et al. 1994). Tadpoles 

were more sensitive; all bullfrog and green frog tadpoles exposed to 2.3 and 4.6 ppm 

triclopyr a.e. died. Leopard frogs were more tolerant and few died, but all were unresponsive 

to prodding at 2.3 and 4.6 ppm a.e. About half the bullfrog and most green frog tadpoles 
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

became unresponsive to prodding when exposed to 1.1 ppm a.e. Surviving tadpoles 

recovered after exposure was terminated. 

Water concentrations from application of triclopyr acid at the typical application rate are 

below 1 mg/L (1 ppm), so acute and chronic risks to aquatic animals are low (SERA, 2003-

Triclopyr, Worksheet G03). At the highest application rate, acute exposure from runoff 

could adversely affect responsiveness of some tadpoles, increasing the risk of predation. 

Despite the difference in toxicity, the conclusion is the same for triclopyr BEE, due to the 

difference in estimated water concentration. 

2,4-D 

Unlike other herbicides in this analysis, 2,4-D may be more toxic to some species of 

amphibians than to fish. The effects of 2,4-D on amphibians have been studied for African 

clawed frog, toads (Bufo melanostictus), and crested newts (Triturus cristatus carnifex) 

(SERA, 1998). Malformations in Xenopus occur a concentration greater than 200 mg/L, but 

this concentration may also be a lethal dose (SERA, 1998). At this concentration, all adult 

crested newts were dead after three hours exposure to the isoctyl ester of 2,4-D in water 

(Zaffaroni et al. 1986, cited in SERA, 1998). All male newts died after 31 days exposure to 

50 mg/L, while none of the females died. One newt died after 21 days exposure to 25 mg/L. 

The 96-hour LC50 for toads was 8.05 mg/L and mortality began to appear at 6.1 mg/L 

(Vardia et al., 1984, cited in SERA, 1998). Concentrations of 2,4-D in ambient water are 

estimated to be 0.002 mg/L in a runoff scenario and 6 mg/L after an accidental spill. Water 

concentration from runoff is well below any dose reported to cause mortality in amphibians. 

However, mortality to amphibians could result from an accidental spill of a large volumn of 

2,4-D (SERA, 1998). 

The actual likelihood of exposing amphibians depends on the application method, habitat 

treated, and season of application, and must be analyzed at the site-specific level. 

Herbicide Effects on Invertebrates 

Manufacturers are required to conduct toxicity tests on honeybees as part of the registration 

process. The estimated doses and toxicity values of the herbicides to honey bees are listed in 

Table 7. The inclusion of other terrestrial invertebrates in toxicity studies varies for each 

herbicide. However, even the most well-studied will include effects on only a small fraction 

of terrestrial invertebrate species potentially found in any diverse ecosystem. Risk to 

invertebrates can only be inferred based on the few test species for which data are available. 

Effects of chlorsulfuron to terrestrial invertebrates have been studied using a leaf beetle 

(Gastrophysa polygoni), large whitebutterfly (Pieris brassicae), and nemotodes (SERA, 

2003-Chlorsulfuron). Direct spray of first-instar larva and feeding of larva on treated plants 

did not produce significant changes in mortality, but did delay development of those feeding 

on treated plants. Placing eggs of the leaf beetle on treated plants significantly decreased 

survival (Kjaer and Elmegaard, 1996; cited in SERA, 2003-Chlorsulfuron). In another study 

(Kjaer and Heimbach, 2001), newly hatched larvae of the leaf beetle and whitebutterfly were 

placed on treated plants and no significant effects on survival or relative growth rates were 

found. Two species of nematodes (Steinernema carpocapsae and S. feltiae) were exposed to 

chlorsulfuron in soil and no effect was observed on reproduction, viability or movement 

31
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

(Rovesti and Desco, 1990; cited in SERA 2003-Chlorsulfuron). A British publication 

(Tomlin, 2000) reports an LD50 > 25mg/kg for honey bees, but it is not clear what research 

provides the basis for this value. 

Clopyralid has been tested on a variety of terrestrial invertebrates. Standard bioassays on 

honeybees (LD50 >90 mg/kg) have been conducted as well as exposure of earthworms to 

clopyralid in soil (LC50 >1000 ppm). Also, Hassan et al. (1994) provided a summary of 

several bioassays and field trials using a variety of terrestrial invertebrates. Clopyralid 

produced some mortality in insect parasites, predatory mites, Semiadalia 11-notata

(Coccinellidae), Anthocoris nemoralis (Anthocoridae), and Chrysoperla carnea

(Chrysopidae). Pekar et al. (2002; cited in SERA 2003 Clopyralid) reported that clopyralid 

was “harmless” to wild immature spiders (Theridion impressum). 

Table 7. Potential herbicide doses for bees in a direct spray scenario, assuming 

100% absorption. 

Herbicide Typical Application Rate Dose for Bee Toxicity Index for Bee 

Chlorsulfuon 0.056 lb/ac 8.98 mg/kg >25 mg/kg (LD50) 

Clopyralid 0.35 lb/ac 56.1 mg/kg 909 mg/kg (no mortality) 

Dicamba 0.3 lb/ac 48.1 mg/kg 1000 mg/kg (no mortality) 

Glyphosate 2.0 lb/ac 321 mg/kg 540 mg/kg (NOAEC) 

Imazapic 0.13 lb/ac 16 mg/kg 387 mg/kg (no mortality) 

Imazapyr 0.45 lb/ac 72.1 mg/kg 1000 mg/kg (no mortality) 

Metsulfuron Methyl 0.03 lb/ac 4.81 mg/kg 270 mg/kg (NOEC) 

Picloram 0.35 lb/ac 56.1 mg/kg 1,000 mg/kg (no mortality) 

Sethoxydim 0.3 lb/ac 60.1 mg/kg 107 mg/kg (NOAEL) 

Sulfometuron Methyl 0.045 lb/ac 7.21 mg/kg 1,075 mg/kg (NOEC) 

Triclopyr BEE 1.0 lb/ac 160 mg/kg >1,075 mg/kg (LD50) 

Triclopyr TEA 1.0 lb/ac 160 mg/kg >1,075 mg/kg (LD50) 

2,4-D 1.0 lb/ac 163 mg/kg 124 mg/kg (LD50) 

NP9E 1.67 lbs/ac 268.00 mg/kg unknown 

Source: SERA 1996-2003 and USDA FS 2003. 

1 Standard acute toxicity studies using bees were not identified in a complete search of studies submitted to 

EPA. Tomlin (2000) reports bee LD50 > 25 mg/kg in a British pesticide manual. Another study found no 

mortality to a leaf-eating beetle directly sprayed at a rate corresponding to 107 lb/ac (SERA 2003 

Chlorsulfuron). 

Dicamba is not particularly toxic to honeybees (LD50 >1000mg/kg). Hassan et al. (1998; 

cited in SERA 2003 Dicamba) classified the formualation Banvel as harmless to the 

beneficial parasite, Trichogramma cacoeciae. Potter et al. (1990; cited in SERA 2003 

Dicamba) observed no toxic effects to earthworms in a field study after an application of 

about 0.1 lb/acre. This rate is below the typical application rate however. 

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DRAFT 

There is a low potential for glyphosate to adversely affect terrestrial invertebrates. The 

honeybee LD50 for glyphosate is greater than 1075 mg/kg and the NOEC is 540 mg/kg. 

Mortality at 134 mg/kg in one study was attributed to equipment failure (SERA, 2003-

Glyphosate). Direct foliar spray had no effect on the spider mite (Tetranchys urticae). Onehundred percent mortality to spider mites was reported after application of RoundUp ULTRA 

at 3.6 kg a.i./ha, but it was attributed to the solution causing the mites to stick to the glass 

plates. Studies of the effects of glyphosate on the spider Lepthyphantes tenuis resulted in no 

effects that could be attributed to glyphosate toxicity. No significant effects were noted in 

studies on rove beetles, butterflies, or terrestrial snail (Helix aspersa). The soil LC50 for a 

worm common in Libya, Aporrectodea caliginosa, is 177-246 mg glyphosate/kg soil 

(Mohamed et al., 1995; cited in SERA, 2003-Glyphosate). 

The standard acute toxicity study to honeybees is the only study found on the effects of 

imazapic to terrestrial invertebrates. At 387 mg/kg, mortality was not statistically significant 

(SERA, 2003-Imazapic). 

Imazapyr has a low acute toxicity to bees with an LD50 >1000 mg/kg. No information on 

effects to other terrestrial invertebrates is available. 

Standard bioassays on effects of metsulfuron methyl to honeybees reported LD50 > 1075 

mg/kg and a NOAEL of at least 270 mg/kg. Very high application rates (almost five times 

higher than the highest labeled application rate) resulted in a 15 percent reduction in eff 

hatching for rove beetle (Samsoe-Petersen 1995; cited in SERA 2003 Metsulfuron methyl). 

Data on the toxicity of picloram to terrestrial invertebrates is available only for the honeybee 

and the brown garden snail (Helix aspersa). The honeybee LD50 is greater than 1000 mg/kg 

and dietary concentration of 5000 mg/kg over a 14-day period did not increase mortality for 

the snail. 

For sethoxydim, the honeybee NOAEL is 107 mg/kg. The only other study on invertebrates 

investigated effects to Mexican bean beetle (Epilachna varivestis) feeding on soybean and 

lima bean plants treated with the equivalent of 5-6 lbs/acre (15 times higher than the highest 

labeled application rate). There was a slight increase in days to pupation for larvae, but also 

significant increases in both the number of egg masses as well as total number of eggs 

produced by beetles feeding on sethoxydim treated plants (Agnello et al. 1986; cited in 

SERA 2001 Sethoxydim). 

Only two studies are available on the toxicity of sulfometuron methyl to terrestrial 

invertebrates and they both looked at effects to the honeybee. Sulfometuron methyl has a 

very low potential to adversely affect bees, with an acute NOAEL of 1075 mg/kg (SERA, 

2001-Sulfometuron methyl). No mortality was reported at the highest doses tested. 

Honeybee assays provide the only information on the effects of triclopyr acid and triclopyr 

TEA to terrestrial invertebrates. In both bioassays, the LD50 is greater than 1075 mg/kg 

(SERA, 2003-Triclopyr). 

33

The effects of 2,4-D have been studied for a limited variety of terrestrial invertebrates. 

Reported LD50 for honeybees range from 124 mg/kg to 1129 mg/kg (SERA, 1998-2,4-D). 
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Mortality may occur 5-7 days after exposure to toxic levels. 2,4-D is reported to cause 

mortality or other adverse effects to southern armyworm (Spodoptera eridania), wheat 

sawfly larvae, millipedes (Scytonotus simplex), coccinellid larvae, various beetle species, 

parasitic wasps, and earthworms (Hassan et al., 1991; and Roberts and Dorough 1984 – both 

cited in SERA, 1998-2,4-D; see also Table 4 in Norris and Kogan 2000). Response of 

earthworms is variable with no measurable effect in the field or in a microcosm for some 

studies (SERA, 1998-2,4-D). Other soil invertebrates were not affected by application of the 

sodium salt of 2,4-D at rates of 1.34 and 2.68 lbs/acre (Prasse, 1979; cited in SERA, 1998-

2,4-D). Terrestrial slugs (Deroceras reticulatum) may absorb 2,4-D through contact with 

contaminated soil (Haqu and Ebing, 1983; cited in SERA, 1998-2,4-D). 

The actual likelihood of exposing invertebrates depends on the application method, size of 

treatment area, habitat treated, and season of application, and must be analyzed at the sitespecific level. 

Likelihood these exposures and effects will actually occur 

While the above exposure scenarios consider animal sizes, feeding habits, herbicide 

application rates, and toxicity data, they cannot account for all the variables found in the field 

during actual applications. Such factors as foliar interception, animal behavior (e.g. 

nocturnal versus diurnal activity), season of use, and selective application methods can 

significantly reduce or eliminate actual exposure to herbicides in field conditions. For 

example, while toxicity of some herbicides could pose a concern for the early stages of 

amphibian development, an actual application of herbicide occurring after mid-summer, well 

after this stage of development might be present at a specific location, could significantly 

reduce risk (Perkins et al., 2000). 

Direct spray of small mammals is very unlikely to occur, since they are typically nocturnal 

and spend the day in burrows, nests, or underneath dense vegetation. Diurnal small 

mammals, like ground squirrels, may be active in treatment areas, but would likely seek 

shelter or move away from the treatment activity. Aerial application could directly spray 

some diurnal small mammals. The likelihood that a predatory bird or mammal would prey 

on the same small mammal that had been directly sprayed is remote, and an entire day’s diet 

of contaminated small mammals is very remote. 

34

Direct spray of insects could occur, as they are present in vegetation and would not 

necessarily flee during treatment operations. However, foliar interception would reduce the 

actual amount sprayed on almost all insects present. Insectivorous birds may establish 

territories during the breeding season. If the treatment area involved most of one or several 

territories, it could be feasible for an insectivorous bird to consume all or most of its daily 

diet within the treatment area. The young of even herbivorous bird species are highly 

dependant upon insects for their growth and development. Therefore, while the actual doses 

received by insectivorous birds may be lower than the exposure scenarios predict, due to 

foliar interception, application method and other variables, the consumption of contaminated 

insects by young birds may offset this advantage. Consumption of contaminated insects 

remains a concern for some herbicides, and likelihood of exposure must be evaluated at the 

site-specific level. Insectivorous mammals may be less likely to consume a large amount of 

contaminated invertebrates, because they either forage over very large areas, like bats, or 

may forage on fossorial invertebrates, like shrews. 
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Consumption of contaminated grass by large birds or mammals would depend on the habitattype in the treatment area and whether these animals are likely to forage there. The 

application method would be very important in determining the amount of exposure. 

Selective foliar applications to target invasive plants are not likely to lead to exposure. But 

broadcast foliar applications of large areas, particularly aerial applications, could contaminate 

forage. Consumption of contaminated vegetation is a substantial concern for some 

herbicides, but the specific application methods and timing may easily avoid exposure to 

these animals. 

In order to evaluate how actual implementation can influence effects to wildlife, field studies 

for many of the above herbicides have been conducted. 

Field Studies

Field studies can help evaluate the likelihood of population effects to wildlife from 

herbicides as applied. Some herbicides have been tested in many field studies on several 

groups of species with results published in open literature, while other herbicides have few or 

no field studies reported. 

Most field studies could only detect changes in population numbers and are not sensitive 

enough to detect sublethal effects to wildlife. Some studies have investigated sub-lethal 

effects (e.g. Sullivan et al., 1998). However, sublethal effects that resulted in indirect 

mortality or other population changes would produce effects that could be detected by most 

longer-term field studies. 

Chlorsulfuron 

No field studies are available. 

Clopyralid 

Rice et al. (1997) published results from an 8-year field study that found no significant 

effects on plant species diversity from the use of clopyralid, clopyralid plus 2,4-D, or 

picloram. Hassan et al. (1994) reported summary of effects to terrestrial invertebrates in field 

trials. 

Dicamba 

Potter et al. (1990; cited in SERA, 2003-Dicamba) observed no toxic effects to earthworms 

in a field study after an application of about 0.1 lb/acre. This rate is below the typical 

application rate however. 

Glyphosate 

Sullivan et al. (1998) looked at long-term influence of glyphosate treatment in a spruce forest 

on reproduction, survival, and growth attributes of deer mouse (Peromyscus maniculatus) 

and southern red-backed vole (Clethrionomys gapperi) populations. For all statistically 

significant differences in their study (e.g. successful pregnancies, survival), the differences 

between treated and untreated populations were within the range of natural fluctuations for 

these small mammal populations over a 5-year period. 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

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Sullivan et al. (1997) investigated the influence of aerial herbicide treatments on small 

mammal populations 9 and 11 years post-treatment. They found that glyphosate did not 

adversely affect reproduction, survival, or growth of deer mice or Oregon voles (Microtus 

oregoni) in coastal forest a decade after application. Species richness and diversity changed 

little over the decade after treatment and concluded that post-harvest successional change had 

more impact than that induced by herbicide treatment. 

A field study on effects to the spider Lepthyphantes tenuis attributed population decrease to 

the secondary effects from changes in vegetation (Haughton et al., 2001; cited in SERA, 

2003-Glyphosate). Bramble et al. (1997) investigated butterfly diversity and abundance on 

electric transmission right-of-ways treated with herbicides versus those treated with only 

mechanical methods. Herbicides used in the right-of-way treatments included a mixture of 

picloram and triclopyr, a mixture of triclopyr and metsulfuron methyl, a mixture of 

glyphosate and fosamine, a mixture of triclopyr and imazapyr, and glyphosate alone. They 

found no significant differences in diversity or abundance of butterflies between herbicide 

and no-herbicide units. 

Cole et al. (1998) found that small mammal capture rates in Oregon forests that were logged, 

burned and then sprayed with glyphosate did not differ from those that were just logged and 

burned. Other studies have found that numbers of some species appear to increase or remain 

the same after treatment with herbicides, while other species decrease (Anthony and 

Morrison 1985; Lautenschlager, 1993; Ritchie et al., 1987; Sullivan, 1990a). The same 

species might show all three responses in different studies with the same herbicide (see 

Sullivan, 1990a). In these studies, effects to small mammals occurred from habitat changes 

created by herbicide treatment, rather than from direct effects of herbicides (Santillo et al., 

1989; Sullivan 1990a; Sullivan 1990b; Sullivan and Sullivan, 1981). 

Santillo et al. (1989) found a substantial decrease in herbivorous insects on glyphosate 

treated sites, while there was clearcut verses untreated, but no trend between treated and 

untreated sites for predatory insects. The overall decrease in insect numbers decreased 

available food for shrews. Cole et al. (1997) sampled amphibians in Oregon clearcuts with 

and without glyphosate applications. Capture rates did not differ between treated and 

untreated plots for rough-skinned newt, ensatina, Pacific giant salamander, Dunn’s 

salamander, western redback salamander, and red-legged frog. 

Imazapic, Sethoxydim, Sulfometuron methyl 

No field studies available. 

Imazapyr 

Imazapyr was used on a low volume retreatment in the Bramble et al. (1997) study 

mentioned above (see glyphosate) without apparent adverse effects to butterfly diversity and 

abundance on electric transmission right-of-ways. 

Metsulfuron methyl 

Metsulfuron methyl was in one of the mixtures used to treat electric transmission right-ofways in the Bramble et al. (1997) study mentioned above (see glyphosate), which found no 

apparent adverse effects to butterfly diversity and abundance. 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

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Picloram 

Rice et al. (1997) published results from an 8-year field study that found no significant 

effects on plant species diversity from the use of clopyralid, clopyralid plus 2,4-D, or 

picloram. Brooks et al. 1995 studied effects of picloram, imazapyr, and triclopyr mixtures on 

small mammals and found reduced numbers on sites after herbicide treatments. However, no 

control site (i.e. non-treated) was used so it is not possible to discern herbicide effects from 

normal population fluctuations that are common with small mammals. Nolte and Fulbright 

(1997) studied effects of an aerial application of picloram/triclopyr mixture on small 

mammals, birds, and rare plants. Effects to animal diversity or plant species richness or 

evenness were not found. 

Picloram was in some of the mixtures used to treat electric transmission right-of-ways in 

studies by Bramble et al. (1997, 1999). The 1997 study found no significant differences to 

butterfly diversity and abundance, while the 1999 study found significantly higher diversity 

and abundance of butterflies on herbicide-treated units than on handcutting units. 

Triclopyr 

There are a number of field studies reported in the open literature, most of which indicate no 

or beneficial effects (SERA 2003 Triclopyr). Refer also to the study by Brooks et al. (1995) 

mentioned above. In contrast, Leslie et al. 1996 found that white-tailed deer avoid areas that 

used a “brown and burn” technique, where the site is treated with herbicide followed by a 

prescribed burn. McMurray et al. (1993a; 1993b; 1994) reported no adverse effects to 

reproductivity in mammals. 

Triclopyr was in some of the mixtures used to treat electric transmission right-of-ways in 

studies by Bramble et al. (1997, 1999). The 1997 study found no significant differences to 

butterfly diversity and abundance, while the 1999 study found significantly higher diversity 

and abundance of butterflies on herbicide-treated units than on handcutting units. 

2,4-D 

Rice et al. (1997) published results from an 8-year field study that found no significant 

effects on plant species diversity from the use of clopyralid, clopyralid plus 2,4-D, or 

picloram. Response of earthworms is variable with no measurable effect in the field or in a 

microcosm for some studies (Potter et al., 1990; and Gile, 1983; cited in SERA, 1998). 

2,4-D was one of the herbicides used in a study by Bramble et al. (1999), which found 

significantly higher diversity and abundance of butterflies on herbicide-treated units than on 

handcutting units in electric transmission right-of-ways. 

Johnson and Hansen (1969) found no significant difference in density or litter size of deer 

mouse populations between areas treated with 2,4-D and untreated areas. They also found 

that treatment with 2,4-D reduced density of northern pocket gophers (Thomomys talpoides) 

and least chipmunks (Eutamias minimus) and increased abundance of Montane vole 

(Microtus montanus). Changes in density and abundance were attributed to changes in food 

and cover produced by the herbicide treatment. 

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Results of Exposure Analysis for Each Herbicide 

Calculated doses for each herbicide at typical and highest application rates for each scenario 

are included in Appendix 1. 

CHLORSULFURON

Small Mammal Directly Sprayed

The acute NOAEL for mammals in laboratory toxicity tests is 75 mg/kg. For exposure 

scenarios that use the typical application rate of 0.056 lb/acre, if a small mammal is directly 

sprayed, and 100 percent absorption is assumed, the animal would receive an acute dose of 

1.36 mg/kg (SERA, 2003-Chlorsulfuron, Worksheet F02a). This dose is 0.018 of the acute 

NOAEL, so there is no basis for asserting or predicting that adverse effects to small 

herbivorous mammals are plausible (SERA 2003 Chlorsulfuron, p. 4-27). 

At the highest application rate of 0.25 lb/acre, the animal would receive an acute dose of 6.06 

mg/kg (project file). This dose is 0.08 of the acute NOAEL, so there is no basis for asserting 

or predicting that adverse effects to mammals are plausible at any application rate. 

Small Mammal Drinking Contaminated Water

The acute NOAEL for mammals in laboratory toxicity tests is 75 mg/kg. The estimated dose 

to a small mammal from drinking water contaminated by an accidental spill, assuming the 

highest levels of contamination, is 0.11 mg/kg for acute exposure (SERA, 2003-

Chlorsulfuron, Worksheet F05). If a small mammal consumes contaminated water over time, 

accounting for dissipation, degradation, and other processes, the animal would receive a 

chronic dose of 0.0000074 mg/kg/day (SERA, 2003-Chlorsulfuron, Worksheet F07). Doses 

to a large mammal would be even lower on a per kg body weight basis. These doses are 

0.0015 of the acute NOAEL, and 0.000001 of the chronic NOAEL, respectively, so there is 

no basis for asserting or predicting that adverse effects to mammals are plausible (SERA, 

2003-Chlorsulfuron, p. 4-27). 

At the highest application rate of 0.25 lb/acre, the acute dose from drinking water 

contaminated by a spill is 0.495 mg/kg (project file). This dose is 0.007 of the acute 

NOAEL. The chronic dose is also below the chronic NOAEL, so there is no basis for 

asserting or predicting that adverse effects to mammals are plausible, even in a worst-case 

scenario. 

Large Herbivorous Mammal 

The acute NOAEL for mammals in laboratory toxicity tests is 75 mg/kg. For exposure 

scenarios that use the typical application rate of 0.056 lb/acre, if a 70 kg mammal consumed 

contaminated vegetation on site shortly after application, assuming the highest residue rates 

and 100 percents of the diet contaminated, it would receive an acute dose of 2.72 mg/kg 

(SERA 2003 Chlorsulfuron, Worksheet F10). This dose is 0.036 of the acute NOAEL, so 

there is no basis for asserting or predicting that adverse effects to large herbivorous mammals 

are plausible (SERA, 2003-Chlorsulfuron, p. 4-27). 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

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Chlorsulfuron, cont’d. 

The chronic NOAEL for mammals in laboratory toxicity tests is 5 mg/kg/day. Chronic 

exposure from the consumption of contaminated vegetation for 90 days at the treatment site, 

assuming the highest residue rates, results in a dose of 1.14 mg/kg (SERA, 2003-

Chlorsulfuron, Worksheet F11a). This dose is 0.228 of the chronic NOAEL, so there is no 

basis for asserting or predicting that adverse effects to large herbivorous mammals are 

plausible (SERA, 2003-Chlorsulfuron, p. 4-27). 

Estimated doses using the highest application rate (0.25 lb/acre) are less than the acute 

NOAEL and equal to the chronic NOAEL for mammals. No exposure exceeds the NOAEL, 

so no adverse effects are plausible from acute or chronic dietary exposures. The assumptions 

in the chronic exposure scenario are very unlikely to occur in field conditions, so the weight 

of evidence suggests that no adverse effects are plausible using typical or worst-case 

exposure assumptions (SERA, 2003-Chlorsulfuron, p. 4-28). 

Medium Carnivorous Mammal 

The acute NOAEL for mammals in laboratory toxicity tests is 75 mg/kg. For exposure 

scenarios that use the typical application rate of 0.056 lb/acre, if a 5 kg mammal consumed 

small mammal prey that has been contaminated by direct spray, assuming 100 percent 

absorption for the prey, it would receive an acute dose of 0.118 mg/kg (SERA, 2003-

Chlorsulfuron, Worksheet F16a). This dose is 0.0016 of the acute NOAEL, so there is no 

basis for asserting or predicting that adverse effects to carnivorous mammals are plausible 

(SERA, 2003-Chlorsulfuron, p. 4-27). Doses to larger mammals would be even lower on a 

per kg body weight basis. 

Chlorsulfuron does not appear to accumulate or persist in animals following either single or 

multiple doses. The elimination of chlorsulfuron has been studied in rats, goats, cows, and 

hens (SERA, 2003-Chlorsulfuron). A combination of elimination and metabolism 

extensively and rapidly eliminated chlorsulfuron and its metabolites from the bodies of all 

mammalian species studied. The half-life for elimination in rats is less than six hours 

(Shrivastava, 1979 cited in SERA, 2003-Chlorsulfuron). Therefore, chronic exposures from 

contaminated mammal prey due to a single application of chlorsulfuron are unlikely to cause 

any adverse effect. In addition, the acute dose is much less than the chronic NOAEL for 

mammals, so there is no basis for asserting or predicting that adverse effects from repeated 

acute exposures from multiple applications of chlorsulfuron over time are plausible. 

Estimated doses using the highest application rate (0.25 lb/acre) are less than the acute and 

chronic NOAELs for mammals, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions (SERA, 2003-

Chlorsulfuron, p. 4-28). 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

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Chlorsulfuron, cont’d. 

Small Herbivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 75 mg/kg. If a small mammal 

consumes contaminated vegetation shortly after application, assuming the highest residue 

rates, the acute dose received is 0.15 mg/kg (SERA, 2003-Chlorsulfuron, Worksheet F03). 

This estimated dose is 0.002 of the acute NOAEL, so there is no basis for asserting or 

predicting that adverse effects to small herbivorous mammals are plausible (SERA, 2003-

Chlorsulfuron, p. 4-27). 

The chronic NOAEL for mammals in laboratory toxicity tests is 5 mg/kg/day. If a small 

mammal consumes contaminated vegetation at the treatment site for 90-days, assuming the 

highest residue rates, the animal would receive a chronic dose of 0.013 mg/kg/day (SERA, 

2003-Chlorsulfuron, Worksheet F04a). This dose is 0.0026 of the chronic NOAEL, so there 

is no basis for asserting or predicting that adverse effects to small herbivorous mammals are 

plausible (SERA, 2003-Chlorsulfuron, p. 4-27). 

Estimated doses using the highest application rate (0.25 lb/acre) are less than the acute and 

chronic NOAELs for mammals, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions (SERA 2003 

Chlorsulfuron, p. 4-28). 

Small Insectivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 75 mg/kg. For exposure 

scenarios that use the typical application rate of 0.056 lb/acre, if a small mammal consumes 

contaminated insects shortly after application, assuming the highest residue rates, the acute 

dose received is 3.89 mg/kg (SERA, 2003-Chlorsulfuron, Worksheet 14a). This dose is 0.052 

of the acute NOAEL, so there is no basis for asserting or predicting that adverse effects to 

insectivorous mammals are plausible (SERA, 2003-Chlorsulfuron, p. 4-27). 

Data on degradation of herbicide residues from insects is not available, so no chronic 

exposure scenario has been developed. However, the acute dose is much less than the 

chronic NOAEL as well, and chronic doses are much lower than acute doses. Therefore, 

there is no basis for asserting or predicting that adverse effects to insectivorous mammals 

from chronic exposures are plausible (SERA, 2003-Chlorsulfuron, p. 4-27). 

The estimated dose (17.3 mg/kg) using the highest application rate (0.25 lb/acre) is less than 

the acute and chronic NOAELs for mammals, so there is no basis for asserting or predicting 

that adverse effects are plausible using typical or worst-case exposure assumptions (SERA, 

2003-Chlorsulfuron, p. 4-28). 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

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Chlorsulfuron, cont’d. 

Large Herbivorous Bird

The acute NOAEL for birds in laboratory toxicity tests is 1686 mg/kg. For exposure 

scenarios that use the typical application rate of 0.056 lb/acre, if a 4 kg bird consumed 

contaminated grass on site shortly after application, assuming the highest residue rates and 

100 percent of diet is contaminated, it would receive an acute dose of 4.26 mg/kg (SERA, 

2003-Chlorsulfuron, Worksheet F12). This dose is 0.0025 of the acute NOAEL, so there is 

no basis for asserting or predicting that adverse effects to large grass-eating birds are 

plausible (SERA, 2003-Chlorsulfuron, p. 4-27). 

The chronic NOAEL for birds in laboratory toxicity tests is 140 mg/kg/day. Chronic 

exposure from the consumption of contaminated grass for 90 days at the treatment site, 

assuming the highest residue rates and 100 percent of diet is contaminated, results in a dose 

of 1.79 mg/kg/day (SERA, 2003-Chlorsulfuron, Worksheet F13a). This dose is 0.013 of the 

chronic NOAEL, so there is no basis for asserting or predicting that adverse effects to large 

grass-eating birds are plausible (SERA, 2003-Chlorsulfuron, p. 4-27). 

Estimated doses using the highest application rate (0.25 lb/acre) are less than the acute and 

chronic NOAELs for birds, so there is no basis for asserting or predicting that adverse effects 

are plausible using typical or worst-case exposure assumptions (SERA, 2003-Chlorsulfuron, 

p.4-28). 

Large Fish-eating Bird

Many chemicals may be concentrated or partitioned from water into the tissues of animals in 

the water. This process is referred to as bioconcentration. The potential for bioconcentration 

of chlorsulfuron in fish was studied in bluegill and channel catfish exposed to 14Cchlorsulfuron for 28 days (Han 1981 and Priester et al., 1991, cited in SERA, 2003 

Chlorsulfuron). In the SERA risk assessments, concentrations in viscera are considered to 

reflect concentration in whole fish. Bioconcentration factors (BCF) for bluegill were <1 L/kg 

in muscle and 4-6 L/kg in viscera and liver (SERA, 2003-Chlorsulfuron, Appendix 9). BCF 

for channel catfish were 1.5 L/kg in muscle and < 12 L/kg in viscera and liver (SERA, 2003-

Chlorsulfuron, Appendix 9). In both studies, residue levels in live fish dropped 70-90 

percent during a two-week cleansing period. No adverse effects on fish were observed 

during the studies. The exposure scenarios in the SERA risk assessment use a whole-fish 

BCF of 2.6 L/kg for acute exposure and 12 L/kg for chronic exposure. 

The acute NOAEL for birds in laboratory toxicity tests is 1686 mg/kg. For exposure 

scenarios that use the typical application rate of 0.056 lb/acre, if a predatory bird consumed 

fish from a pond contaminated by an accidental spill, assuming the highest concentrations in 

fish and highest intake on a body weight basis, it would receive an acute dose of 0.295 mg/kg 

(SERA 2003 Chlorsulfuron, Worksheet F08). This dose is 0.00017 of the acute NOAEL, so 

there is no basis for asserting or predicting that adverse effects to fish-eating birds are 

plausible (SERA 2003 Chlorsulfuron, p. 4-27). 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

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Chlorsulfuron, cont’d.

The chronic NOAEL for birds in laboratory toxicity tests is 140 mg/kg/day. If a predatory 

bird consumed fish contaminated by runoff for a lifetime, assuming the highest 

concentrations in fish and highest intake on a body weight basis, it would receive a chronic 

dose of 0.00009 mg/kg/day (SERA, 2003-Chlorsulfuron, Worksheet F09). This dose is 

0.00000064 of the chronic NOAEL, so there is no basis for asserting or predicting that 

adverse effects to fish-eating birds are plausible (SERA, 2003-Chlorsulfuron, p. 4-27). 

Estimated doses using the highest application rate (0.25 lb/acre) are much less than the acute 

and chronic NOAELs for birds, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions (SERA, 2003-

hlorsulfuron, p.4-28). 

Large Predatory Bird

The acute NOAEL for birds in laboratory toxicity tests is 1686 mg/kg. For exposure 

scenarios that use the typical application rate of 0.056 lb/acre, if a 0.6 kg bird consumed 

small mammal prey that has been contaminated by direct spray, assuming 100 percent 

absorption for the prey, it would receive an acute dose of 0.181 mg/kg (SERA, 2003-

Chlorsulfuron, Worksheet F16b). This dose is 0.0001 of the acute NOAEL, so there is no 

basis for asserting or predicting that adverse effects to predatory birds are plausible (SERA, 

2003-Chlorsulfuron, p. 4-27). 

Chlorsulfuron does not appear to bioconcentrate or persist in animals following either single 

or multiple doses. The elimination of chlorsulfuron has been studied in rats, goats, cows, and 

hens (SERA, 2003-Chlorsulfuron). A combination of elimination and metabolism 

extensively and rapidly eliminated chlorsulfuron and its metabolites from the bodies of all 

mammalian species studied. The half-life for elimination in rats is less than six hours 

(Shrivastava 1979 cited in SERA, 2003-Chlorsulfuron). Therefore, chronic exposures from 

contaminated mammal prey due to a single application of chlrosulfuron are unlikely to cause 

any adverse effect. In addition, the acute dose is much less than the chronic NOAEL for 

birds, so there is no basis for asserting or predicting that adverse effects are plausible (SERA, 

2003-Chlorsulfuron, p. 4-27). 

Estimated doses using the highest application rate (0.25 lb/acre) are much less than the acute 

and chronic NOAELs for birds, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions (SERA, 2003-

Chlorsulfuron, p.4-28). 

Small Insectivorous Bird

The acute NOAEL for birds in laboratory toxicity tests is 1686 mg/kg. For exposure 

scenarios that use the typical application rate of 0.056 lb/acre, if a 10 g bird consumed 

contaminated insects on site shortly after application, assuming the highest residue rates, it 

would receive an acute dose of 6.32 mg/kg (SERA, 2003-Chlorsulfuron, Worksheet F14b). 

This dose is 0.004 of the acute NOAEL, so there is no basis for asserting or predicting that 

adverse effects to insectivorous birds are plausible (SERA, 2003-Chlorsulfuron, p. 4-27). 

42
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Data on degradation of herbicide residues from insects is not available, so no chronic 

exposure scenario has been developed. However, the acute dose is much less than the 

chronic NOAEL as well, and chronic doses are much lower than acute doses. Therefore, 

there is no basis for asserting or predicting that adverse effects are plausible (SERA, 2003-

Chlorsulfuron, p. 4-27). 

Estimated doses using the highest application rate (0.25 lb/acre) are much less than the acute 

and chronic NOAELs for birds, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions (SERA, 2003-

Chlorsulfuron, p.4-28). 

CLOPYRALID

Small Mammal Directly Sprayed

The acute NOAEL for mammals in laboratory toxicity tests is 75 mg/kg. For, exposure 

scenarios that use the typical application rate of 0.35 lb/acre, if a small mammal is directly 

sprayed, and 100 percent absorption is assumed, the animal would receive an acute dose of 

8.49 mg/kg (SERA, 2003-Clopyralid, Worksheet F02a). This estimated dose is 0.10 of the 

acute NOAEL, so there is no basis for asserting or predicting that adverse effects to 

mammals are plausible (SERA, 2003-Clopyralid, p. 4-23). 

At the highest application rate of 0.5 lb/acre, the animal would receive an acute dose of 12.1 

mg/kg (project file). This dose is 0.2 of the acute NOAEL, so there is no basis for asserting 

or predicting that adverse effects to mammals are plausible at any application rate. 

Small Mammal Drinking Contaminated Water

The estimated doses to a small mammal from drinking water contaminated by an accidental 

spill, assuming the highest levels of contamination, are 2.33 mg/kg for acute exposure 

(SERA, 2003-Clopryalid, Worksheet F05). If a small mammal consumes contaminated 

water over time, accounting for dissipation, degradation, and other processes, the animal 

would receive a chronic dose of 0.00067 mg/kg/day (SERA, 2003-Clopyralid, Worksheet 

F07). Doses to a large mammal would be even lower on a per kg body weight basis. These 

doses are 0.03 of the acute NOAEL, and 0.00004 of the chronic NOAEL, respectively, so 

there is no basis for asserting or predicting that adverse effects to mammals are plausible

(SERA, 2003-Clopyralid, p. 4-23). 

At the highest application rate of 0.5 lb/acre, the acute dose from drinking water 

contaminated by a spill is 3.32 mg/kg (project file). This dose is 0.04 of the acute NOAEL. 

The chronic dose is also below the chronic NOAEL, so there is no basis for asserting or 

predicting that adverse effects to mammals are plausible, even in a worst-case scenario. 

43
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Clopyralid, cont’d.

Large Herbivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 75 mg/kg. For exposure 

scenarios that use the typical application rate of 0.35 lb/acre, if a 70 kg mammal consumed 

contaminated vegetation on site shortly after application, assuming the highest residue rates 

and 100 percents of the diet contaminated, it would receive an acute dose of 17.0 mg/kg 

(SERA, 2003-Clopyralid, Worksheet F10). This dose is 0.2 of the acute NOAEL, so there is 

no basis for asserting or predicting that adverse effects to large herbivorous mammals are 

plausible (SERA, 2003-Clopyralid, p. 4-23). 

The chronic NOAEL for mammals in laboratory toxicity tests is 15 mg/kg/day. Chronic 

exposure from the consumption of contaminated vegetation for 90 days at the treatment site, 

assuming the highest residue rates, results in a dose of 8.95 mg/kg/day (SERA, 2003-

Clopyralid, Worksheet F11a). This dose is 0.6 of the chronic NOAEL, so there is no basis for 

asserting or predicting that adverse effects to large herbivorous mammals are plausible 

(SERA, 2003-Clopyralid, p. 4-23). 

Estimated doses using the highest application rate (0.50 lb/acre) are less than the acute and 

chronic NOAELs for mammals, although only marginally so for the chronic NOAEL. Since 

both doses are still below the NOAEL, there is no basis for asserting or predicting that 

adverse effects are plausible using typical or worst-case exposure assumptions (SERA, 2003-

Clopyralid, p. 4-23). 

Medium Carnivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 75 mg/kg. For exposure 

scenarios that use the typical application rate of 0.35 lb/acre, if a 5 kg mammal consumed 

small mammal prey that has been contaminated by direct spray, assuming 100 percent 

absorption for the prey, it would receive an acute dose of 0.734 mg/kg (SERA, 2003-

Clopyralid, Worksheet F16a). Doses to a large mammal would be even lower on a per kg 

body weight basis. This dose is 0.02 of the acute NOAEL, so there is no basis for asserting 

or predicting that adverse effects to carnivorous mammals are plausible (SERA, 2003-

Clopyralid, p. 4-23). 

Clopyralid does not appear to accumulate in animal tissues. The elimination and metabolism 

of clopyralid has been studied in rats, hens, lambs, and goats (SERA, 2003-Clopyralid). 

These animals rapidly excreted largely unmetabolized clopyralid. The half-life for 

elimination in rats is three hours (Dow AgroSciences 1998 cited in SERA, 2003-Clopyralid). 

Therefore, chronic exposures from contaminated mammal prey due to a single application of 

clopyralid are unlikely to cause any adverse effect. In addition, the acute dose is less than 

the chronic NOAEL of 15 mg/kg/day for mammals, so there is no basis for asserting or 

predicting that adverse effects from repeated acute exposures from multiple applications of 

clopyralid over time are plausible. 

44

Estimated doses using the highest application rate (0.50 lb/acre) are less than the acute and 

chronic NOAELs for mammals, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions (SERA, 2003-

Clopyralid, p. 4-23). 
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Clopyralid, cont’d.

Small Herbivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 75 mg/kg. If a small mammal 

consumes contaminated vegetation shortly after application, assuming the highest residue 

rates, the acute dose received is 0.938 mg/kg (SERA 2003 Clopyralid, Worksheet F03). This 

estimated dose is 0.01 of the acute NOAEL, so there is no basis for asserting or predicting 

that adverse effects to small herbivorous mammals are plausible (SERA 2003 Clopyralid, p. 

4-23). 

The chronic NOAEL for mammals in laboratory toxicity tests is 15 mg/kg/day. If a small 

mammal consumes contaminated vegetation at the treatment site for 90-days, assuming 

highest residue rates, the animal would receive a chronic dose of 0.0987 mg/kg/day (SERA 

2003 Clopyralid, Worksheet F04a). This estimated dose is 0.007 of the chronic NOAEL, so 

there is no basis for asserting or predicting that adverse effects to small herbivorous 

mammals are plausible (SERA 2003 Clopyralid, p. 4-23). 

Estimated doses using the highest application rate (0.50 lb/acre) are than the acute and 

chronic NOAELs for mammals, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions (SERA 2003 

Clopyralid, p. 4-23). 

Small Insectivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 75 mg/kg. For exposure 

scenarios that use the typical application rate of 0.35 lb/acre, if a small mammal consumes 

contaminated insects shortly after application, assuming the highest residue rates, the acute 

dose received is 24.3 mg/kg (SERA 2003 Clopyralid, Worksheet 14a). This dose is 0.30 of 

the acute NOAEL, so there is no basis for asserting or predicting that adverse effects to 

insectivorous mammals are plausible (SERA 2003 Clopyralid, p. 4-23). 

Data on degradation of herbicide residues from insects is not available, so no chronic 

exposure scenario has been developed. Residue on insects likely declines over time, but the 

extent of decline has not been quantified. The acute dose is greater than the chronic 

NOAEL (15 mg/kg/day), so adverse effects to insectivorous mammals appear plausible from 

chronic dietary exposures. The dose is less than the chronic LOAEL of 150 mg/kg/day, 

however. The exposure scenario uses residue rates from small insects, which are 

substantially higher than those for large insects, and assumes that 100 percent of the daily 

diet is composed of insects that have been directly sprayed. For bats, in particular, the 

scenario is unlikely to occur in the field. It seems more plausible for shrews and small 

fossorial insectivores, however 

The estimated dose (34.7 mg/kg) using the highest application rate (0.50 lb/acre) is less than 

the acute NOAEL, but greater than the chronic NOAEL for mammals. The dose is less 

than the chronic LOAEL of 150 mg/kg/day, however. No adverse effects are plausible from 

acute exposures, but adverse effects to insectivorous mammals are plausible from chronic 

dietary exposures. 

45
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Clopyralid, cont’d.

Large Herbivorous Bird

The acute NOAEL for birds in laboratory toxicity tests is 670 mg/kg. For exposure scenarios 

that use the typical application rate of 0.35 lb/acre, if a 4 kg bird consumed contaminated 

grass on site shortly after application, assuming the highest residue rates and 100 percent of 

diet is contaminated, it would receive an acute dose of 26.6 mg/kg (SERA, 2003-Clopyralid, 

Worksheet F12). This dose is 0.04 of the acute NOAEL, so there is no basis for asserting or 

predicting that adverse effects to large grass-eating birds are plausible (SERA, 2003-

Clopyralid, p. 4-23). 

There is no chronic toxicity index available for effects of clopyralid to birds, so the mammal 

chronic NOAEL will be used. In acute dietary exposures, the bird NOAEL is about a factor 

of nine above the mammal NOAEL, suggesting that birds are less sensitive than mammals to 

clopyralid. The chronic NOAEL for mammals in laboratory toxicity tests is 15 mg/kg/day. 

Chronic exposure from the consumption of contaminated grass for 90 days at the treatment 

site, assuming the highest residue rates and 100 percent of diet is contaminated, results in a 

dose of 14.0 mg/kg/day (SERA, 2003-Clopyralid, Worksheet F13a). This estimated dose is 

0.90 of the chronic NOAEL for mammals, and birds appear to be less sensitive to clopyralid 

than mammals, so there is no basis for asserting or predicting that adverse effects to large 

grass-eating birds are plausible (SERA, 2003-Clopyralid, p. 4-23). 

Estimated doses using the highest application rate (0.50 lb/acre) are less than the acute 

NOAEL for birds, but greater than the chronic NOAEL for mammals. The chronic dose is 

less than the chronic LOAEL of 150 mg/kg/day, however. No adverse effects are plausible 

from acute exposures, but adverse effects to large herbivorous birds appear plausible from 

chronic dietary exposures. However, the assumptions in the chronic exposure scenario are 

very unlikely to occur in field conditions, so the weight of evidence suggests that no adverse 

effects are plausible using typical or worst-case exposure assumptions (SERA, 2003-

Clopyralid, p. 4-23). 

Large Fish-eating Bird

Many chemicals may be concentrated or partitioned from water into the tissues of animals in 

the water. This process is referred to as bioconcentration. Clopyralid does not appear to 

bioconcentrate, based on one study in sunfish (Bidlack 1982 as cited in SERA, 2003-

Clopyralid). The exposure scenarios in the SERA risk assessment use a whole-fish BCF of 1 

L/kg for acute and chronic exposures. 

The acute NOAEL for birds in laboratory toxicity tests is 670 mg/kg. For exposure scenarios 

that use the typical application rate of 0.35 lb/acre, if a predatory bird consumed fish from a 

pond contaminated by an accidental spill, assuming the highest concentrations in fish and 

highest intake on a body weight basis, it would receive an acute dose of 2.38 mg/kg (SERA, 

2003-Clopyralid, Worksheet F08). This dose is 0.004 of the acute NOAEL, so there is no 

basis for asserting or predicting that adverse effects to fish-eating birds are plausible (SERA, 

2003-Clopyralid, p. 4-23). 

46
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Clopyralid, cont’d.

There is no chronic toxicity index available for effects of clopyralid to birds, so the mammal 

chronic NOAEL will be used. In acute dietary exposures, the bird NOAEL is about a factor 

of nine above the mammal NOAEL, suggesting that birds are less sensitive than mammals to 

clopyralid. The chronic NOAEL for mammals in laboratory toxicity tests is 15 mg/kg/day. If 

a predatory bird consumed fish contaminated by runoff for a lifetime, assuming the highest 

concentrations in fish and highest intake on a body weight basis, it would receive a chronic 

dose of 0.000683 mg/kg/day (SERA 2003 Clopyralid, Worksheet F09). This estimated dose 

is 0.00005 of the chronic NOAEL for mammals, so there is no basis for asserting or 

predicting that adverse effects to fish-eating birds are plausible (SERA, 2003-Clopyralid, p. 

4-23). 

Estimated doses using the highest application rate (0.50 lb/acre) are less than the acute 

NOAEL for birds and chronic NOAEL for mammals, so there is no basis for asserting or 

predicting that adverse effects are plausible using typical or worst-case exposure 

assumptions. 

Large Predatory Bird

The acute NOAEL for birds in laboratory toxicity tests is 670 mg/kg. For exposure scenarios 

that use the typical application rate of 0.35 lb/acre, if a 0.6 kg bird consumed small mammal 

prey that has been contaminated by direct spray, assuming 100 percent absorption for the 

prey, it would receive an acute dose of 1.13 mg/kg (SERA 2003 Clopyralid, Worksheet 

F16b). This is 0.002 of the acute NOAEL, so there is no basis for asserting or predicting that 

adverse effects to predatory birds are plausible. 

Clopyralid does not appear to bioconcentrate, based on one study in sunfish (Bidlack 1982 as 

cited in SERA 2003 Clopyralid). The elimination and metabolism of clopyralid has been 

studied in rats, hens, lambs, and goats ((SERA, 2003-Clopyralid). These animals rapidly 

excreted largely unmetabolized clopyralid. The half-life for elimination in rats is three hours 

(Dow AgroSciences, 1998 cited in SERA, 2003). Therefore, chronic exposures from 

contaminated mammal prey due to a single application of clopyralid are unlikely to cause any 

adverse effect. In addition, the acute dose is less than the chronic NOAEL for birds, so there 

is no basis for asserting/predicting that adverse effects from repeated acute exposures from 

multiple applications of clopyralid over time are plausible. 

Estimated doses using the highest application rate (0.50 lb/acre) are less than the acute 

NOAEL for birds, and the chronic NOAEL for mammals, so there is no basis for asserting or 

predicting that adverse effects to predatory birds are plausible. 

Small Insectivorous Bird

The acute NOAEL for birds in laboratory toxicity tests is 670 mg/kg. For exposure scenarios 

that use the typical application rate of 0.35 lb/acre, if a 10 g bird consumed contaminated 

insects on site shortly after application, assuming the highest residue rates, it would receive 

an acute dose of 39.5 mg/kg (SERA, 2003-Clopyralid, Worksheet F14b). This dose is 0.06 

of the acute NOAEL, so there is no basis for asserting or predicting that adverse effects to 

insectivorous birds are plausible (SERA, 2003-Clopyralid, p. 4-23). 

47
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Clopyralid, cont’d.

Data on degradation of herbicide residues from insects is not available, so no chronic 

exposure scenario has been developed. Residue on insects likely declines over time, but the 

extent of decline has not been quantified. The acute dose is greater than the chronic NOAEL 

(15 mg/kg/day) for mammals, so adverse effects to insectivorous birds appear plausible from 

chronic dietary exposures. The dose is less than the chronic LOAEL of 150 mg/kg/day, 

however. 

The estimated dose (56.4 mg/kg) using the highest application rate (0.50 lb/acre) is less than 

the acute NOAEL for birds but greater than the chronic NOAEL for mammals. The dose is 

less than the chronic LOAEL of 150 mg/kg/day, however. No adverse effects are plausible 

from acute exposures, but adverse effects to insectivorous birds appear plausible from 

chronic dietary exposures. 

DICAMBA

Dicamba has a relatively low acute toxicity to adult animals, in terms of direct lethal doses, 

but adverse effects on reproduction and nervous systems occur at much lower doses. 

Dicamba shows a consistent pattern of increased toxicity to larger sized animals, across 

several species and animal types (i.e. birds and mammals). 

The following results are based on a very protective reference dose from EPA that is disputed 

by more recent information from EPA’s Office of Pesticide Programs (OPP) (Durkin, pers. 

com.). The appropriateness of the toxicity index is currently being peer reviewed, and may 

change with the final risk assessment for dicamba. If the value used by OPP becomes the 

toxicity index used for the FS/SERA risk assessment, the analysis will show a lower potential 

for adverse effects to mammals (Durkin, pers. com). 

Small Mammal Directly Sprayed

The acute NOAEL for small mammals in laboratory toxicity tests is 30 mg/kg, and it is 3 

mg/kg for larger mammals. For, exposure scenarios that use the typical application rate of 

0.3 lb/acre, if a small mammal is directly sprayed, and 100 percent absorption is assumed, the 

animal would receive an acute dose of 7.27 mg/kg (SERA, 2003-Dicamba, Worksheet F02a). 

If a mammal the size of a rabbit is directly sprayed, it would receive an acute dose of 1.69 

mg/kg (SERA, 2003-Dicamba, Worksheet F02c). These estimated doses are 0.2 and 0.6 of 

their respective NOAELs, so there is no basis for predicting or asserting that adverse effects 

to smaller herbivorous mammals are plausible (SERA, 2003-Dicamba, p. 4-32). 

48

At the highest application rate of 2.0 lb/acre, the acute dose is 48.5 mg/kg for a small 

mammal, and 11.2 for a rabbit-sized mammal (project file). These doses are 1.6 times 

greater than the acute NOAEL for small mammals, and 3.7 times greater than the acute 

NOAEL for larger mammals. The dose in the rabbit-sized mammal (about 12 mg/kg) 

exceeds the LOAEL for adverse reproductive effects in larger mammals. The dose for the 

mouse-sized mammal (60 mg/kg) is less than the LOAEL for neurotoxic effects in smaller 

mammals. Therefore, adverse effects to reproduction of rabbit-sized mammals are plausible 

and adverse effects to nervous system responses in mouse-sized mammals may be plausible, 

from direct spray exposure at the highest application rate.
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Dicamba, cont’d.

Small Mammal Drinking Contaminated Water

The estimated doses to a small mammal from drinking water contaminated by an accidental 

spill, assuming the highest levels of contamination, are 1.33 mg/kg for acute exposure 

(SERA, 2003-Dicamba, Worksheet F05). If a small mammal consumes contaminated water 

over time, accounting for dissipation, degradation, and other processes, the animal would 

receive a chronic dose of 0.00000132 mg/kg/day (SERA, 2003-Dicamba, Worksheet F07). 

Doses to a large mammal would be even lower on a per kg body weight basis, but dicamba is 

more toxic to larger animals. These doses are 0.44 of the acute NOAEL for large mammals, 

and 0.0000004 of the chronic NOAEL, respectively, so there is no basis for asserting or 

predicting that adverse effects to mammals are plausible (SERA, 2003-Dicamba, p. 4.32). 

At the highest application rate of 2.0 lb/acre, the acute dose to a small mammal from drinking 

water contaminated by a spill is 8.87 mg/kg (project file). This dose is 0.3 of the acute 

NOAEL. The chronic dose is also below the chronic NOAEL, so there is no basis for 

asserting or predicting that adverse effects to mammals are plausible, even in a worst-case 

scenario. 

Large Herbivorous Mammal

The acute NOAEL for large mammals in laboratory toxicity tests is 3 mg/kg. For exposure 

scenarios that use the typical application rate of 0.3 lb/acre, if a 70 kg mammal consumed 

contaminated vegetation on site shortly after application, assuming the highest residue rates 

and 100 percents of the diet contaminated, it would receive an acute dose of 14.6 mg/kg 

(SERA, 2003-Dicamba, Worksheet F10). This dose is greater than the acute NOAEL and 

also exceeds the acute LOAEL for large mammals (10 mg/kg). Since the toxicity index is 

based on reproductive effects, the interpretation of risk is made with respect to the toxicity 

studies on which the NOAEL is based (SERA, 2003-Dicamba, p. 4-33). Therefore, adverse 

effects to the reproductive ability of large grass-eating mammals are plausible at the typical 

application rate (SERA, 2003-Dicamba, p. 4-31). 

The chronic NOAEL for both large and small mammals in laboratory toxicity tests is 3 

mg/kg/day, based on the same studies used to determine the acute NOAEL for large 

mammals. Chronic exposure from the consumption of contaminated vegetation for 90 days 

at the treatment site, assuming the highest residue rates, results in a dose of 2.10 mg/kg/day 

(SERA 2003 Dicamba, Worksheet F11a). This dose is 0.7 of the chronic NOAEL, so there is 

no basis for asserting or predicting that adverse effects to large grass-eating mammals are 

plausible (SERA, 2003-Dicamba, p. 4-32). 

49

Estimated doses using the highest application rate (2.0 lb/acre) are greater than the acute 

NOAEL and greater than the chronic NOAEL for mammals. The acute dose (97.3 mg/kg) 

is intermediate between the NOAEL for neurotoxicity (30 mg/kg) and the LOAEL for 

neurotoxicity, so adverse effects to nervous systems are not expected, but are plausible 

(SERA 2003 Dicamba, p. 4-33). However, the acute dose is a factor of 10 above the LOAEL 

for reproductive effects, so adverse effects to reproduction would not only be plausible, they 

are expected at the highest application rate (SERA, 2003-Dicamba, p. 4-33). The chronic 

dose (14.0 mg/kg/day) is greater than the chronic LOAEL (10 mg/kg/day) for reproductive 

effects. Adverse effects to reproduction are plausible for the chronic exposure.
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Dicamba, cont’d.

Medium Carnivorous Mammal

The acute NOAEL for small mammals in laboratory toxicity tests is 30 mg/kg. For exposure 

scenarios that use the typical application rate of 0.3 lb/acre, if a 5 kg mammal consumed 

small mammal prey that has been contaminated by direct spray, assuming 100 percent 

absorption for the prey, it would receive an acute dose of 0.629 mg/kg (SERA, 2003-

Dicamba, Worksheet F16a). Doses to a large mammal would be even lower on a per kg body 

weight basis. This dose is 0.02 of the acute NOAEL for smaller mammals, so there is no 

basis for asserting or predicting that adverse effects to carnivorous mammals are plausible

(SERA, 2003-Dicamba, p. 4-32). 

Dicamba does not appear to accumulate or persist in animal tissues. The elimination of 

dicamba has been studied in rats, mice, rabbits, and dogs (SERA 2003 Dicamba). A 

combination of elimination and metabolism extensively and rapidly eliminated dicamba and 

its metabolites from the bodies of all mammalian species studied. With dietary exposure, 

urinary and fecal excretion approached 96 percent and 4 percent, respectively (SERA, 2003-

Dicamba ). Following a single oral dose of 100 mg/kg, 67-83 percent of the dose was 

excreted as parent compound within 48 hours in rats, mice, rabbits and dogs (SERA, 2003-

Dicamba, citing Atallah et al., 1980). However, renal saturation can occur at doses above 

approximately 150 mg/kg, presumably increasing the time it takes for dicamba to be 

excreted. Therefore, chronic exposures from contaminated mammal prey due to a single 

application of dicamba are unlikely to cause any adverse effect. In addition, the acute dose 

is less than the chronic NOAEL for mammals, so there is no basis for asserting or predicting 

that adverse effects from repeated acute exposures from multiple applications of carnivorous 

mammals over time are plausible. 

The estimated dose using the highest application rate (2 lb/acre) is less than the acute 

NOAEL for small mammals, and equal to the chronic NOAEL, so there is no basis for 

asserting or predicting that adverse effects are plausible using typical or worst-case exposure 

assumptions. 

Small Herbivorous Mammal

The acute NOAEL for small mammals in laboratory toxicity tests is 30 mg/kg, and it is 3 

mg/kg for larger mammals. If a small mammal consumes contaminated vegetation shortly 

after application, assuming the highest residue rates, the acute dose received is 0.804 mg/kg 

(SERA, 2003-Dicamba, Worksheet F03). This estimated doses is 0.03 of the acute NOAEL, 

respectively, so there is no basis for asserting or predicting that adverse effects to small 

herbivorous mammals are plausible (SERA, 2003-Name, p. 4-32). 

The chronic NOAEL for mammals in laboratory toxicity tests is 3 mg/kg/day. If a small 

mammal consumes contaminated vegetation at the treatment site for 90-days, assuming 

highest residue rates, the animal would receive a chronic dose of 0.0232 mg/kg/day (SERA, 

2003-Dicamba, Worksheet F04a). This estimated dose is 0.008 of the chronic NOAEL, so 

there is no basis for asserting or predicting that adverse effects to small herbivorous 

mammals are plausible. 

50
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Dicamba, cont’d.

Estimated doses using the highest application rate (2 lb/acre) are less than the acute and 

chronic NOAEL for small mammals for the consumption of contaminated vegetation, so 

there is no basis for asserting or predicting that adverse effects are plausible using typical or 

worst-case exposure assumptions. 

Small Insectivorous Mammal

The acute NOAEL for small mammals in laboratory toxicity tests is 30 mg/kg. For exposure 

scenarios that use the typical application rate of 0.3 lb/acre, if a small mammal consumes 

contaminated insects shortly after application, assuming the highest residue rates, the acute 

dose received is 20.8 mg/kg (SERA, 2003-Dicamba, Worksheet 14a). This dose is 0.7 of the 

acute NOAEL, so there is no basis for asserting or predicting that adverse effects to 

insectivorous mammals are plausible (SERA, 2003-Dicamba, p. 4-32). 

Data on degradation of herbicide residues from insects is not available, so no chronic 

exposure scenario has been developed. Residue on insects likely declines over time, but the 

extent of decline has not been quantified. The acute dose is greater than the chronic 

NOAEL and also exceeds the chronic LOAEL for effects to reproductions, so adverse effects 

to insectivorous mammals appear plausible from chronic dietary exposures. The exposure 

scenario uses residue rates from small insects, which are substantially higher than those for 

large insects, and assumes that 100 percent of the daily diet is composed of insects that have 

been directly sprayed. For bats, in particular, the scenario is unlikely to occur in the field. It 

seems more plausible for shrews and small fossorial insectivores, however. 

The estimated dose using the highest application rate (2 lb/acre) is greater than the acute 

NOAEL, and greater than the chronic NOAEL for mammals. The estimated dose (150 

mg/kg) is equal to the LOAEL for neurotoxicity, but a factor of 15 greater than the LOAEL 

for reproductive effects (10 mg/kg). Therefore, adverse effects to nervous system responses 

are plausible and adverse effects to reproduction would not only be plausible, they are 

expected at the highest application rate. 

Large Herbivorous Bird

The acute NOAEL for birds in laboratory toxicity tests is 13.6 mg/kg. For exposure 

scenarios that use the typical application rate of 0.3 lb/acre, if a 4 kg bird consumed 

contaminated grass on site shortly after application, assuming the highest residue rates and 

100 percent of diet is contaminated, it would receive an acute dose of 22.8 mg/kg (SERA, 

2003-Dicamba, Worksheet F12). This dose is greater than the acute NOAEL, and about 

equal to the LOAEL for neurotoxic effects (27 mg/kg). Therefore, adverse effects to grasseating birds are plausible at the typical application rate (SERA, 2003-Dicamba, p. 4-34). 

The chronic NOAEL for birds in laboratory toxicity tests is 13.6 mg/kg/day. Chronic 

exposure from the consumption of contaminated grass for 90 days at the treatment site, 

assuming the highest residue rates and 100 percent of diet is contaminated, results in a dose 

of 3.29 mg/kg/day (SERA 2003 Dicamba, Worksheet F13a). This estimated dose is 0.2 of 

the chronic NOAEL, so there is no basis for asserting or predicting that adverse effects to 

grass-eating birds are plausible (SERA, 2003-Dicamba, p. 4-32). 

51
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Dicamba, cont’d.

Estimated doses using the highest application rate (2 lb/acre) are greater than the acute 

NOAEL and greater than the chronic NOAEL for birds. The acute dose (150 mg/kg) is 5 

times greater than the LOAEL for neurotoxic effects, so adverse effects to nervous system 

responses are expected. Adverse effects to reproductive ability are also plausible at this dose 

(LOAEL = 184 mg/kg) (SERA 2003 Dicamba, p.4-34). 

The chronic dose is equal to the LOAEL for neurotoxic effects, so adverse effects to nervous 

system responses are plausible from chronic exposures. 

Large Fish-eating Bird

Many chemicals may be concentrated or partitioned from water into the tissues of animals in 

the water. This process is referred to as bioconcentration. Because of its low octanol water 

partition coefficient, dicamba has a very low potential to bioconcentrate in fish (SERA, 

2003-Dicamba, p. 3-23). Yu et al. (1975) and Francis et al. (1985), as cited in SERA 2004 

Dicamba, conducted microcosm studies to measure the bioconcentration of dicamba in 

aquatic species. Both studies indicated that bioconcentration did not occur. The 

bioconcentration factor (BCF) of a substance can be estimated using a formula discussed in 

Calabrese and Baldwin (1993). This formula yields a BCF of 0.66 for dicamba in whole fish, 

which is higher than the values from the microcosm studies. The exposure scenarios in the 

SERA risk assessment use a whole-fish BCF of 0.66 L/kg for acute and chronic exposure. 

The acute NOAEL for birds in laboratory toxicity tests is 13.6 mg/kg. For exposure 

scenarios that use the typical application rate of 0.3 lb/acre, if a predatory bird consumed fish 

from a pond contaminated by an accidental spill, assuming the highest concentrations in fish 

and highest intake on a body weight basis, it would receive an acute dose of 0.899 mg/kg 

(SERA, 2003-Dicamba, Worksheet F08). This dose is 0.07 of the acute NOAEL, so there is 

no basis for asserting or predicting that adverse effects to fish-eating birds are plausible

(SERA, 2003-Dicamba, p. 4-32). 

The chronic NOAEL for birds in laboratory toxicity tests is 13.6 mg/kg/day. If a predatory 

bird consumed fish contaminated by runoff for a lifetime, assuming the highest 

concentrations in fish and highest intake on a body weight basis, it would receive a chronic 

dose of 0.000000891 mg/kg/day (SERA 2003 Dicamba, Worksheet F09). This estimated 

dose is 0.00000007 of the chronic NOAEL, so there is no basis for asserting or predicting 

that adverse effects to fish-eating birds are plausible (SERA 2003 Dicamba, p. 4-32). 

Estimated doses using the highest application rate (2 lb/acre) are less than the acute and 

chronic NOAEL for birds, so there is no basis for asserting or predicting that adverse effects 

are plausible using typical or worst-case exposure assumptions. 

52
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Dicamba, cont’d.

Large Predatory Bird

The acute NOAEL for birds in laboratory toxicity tests is 13.6 mg/kg. For exposure 

scenarios that use the typical application rate of 0.3 lb/acre, if a 0.6 kg bird consumed small 

mammal prey that has been contaminated by direct spray, assuming 100 percent absorption 

for the prey, it would receive an acute dose of 0.97 mg/kg (SERA 2003 Dicamba, Worksheet 

F16b). This is 0.07 of the acute NOAEL, so there is no basis for asserting or predicting that 

adverse effects to predatory birds are plausible. 

Dicamba does not appear to accumulate or persist in animal tissues. The elimination of 

dicamba has been studied in rats, mice, rabbits, and dogs (SERA 2003 Dicamba). A 

combination of elimination and metabolism extensively and rapidly eliminated dicamba and 

its metabolites from the bodies of all mammalian species studied. With dietary exposure, 

urinary and fecal excretion approached 96 percent and 4 percent, respectively (SERA, 2003-

Dicamba ). Following a single oral dose of 100 mg/kg, 67-83 percent of the dose was 

excreted as parent compound within 48 hours in rats, mice, rabbits and dogs (SERA, 2003-

Dicamba, citing Atallah et al. 1980). However, renal saturation can occur at doses above 

approximately 150 mg/kg, presumably increasing the time it takes for dicamba to be 

excreted. Therefore, chronic exposures from contaminated mammal prey due to a single 

application of dicamba are unlikely to cause any adverse effect. In addition, the acute dose 

is less than the chronic NOAEL for birds, so there is no basis for asserting or predicting that 

adverse effects from repeated acute exposures from multiple applications of predatory birds 

over time are plausible. 

Estimated doses using the highest application rate (2 lb/acre) also result in an exposure less 

than the acute and chronic NOAEL for birds/mammals, so there is no basis for asserting or 

predicting that adverse effects are plausible using typical or worst-case exposure 

assumptions. 

Small Insectivorous Bird

The acute NOAEL for birds in laboratory toxicity tests is 13.6 mg/kg. For exposure 

scenarios that use the typical application rate of 0.3 lb/acre, if a 10 g bird consumed 

contaminated insects on site shortly after application, assuming the highest residue rates, it 

would receive an acute dose of 33.8 mg/kg (SERA, 2003-Dicamba, Worksheet F14b). This 

dose is greater than the acute NOAEL. This dose is equal to the LOAEL for neurotoxic 

effects, so adverse effects to nervous system responses in insectivorous birds are plausible 

(SERA, 2003-Dicamba, p. 4-34). 

Data on degradation of herbicide residues from insects is not available, so no chronic 

exposure scenario has been developed. The acute dose is greater than the chronic NOAEL 

for birds (13.6 mg/kg/day) and also greater than the chronic LOAEL for neurotoxic effects 

(27 mg/kg/day). So adverse effects to nervous system responses are plausible from chronic 

exposures. 

53
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Dicamba, cont’d. 

The estimated dose (226 mg/kg) using the highest application rate (2 lb/acre) is greater than

the acute and chronic NOAEL for birds. This dose is also almost 9 times greater than the 

LOAEL for neurotoxic effects, and greater than the LOAEL for reproductive effects (184 

mg/kg/day), so adverse effects to insectivorous birds are expected at the highest application 

rate. 

GLYPHOSATE

Small Mammal Directly Sprayed

The acute NOAEL for mammals in laboratory toxicity tests is 175 mg/kg. For, exposure 

scenarios that use the typical application rate of 2 lb/acre, if a small mammal is directly 

sprayed, and 100 percent absorption is assumed, the animal would receive an acute dose of 

48.5 mg/kg (SERA, 2003-Glyphosate, Worksheet F02a). This estimated dose is 0.3 of the 

acute NOAEL, so there is no basis for asserting or predicting that adverse effects to 

mammals are plausible (SERA, 2003-Glyphosate, p. 4-43). 

At the highest application rate of 7 lb/acre, the animal would receive an acute dose of 170 

mg/kg (project file). This dose is 0.97 of the acute NOAEL, so there is no basis for asserting 

or predicting that adverse effects to mammals are plausible at any application rate. 

Small Mammal Drinking Contaminated Water

The acute NOAEL for mammals in laboratory toxicity tests is 175 mg/kg. The estimated 

doses to a small mammal from drinking water contaminated by an accidental spill, assuming 

the highest levels of contamination, are 5.32 mg/kg for acute exposure (SERA, 2003-

Glyphosate, Worksheet F05). If a small mammal consumes contaminated water over time, 

accounting for dissipation, degradation, and other processes, the animal would receive a 

chronic dose of 0.00234 mg/kg/day (SERA 2003 Glyphosate, Worksheet F07). Doses to a 

large mammal would be even lower on a per kg body weight basis. These doses are 0.03 of 

the acute NOAEL, and 0.00001 of the chronic NOAEL, respectively, so there is no basis for 

asserting or predicting that adverse effects to mammals are plausible (SERA, 2003-

Glyphosate, p. 4-43). 

At the highest application rate of 7 lb/acre, the acute dose from drinking water contaminated 

by a spill is 18.6 mg/kg (project file). This dose is 0.1 of the acute NOAEL. The chronic 

dose is also below the chronic NOAEL, so there is no basis for asserting or predicting that 

adverse effects to mammals are plausible, even in a worst-case scenario. 

Large Herbivorous Mammal

54

The acute NOAEL for mammals in laboratory toxicity tests is 175 mg/kg. For exposure 

scenarios that use the typical application rate of 2 lb/acre, if a 70 kg mammal consumed 

contaminated vegetation on site shortly after application, assuming the highest residue rates 

and 100 percents of the diet contaminated, it would receive an acute dose of 97.1 mg/kg 

(SERA, 2003-Glyphosate, Worksheet F10). This dose is 0.6 of the acute NOAEL, so there is 

no basis for asserting or predicting that adverse effects to large grass-eating mammals are 

plausible (SERA, 2003-Glyphosate, p. 4-43). 
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Glyphosate, cont’d. 

The chronic NOAEL for mammals in laboratory toxicity tests is 175 mg/kg/day. Chronic 

exposure from the consumption of contaminated vegetation for 90 days at the treatment site, 

assuming the highest residue rates, results in a dose of 53.2 mg/kg/day (SERA, 2003-

Glyphosate, Worksheet F11a). This dose is 0.3 of the chronic NOAEL, so there is no/ basis 

for asserting or predicting that adverse effects to large grass-eating mammals are plausible

(SERA, 2003-Glyphosate, p. 4-43). 

Estimated doses using the highest application rate (7 lb/acre) result in doses greater than the 

acute and equal to the chronic NOAEL for mammals. The acute dose is equal to a LOAEL 

that resulted in some mortality to pregnant rabbits. Thus, while the acute dose to herbivorous 

mammals at the highest application rate is well below the LD50 (2,000 mg/kg), mortality in 

some animals would be plausible (SERA, 2003-Glyphosate, p. 4-44). 

Medium Carnivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 175 mg/kg. For exposure 

scenarios that use the typical application rate of 2 lb/acre, if a 5 kg mammal consumed small 

mammal prey that has been contaminated by direct spray, assuming 100 percent absorption 

for the prey, it would receive an acute dose of 4.2 mg/kg (SERA, 2003-Glyphosate, 

Worksheet F16a). Doses to a large mammal would be even lower on a per kg body weight 

basis. This dose is 0.024 of the acute NOAEL, so there is no basis for asserting or predicting 

that adverse effects to carnivorous mammals are plausible (SERA, 2003-Glyphosate, p. 4-

43). 

Glyphosate does not appear to accumulate or persist in animal tissues. Only about 30 percent 

of ingested glyphosate is absorbed from the gastrointestinal tract (several studies by Davies 

1996 cited in SERA, 2003-Glyphosate). The glyphosate that is absorbed is distributed 

widely throughout the body, and then efficiently excreted. More than 97 percent of the 

administered dose is excreted unchanged, and glyphosate does not substantially concentrate 

or persist in any tissue (SERA, 2003-Glyphosate, p. 3-5). These conclusions are consistent 

with data from a field study that measured glyphosate residues in several small mammal 

species after an aerial application in Oregon (Newton et al. 1984). Newton et al. (1984) 

found that residues in small mammals were below 1 mg/kg for deermice and shrews, and 

below 2 mg/kg for voles, three days after treatment. Therefore, chronic exposures from 

contaminated mammal prey due to a single application of glyphosate are unlikely to cause 

any adverse effect. In addition, the acute dose is much less than the chronic NOAEL for 

mammals, so there is no basis for asserting or predicting that adverse effects from repeated 

acute exposures from multiple applications of glyphosate over time are plausible. 

The estimated dose using the highest application rate (7 lb/acre) is much less than the acute 

and chronic NOAEL for mammals, so there is no basis for asserting or predicting that 

adverse effects are plausible using typical or worst-case exposure assumptions. 

55
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Glyphosate, cont’d. 

Small Herbivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 175 mg/kg. If a small 

mammal consumes contaminated vegetation shortly after application, assuming the highest 

residue rates, the acute dose received is 2.11 mg/kg (SERA, 2003-Glyphosate, Worksheet 

F03). This estimated dose is 0.01 of the acute NOAEL, so there is no basis for asserting or 

predicting that adverse effects to small herbivorous mammals are plausible (SERA, 2003-

Glyphosate, p. 4-43). 

The chronic NOAEL for mammals in laboratory toxicity tests is 175 mg/kg/day. If a small 

mammal consumes contaminated vegetation at the treatment site for 90-days, assuming 

highest residue rates, the animal would receive a chronic dose of 0.231 mg/kg/day (SERA 

2003-Glyphosate, Worksheet F04a). This estimated dose is 0.001 of the chronic NOAEL, so 

there is no basis for asserting or predicting that adverse effects to small herbivorous 

mammals are plausible (SERA, 2003-Glyphosate, p. 4-43). 

Estimated doses using the highest application rate (7 lb/acre) are less than the acute and 

chronic NOAEL for mammals, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions. 

Small Insectivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 175 mg/kg. For exposure 

scenarios that use the typical application rate of 2 lb/acre, if a small mammal consumes 

contaminated insects shortly after application, assuming the highest residue rates, the acute 

dose received is 139 mg/kg (SERA, 2003-Glyphosate, Worksheet 14a). This dose is 0.793 of 

the acute NOAEL, so there is no basis for asserting or predicting that adverse effects to small 

insectivorous mammals are plausible (SERA, 2003-Glyphosate, p. 4-43). 

Data on degradation of herbicide residues from insects is not available, so no chronic 

exposure scenario has been developed. Residue on insects likely declines over time, but the 

extent of decline has not been quantified. However, the acute dose is less than the chronic 

NOAEL as well, and chronic doses are much lower than acute doses. Therefore, there is no 

basis for asserting or predicting that adverse effects to insectivorous mammals from chronic 

exposures are plausible. 

The estimated dose (486 mg/kg) using the highest application rate (7 lb/acre) is greater than

the acute and chronic NOAELs for mammals, so adverse effects to insectivorous mammals

are plausible. This dose also exceeds the acute and chronic LOAEL (350 mg/kg) for diarrhea 

in mammals. The exposure scenario uses residue rates from small insects, which are 

substantially higher than those for large insects, and assumes that 100 percent of the daily 

diet is composed of insects that have been directly sprayed. For bats, in particular, the 

scenario is unlikely to occur in the field. It seems more plausible for shrews and small 

fossorial insectivores, however. (Check Newton et al 1984 paper). 

56
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Glyphosate, cont’d.

Large Herbivorous Bird

The acute NOAEL for birds in laboratory toxicity tests is 562 mg/kg. For exposure scenarios 

that use the typical application rate of 2 lb/acre, if a 4 kg bird consumed contaminated grass 

on site shortly after application, assuming the highest residue rates and 100 percent of diet is 

contaminated, it would receive an acute dose of 152 mg/kg (SERA, 2003-Glyphosate, 

Worksheet F12). This dose is 0.3 of the acute NOAEL, so there is no basis for asserting or 

predicting that adverse effects to large grass-eating birds are plausible (SERA, 2003-

Glyphosate, p. 4-43). 

The chronic NOAEL for birds in laboratory toxicity tests is 100 mg/kg/day. Chronic 

exposure from the consumption of contaminated grass for 90 days at the treatment site, 

assuming the highest residue rates and 100 percent of diet is contaminated, results in a dose 

of 83.2 mg/kg/day (SERA, 200X-Name, Worksheet F13a). This estimated dose is 0.8 of the 

chronic NOAEL, so there is no/ basis for asserting or predicting that adverse effects to large 

grass-eating birds are plausible (SERA, 2003-Glyphosate, p. 4-43). 

Estimated doses using the highest application rate (7 lb/acre) are less than the acute NOAEL, 

but greater than the chronic NOAEL for birds. LOAEL’s are not reported for birds in the 

sources I reviewed, presumably because of a lack of toxic responses in laboratory tests. No 

adverse effects are plausible from acute exposures, but adverse effects to large herbivorous 

birds appear plausible from chronic dietary exposures, based on dose exceeding the NOAEL. 

The assumptions in the chronic exposure scenario are unlikely to occur in field conditions, 

particularly because glyphosate is a non-selective herbicide and would kill most forage 

species at this application rate, making the forage unavailable or unpalatable. However, 

some monitored values for glyphosate residues on vegetation (Newton et al. 1994) are higher 

than those used in the SERA risk assessments. Therefore, the higher residue rates may offset 

the lack of forage availability, and adverse effects to herbivorous birds are plausible. 

Large Fish-eating Bird

Many chemicals may be concentrated or partitioned from water into the tissues of animals in 

the water. This process is referred to as bioconcentration. The EPA uses a BCF for whole 

fish of 0.52 L/kg based on a study by Forbis (1989 as cited in SERA, 2003-Glyphosate) and 

corroborated by Chamberlain et al. (1996, as cited in SERA, 2003). Therefore, exposure 

scenarios in the SERA risk assessment use a whole-fish BCF of 0.52 L/kg for acute and 

chronic exposures. 

The acute NOAEL for birds in laboratory toxicity tests is 562 mg/kg. For exposure scenarios 

that use the typical application rate of 2 lb/acre, if a predatory bird consumed fish from a 

pond contaminated by an accidental spill, assuming the highest concentrations in fish and 

highest intake on a body weight basis, it would receive an acute dose of 2.83 mg/kg (SERA, 

2003-Glyphosate, Worksheet F08). This dose is 0.005 of the acute NOAEL, so there is no 

basis for asserting or predicting that adverse effects to fish-eating birds are plausible (SERA, 

2003-Glyphosate, p. 4-43). 

57
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Glyphosate, cont’d.

The chronic NOAEL for birds in laboratory toxicity tests is 100 mg/kg/day. If a predatory 

bird consumed fish contaminated by runoff for a lifetime, assuming the highest 

concentrations in fish and highest intake on a body weight basis, it would receive a chronic 

dose of 0.00125 mg/kg/day (SERA, 2003-Glyphosate, Worksheet F09). This estimated dose 

is 0.00001 of the chronic NOAEL, so there is no basis for asserting/predicting that adverse 

effects to fish-eating birds are plausible. 

Estimated doses using the highest application rate (7 lb/acre) are much less than the acute 

and chronic NOAELs for birds, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions. 

Large Predatory Bird

The acute NOAEL for birds in laboratory toxicity tests is 562mg/kg. For exposure scenarios 

that use the typical application rate of 2 lb/acre, if a 0.6 kg bird consumed small mammal 

prey that has been contaminated by direct spray, assuming 100 percent absorption for the 

prey, it would receive an acute dose of 6.46 mg/kg (SERA, 2003-Glyphosate, Worksheet 

F16b). This is 0.0115 of the acute NOAEL, so there is no basis for asserting or predicting 

that adverse effects to predatory birds are plausible. 

Glyphosate does not appear to accumulate or persist in animals. Only about 30 percent of 

ingested glyphosate is absorbed from the gastrointestinal tract (several studies by Davies 

1996 cited in SERA, 2003-Glyphosate). The glyphosate that is absorbed is distributed 

widely throughout the body, and then efficiently excreted. More than 97 percent of the 

administered dose is excreted unchanged, and glyphosate does not substantially concentrate 

or persist in any tissue (SERA 2003 Glyphosate, p. 3-5). These conclusions are consistent 

with data from a field study that measured glyphosate residues in several small mammal 

species after an aerial application in Oregon (Newton et al., 1984). Newton et al. (1984) 

found that residues in small mammals were below 1 mg/kg for deermice and shrews, and 

below 2 mg/kg for voles, three days after treatment. Therefore, chronic exposures from 

contaminated mammal prey due to a single application of glyphosate are unlikely to cause 

any adverse effect. In addition, the acute dose is much less than the chronic NOAEL for 

birds, so there is no basis for asserting or predicting that adverse effects from repeated acute 

exposures from multiple applications of glyphosate over time are plausible. 

Estimated doses using the highest application rate (7 lb/acre) are less than the acute and 

chronic NOAELs for birds, so there is no basis for asserting or predicting that adverse effects 

are plausible using typical or worst-case exposure assumptions. 

Small Insectivorous Bird

The acute NOAEL for birds in laboratory toxicity tests is 562 mg/kg. For exposure scenarios 

that use the typical application rate of 2 lb/acre, if a 10 g bird consumed contaminated insects 

on site shortly after application, assuming the highest residue rates, it would receive an acute 

dose of 226 mg/kg (SERA, 2003-Glyphosate, Worksheet F14b). This dose is 0.4 of the acute 

NOAEL, so there is no basis for asserting or predicting that adverse effects to insectivorous 

birds are plausible (SERA, 2003-Glyphosate, p. 4-43). 

58
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Glyphosate, cont’d.

Data on degradation of herbicide residues from insects is not available, so no chronic 

exposure scenario has been developed. However, the acute dose is greater than the chronic 

NOAEL for birds. LOAEL’s are not reported for birds in the sources I reviewed, presumably 

because of a lack of toxic responses in laboratory tests. Adverse effects to insectivorous 

birds appear plausible from chronic dietary exposures, based on dose exceeding the NOAEL. 

The estimated dose using the highest application rate (7 lb/acre) is greater than the acute 

and chronic NOAELs for birds, so adverse effects to insectivorous birds appear plausible at 

the highest application rate. 

IMAZAPIC

Small Mammal Directly Sprayed

For, exposure scenarios that use the typical application rate of 0.1 lb/acre, if a small mammal 

is directly sprayed, and 100 percent absorption is assumed, the animal would receive an acute 

dose of 2.42 mg/kg (SERA, 2003-Imazapic, Worksheet F02a). This estimated dose is 0.007 

of the acute NOAEL, so there is no basis for asserting or predicting that adverse effects to 

mammals are plausible (SERA, 2003-Imazapic, p. 4-21). 

At the highest application rate of 0.19 lb/acre, the animal would receive an acute dose of 4.36 

mg/kg (project file). This dose is 0.01 of the acute NOAEL, so there is no basis for asserting 

or predicting that adverse effects to mammals are plausible at any application rate. 

Small Mammal Drinking Contaminated Water

The acute NOAEL for mammals in laboratory toxicity tests is 350 mg/kg. The estimated 

doses to a small mammal from drinking water contaminated by an accidental spill, assuming 

the highest levels of contamination, are 0.665 mg/kg for acute exposure (SERA, 2003-

Imazapic, Worksheet F05). If a small mammal consumes contaminated water over time, 

accounting for dissipation, degradation, and other processes, the animal would receive a 

chronic dose of 0.000000439 mg/kg/day (SERA, 2003-Imazapic, Worksheet F07). Doses to a 

large mammal would be even lower on a per kg body weight basis. These doses are 0.002 of 

the acute NOAEL, and 0.000000009 of the chronic NOAEL, respectively, so there is no basis 

for asserting or predicting that adverse effects to mammals are plausible (SERA, 2003-

Imazapic, p. 4-21). 

At the highest application rate of 0.19 lb/acre, the acute dose from drinking water 

contaminated by a spill is 1.26 mg/kg (project file). This dose is 0.004 of the acute NOAEL. 

The chronic dose is also below the chronic NOAEL, so there is no basis for asserting or 

predicting that adverse effects to mammals are plausible, even in a worst-case scenario. 

59
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Imazapic, cont’d.

Large Herbivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 350 mg/kg. For exposure 

scenarios that use the typical application rate of 0.1 lb/acre, if a 70 kg mammal consumed 

contaminated vegetation on site shortly after application, assuming the highest residue rates 

and 100 percents of the diet contaminated, it would receive an acute dose of 4.86 mg/kg 

(SERA, 2003-Imazapic, Worksheet F10). This dose is 0.01 of the acute NOAEL, so there is 

no basis for asserting or predicting that adverse effects to large grass-eating mammals are 

plausible (SERA 2003 Imazapic, p. 4-21). 

The chronic NOAEL for mammals in laboratory toxicity tests is 45 mg/kg/day. Chronic 

exposure from the consumption of contaminated vegetation for 90 days at the treatment site, 

assuming the highest residue rates, results in a dose of 0.929 mg/kg/day (SERA, 2003-

Imazapic, Worksheet F11a). This dose is 0.02 of the chronic NOAEL, so there is no/ basis 

for asserting or predicting that adverse effects to large grass-eating mammals are plausible

(SERA, 2003-Imazapic, p. 4-21). 

Estimated doses using the highest application rate (0.1875 lb/acre) are less than the acute and 

chronic NOAELs for mammals, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions (SERA, 20030-

Imazapic, p. 4-21). 

Medium Carnivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 350 mg/kg. For exposure 

scenarios that use the typical application rate of 0.1 lb/acre, if a 5 kg mammal consumed 

small mammal prey that has been contaminated by direct spray, assuming 100 percent 

absorption for the prey, it would receive an acute dose of 0.21 mg/kg (SERA, 2003-Imazapic, 

Worksheet F16a). Doses to a large mammal would be even lower on a per kg body weight 

basis. This dose is 0.0006 of the acute NOAEL, so there is no basis for asserting or 

predicting that adverse effects to carnivorous mammals are plausible (SERA, 2003=-

Imazapic, p. 4-21). 

Imazapic does not appear to accumulate or persist in animals following either single or 

multiple doses. The elimination of imazapic has been studied in rats, hens, and goats (Afzal, 

1994; Cheng, 1993; Gatterdam 1993a,b; Kao 1993a,b; Sharp and Thalacker, 1999; all as 

cited in SERA, 2003-Imazapic). A combination of elimination and metabolism extensively 

and rapidly eliminated imazapic and its metabolites from the bodies of all species studied. 

Therefore, chronic exposures from contaminated mammal prey due to a single application of 

imazapic are unlikely to cause any adverse effect. In addition, the acute dose is much less 

than the chronic NOAEL for mammals, so there is no basis for asserting or predicting that 

adverse effects from repeated acute exposures from multiple applications of imazapic over 

time are plausible. 

60
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Imazapic, cont’d.

The estimated dose using the highest application rate (0.1875 lb/acre) is less than the acute 

and chronic NOAELs for mammals, so there is no basis for asserting or predicting that 

adverse effects are plausible using typical or worst-case exposure assumptions (SERA, 2003-

Imazapic, p. 4-21). 

Small Herbivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 350 mg/kg. If a small 

mammal consumes contaminated vegetation shortly after application, assuming the highest 

residue rates, the acute dose received is 0.268 mg/kg (SERA, 2003-Imazapic, Worksheet 

F03). This estimated dose is 0.0008 of the acute NOAEL, so there is no basis for asserting or 

predicting that adverse effects to herbivorous mammals are plausible (SERA, 2003-Imazapic, 

p. 4-21). 

The chronic NOAEL for mammals in laboratory toxicity tests is 45 mg/kg/day. If a small 

mammal consumes contaminated vegetation at the treatment site for 90-days, assuming 

highest residue rates, the animal would receive a chronic dose of 0.0102 mg/kg/day (SERA, 

2003-Imazapic, Worksheet F04a). This estimated dose is 0.0002 of the chronic NOAEL, so 

there is no basis for asserting or predicting that adverse effects to herbivorous mammals are 

plausible (SERA, 2003-Imazapic, p. 4-21). 

Estimated doses using the highest application rate (0.1875 lb/acre) are less than the acute and 

chronic NOAELs for mammals, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions (SERA, 2003-

Imazapic, p. 4-21). 

Small Insectivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 350 mg/kg. For exposure 

scenarios that use the typical application rate of 0.1 lb/acre, if a small mammal consumes 

contaminated insects shortly after application, assuming the highest residue rates, the acute 

dose received is 6.94 mg/kg (SERA, 2003-Imazapic, Worksheet 14a). This dose is 0.02 of 

the acute NOAEL, so there is no basis for asserting or predicting that adverse effects to 

insectivorous mammals are plausible (SERA, 2003-Imazapic, p. 4-21). 

Data on degradation of herbicide residues from insects is not available, so no chronic 

exposure scenario has been developed. Residue on insects likely declines over time, but the 

extent of decline has not been quantified. However, the acute dose is less than the chronic 

NOAEL for mammals as well, and chronic doses are much lower than acute doses. 

Therefore, there is no basis for asserting or predicting that adverse effects to insectivorous 

mammals from chronic exposures are plausible. 

The estimated dose using the highest application rate (0.1875 lb/acre) is less than the acute 

and chronic NOAELs for mammals, so there is no basis for asserting or predicting that 

adverse effects are plausible using typical or worst-case exposure assumptions (SERA, 2003-

Imazapic, p. 4-21). 

61
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Imazapic, cont’d.

Large Herbivorous Bird

The acute NOAEL for birds in laboratory toxicity tests is 1100 mg/kg. For exposure 

scenarios that use the typical application rate of 0.1 lb/acre, if a 4 kg bird consumed 

contaminated grass on site shortly after application, assuming the highest residue rates and 

100 percent of diet is contaminated, it would receive an acute dose of 7.6 mg/kg (SERA, 

2003-Imazapic, Worksheet F12). This dose is 0.007 of the acute NOAEL, so there is no 

basis for asserting or predicting that adverse effects to large grass-eating birds are plausible 

(SERA, 2003-Imazapic, p. 4-21). 

The chronic NOAEL for birds in laboratory toxicity tests is 113 mg/kg/day. Chronic 

exposure from the consumption of contaminated grass for 90 days at the treatment site, 

assuming the highest residue rates and 100 percent of diet is contaminated, results in a dose 

of 1.45 mg/kg/day (SERA, 2003-Imazapic, Worksheet F13a). This estimated dose is 0.01 of 

the chronic NOAEL, so there is no/ basis for asserting or predicting that adverse effects to 

large grass-eating birds are plausible (SERA, 2003-Imazapic, p. 4-21). 

Estimated doses using the highest application rate (0.1875 lb/acre) are less than the acute and 

chronic NOAELs for birds, so there is no basis for asserting or predicting that adverse effects 

are plausible using typical or worst-case exposure assumptions (SERA 2003 Imazapic, p. 4-

21). 

Large Fish-eating Bird

Many chemicals may be concentrated or partitioned from water into the tissues of animals in 

the water. This process is referred to as bioconcentration. The potential for bioconcentration 

of imazapic in fish was studied in bluegill sunfish exposed to 14C-labeled imazapic for 28 

days (Robinson, 1994, cited in SERA, 2003-Imazapic). In the SERA risk assessments, 

concentrations in viscera are considered to reflect concentration in whole fish. 

Bioconcentration factors (BCF) for bluegill were 0.11 L/kg in whole fish, indicating that the 

concentration of imazapic in the fish was less than the concentration of imazapic in the water 

(SERA, 2003-Imazapic). The exposure scenarios in the SERA risk assessment use a wholefish BCF of 0.11 L/kg for acute and chronic exposures because of the rapid time it takes to 

reach a steady state and the very low BCF. 

The acute NOAEL for birds in laboratory toxicity tests is 1100 mg/kg. For exposure 

scenarios that use the typical application rate of 0.1 lb/acre, if a predatory bird consumed fish 

from a pond contaminated by an accidental spill, assuming the highest concentrations in fish 

and highest intake on a body weight basis, it would receive an acute dose of 0.0749 mg/kg 

(SERA, 2003-Imazapic, Worksheet F08). This dose is 0.00007 of the acute NOAEL, so there 

is no basis for asserting or predicting that adverse effects to fish-eating birds are plausible

(SERA, 2003-Imazapic, p. 4-21). 

62
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Imazapic, cont’d.

The chronic NOAEL for birds in laboratory toxicity tests is 113 mg/kg/day. If a predatory 

bird consumed fish contaminated by runoff for a lifetime, assuming the highest 

concentrations in fish and highest intake on a body weight basis, it would receive a chronic 

dose of 0.0000000495 mg/kg/day (SERA, 200X-Worksheet F09). This estimated dose is 

0.0000000004 of the chronic NOAEL, so there is no basis for asserting/predicting that 

adverse effects to fish-eating birds are plausible (SERA, 2003-Imazapic, p. 4-21). 

Estimated doses using the highest application rate (0.1875 lb/acre) also result in exposures 

much less than the acute and chronic NOAELs for birds, so there is no basis for asserting or 

predicting that adverse effects are plausible using typical or worst-case exposure assumptions 

(SERA, 2003-Imazapic, p. 4-21). 

Large Predatory Bird

The acute NOAEL for birds in laboratory toxicity tests is 1100 mg/kg. For exposure 

scenarios that use the typical application rate of 0.1 lb/acre, if a 0.6 kg bird consumed small 

mammal prey that has been contaminated by direct spray, assuming 100 percent absorption 

for the prey, it would receive an acute dose of 0.323 mg/kg (SERA, 2003-Imazapic, 

Worksheet F16b). This is 0.0003 of the acute NOAEL, so there is no basis for asserting or 

predicting that adverse effects to predatory birds are plausible (SERA, 2003-Imazapic, p. 4-

21). 

Imazapic does not appear to accumulate or persist in animals following either single or 

multiple doses. The elimination of imazapic has been studied in rats (Cheng 1993), hens 

(Afzal, 1994; Gatterdam, 1993a,b), and goats (Kao 1993a,b; Sharp and Thalacker, 1999; 

cited in SERA, 2003-Imazapic). A combination of elimination and metabolism extensively 

and rapidly eliminated imazapic and its metabolites from the bodies of all species studied. 

Therefore, chronic exposures from contaminated mammal prey due to a single application of 

imazapic are unlikely to cause any adverse effect. In addition, the acute dose is much less 

than the chronic NOAEL for birds, so there is no basis for asserting or predicting that adverse 

effects from repeated acute exposures from multiple applications of imazapic over time are 

plausible. 

The estimated dose using the highest application rate (0.1875 lb/acre) is less than the acute 

and chronic NOAELs for birds, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions (SERA, 2003-

Imazapic, p. 4-21). 

Small Insectivorous Bird

The acute NOAEL for birds in laboratory toxicity tests is 1100 mg/kg. For exposure 

scenarios that use the typical application rate of 0.1 lb/acre, if a 10 g bird consumed 

contaminated insects on site shortly after application, assuming the highest residue rates, it 

would receive an acute dose of 11.3 mg/kg (SERA, 2003-Imazapic, Worksheet F14b). This 

dose is 0.01 of the acute NOAEL, so there is no basis for asserting or predicting that adverse 

effects to insectivorous birds are plausible (SERA, 2003-Imazapic, p. 4-21). 

63
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Imazapic, cont’d.

Data on degradation of herbicide residues from insects is not available, so no chronic 

exposure scenario has been developed. Residue on insects likely declines over time, but the 

extent of decline has not been quantified. However, the acute dose is less than the chronic 

NOAEL for birds as well, and chronic doses are much lower than acute doses. Therefore, 

there is no basis for asserting or predicting that adverse effects to insectivorous birds from 

chronic exposures are plausible. 

The estimated dose using the highest application rate (0.1875 lb/acre) is less than the acute 

and chronic NOAELs for birds, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions (SERA, 2003-

Imazapic, p. 4-21). 

IMAZAPYR

Small Mammal Directly Sprayed

The acute NOAEL for mammals in laboratory toxicity tests is 250 mg/kg. For, exposure 

scenarios that use the typical application rate of 0.45 lb/acre, if a small mammal is directly 

sprayed, and 100 percent absorption is assumed, the animal would receive an acute dose of 

10.9 mg/kg (SERA, 2003-Imazapyr, Worksheet F02a). This estimated dose is 0.04 of the 

acute NOAEL, so there is no basis for asserting or predicting that adverse effects to 

herbivorous mammals are plausible (SERA, 2003-Imazapyr, p. 4-25). 

At the highest application rate of 1.25 lb/acre, the animal would receive an acute dose of 30.3 

mg/kg (project file). This dose is 0.1 of the acute NOAEL, so there is no basis for asserting 

or predicting that adverse effects to mammals are plausible at any application rate. 

Small Mammal Drinking Contaminated Water

The estimated doses to a small mammal from drinking water contaminated by an accidental 

spill, assuming the highest levels of contamination, are 1.22 mg/kg for acute exposure 

(SERA, 2003-Imazapyr, Worksheet F05). If a small mammal consumes contaminated water 

over time, accounting for dissipation, degradation, and other processes, the animal would 

receive a chronic dose of 0.0000659 mg/kg/day (SERA 2003 Imazapyr, Worksheet F07). 

Doses to a large mammal would be even lower on a per kg body weight basis. These doses 

are 0.005 of the acute NOAEL, and 0.0000003 of the chronic NOAEL, respectively, so there 

is no basis for asserting or predicting that adverse effects to mammals are plausible (SERA, 

2003-Imazapyr, p. 4-25). 

At the highest application rate of 1.25 lb/acre, the acute dose from drinking water 

contaminated by a spill is 3.39 mg/kg (project file). This dose is 0.005 of the acute NOAEL. 

The chronic dose is also below the chronic NOAEL, so there is no basis for asserting or 

predicting that adverse effects to mammals are plausible, even in a worst-case scenario. 

64
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Imazapyr, cont’d. 

Large Herbivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 250 mg/kg. For exposure 

scenarios that use the typical application rate of 0.45 lb/acre, if a 70 kg mammal consumed 

contaminated vegetation on site shortly after application, assuming the highest residue rates 

and 100 percents of the diet contaminated, it would receive an acute dose of 21.9 mg/kg 

(SERA, 2003-Imazapyr, Worksheet F10). This dose is 0.09 of the acute NOAEL, so there is 

no basis for asserting or predicting that adverse effects to large grass-eating mammals are 

plausible (SERA, 2003-Imazapyr, p. 4-25). 

The chronic NOAEL for mammals in laboratory toxicity tests is 250 mg/kg/day. Chronic 

exposure from the consumption of contaminated vegetation for 90 days at the treatment site, 

assuming the highest residue rates, results in a dose of 10.6 mg/kg/day (SERA, 200X-Name, 

Worksheet F11a). This dose is 0.04 of the chronic NOAEL, so there is no basis for asserting 

or predicting that adverse effects to large grass-eating mammals are plausible (SERA, 2003-

Imazapyr, p. 4-25). 

Estimated doses using the highest application rate (1.25 lb/acre) are less than the acute and 

chronic NOAEL for mammals, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions (SERA, 2003-

Imazapyr, p. 4.25). 

Medium Carnivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 250 mg/kg. For exposure 

scenarios that use the typical application rate of 0.45 lb/acre, if a 5 kg mammal consumed 

small mammal prey that has been contaminated by direct spray, assuming 100 percent 

absorption for the prey, it would receive an acute dose of 0.944 mg/kg (SERA, 2003-

Imazapyr, Worksheet F16a). (Doses to a large mammal would be even lower on a per kg 

body weight basis). This dose is 0.004 of the acute NOAEL, so there is no basis for asserting 

or predicting that adverse effects to carnivorous mammals are plausible (SERA, 2003-

Imazapyr, p. 4-25). 

Imazapyr does not appear to accumulate or persist in animals following either single or 

multiple doses (SERA, 2003-Imazapyr, p. 3-2). The elimination of imazapyr has been 

studied in rats and lactating goats and the studies reported that it is rapidly excreted, 

unchanged, in urine and feces (Mallipudi et al., 1983; and Zdybak, 1992 as cited in SERA, 

2003-Imazapyr). No metabolites were identified. Therefore, chronic exposures from 

contaminated mammal prey due to a single application of imazapyr are unlikely to cause any 

adverse effect. In addition, the acute dose is much less than the chronic NOAEL for 

mammals, so there is no basis for asserting or predicting that adverse effects from repeated 

acute exposures from multiple applications of imazapyr over time are plausible. 

Estimated doses using the highest application rate (1.25 lb/acre) are less than the acute and 

chronic NOAEL for mammals, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions (SERA, 2003-

mazapyr, p. 4-25). 

65
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Imazapyr, cont’d. 

Small Herbivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 250 mg/kg. If a small 

mammal consumes contaminated vegetation shortly after application, assuming the highest 

residue rates, the acute dose received is 1.21 mg/kg (SERA, 2003-Imazapyr, Worksheet 

F03). This estimated dose is 0.005 of the acute NOAEL, so there is no basis for asserting or 

predicting that adverse effects to herbivorous mammals are plausible (SERA, 2003-

Imazapyr, p. 4-25). 

The chronic NOAEL for mammals in laboratory toxicity tests is 250 mg/kg/day. If a small 

mammal consumes contaminated vegetation at the treatment site for 90-days, assuming 

highest residue rates, the animal would receive a chronic dose of 0.117 mg/kg/day (SERA, 

2003-Imazapyr, Worksheet F04a). This estimated dose is 0.0005 of the chronic NOAEL, so 

there is no basis for asserting or predicting that adverse effects to herbivorous mammals are 

plausible. 

Estimated doses using the highest application rate (1.25 lb/acre) are less than the acute and 

chronic NOAEL for mammals, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions (SERA, 2003-

Imazapyr, p. 4-25). 

Small Insectivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 250 mg/kg. For exposure 

scenarios that use the typical application rate of 0.45 lb/acre, if a small mammal consumes 

contaminated insects shortly after application, assuming the highest residue rates, the acute 

dose received is 31.2 mg/kg (SERA, 2003-Imazapyr, Worksheet 14a). This dose is 0.1 of the 

acute NOAEL, so there is no basis for asserting or predicting that adverse effects to 

insectivorous mammals are plausible (SERA, 2003-Imazapyr, p. 4-25). 

Data on degradation of herbicide residues from insects is not available, so no chronic 

exposure scenario has been developed. Residue on insects likely declines over time, but the 

extent of decline has not been quantified. However, the acute dose is less than the chronic 

NOAEL for mammals as well, and chronic doses are much lower than acute doses. 

Therefore, there is no basis for asserting or predicting that adverse effects to insectivorous 

mammals from chronic exposures are plausible. 

The estimated dose using the highest application rate (1.25 lb/acre) is less than the acute and 

chronic NOAEL for mammals, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions (SERA, 2003-

Imazapyr, p. 4-25). 

66
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Imazapyr, cont’d. 

Large Herbivorous Bird

The acute NOAEL for birds in laboratory toxicity tests is 674 mg/kg. For exposure scenarios 

that use the typical application rate of 0.45 lb/acre, if a 4 kg bird consumed contaminated 

grass on site shortly after application, assuming the highest residue rates and 100 percent of 

diet is contaminated, it would receive an acute dose of 34.2 mg/kg (SERA, 2003-Imazapyr, 

Worksheet F12). This dose is 0.05 of the acute NOAEL, so there is no basis for asserting or 

predicting that adverse effects to large grass-eating birds are plausible (SERA, 2003-

Imazapyr, p. 4-25). 

The chronic NOAEL for birds in laboratory toxicity tests is 200 mg/kg/day. Chronic 

exposure from the consumption of contaminated grass for 90 days at the treatment site, 

assuming the highest residue rates and 100 percent of diet is contaminated, results in a dose 

of 16.5 mg/kg/day (SERA, 2003-Imazapyr, Worksheet F13a). This estimated dose is 0.08 of 

the chronic NOAEL, so there is no/ basis for asserting or predicting that adverse effects to 

large grass-eating birds are plausible (SERA, 2003-Imazapyr, p. 4-25). 

Estimated doses using the highest application rate (1.25 lb/acre) are less than the acute and 

chronic NOAEL for mammals, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions (SERA, 2003-

Imazapyr, p. 4-25). 

Large Fish-eating Bird

Many chemicals may be concentrated or partitioned from water into the tissues of animals in 

the water. This process is referred to as bioconcentration. The potential for bioconcentration 

of imazapyr in fish was studied in bluegill sunfish exposed to 14C-labeled imazapyr for 28 

days (McAllister et al., 1985, cited in SERA, 2003-Imazapyr). In the SERA risk 

assessments, concentrations in viscera are considered to reflect concentration in whole fish. 

Bioconcentration factors (BCF) for bluegill were 0.5 L/kg, indicating that the concentration 

of imazapyr in the fish was less than the concentration of imazapyr in the water (SERA, 

2003-Imazapyr, p. 3-20). The exposure scenarios in the SERA risk assessment use a wholefish BCF of 0.5 L/kg for acute and chronic exposures. 

The acute NOAEL for birds in laboratory toxicity tests is 674 mg/kg. For exposure scenarios 

that use the typical application rate of 0.45 lb/acre, if a predatory bird consumed fish from a 

pond contaminated by an accidental spill, assuming the highest concentrations in fish and 

highest intake on a body weight basis, it would receive an acute dose of 0.625 mg/kg (SERA, 

2003-Imazapyr, Worksheet F08). This dose is 0.0009 of the acute NOAEL, so there is no 

basis for asserting or predicting that adverse effects to fish-eating birds are plausible (SERA, 

2003-Imazapyr, p. 4-25). 

67
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Imazapyr, cont’d. 

The chronic NOAEL for birds in laboratory toxicity tests is 200 mg/kg/day. If a predatory 

bird consumed fish contaminated by runoff for a lifetime, assuming the highest 

concentrations in fish and highest intake on a body weight basis, it would receive a chronic 

dose of 0.0000338 mg/kg/day (SERA, 2003-Imazapyr, Worksheet F09). This estimated dose 

is 0.0000002 of the chronic NOAEL, so there is no basis for asserting/predicting that adverse 

effects to fish-eating birds are plausible. 

Estimated doses using the highest application rate (1.25 lb/acre) are less than the acute and 

chronic NOAEL for birds, so there is no basis for asserting or predicting that adverse effects 

are plausible using typical or worst-case exposure assumptions (SERA, 2003-Imazapyr, p. 4-

25). 

Large Predatory Bird

The acute NOAEL for birds in laboratory toxicity tests is 674 mg/kg. For exposure scenarios 

that use the typical application rate of 0.45 lb/acre, if a 0.6 kg bird consumed small mammal 

prey that has been contaminated by direct spray, assuming 100 percent absorption for the 

prey, it would receive an acute dose of 1.45 mg/kg (SERA, 2003-Imazapyr, Worksheet 

F16b). This is 0.002 of the acute NOAEL, so there is no basis for asserting or predicting that 

adverse effects to predatory birds are plausible. 

Imazapyr does not appear to accumulate or persist in animals following either single or 

multiple doses (SERA, 2003-Imazapyr, p. 3-2). The elimination of imazapyr has been 

studied in rats and lactating goats and the studies reported that it is rapidly excreted, 

unchanged, in urine and feces (Mallipudi et al., 1983; and Zdybak, 1992 as cited in SERA, 

2003-Imazapyr). No metabolites were identified. Therefore, chronic exposures from 

contaminated mammal prey due to a single application of imazapyr are unlikely to cause any 

adverse effect. In addition, the acute dose is much less than the chronic NOAEL for birds, 

so there is no basis for asserting or predicting that adverse effects from repeated acute 

exposures from multiple applications of imazapyr over time are plausible. 

The estimated dose using the highest application rate (1.25 lb/acre) is less than the acute and 

chronic NOAEL for mammals, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions (SERA, 2003-

Imazapyr, p. 4-25). 

Small Insectivorous Bird

The acute NOAEL for birds in laboratory toxicity tests is 674 mg/kg. For exposure scenarios 

that use the typical application rate of 0.45 lb/acre, if a 10 g bird consumed contaminated 

insects on site shortly after application, assuming the highest residue rates, it would receive 

an acute dose of 50.8 mg/kg (SERA, 2003-Imazapyr, Worksheet F14b). This dose is 0.08 of 

the acute NOAEL, so there is no basis for asserting or predicting that adverse effects to 

insectivorous birds are plausible (SERA, 2003-Imazapyr, p. 4-25). 

68
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Imazapyr, cont’d. 

Data on degradation of herbicide residues from insects is not available, so no chronic 

exposure scenario has been developed. Residue on insects likely declines over time, but the 

extent of decline has not been quantified. However, the acute dose is less than the chronic 

NOAEL for birds as well, and chronic doses are much lower than acute doses. Therefore, 

there is no basis for asserting or predicting that adverse effects to insectivorous birds from 

chronic exposures are plausible. 

The estimated dose using the highest application rate (1.25 lb/acre) is less than the acute and 

chronic NOAEL for birds, so there is no basis for asserting or predicting that adverse effects 

are plausible using typical or worst-case exposure assumptions (SERA, 2003-Imazapyr, p. 4-

25). 

METSULFURON METHYL

Small Mammal Directly Sprayed

The acute NOAEL for mammals in laboratory toxicity tests is 25 mg/kg. For, exposure 

scenarios that use the typical application rate of 0.03 lb/acre, if a small mammal is directly 

sprayed, and 100 percent absorption is assumed, the animal would receive an acute dose of 

0.727 mg/kg (SERA, 2003-Metsulfuron methyl, Worksheet F02a). This estimated dose is 

0.03 of the acute NOAEL, so there is no basis for asserting or predicting that adverse effects 

to herbivorous mammals are plausible (SERA, 2003-Metsulfuron methyl, p. 4-26). 

At the highest application rate of 0.15 lb/acre, the animal would receive an acute dose of 3.64 

mg/kg (project file). This dose is 0.1 of the acute NOAEL, so there is no basis for asserting 

or predicting that adverse effects to mammals are plausible at any application rate. 

Small Mammal Drinking Contaminated Water

The estimated doses to a small mammal from drinking water contaminated by an accidental 

spill, assuming the highest levels of contamination, are 0.0443 mg/kg for acute exposure 

(SERA, 2003-Metsulfuron methyl, Worksheet F05). If a small mammal consumes 

contaminated water over time, accounting for dissipation, degradation, and other processes, 

the animal would receive a chronic dose of 0.00000176 mg/kg/day (SERA 2003 Metsulfuron 

methyl, Worksheet F07). Doses to a larger mammal would be even lower on a per kg body 

weight basis. These doses are 0.002 of the acute NOAEL, and 0.00000007 of the chronic 

NOAEL, respectively, so there is no basis for asserting or predicting that adverse effects to 

mammals are plausible (SERA, 2003-Metsulfuron methyl, p. 4-26, 4-27). 

At the highest application rate of 0.15 lb/acre, the acute dose from drinking water 

contaminated by a spill is 0.222 mg/kg (project file). This dose is 0.009 of the acute NOAEL. 

The chronic dose is also below the chronic NOAEL, so there is no basis for asserting or 

predicting that adverse effects to mammals are plausible, even in a worst-case scenario. 

69
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Metsulfuron methyl, cont’d. 

Large Herbivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 25 mg/kg. For exposure 

scenarios that use the typical application rate of 0.03 lb/acre, if a 70 kg mammal consumed 

contaminated vegetation on site shortly after application, assuming the highest residue rates 

and 100 percents of the diet contaminated, it would receive an acute dose of 1.46 mg/kg 

(SERA, 2003-Metsulfuron methyl, Worksheet F10). This dose is 0.06 of the acute NOAEL, 

so there is no basis for asserting or predicting that adverse effects to large grass-eating 

mammals are plausible (SERA, 2003-Metsulfuron methyl, p. 4-26). The chronic NOAEL for 

mammals in laboratory toxicity tests is 25 mg/kg/day. Chronic exposure from the 

consumption of contaminated vegetation for 90 days at the treatment site, assuming the 

highest residue rates, results in a dose of 0.613 mg/kg/day (SERA, 2003-Metsulfuron methyl, 

Worksheet F11a). This dose is 0.02 of the chronic NOAEL, so there is no basis for asserting 

or predicting that adverse effects to large grass-eating mammals are plausible (SERA, 2003-

Metsulfuron methyl, p. 4-27). 

Estimated doses using the highest application rate (0.15 lb/acre) are less than the acute and 

chronic NOAEL for mammals, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions (SERA 2003 

Metsulfuron methyl, p. 4-27). 

Medium Carnivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 25 mg/kg. For exposure 

scenarios that use the typical application rate of 0.03 lb/acre, if a 5 kg mammal consumed 

small mammal prey that has been contaminated by direct spray, assuming 100 percent 

absorption for the prey, it would receive an acute dose of 0.0629 mg/kg (SERA, 2003-

Metsulfuron methyl, Worksheet F16a). Doses to a large mammal would be even lower on a 

per kg body weight basis. This dose is 0.003 of the acute NOAEL, so there is no basis for 

asserting or predicting that adverse effects to carnivorous mammals are plausible (SERA, 

2003-Metsulfuron methyl, p. 4-26). 

Metsulfuron methyl does not appear to accumulate or persist in animal tissues. The 

elimination of metsulfuron methyl has been studied in rats, hens cows, and goats (SERA 

2003 Metsulfuron methyl, citing Charlton and Bookhart, 1996; USEPA, 1998; Hershberger 

and Moore, 1985; Hundley, 1985; Hunt, 1984). A combination of elimination of the 

unchanged compound and metabolism rapidly eliminated metsulfuron methyl from the 

bodies of all species studied. The half-life for elimination in all species is one day or less 

(SERA, 2003-Metsulfuron methyl, p. 3-3). Therefore, chronic exposures from contaminated 

mammal prey due to a single application of metsulfuron methyl are unlikely to cause any 

adverse effect. In addition, the acute dose is much less than the chronic NOAEL for 

mammals, so there is no basis for asserting or predicting that adverse effects from repeated 

acute exposures from multiple applications of metsulfuron methyl over time are plausible. 

70
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Metsulfuron methyl, cont’d. 

The estimated dose using the highest application rate (0.15 lb/acre) is less than the acute and 

chronic NOAEL for mammals, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions (SERA, 2003-

etsulfuron methyl, p. 4-27). 

Small Herbivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 25 mg/kg. If a small mammal 

consumes contaminated vegetation shortly after application, assuming the highest residue 

rates, the acute dose received is 0.0804 mg/kg (SERA, 200- Metsulfuron methyl, Worksheet 

F03). This estimated dose is 0.003 of the acute NOAEL, so there is no basis for asserting or 

predicting that adverse effects to herbivorous mammals are plausible (SERA, 2003-

Metsulfuron methyl, p. 4-26). 

The chronic NOAEL for mammals in laboratory toxicity tests is 25 mg/kg/day. If a small 

mammal consumes contaminated vegetation at the treatment site for 90-days, assuming 

highest residue rates, the animal would receive a chronic dose of 0.00676 mg/kg/day (SERA, 

2003-Metsulfuron methyl, Worksheet F04a). This estimated dose is 0.0003 of the chronic 

NOAEL, so there is no basis for asserting or predicting that adverse effects to small 

herbivorous mammals are plausible (SERA, 2003-Metsulfuron methyl, p. 4-27). 

Estimated doses using the highest application rate (0.15 lb/acre) are less than the acute and 

chronic NOAEL for mammals, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions (SERA 2003 

Metsulfuron methyl, p. 4-27). 

Small Insectivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 25 mg/kg. For exposure 

scenarios that use the typical application rate of 0.03 lb/acre, if a small mammal consumes 

contaminated insects shortly after application, assuming the highest residue rates, the acute 

dose received is 2.08 mg/kg (SERA, 2003-Metsulfuron methyl, Worksheet 14a). This dose is 

0.08 of the acute NOAEL, so there is no basis for asserting or predicting that adverse effects 

to insectivorous mammals are plausible (SERA, 2003-Metsulfuron methyl, p. 4-26). 

Data on degradation of herbicide residues from insects is not available, so no chronic 

exposure scenario has been developed. Residue on insects likely declines over time, but the 

extent of decline has not been quantified. However, the acute dose is less than the chronic 

NOAEL as well, and chronic doses are much lower than acute doses. Therefore, there is no 

basis for asserting or predicting that adverse effects to insectivorous mammals from chronic 

exposures are plausible. 

Estimated doses using the highest application rate (0.15 lb/acre) also result in an exposure 

less than the acute and chronic NOAEL for mammals, so there is no basis for asserting or 

predicting that adverse effects are plausible using typical or worst-case exposure 

assumptions. 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Metsulfuron methyl, cont’d. 

Large Herbivorous Bird

The acute NOAEL for birds in laboratory toxicity tests is 1043 mg/kg. For exposure 

scenarios that use the typical application rate of 0.03 lb/acre, if a 4 kg bird consumed 

contaminated grass on site shortly after application, assuming the highest residue rates and 

100 percent of diet is contaminated, it would receive an acute dose of 2.28 mg/kg (SERA, 

2003-Metsulfuron methyl, Worksheet F12). This dose is 0.002 of the acute NOAEL, so there 

is no basis for asserting or predicting that adverse effects to large grass-eating birds are 

plausible (SERA, 2003-Metsulfuron methyl, p. 4-26). 

The chronic NOAEL for birds in laboratory toxicity tests is 120 mg/kg/day. Chronic 

exposure from the consumption of contaminated grass for 90 days at the treatment site, 

assuming the highest residue rates and 100 percent of diet is contaminated, results in a dose 

of 0.96 mg/kg/day (SERA, 2003-Metsulfuron methyl, Worksheet F13a). This estimated dose 

is 0.008 of the chronic NOAEL, so there is no basis for asserting or predicting that adverse 

effects to large grass-eating birds are plausible (SERA, 2003-Metsulfuron methyl, p. 4-27). 

Estimated doses using the highest application rate (0.15 lb/acre) are less than the acute and 

chronic NOAELs for birds, so there is no basis for asserting or predicting that adverse effects 

are plausible using typical or worst-case exposure assumptions (SERA, 2003-Metsulfuron 

methyl, p. 4-27). 

Large Fish-eating Bird

Many chemicals may be concentrated or partitioned from water into the tissues of animals in 

the water. This process is referred to as bioconcentration. The potential for bioconcentration 

of metsulfuron methyl in fish was studied in bluegill sunfish exposed to 14C-metsulfuron 

methyl for 28 days (Han 1982, cited in SERA, 2003-Metsulfuron methyl). In the SERA risk 

assessments, concentrations in viscera are considered to reflect concentration in whole fish. 

Bioconcentration factors (BCF) reported for bluegill viscera were 0.21 L/kg after 24 hours 

and the highest BCF reported was 2.11 L/kg after 14 days (SERA, 2003-Metsulfuron methyl, 

Appendix 8). The exposure scenarios in the SERA risk assessment use a whole-fish BCF of 

0.21 L/kg for acute exposure and 2.11 L/kg for chronic exposure. 

The acute NOAEL for birds in laboratory toxicity tests is 1043 mg/kg. For exposure 

scenarios that use the typical application rate of 0.03 lb/acre, if a predatory bird consumed 

fish from a pond contaminated by an accidental spill, assuming the highest concentrations in 

fish and highest intake on a body weight basis, it would receive an acute dose of 0.00954 

mg/kg (SERA, 2003-Metsulfuron methyl, Worksheet F08). This dose is 0.000009 of the 

acute NOAEL, so there is no basis for asserting or predicting that adverse effects to fisheating birds are plausible (SERA, 2003-Metsulfuron methyl, p. 4-26). 

72
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Metsulfuron methyl, cont’d. 

The chronic NOAEL for birds in laboratory toxicity tests is 120 mg/kg/day. If a predatory 

bird consumed fish contaminated by runoff for a lifetime, assuming the highest 

concentrations in fish and highest intake on a body weight basis, it would receive a chronic 

dose of 0.0000038 mg/kg/day (SERA, 2003-Metsulfuron methyl, Worksheet F09). This 

estimated dose is 0.00000003 of the chronic NOAEL, so there is no basis for 

asserting/predicting that adverse effects to fish-eating birds are plausible (SERA 2003 

Metsulfuron methyl, p. 4-27). 

Estimated doses using the highest application rate (0.15 lb/acre) are much less than the acute 

and chronic NOAELs for birds, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions. 

Large Predatory Bird

The acute NOAEL for birds in laboratory toxicity tests is 1043mg/kg. For exposure 

scenarios that use the typical application rate of 0.03 lb/acre, if a 0.6 kg bird consumed small 

mammal prey that has been contaminated by direct spray, assuming 100 percent absorption 

for the prey, it would receive an acute dose of 0.097 mg/kg (SERA, 2003-Metsulfuron 

methyl, Worksheet F16b). This is 0.00009 of the acute NOAEL, so there is no basis for 

asserting or predicting that adverse effects to predatory birds are plausible (SERA, 2003-

Metsulfuron methyl, p. 4-26). 

Metsulfuron methyl does not appear to accumulate or persist in animal tissues. The 

elimination of metsulfuron methyl has been studied in rats, hens cows, and goats (SERA, 

2003-Metsulfuron methyl, citing Charlton and Bookhart, 1996; USEPA, 1998; Hershberger 

and Moore, 1985; Hundley, 1985; Hunt, 1984). A combination of elimination of the 

unchanged compound and metabolism rapidly eliminated metsulfuron methyl from the 

bodies of all species studied. The half-life for elimination in all species is one day or less 

(SERA, 2003-Metsulfuron methyl, p. 3-3). Therefore, chronic exposures from contaminated 

mammal prey due to a single application of metsulfuron methyl are unlikely to cause any 

adverse effect. In addition, the acute dose is much less than the chronic NOAEL for birds, so 

there is no basis for asserting or predicting that adverse effects from repeated acute exposures 

from multiple applications of metsulfuron methyl over time are plausible. 

The estimated dose using the highest application rate (0.15 lb/acre) is less than the acute and 

chronic NOAELs for birds, so there is no basis for asserting or predicting that adverse effects 

are plausible using typical or worst-case exposure assumptions. 

Small Insectivorous Bird

The acute NOAEL for birds in laboratory toxicity tests is 1043 mg/kg. For exposure 

scenarios that use the typical application rate of 0.03 lb/acre, if a 10 g bird consumed 

contaminated insects on site shortly after application, assuming the highest residue rates, it 

would receive an acute dose of 3.38 mg/kg (SERA, 2003-Metsulfuron methyl, Worksheet 

F14b). This dose is 0.003 of the acute NOAEL, so there is no basis for asserting or predicting 

that adverse effects to insectivorous birds are plausible (SERA, 2003-Metsulfuron methyl, p. 

4-26). 

73
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Metsulfuron methyl, cont’d. 

Data on degradation of herbicide residues from insects is not available, so no chronic 

exposure scenario has been developed. However, the acute dose is less than the chronic 

NOAEL for birds as well, and chronic doses are much less than acute doses. Therefore, there 

is no basis for asserting or predicting that adverse effects to insectivorous birds from chronic 

exposures are plausible. 

The estimated doses using the highest application rate (0.15 lb/acre) is less than the acute and 

chronic NOAELs for birds, so there is no basis for asserting or predicting that adverse effects 

are plausible using typical or worst-case exposure assumptions. 

PICLORAM

Small Mammal Directly Sprayed

The acute NOAEL for mammals in laboratory toxicity tests is 34 mg/kg. For, exposure 

scenarios that use the typical application rate of 0.35 lb/acre, if a small mammal is directly 

sprayed, and 100 percent absorption is assumed, the animal would receive an acute dose of 

8.49 mg/kg (SERA, 2003-Picloram, Worksheet F02a). This estimated dose is 0.2 of the 

acute NOAEL, so there is no basis for asserting or predicting that adverse effects to 

herbivorous mammals are plausible (SERA, 2003-Picloram, p. 4-29). 

At the highest application rate of 1 lb/acre, the animal would receive an acute dose of 24.2 

mg/kg (project file). This dose is 0.7 of the acute NOAEL, so there is no basis for asserting 

or predicting that adverse effects to mammals are plausible at any application rate. 

Small Mammal Drinking Contaminated Water

The estimated doses to a small mammal from drinking water contaminated by an accidental 

spill, assuming the highest levels of contamination, are 0.887 mg/kg for acute exposure 

(SERA, 2003-Picloram, Worksheet F05). If a small mammal consumes contaminated water 

over time, accounting for dissipation, degradation, and other processes, the animal would 

receive a chronic dose of 0.000205 mg/kg/day (SERA, 2003-Picloram, Worksheet F07). 

Doses to a large mammal would be even lower on a per kg body weight basis. These doses 

are 0.03 of the acute NOAEL, and 0.00003 of the chronic NOAEL, respectively, so there is 

no basis for asserting or predicting that adverse effects to mammals are plausible (SERA, 

2003-Picloram, p. 4-29). 

At the highest application rate of 1 lb/acre, the acute dose from drinking water contaminated 

by a spill is 2.53 mg/kg (project file). This dose is 0.07 of the acute NOAEL. The chronic 

dose is also below the chronic NOAEL, so there is no basis for asserting or predicting that 

adverse effects to mammals are plausible, even in a worst-case scenario. 

74
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Picloram, cont’d.

Large Herbivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 34 mg/kg. For exposure 

scenarios that use the typical application rate of 0.35 lb/acre, if a 70 kg mammal consumed 

contaminated vegetation on site shortly after application, assuming the highest residue rates 

and 100 percents of the diet contaminated, it would receive an acute dose of 17.0 mg/kg 

(SERA, 2003-Picloram, Worksheet F10). This dose is 0.5 of the acute NOAEL, so there is 

no basis for asserting or predicting that adverse effects to large grass-eating mammals are 

plausible (SERA, 2003-Picloram, p. 4-29). The chronic NOAEL for mammals in laboratory 

toxicity tests is 7 mg/kg/day. Chronic exposure from the consumption of contaminated 

vegetation for 90 days at the treatment site, assuming the highest residue rates, results in a 

dose of 2.18 mg/kg/day (SERA 2003 Picloram, Worksheet F11a). This dose is 0.3 of the 

chronic NOAEL, so there is no basis for asserting or predicting that adverse effects to large 

grass-eating mammals are plausible (SERA, 2003-Picloram, p. 4-29). 

Estimated doses using the highest application rate (1 lb/acre) are greater than the acute 

NOAEL and about equal to the chronic NOAEL for mammals. The acute dose (48.6 mg/kg) 

is less than the acute LOAEL for decreased weight gain in rabbits (USEPA/OPP, 1998). No 

adverse effects are plausible from chronic exposures, but adverse effects to large herbivorous 

mammals may be plausible from acute dietary exposures. 

Medium Carnivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 34 mg/kg. For exposure 

scenarios that use the typical application rate of 0.35 lb/acre, if a 5 kg mammal consumed 

small mammal prey that has been contaminated by direct spray, assuming 100 percent 

absorption for the prey, it would receive an acute dose of 0.734 mg/kg (SERA, 2003-

Picloram, Worksheet F16a). Doses to a larger mammal would be even lower on a per kg 

body weight basis. This dose is 0.0216 of the acute NOAEL, so there is no basis for 

asserting or predicting that adverse effects to carnivorous mammals are plausible (SERA, 

2003-Picloram, p. 4-29). 

Picloram does not appear to accumulate or persist in animals. The elimination of picloram 

has been studied in humans, rats, dogs, and cattle (SERA 2003 Picloram). In humans, over 

75 percent of the administered picloram was eliminated after six hours and over 90 percent 

was eliminated after 72 hours (SERA, 2003-Picloram citing Nolan et al. 1984). Therefore, 

chronic exposures from contaminated mammal prey due to a single application of picloram 

are unlikely to cause any adverse effect. In addition, the acute dose is much less than the 

chronic NOAEL for mammals, so there is no basis for asserting or predicting that adverse 

effects from repeated acute exposures from multiple applications of carnivorous mammals 

over time are plausible. 

The estimated dose using the highest application rate (1 lb/acre) is less than the acute and 

chronic NOAELs for mammals, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions. 

75
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Picloram, cont’d.

Small Herbivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 34 mg/kg. If a small mammal 

consumes contaminated vegetation shortly after application, assuming the highest residue 

rates, the acute dose received is 0.938 mg/kg (SERA, 2003-Picloram, Worksheet F03). This 

estimated dose is 0.03 of the acute NOAEL, so there is no basis for asserting or predicting 

that adverse effects to herbivorous mammals are plausible (SERA, 2003-Picloram, p. 4-29). 

The chronic NOAEL for mammals in laboratory toxicity tests is 7 mg/kg/day. If a small 

mammal consumes contaminated vegetation at the treatment site for 90-days, assuming 

highest residue rates, the animal would receive a chronic dose of 0.024 mg/kg/day (SERA, 

2003-Picloram, Worksheet F04a). This estimated dose is 0.003 of the chronic NOAEL, so 

there is no basis for asserting or predicting that adverse effects to small herbivorous 

mammals are plausible (SERA, 2003-Picloram, p. 4-29). 

Estimated doses using the highest application rate (1 lb/acre) are less than the acute and 

chronic NOAELs for mammals, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions. 

Small Insectivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 34 mg/kg. For exposure 

scenarios that use the typical application rate of 0.35 lb/acre, if a small mammal consumes 

contaminated insects shortly after application, assuming the highest residue rates, the acute 

dose received is 24.3 mg/kg (SERA, 2003-Picloram, Worksheet 14a). This dose is 0.714 of 

the acute NOAEL, so there is no basis for asserting or predicting that adverse effects to 

insectivorous mammals are plausible (SERA, 2003-Picloram, p. 4-29). 

Data on degradation of herbicide residues from insects is not available, so no chronic 

exposure scenario has been developed. Residue on insects likely declines over time, but the 

extent of decline has not been quantified. The acute dose is greater than the chronic 

NOAEL (7 mg/kg), and near the chronic LOAEL (35 mg/kg/day) for increased liver weight. 

So adverse effects to insectivorous mammals appear plausible from chronic dietary 

exposures. The exposure scenario uses residue rates from small insects, which are 

substantially higher than those for large insects, and assumes that 100 percent of the daily 

diet is composed of insects that have been directly sprayed. For bats, in particular, the 

scenario is unlikely to occur in the field. It seems more plausible for shrews and small 

fossorial insectivores, however. 

The estimated dose (69.4 mg/kg) using the highest application rate (1 lb/acre) is greater 

than the acute and chronic NOAELs for mammals. It is less than the acute LOAEL for 

decreased weight gain, but is almost twice the chronic LOAEL for increased liver weight. So 

adverse effects to insectivorous mammals appear plausible from acute or chronic dietary 

exposures. 

76
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Picloram, cont’d.

Large Herbivorous Bird

The acute NOAEL for birds in laboratory toxicity tests is 1500 mg/kg. For exposure 

scenarios that use the typical application rate of 0.35 lb/acre, if a 4 kg bird consumed 

contaminated grass on site shortly after application, assuming the highest residue rates and 

100 percent of diet is contaminated, it would receive an acute dose of 26.6 mg/kg (SERA, 

2003-Name, Worksheet F12). This dose is 0.02 of the acute NOAEL, so there is no basis for 

asserting or predicting that adverse effects to large grass-eating birds are plausible (SERA, 

2003-Picloram, p. 4-29). 

There is no chronic toxicity index available for effects of picloram to birds, so the mammal 

chronic NOAEL will be used. Since the acute NOAEL for birds is greater than the acute 

NOAEL for mammals, the use of the chronic figure from mammals is likely to over-estimate 

risk to birds. The chronic NOAEL for mammals in laboratory toxicity tests is 7 mg/kg/day. 

Chronic exposure from the consumption of contaminated grass for 90 days at the treatment 

site, assuming the highest residue rates and 100 percent of diet is contaminated, results in a 

dose of 3.41 mg/kg/day (SERA, 2003-Picloram, Worksheet F13a). This estimated dose is 

0.5 of the chronic NOAEL, so there is no/ basis for asserting or predicting that adverse 

effects to large grass-eating birds are plausible (SERA, 2003-Picloram, p. 4-29). 

Estimated doses using the highest application rate (1 lb/acre) are less than the acute NOAEL 

for birds, but greater than the chronic NOAEL for mammals. The chronic dose is less than 

the chronic LOAEL for mammals. No adverse effects are plausible from acute exposures, 

but adverse effects to large herbivorous birds appear plausible from chronic dietary 

exposures, based on dose exceeding the NOAEL. Since picloram does not kill grass, 

herbicide residues on grass may be more available for chronic ingestion than non-selective 

herbicides. 

Large Fish-eating Bird

Many chemicals may be concentrated or partitioned from water into the tissues of animals in 

the water. This process is referred to as bioconcentration. The potential for bioconcentration 

of picloram in fish was studied in bluegill and channel catfish exposed to 14C-picloram for 28 

days (Bidlack 1980a,b cited in SERA, 2003-Picloram). Only trace amounts of 14C-picloram 

were recovered in the fish, so the BCF for picloram appears to be substantially less than one 

(SERA 2003 Picloram). The exposure scenarios in the SERA risk assessment use a wholefish BCF of 1 L/kg for acute and chronic exposures, which will over-estimate exposure. 

The acute NOAEL for birds in laboratory toxicity tests is 1500 mg/kg. For exposure 

scenarios that use the typical application rate of 0.35 lb/acre, if a predatory bird consumed 

fish from a pond contaminated by an accidental spill, assuming the highest concentrations in 

fish and highest intake on a body weight basis, it would receive an acute dose of 0.908 mg/kg 

(SERA, 2003-Picloram, Worksheet F08). This dose is 0.0006 of the acute NOAEL, so there 

is no basis for asserting or predicting that adverse effects to fish-eating birds are plausible

(SERA, 2003-Picloram, p. 4-29). 

77
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Picloram, cont’d.

There is no chronic toxicity index available for effects of picloram to birds, so the mammal 

chronic NOAEL will be used. Since the acute NOAEL for birds is greater than the acute 

NOAEL for mammals, the use of the chronic figure from mammals is likely to over-estimate 

risk to birds. The chronic NOAEL for mammals in laboratory toxicity tests is 7 mg/kg/day. 

If a predatory bird consumed fish contaminated by runoff for a lifetime, assuming the highest 

concentrations in fish and highest intake on a body weight basis, it would receive a chronic 

dose of 0.000214 mg/kg/day (SERA, 2003-Picloram, Worksheet F09). This estimated dose is 

0.00003 of the chronic NOAEL, so there is no basis for asserting/predicting that adverse 

effects to fish-eating birds are plausible (SERA, 2003-Picloram, p. 4-29). 

Estimated doses using the highest application rate (1 lb/acre) are less than the acute NOAEL 

for birds and chronic NOAEL for mammals, so there is no basis for asserting or predicting 

that adverse effects are plausible using typical or worst-case exposure assumptions. 

Large Predatory Bird

The acute NOAEL for birds in laboratory toxicity tests is 1500 mg/kg. For exposure 

scenarios that use the typical application rate of 0.35 lb/acre, if a 0.6 kg bird consumed small 

mammal prey that has been contaminated by direct spray, assuming 100 percent absorption 

for the prey, it would receive an acute dose of 1.13 mg/kg (SERA 2003 Picloram, Worksheet 

F16b). This is 0.000754 of the acute NOAEL, so there is no basis for asserting or predicting 

that adverse effects to predatory birds are plausible (SERA, 2003-Picloram, p. 4-29). 

Picloram does not appear to accumulate or persist in animals. The elimination of picloram 

has been studied in humans, rats, dogs, and cattle (SERA, 2003-Picloram). In humans, over 

75 percent of the administered picloram was eliminated after six hours and over 90 percent 

was eliminated after 72 hours (SERA, 2003-Picloram citing Nolan et al. 1984). Therefore, 

chronic exposures from contaminated mammal prey due to a single application of picloram 

are unlikely to cause any adverse effect. In addition, the acute dose is less than the chronic 

NOAEL for mammals, so there is no basis for asserting or predicting that adverse effects 

from repeated acute exposures from multiple applications of picloram over time are 

plausible. 

The estimated dose using the highest application rate (1 lb/acre) is less than the acute 

NOAEL for birds and chronic NOAEL mammals, so there is no basis for asserting or 

predicting that adverse effects are plausible using typical or worst-case exposure 

assumptions. 

Small Insectivorous Bird

The acute NOAEL for birds in laboratory toxicity tests is 1500 mg/kg. For exposure 

scenarios that use the typical application rate of 0.35 lb/acre, if a 10 g bird consumed 

contaminated insects on site shortly after application, assuming the highest residue rates, it 

would receive an acute dose of 39.5 mg/kg (SERA, 2003-Picloram, Worksheet F14b). This 

dose is 0.03 of the acute NOAEL, so there is no basis for asserting or predicting that adverse 

effects to insectivorous birds are plausible (SERA, 2003-Picloram, p. 4-29). 

78
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Picloram, cont’d.

Data on degradation of herbicide residues from insects is not available, so no chronic 

exposure scenario has been developed. Residue on insects likely declines over time, but the 

extent of decline has not been quantified. However, the acute dose is greater than the 

chronic NOAEL for mammals, so adverse effects to insectivorous birds appear plausible 

from chronic dietary exposures. 

The estimated dose using the highest application rate (1 lb/acre) is less than the acute 

NOAEL for birds, but greater than the chronic NOAEL for mammals. The acute dose (113 

mg/kg) is also greater than the chronic LOAEL for mammals (35 mg/kg/day), so adverse 

effects to insectivorous birds appear plausible from chronic dietary exposures. 

SETHOXYDIM

Small Mammal Directly Sprayed

The acute NOAEL for mammals in laboratory toxicity tests is 160 mg/kg. For, exposure 

scenarios that use the typical application rate of 0.30 lb/acre, if a small mammal is directly 

sprayed, and 100 percent absorption is assumed, the animal would receive an acute dose of 

7.27 mg/kg (Project file, Sethoxdim Worksheet F02a). This estimated dose is 0.05 and 0.005 

of the acute NOAEL, so there is no basis for asserting or predicting that adverse effects to 

herbivorous mammals are plausible (SERA 2001 Sethoxydim, p. 4-19). 

Small Mammal Drinking Contaminated Water

The estimated doses to a small mammal from drinking water contaminated by an accidental 

spill, assuming the highest levels of contamination, are 0.997 mg/kg for acute exposure 

(Project file, Sethoxdim Worksheet F05). If a small mammal consumes contaminated water 

over time, accounting for dissipation, degradation, and other processes, the animal would 

receive a chronic dose of 0.0000527 mg/kg/day (Project file, Sethoxdim Worksheet F07). 

Doses to a large mammal would be even lower on a per kg body weight basis. These doses 

are 0.006 of the acute NOAEL, and 0.000006 of the chronic NOAEL, respectively, so there 

is no basis for asserting or predicting that adverse effects to mammals are plausible (SERA 

2001 Sethoxydim, p. 4-19). 

At the highest application rate of 0.375 lb/acre, the acute dose from drinking water 

contaminated by a spill is 0.997 mg/kg (project file). This dose is 0.006 of the acute NOAEL. 

The chronic dose is also below the chronic NOAEL, so there is no basis for asserting or 

predicting that adverse effects to mammals are plausible, even in a worst-case scenario. 

Large Herbivorous Mammal

79

The acute NOAEL for mammals in laboratory toxicity tests is 160 mg/kg. For exposure 

scenarios that use the typical application rate of 0.30 lb/acre, if a 70 kg mammal consumed 

contaminated vegetation on site shortly after application, assuming the highest residue rates 

and 100 percent of the diet contaminated, it would receive an acute dose of 14.6 mg/kg 

(Project file, Sethoxdim Worksheet F10). This dose is 0.09 of the acute NOAEL, so there is 

no basis for asserting or predicting that adverse effects to large grass-eating mammals are 

plausible (SERA, 2001-Sethoxydim, p. 4-19). 
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Sethoxydim, cont’d. 

The chronic NOAEL for mammals in laboratory toxicity tests is 9 mg/kg/day. Chronic 

exposure from the consumption of contaminated vegetation for 90 days at the treatment site, 

assuming the highest residue rates, results in a dose of 0.701 mg/kg/day (Project file, 

Sethoxdim Worksheet F11a). This dose is 0.08 of the chronic NOAEL, so there is no basis 

for asserting or predicting that adverse effects to large grass-eating mammals are plausible

(SERA, 2001-Sethoxydim, p. 4-19). 

Estimated doses using the highest application rate (0.375 lb/acre) are less the acute and 

chronic NOAELs for mammals, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions (SERA 2001 

Sethoxydim, p. 4-19). 

Medium Carnivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 160 mg/kg. For exposure 

scenarios that use the typical application rate of 0.30 lb/acre, if a 5 kg mammal consumed 

small mammal prey that has been contaminated by direct spray, assuming 100 percent 

absorption for the prey, it would receive an acute dose of 0.629 mg/kg (Project file, 

Sethoxdim Worksheet F16a). Doses to a large mammal would be even lower on per kg body 

weight basis. This dose is 0.004 of the acute NOAEL, so there is no basis for asserting or 

predicting that adverse effects to carnivorous mammals are plausible (SERA 2001 

Sethoxydim, p. 4-19). 

There is no information in the risk assessment (SERA 2001 Sethoxydim) on accumulation or 

elimination of sethoxydim in mammals. Therefore, the potential for chronic exposures from 

contaminated mammal prey due to a single application of sethoxydim cannot be deduced. 

However, the acute dose is less than the chronic NOAEL for mammals, so there is no basis 

for asserting or predicting that adverse effects from repeated acute exposures from multiple 

applications of sethoxydim over time are plausible. 

Estimated doses using the highest application rate (0.375 lb/acre) are less than the acute and 

chronic NOAELs for mammals, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions. 

Small Herbivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 160 mg/kg. If a small 

mammal consumes contaminated vegetation shortly after application, assuming the highest 

residue rates, the acute dose received is 0.804 mg/kg (Project file, Sethoxdim Worksheet 

F03). This estimated dose is 0.005 of the acute NOAEL, so there is no basis for asserting or 

predicting that adverse effects to herbivorous mammals are plausible (SERA, 2001-

Sethoxydim, p. 4-19). 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Sethoxydim, cont’d. 

The chronic NOAEL for mammals in laboratory toxicity tests is 9 mg/kg/day. If a small 

mammal consumes contaminated vegetation at the treatment site for 90-days, assuming 

highest residue rates, the animal would receive a chronic dose of 0.00773 mg/kg/day (Project 

file, Sethoxdim Worksheet F04a). This estimated dose is 0.0009 of the chronic NOAEL, so 

there is no basis for asserting or predicting that adverse effects to herbivorous mammals are 

plausible (SERA, 2001-Sethoxydim, p. 4-19). 

Estimated doses using the highest application rate (0.375 lb/acre) are less than the acute and 

chronic NOAELs for mammals, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions (SERA, 2001-

Sethoxydim, p. 4-19). 

Small Insectivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 160 mg/kg. For exposure 

scenarios that use the typical application rate of 0.30 lb/acre, if a small mammal consumes 

contaminated insects shortly after application, assuming the highest residue rates, the acute 

dose received is 20.8 mg/kg (Project file, Sethoxdim Worksheet 14a). This dose is 0.10 of the 

acute NOAEL, so there is no basis for asserting or predicting that adverse effects to 

insectivorous mammals are plausible. 

Data on degradation of herbicide residues from insects is not available, so no chronic 

exposure scenario has been developed. Residue on insects likely declines over time, but the 

extent of decline has not been quantified. However, the acute dose is greater than the 

chronic NOAEL and the chronic LOAEL (18 mg/kg/day) for mild anemia. So adverse 

effects to insectivorous mammals appear plausible from chronic dietary exposures. The 

exposure scenario uses residue rates from small insects, which are substantially higher than 

those for large insects, and assumes that 100 percent of the daily diet is composed of insects 

that have been directly sprayed. For bats, in particular, the scenario is unlikely to occur in 

the field. It seems more plausible for shrews and small fossorial insectivores, however. 

The estimated dose using the highest application rate (0.375 lb/acre) is less than the acute 

NOAEL, but greater than the chronic NOAEL for mammals, so adverse effects to 

insectivorous mammals are plausible from chronic dietary exposures. 

Large Herbivorous Bird

The acute NOAEL for birds in laboratory toxicity tests is 500 mg/kg. For exposure scenarios 

that use the typical application rate of 0.30 lb/acre, if a 4 kg bird consumed contaminated 

grass on site shortly after application, assuming the highest residue rates and 100 percent of 

diet is contaminated, it would receive an acute dose of 22.8 mg/kg (Project file, Sethoxdim 

Worksheet F12). This dose is 0.05 of the acute NOAEL, so there is no basis for asserting or 

predicting that adverse effects to large grass-eating birds are plausible (SERA, 2001-

Sethoxydim, p. 4-19). 

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DRAFT 

Sethoxydim, cont’d. 

The chronic LOAEL for birds in laboratory toxicity tests is 10 mg/kg/day. Chronic exposure 

from the consumption of contaminated grass for 90 days at the treatment site, assuming the 

highest residue rates and 100 percent of diet is contaminated, results in a dose of 1.10 

mg/kg/day (Project file, Sethoxdim Worksheet F13a). This estimated dose is 0.1 of the 

chronic LOAEL. If we apply the standard EPA conversion for extrapolating from a LOAEL 

to a NOAEL, the NOAEL becomes 1 mg/kg, and the dose is equal to the chronic NOAEL. 

At this dose, adverse reproductive effects to large grass-eating birds are not likely. 

Estimated doses using the highest application rate (0.375 lb/acre) are less than the acute 

NOAEL and chronic LOAEL. But the estimated dose is greater than the extrapolated

chronic NOAEL for birds, so adverse effects to grass-eating birds is plausible from chronic 

dietary exposures at the highest application rate. 

Large Fish-eating Bird

Many chemicals may be concentrated or partitioned from water into the tissues of animals in 

the water. This process is referred to as bioconcentration. The potential for bioconcentration 

of sethoxydim in fish was studied in bluegill and catfish. Bioconcentration factors (BCF) for 

catfish were 0.71 L/kg in muscle and 0.75 L/kg in whole fish (SERA, 2001-Sethoxydim, 

Appendix 3). BCF for bluegill sunfish were substantially higher, measuring 7 L/kg in muscle 

and 21 L/kg in whole fish (SERA, 2001-Sethoxydim, Appendix 3). The BCF for acute 

exposure is calculated using the elimination half-life of sethoxydim residue in fish, to adjust 

for the expected bioconcentration after one day (SERA, 2001-Sethoxydim, p. 3-16). The 

exposure scenarios in the SERA risk assessment use a whole-fish BCF of 3.6 L/kg for acute 

exposure and 21 L/kg for chronic exposure. 

The acute NOAEL for birds in laboratory toxicity tests is 500 mg/kg. For exposure scenarios 

that use the typical application rate of 0.30 lb/acre, if a predatory bird consumed fish from a 

pond contaminated by an accidental spill, assuming the highest concentrations in fish and 

highest intake on a body weight basis, it would receive an acute dose of 3.68 mg/kg (Project 

file, Sethoxdim Worksheet F08). This dose is 0.007 of the acute NOAEL, so there is no basis 

for asserting or predicting that adverse effects to fish-eating birds are plausible (SERA, 2001-

Sethoxydim, p. 4-19). 

The chronic LOAEL for birds in laboratory toxicity tests is 10 mg/kg/day. If a predatory bird 

consumed fish contaminated by runoff for a lifetime, assuming the highest concentrations in 

fish and highest intake on a body weight basis, it would receive a chronic dose of 0.00113 

mg/kg/day (Project file, Sethoxdim Worksheet F09). This estimated dose is 0.0001 of the 

chronic LOAEL. If we apply the standard EPA safety factor for extrapolating from a 

LOAEL to a NOAEL, the NOAEL becomes 1 mg/kg. The dose is 0.001of the chronic 

NOAEL, so there is no basis for asserting/predicting that adverse effects to fish-eating birds 

are plausible (SERA, 2001-Sethoxydim, p. 4-19). 

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DRAFT 

Sethoxydim, cont’d. 

Estimated doses using the highest application rate (0.375 lb/acre) also result in exposures less 

than the acute and extrapolated chronic NOAELs for birds, so there is no basis for asserting 

or predicting that adverse effects are plausible using typical or worst-case exposure 

assumptions. 

Large Predatory Bird

The acute NOAEL for birds in laboratory toxicity tests is 500 mg/kg. For exposure scenarios 

that use the typical application rate of 0.30 lb/acre, if a 0.6 kg bird consumed small mammal 

prey that has been contaminated by direct spray, assuming 100 percent absorption for the 

prey, it would receive an acute dose of 0.97 mg/kg (Project file, Sethoxdim Worksheet 

F16b). This is 0.002 of the acute NOAEL, so there is no basis for asserting or predicting that 

adverse effects to predatory birds are plausible. 

There is no information in the risk assessment (SERA, 2001-Sethoxydim) on accumulation 

or elimination of sethoxydim in mammals. Therefore, the potential for chronic exposures 

from contaminated mammal prey due to a single application of sethoxydim cannot be 

deduced. However, the acute dose is less than the chronic LOAEL, and the extrapolated 

NOAEL, for birds, so there is no basis for asserting/predicting that adverse effects from 

repeated acute exposures from multiple applications of sethoxydim over time are plausible. 

The estimated dose using the highest application rate (0.375 lb/acre) is less than the acute 

NOAEL and less than the chronic LOAEL. The dose (1.21 mg/kg) is greater than the 

extrapolated chronic NOAEL for birds. Therefore, adverse effects to predatory birds appear 

plausible from chronic dietary exposures at the highest application rate, base on dose 

exceeding an extrapolated chronic NOAEL. 

Small Insectivorous Bird

The acute NOAEL for birds in laboratory toxicity tests is 500 mg/kg. For exposure scenarios 

that use the typical application rate of 0.30 lb/acre, if a 10 g bird consumed contaminated 

insects on site shortly after application, assuming the highest residue rates, it would receive 

an acute dose of 33.8 mg/kg (Project file, Sethoxdim Worksheet F14b). This dose is 0.07 of 

the acute NOAEL, so there is no basis for asserting or predicting that adverse effects to 

insectivorous birds are plausible (SERA, 2001-Sethoxydim, p. 4-19). 

Data on degradation of herbicide residues from insects is not available, so no chronic 

exposure scenario has been developed. Residue on insects likely declines over time, but the 

extent of decline has not been quantified. However, the acute dose is 3 times greater than

the chronic LOAEL for birds, so adverse effects to reproduction of insectivorous birds are 

expected from chronic dietary exposures. 

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DRAFT 

Sethoxydim, cont’d. 

The estimated dose using the highest application rate (0.375 lb/acre) is less than the acute 

NOAEL, but 4 times greater than the chronic LOAEL for birds. Therefore, adverse effects 

to reproduction of insectivorous birds are expected from chronic dietary exposures at the 

highest application rate. 

SULFOMETURON METHYL

Small Mammal Directly Sprayed

The acute NOAEL for mammals in laboratory toxicity tests is 87 mg/kg. For, exposure 

scenarios that use the typical application rate of 0.045 lb/acre, if a small mammal is directly 

sprayed, and 100 percent absorption is assumed, the animal would receive an acute dose of 

1.09 mg/kg (SERA 2003 Sulfometuron methyl, Worksheet F02a). This estimated dose is 

0.01 of the acute NOAEL, so there is no basis for asserting or predicting that adverse effects 

to mammals are plausible (SERA, 2003-Sulfometuron methyl, p. 4-30). 

At the highest application rate of 0.38 lb/acre, the animal would receive an acute dose of 9.21 

mg/kg (project file). This dose is 0.1 of the acute NOAEL, so there is no basis for asserting 

or predicting that adverse effects to mammals are plausible at any application rate. 

Small Mammal Drinking Contaminated Water

The estimated doses to a small mammal from drinking water contaminated by an accidental 

spill, assuming the highest levels of contamination, are 0.122 mg/kg for acute exposure 

(SERA 2003 Sulfometuron methyl, Worksheet F05). If a small mammal consumes 

contaminated water over time, accounting for dissipation, degradation, and other processes, 

the animal would receive a chronic dose of 0.461 mg/kg/day (SERA 2003 Sulfometuron 

methyl, Worksheet F07). Doses to a large mammal would be even lower on a per kg body 

weight basis. These doses are 0.001 of the acute NOAEL, and 0.0000002 of the chronic 

NOAEL, respectively, so there is no basis for asserting or predicting that adverse effects to 

mammals are plausible (SERA 2003 Sulfometuron methyl, p. 4-30 and 4-31). 

At the highest application rate of 0.38 lb/acre, the acute dose from drinking water 

contaminated by a spill is 1.03 mg/kg (project file). This dose is 0.01 of the acute NOAEL. 

The chronic dose is also below the chronic NOAEL, so there is no basis for asserting or 

predicting that adverse effects to mammals are plausible, even in a worst-case scenario. 

Large Herbivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 87 mg/kg. For exposure 

scenarios that use the typical application rate of 0.045 lb/acre, if a 70 kg mammal consumed 

contaminated vegetation on site shortly after application, assuming the highest residue rates 

and 100 percents of the diet contaminated, it would receive an acute dose of 2.19 mg/kg 

(SERA, 2003-Sulfometuron methyl, Worksheet F10). This dose is 0.03 of the acute 

NOAEL, so there is no basis for asserting or predicting that adverse effects to large grasseating mammals are plausible (SERA, 2003-Sulfometuron methyl, p. 4-30). 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Sulfometuron methyl, cont’d. 

The chronic NOAEL for mammals in laboratory toxicity tests is 2 mg/kg/day. Chronic 

exposure from the consumption of contaminated vegetation for 90 days at the treatment site, 

assuming the highest residue rates, results in a dose of 0.35 mg/kg/day (SERA, 2003-

Sulfometuron methyl, Worksheet F11a). This dose is 0.2 of the chronic NOAEL, so there is 

no basis for asserting or predicting that adverse effects to large grass-eating mammals are 

plausible (SERA, 2003-Sulfometuron methyl, p. 4-30). 

Estimated doses using the highest application rate (0.38 lb/acre) are less than the acute 

NOAEL, but greater than the chronic NOAEL for mammals. The chronic dose (2.95 

mg/kg) is less than the chronic LOAEL (20 mg/kg/day) for effects to blood and bile ducts. 

No adverse effects are plausible from acute exposures, but adverse effects to large 

herbivorous mammals appear plausible from chronic dietary exposures, based on dose 

exceeding the chronic NOAEL. However, the assumptions in the chronic exposure scenario 

are very unlikely to occur in field conditions, so the weight of evidence suggests that no 

adverse effects are plausible using typical or worst-case exposure assumptions (SERA 2003 

Sulfometuron methyl, p. 4-31). 

Medium Carnivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 87 mg/kg. For exposure 

scenarios that use the typical application rate of 0.045 lb/acre, if a 5 kg mammal consumed 

small mammal prey that has been contaminated by direct spray, assuming 100 percent 

absorption for the prey, it would receive an acute dose of 0.0944 mg/kg (SERA, 2003 

Sulfometuron methyl, Worksheet F16a). Doses to a larger mammal would be even lower on a 

per kg body weight basis. This dose is 0.001 of the acute NOAEL, so there is no basis for 

asserting or predicting that adverse effects to carnivorous mammals are plausible SERA, 

2003 -ulfometuron methyl, p. 4-30. 

Sulfometuron methyl is eliminated fairly rapidly and does not appear to accumulate in animal 

tissues (SERA, 2003-Sulfometuron methyl). The metabolism of sulfometuron methyl has 

been studied in lactating goats and rats. Goats eliminated 94-99 percent in the urine (Keoppe 

and Mucha, 1991 cited in SERA, 2003-Sulfometuron methyl). The half-life for metabolism 

in rats is 28 hours after a gavage dose of 16 mg/kg and 40 hours after a dose of 3000 mg/kg 

(DuPont, 1989 cited in SERA, 2003-Sulfometuron methyl). Therefore, chronic exposures 

from contaminated mammal prey due to a single application of sulfometuron methyl are 

unlikely to cause any adverse effect. In addition, the acute dose is much less than the chronic 

NOAEL for mammals, so there is no basis for asserting or predicting that adverse effects 

from repeated acute exposures from multiple applications of sulfometuron methyl over time 

are plausible. 

The estimated dose using the highest application rate (0.38 lb/acre) is less than the acute and 

chronic NOAELs for mammals, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions. 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Sulfometuron methyl, cont’d. 

Small Herbivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 87 mg/kg. If a small mammal 

consumes contaminated vegetation shortly after application, assuming the highest residue 

rates, the acute dose received is 0.121 mg/kg (SERA, 2003-Sulfometuron methyl, Worksheet 

F03). This estimated dose is 0.001 of the acute NOAEL, so there is no basis for asserting or 

predicting that adverse effects to herbivorous mammals are plausible (SERA, 2003-

Sulfometuron methyl, p. 4-30). 

The chronic NOAEL for mammals in laboratory toxicity tests is 2 mg/kg/day. If a small 

mammal consumes contaminated vegetation at the treatment site for 90-days, assuming 

highest residue rates, the animal would receive a chronic dose of 0.00386 mg/kg/day (SERA, 

2003-Sulfometuron methyl, Worksheet F04a). This estimated dose is 0.002 of the chronic 

NOAEL, so there is no basis for asserting or predicting that adverse effects to herbivorous 

mammals are plausible (SERA, 2003-Sulfometuron methyl, p. 4-31). 

Estimated doses using the highest application rate (0.38 lb/acre) are less than the acute and 

chronic NOAELs for mammals, so there is no basis for asserting or predicting that adverse 

effects are plausible using typical or worst-case exposure assumptions. 

Small Insectivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 87 mg/kg. For exposure 

scenarios that use the typical application rate of 0.045 lb/acre, if a small mammal consumes 

contaminated insects shortly after application, assuming the highest residue rates, the acute 

dose received is 3.12 mg/kg (SERA, 2003-Sulfometuron methyl, Worksheet 14a). This dose 

is 0.04 of the acute NOAEL, so there is no basis for asserting or predicting that adverse 

effects to mammal insectivores are plausible (SERA, 2003-Sulfometuron methyl, p. 4-30). 

Data on degradation of herbicide residues from insects is not available, so no chronic 

exposure scenario has been developed. Residue on insects likely declines over time, but the 

extent of decline has not been quantified. The acute dose is greater than the chronic 

NOAEL (2 mg/kg/day), but less than the chronic LOAEL (20 mg/kg/day) for effects to blood 

and bile ducts. So adverse effects to insectivorous mammals appear plausible from chronic 

dietary exposures, based on dose exceeding the chronic NOAEL. The exposure scenario 

uses residue rates from small insects, which are substantially higher than those for large 

insects, and assumes that 100 percent of the daily diet is composed of insects that have been 

directly sprayed. For bats, in particular, the scenario is unlikely to occur in the field. It 

seems more plausible for shrews and small fossorial insectivores, however. 

The estimated dose (26.4 mg/kg) using the highest application rate (0.38 lb/acre) is less than 

the acute NOAEL. But the acute dose is greater than the chronic NOAEL and the chronic 

LOAEL (20 mg/kg/day) for effects to blood and bile ducts. No adverse effects are plausible 

from acute exposures, but adverse effects to insectivorous mammals are plausible, and may 

be expected, from chronic dietary exposures at the maximum application rate. 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Sulfometuron methyl, cont’d. 

Large Herbivorous Bird

The acute NOAEL for birds in laboratory toxicity tests is 312 mg/kg. For exposure scenarios 

that use the typical application rate of 0.045 lb/acre, if a 4 kg bird consumed contaminated 

grass on site shortly after application, assuming the highest residue rates and 100 percent of 

diet is contaminated, it would receive an acute dose of 3.42 mg/kg (SERA, 2003-

Sulfometuron methyl, Worksheet F12). This dose is 0.01 of the acute NOAEL, so there is no 

basis for asserting or predicting that adverse effects to large grass-eating birds are plausible 

(SERA, 2003-Sulfometuron methyl, p. 4-30). 

There is no chronic toxicity index available for effects of sulfometuron methyl to birds, so 

the mammal chronic NOAEL will be used (acute toxicities of sulfometuron methyl to 

mammals and birds are of similar magnitude (SERA 2003 Sulfometuron methyl, p. 4-24)). 

The chronic NOAEL for mammals in laboratory toxicity tests is 2 mg/kg/day. Chronic 

exposure from the consumption of contaminated grass for 90 days at the treatment site, 

assuming the highest residue rates and 100 percent of diet is contaminated, results in a dose 

of 0.547 mg/kg/day (SERA, 2003-Sulfometuron methyl, Worksheet F13a). This estimated 

dose is 0.3 of the chronic NOAEL for mammals, so there is no basis for asserting or 

predicting that adverse effects to large grass-eating birds are plausible (SERA, 2003-

Sulfometuron methyl, p. 4-31). 

Estimated doses using the highest application rate (0.38 lb/acre) are less than the acute 

NOAEL for birds, but greater than the chronic NOAEL for mammals. The chronic dose 

(4.62 mg/kg/day) is less than the chronic LOAEL for mammals. No adverse effects are 

plausible from acute exposures, but adverse effects to large herbivorous birds appear 

plausible from chronic dietary exposures, based on dose exceeding a NOAEL. However, the 

assumptions in the chronic exposure scenario are very unlikely to occur in field conditions, 

so the weight of evidence suggests that no adverse effects are plausible using typical or 

worst-case exposure assumptions (SERA, 2003-Sulfometuron methyl, p. 4-31). 

Large Fish-eating Bird

Many chemicals may be concentrated or partitioned from water into the tissues of animals in 

the water. This process is referred to as bioconcentration. The potential for bioconcentration 

of sulfometuron methyl in fish was studied in bluegill sunfish and channel catfish exposed to 

14C-sulformeturon methyl for 28 days (Harvey, 1981, cited in SERA, 2003-Sulfometuron 

methyl, p. 3-21). In the SERA risk assessments, concentrations in viscera are considered to 

reflect concentration in whole fish. No bioaccumulation occurred in either muscle or viscera 

of bluegill. Bioconcentration Factors (BCF) for viscera of channel catfish after one day of 

exposure was 3.5 L/kg, and 6 L/kg after 28 days (SERA, 2003-Sulfometuron methyl, 

Appendix 2). Therefore, exposure scenarios in the SERA risk assessment use a whole-fish 

BCF of 3.5 L/kg for acute exposure and 6 L/kg for chronic exposure. 

87
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Sulfometuron methyl, cont’d. 

The acute NOAEL for birds in laboratory toxicity tests is 312 mg/kg. For exposure scenarios 

that use the typical application rate of 0.045 lb/acre, if a predatory bird consumed fish from a 

pond contaminated by an accidental spill, assuming the highest concentrations in fish and 

highest intake on a body weight basis, it would receive an acute dose of 0.437 mg/kg (SERA, 

200X, Worksheet F08). This dose is 0.001 of the acute NOAEL, so there is no basis for 

asserting or predicting that adverse effects to fish-eating birds are plausible (SERA, 2003-

Sulfometuron methyl, p. 4-30). 

There is no chronic toxicity index available for effects of sulfometuron methyl to birds, so 

the mammal chronic NOAEL will be used (acute toxicities of sulfometuron methyl to 

mammals and birds are of similar magnitude (SERA, 2003-Sulfometuron methyl, p. 4-24)). 

The chronic NOAEL for mammals in laboratory toxicity tests is 2 mg/kg/day. If a predatory 

bird consumed fish contaminated by runoff for a lifetime, assuming the highest 

concentrations in fish and highest intake on a body weight basis, it would receive a chronic 

dose of 0.000003 mg/kg/day (SERA, 200X-Worksheet F09). This estimated dose is 0.000001

of the chronic NOAEL for mammals, so there is no basis for asserting or predicting that 

adverse effects to fish-eating birds are plausible (SERA 2003 Sulfometuron methyl, p. 4-31). 

Estimated doses using the highest application rate (0.38 lb/acre) also result in exposures 

much less than the acute NOAEL for bird and chronic NOAEL for mammals, so there is no 

basis for asserting or predicting that adverse effects are plausible using typical or worst-case 

exposure assumptions (SERA, 2003-Sulfometuron methyl, p. 4-31). 

Large Predatory Bird

The acute NOAEL for birds in laboratory toxicity tests is 312 mg/kg. For exposure scenarios 

that use the typical application rate of 0.045 lb/acre, if a 0.6 kg bird consumed small mammal 

prey that has been contaminated by direct spray, assuming 100 percent absorption for the 

prey, it would receive an acute dose of 0.145 mg/kg (SERA, 2003-Sulfometuron methyl, 

Worksheet F16b). This is 0.0005 of the acute NOAEL, so there is no basis for asserting or 

predicting that adverse effects to predatory birds are plausible. 

Sulfometuron methyl does not appear to accumulate in animal tissues. The elimination of 

this herbicide has been studied in lactating goats and rats (SERA, 2003-Sulfometuron 

methyl). Goats eliminated 94-99 percent in the urine (Keoppe and Mucha 1991 cited in 

SERA, 2003-Sulfometuron methyl). The half-life for metabolism in rats is 28 hours after a 

gavage dose of 16 mg/kg and 40 hours after a dose of 3000 mg/kg (DuPont, 1989 cited in 

SERA, 2003-Sulfometuron methyl). Therefore, chronic exposures from contaminated 

mammal prey due to a single application of sulfometuron methyl are unlikely to cause any 

adverse effect. In addition, the acute dose is less than the chronic NOAEL for mammals, so 

there is no basis for asserting/predicting that adverse effects from repeated acute exposures 

from multiple applications of sulfometuron methyl over time are plausible. 

88
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Sulfometuron methyl, cont’d. 

Estimated doses using the highest application rate (0.38 lb/acre) are less than the acute 

NOAEL for birds and chronic NOAEL for mammals, so there is no basis for asserting or 

predicting that adverse effects are plausible using typical or worst-case exposure assumptions 

(SERA, 2003-Sulfometuron methyl, p. 4-30 and 4-31). 

Small Insectivorous Bird

The acute NOAEL for birds in laboratory toxicity tests is 312 mg/kg. For exposure scenarios 

that use the typical application rate of 0.045 lb/acre, if a 10 g bird consumed contaminated 

insects on site shortly after application, assuming the highest residue rates, it would receive 

an acute dose of 5.08 mg/kg (SERA, 2003-Sulfometuron methyl, Worksheet F14b). This 

dose is 0.02 of the acute NOAEL, so there is no basis for asserting or predicting that adverse 

effects to insectivorous birds are plausible (SERA, 2003-Sulfometuron methyl, p. 4-30). 

There is no chronic toxicity index available for effects of sulfometuron methyl to birds, so 

the mammal chronic NOAEL will be used (acute toxicities of sulfometuron methyl to 

mammals and birds are of similar magnitude (SERA, 2003-Sulfometuron methyl, p. 4-24)). 

Data on degradation of herbicide residues from insects is not available, so no chronic 

exposure scenario has been developed. Residue on insects likely declines over time, but the 

extent of decline has not been quantified. The acute dose is greater than the chronic 

NOAEL for mammals (2 mg/kg/day), but less than the chronic LOAEL (20 mg/kg/day) for 

mammals. So adverse effects to insectivorous birds appear plausible from chronic dietary 

exposures, based on an acute dose exceeding a chronic NOAEL. 

The estimated dose using the highest application rate (0.38 lb/acre) is less than the acute 

NOAEL for birds, but greater than the chronic NOAEL for mammals. The acute dose (42.9 

mg/kg/day) is also two times greater than the chronic mammal LOAEL for effects to blood 

and bile ducts. No adverse effects are plausible from acute exposures, but adverse effects to 

insectivorous birds are plausible, and may be expected, from chronic dietary exposures at the 

maximum application rate. 

TRICLOPYR

89

Toxicity indices and doses are the same for triclopyr acid and triclopyr BEE for mammals, 

but they differ for birds. The EPA has used two different values for a reference dose on the 

effects of triclopyr to mammals. The FS/SERA risk assessment (2003 Triclopyr) relies on a 

chronic toxicity index (NOEL of 5 mg/kg/day) from a rat reproduction study. In this 

analysis, we will use a lower value from a 1-year feeding study of dogs (chronic NOEL of 

0.5 mg/kg/day; Quast et al. 1976, cited in SERA, 2003-Triclopyr). Dogs were not considered 

by EPA to be a good model for human health effects, because they do not excrete weak acids 

as well as other animals (see Timchalk and Nolan 1997; Timchalk et al. 1997). Canids are, 

however, relevant for concerns about effects to wildlife. It may be argued that the use of the 

0.5 mg/kg/day value for the toxicity index in this analysis is overly cautious, because it 

represents competition for excretion rather than a toxic effect (Timchalk et al. 1997), and 

because it is being applied to other animals besides canids. However, it meets the criteria for 

providing a data-based worst-case analysis for potential effects to wildlife, and is therefore 

consistent with the criteria for choice of other indices used in this analysis.
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Triclopyr, cont’d.

Small Mammal Directly Sprayed

The acute NOAEL for mammals in laboratory toxicity tests is 100 mg/kg. For, exposure 

scenarios that use the typical application rate of 1 lb/acre, if a small mammal is directly 

sprayed, and 100 percent absorption is assumed, the animal would receive an acute dose of 

24.2 mg/kg (SERA, 2003-Triclopyr, Worksheet F02a). This estimated dose is 0.2 of the 

acute NOAEL, so there is no basis for asserting or predicting that adverse effects to 

mammals are plausible. 

At the highest application rate of 10 lb/acre, the animal would receive an acute dose of 242 

mg/kg (project file). This dose is greater than the acute NOAEL but less than the acute 

LOAEL for malformed fetuses, although not substantially. So adverse effects are plausible 

from direct spray at the highest application rate, based on dose exceeding the NOAEL. 

Small Mammal Drinking Contaminated Water

The estimated doses to a small mammal from drinking water contaminated by an accidental 

spill, assuming the highest levels of contamination, are 2.66 mg/kg for acute exposure 

(SERA, 2003-Triclopyr, Worksheet F05). If a small mammal consumes contaminated water 

over time, accounting for dissipation, degradation, and other processes, the animal would 

receive a chronic dose of 0.00732 mg/kg/day (SERA, 2003-Triclopyr, Worksheet F07). 

Doses to a large mammal would be even lower on a per kg body weight basis. These doses 

are 0.03 of the acute NOAEL, and 0.01 of the chronic NOAEL, respectively, so there is no 

basis for asserting or predicting that adverse effects to mammals are plausible. 

At the highest application rate of 10 lb/acre, the acute dose from drinking water contaminated 

by a spill is 26.6 mg/kg (project file). This dose is 0.3 of the acute NOAEL. The chronic 

dose is also below the chronic NOAEL, so there is no basis for asserting or predicting that 

adverse effects to mammals are plausible, even in a worst-case scenario. 

Large Herbivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 100 mg/kg. For exposure 

scenarios that use the typical application rate of 1 lb/acre, if a 70 kg mammal consumed 

contaminated vegetation on site shortly after application, assuming the highest residue rates 

and 100 percents of the diet contaminated, it would receive an acute dose of 48.6 mg/kg 

(SERA, 2003-Triclopyr, Worksheet F10). This dose is 0.5 of the acute NOAEL, so there is 

no basis for asserting or predicting that adverse effects to large grass-eating mammals are 

plausible. 

90
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Triclopyr, cont’d.

The chronic NOAEL for mammals in laboratory toxicity tests is 0.5 mg/kg/day. Chronic 

exposure from the consumption of contaminated vegetation for 90 days at the treatment site, 

assuming the highest residue rates, results in a dose of 32.0 mg/kg/day (SERA, 2003-

Triclopyr, Worksheet F11a). This dose is greater than the chronic NOAEL and 13 times 

greater than the LOAEL of 2.5 mg/kg for effects to kidneys. Adverse effects to grasseating mammals are plausible and of substantial concern with the use of triclopyr (SERA, 

2003-Triclopyr, p. 4-28). 

Estimated doses using the highest application rate (10 lb/acre) are greater than the acute and 

chronic NOAELs for mammals. The acute dose is 486 mg/kg; which also exceeds the acute 

LOAEL for malformed fetuses. The chronic dose is 320 mg/kg; which exceeds the chronic 

LOAEL for effects to kidneys. Adverse effects to reproduction and internal organs of grasseating mammals are plausible with acute and chronic exposures at the highest application 

rate. The potential for adverse effects are of substantial concern with the use of triclopyr 

(SERA, 2003-Triclopyr, p. 4-28). 

Medium Carnivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 100 mg/kg. For exposure 

scenarios that use the typical application rate of 1 lb/acre, if a 5 kg mammal consumed small 

mammal prey that has been contaminated by direct spray, assuming 100 percent absorption 

for the prey, it would receive an acute dose of 2.10 mg/kg (SERA 2003 Triclopyr, Worksheet 

F16a). Doses to a larger mammal would be even lower on a per kg body weight basis. This 

dose is 0.021 of the acute NOAEL, so there is no basis for asserting or predicting that 

adverse effects to carnivorous mammals are plausible. 

Triclopyr acid and triclopyr BEE do not appear to accumulate or persist in animals. The 

elimination of triclopyr has been studied in rats and cattle (SERA 2003 Triclopyr). A study 

by Timchalk et al. (1990) found that the half-life for elimination in rats is 3.6 hours and that 

virtually all the ingested dose of triclopyr is excreted unchanged in the urine, although four 

minor metabolites are formed. In cattle, over 86 percent of the ingested dose was eliminated 

unchanged in the urine and almost all the dose was eliminated after 24 hours (Eckerlin et al. 

1987, cited in SERA 2003). Therefore, chronic exposures from contaminated mammal prey 

due to a single application of triclopyr are unlikely to cause any adverse effect. However, the 

acute dose is greater than the chronic NOAEL for mammals, but slightly less than the 

chronic LOAEL, so adverse effects to carnivorous mammals appear plausible from chronic 

dietary exposures. 

The estimated dose using the highest application rate (10 lb/acre) is less than the acute 

NOAEL, but greater than the chronic LOAEL for effects to kidneys of mammals. No 

adverse effects are plausible from acute exposures, but adverse effects to carnivorous 

mammals appear plausible from chronic dietary exposures at the maximum application rate. 

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Triclopyr, cont’d.

Small Herbivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 100 mg/kg. If a small 

mammal consumes contaminated vegetation shortly after application, assuming the highest 

residue rates, the acute dose received is 0.495 mg/kg (SERA, 2003-Triclopyr, Worksheet 

F03). This estimated dose is 0.005 of the acute NOAEL, so there is no basis for asserting or 

predicting that adverse effects to herbivorous mammals are plausible. 

The chronic NOAEL for mammals in laboratory toxicity tests is 0.5 mg/kg/day. If a small 

mammal consumes contaminated vegetation at the treatment site for 90-days, assuming 

highest residue rates, the animal would receive a chronic dose of 0.0652 mg/kg/day (SERA, 

2003-Triclopyr, Worksheet F04a). This estimated dose is 0.1 the chronic NOAEL, so there is 

no basis for asserting or predicting that adverse effects to herbivorous mammals are 

plausible. 

Estimated doses using the highest application rate (10 lb/acre) are less than the acute 

NOAEL, but slightly greater than the chronic NOAELs for mammals. The chronic dose 

(0.65 mg/kg/day) is less than the chronic LOAEL (2.5 mg/kg/day) for effects to kidneys. No 

adverse effects are plausible from acute exposures, but adverse effects to herbivorous 

mammals appear plausible from chronic dietary exposures at the maximum application rate, 

based on dose exceeding a NOAEL. 

Small Insectivorous Mammal

The acute NOAEL for mammals in laboratory toxicity tests is 100 mg/kg. For exposure 

scenarios that use the typical application rate of 1 lb/acre, if a small mammal consumes 

contaminated insects shortly after application, assuming the highest residue rates, the acute 

dose received is 69.4 mg/kg (SERA, 2003-Triclopyr, Worksheet 14a). This dose is 0.694 of 

the acute NOAEL, so there is no basis for asserting or predicting that adverse effects to 

insectivorous mammals are plausible. 

Data on degradation of herbicide residues from insects is not available, so no chronic 

exposure scenario has been developed. Residue on insects likely declines over time, but the 

extent of decline has not been quantified. However, the acute dose is much greater than the 

chronic LOAEL for mammals, so adverse effects to insectivorous mammals appear plausible 

from chronic dietary exposures. The exposure scenario uses residue rates from small insects, 

which are substantially higher than those for large insects, and assumes that 100 percent of 

the daily diet is composed of insects that have been directly sprayed. For bats, in particular, 

the scenario is unlikely to occur in the field. It seems more plausible for shrews and small 

fossorial insectivores, however. 

The estimated dose (694 mg/kg) using the highest application rate (10 lb/acre) is much 

greater than the acute and chronic NOAELs for mammals. The acute dose is more than two 

times greater than the acute LOAEL for malformed fetuses and more than 200 times 

greater than the chronic LOAEL for effects to kidneys. Therefore, adverse effects to 

insectivorous mammals may be expected if they feed on insects contaminated with triclopyr 

applied at the highest application rate. 

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Triclopyr, cont’d.

Large Herbivorous Bird

Triclopyr BEE is slightly more toxic to birds in acute exposures than triclopyr acid. For 

triclopyr acid, the acute LD50 for birds in laboratory toxicity tests is 535 mg/kg and for 

triclopyr BEE the acute LD50 is 388 mg/kg. For exposure scenarios that use the typical 

application rate of 1 lb/acre, if a 4 kg bird consumed contaminated grass on site shortly after 

application, assuming the highest residue rates and 100 percent of diet is contaminated, it 

would receive an acute dose of 76.0 mg/kg (SERA 2003 Triclopyr, Worksheets F12). This 

dose is 0.1 of the acute LD50 for triclopyr acid and 0.2 of the acute LD50 for triclopyr BEE. 

Since the acute exposure scenario for bird is based on an LD50 rather than an acute NOAEL, 

the FS/SERA risk assessments base the level of concern on 0.1 of the LD50 (SERA, 2003-

Triclopyr), a factor used by EPA as a result of data analysis and modeling conducted by their 

Office of Pesticide Programs (Urban and Cook, 1986). Therefore, acute exposure from 

triclopyr acid is equal to the level of concern and that from triclopyr BEE is greater than the 

level of concern (SERA 2003 Triclopyr). Adverse effects to grass-eating birds are plausible 

and of substantial concern with the use of triclopyr (SERA, 2003-Triclopyr, p. 4-28). 

The chronic NOAEL for birds in laboratory toxicity tests is 10 mg/kg/day for both triclopyr 

acid and triclopyr BEE. Chronic exposure from the consumption of contaminated grass for 

90 days at the treatment site, assuming the highest residue rates and 100 percent of diet is 

contaminated, results in a dose of 50.1 mg/kg/day (SERA, 2003-Triclopyr, Worksheets 

F13a). This estimated dose is greater than the chronic NOAEL and more than two times 

greater than the chronic LOAEL for decreased survival of offspring. The assumptions in the 

chronic exposure scenario are unlikely to occur in field conditions, however, adverse effects 

reproduction of grass-eating birds are plausible and of substantial concern with the use of 

triclopyr (SERA, 2003-Triclopyr, p. 4-28). 

At the highest application rate (10 lb/acre), the acute dose is 760 mg/kg, which is greater 

than the acute LD50 for birds, for both triclopyr acid and triclopyr BEE. Mortality could be 

expected for birds feeding on vegetation contaminated with triclopyr applied at the highest 

application rate. In the case of the chronic exposures, the estimated dose (501 mg/kg/day) is 

much greater than the chronic LOAEL for decreased survival of offspring. Adverse effects, 

including mortality and decreased reproduction, to grass-eating birds are plausible and of 

substantial concern with the use of triclopyr (SERA, 2003-Triclopyr, p. 4-28). 

Large Fish-eating Bird

Many chemicals may be concentrated or partitioned from water into the tissues of animals in 

the water. This process is referred to as bioconcentration. The potential for bioconcentration 

of triclopyr in fish was studied in bluegill sunfish exposed to 14C-triclopyr (Rick et al., 1996; 

and Lickly and Murphy, 1987; cited in SERA 2003 Triclopyr). Bioconcentration factors 

(BCF) of triclopyr and its metabolites (primarily TCP) for bluegill were 0.83 L/kg for whole 

fish, which is the figure used in the exposure scenarios in the SERA risk assessment for acute 

and chronic exposures. 

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DRAFT 

Triclopyr, cont’d.

Triclopyr BEE is slightly more toxic to birds in acute exposures than triclopyr acid. For 

triclopyr acid, the acute LD50 for birds in laboratory toxicity tests is 535 mg/kg and for 

triclopyr BEE the acute LD50 is 388 mg/kg. For exposure scenarios that use the typical 

application rate of 1 lb/acre, if a predatory bird consumed fish from a pond contaminated by 

an accidental spill, assuming the highest concentrations in fish and highest intake on a body 

weight basis, it would receive an acute dose of 2.26 mg/kg (SERA, 2003-Triclopyr, 

Worksheet F08). This dose is 0.004 of the acute LD50 for triclopyr acid, and 0.006 of the 

acute LD50 for triclopyr BEE. Since the acute exposure scenario for bird is based on an 

LD50 rather than an acute NOAEL, the FS/SERA risk assessments base the level of concern 

on 0.1 of the LD50 (SERA, 2003-Triclopyr), a factor used by EPA as a result of data analysis 

and modeling conducted by their Office of Pesticide Programs (Urban and Cook 1986). The 

resultant values are much less than the level of concern, so there is no basis for asserting or 

predicting that adverse effects to fish-eating birds are plausible. 

The chronic NOAEL for birds in laboratory toxicity tests is 10 mg/kg/day for both triclopyr 

acid and triclopyr BEE. If a predatory bird consumed fish contaminated by runoff for a 

lifetime, assuming the highest concentrations in fish and highest intake on a body weight 

basis, it would receive a chronic dose of 0.00623 mg/kg/day (SERA, 2003-Triclopyr, 

Worksheet F09). This estimated dose is 0.0006 of the chronic NOAEL, so there is no basis 

for asserting/predicting that adverse effects to fish-eating birds are plausible. 

Estimated doses using the highest application rate (10 lb/acre) are less than 0.1 of the acute 

LD50 and the chronic NOAEL for birds, so there is no basis for asserting or predicting that 

adverse effects are plausible using typical or worst-case exposure assumptions. 

Large Predatory Bird

Triclopyr BEE is slightly more toxic to birds in acute exposures than triclopyr acid. For 

triclopyr acid, the acute LD50 for birds in laboratory toxicity tests is 535 mg/kg and for 

triclopyr BEE the acute LD50 is 388 mg/kg. For exposure scenarios that use the typical 

application rate of 1 lb/acre, if a 0.6 kg bird consumed small mammal prey that has been 

contaminated by direct spray, assuming 100 percent absorption for the prey, it would receive 

an acute dose of 3.23 mg/kg (SERA, 2003-Triclopyr, Worksheet F16b). This is 0.00604 of 

the acute LD50 for triclopyr acid and 0.00833 of the acute LD50 for triclopyr BEE. Since the 

acute exposure scenario for bird is based on an LD50 rather than an acute NOAEL, the 

FS/SERA risk assessments base the level of concern on 0.1 of the LD50 (SERA, 2003-

Triclopyr), a factor used by EPA as a result of data analysis and modeling conducted by their 

Office of Pesticide Programs (Urban and Cook, 1986). The resultant values are much less 

than the level of concern, so there is no basis for asserting or predicting that adverse effects 

to predatory birds are plausible. 

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DRAFT 

Triclopyr, cont’d.

Triclopyr acid and triclopyr BEE do not appear to accumulate or persist in animals. The 

elimination of triclopyr has been studied in rats and cattle (SERA, 2003-Triclopyr). A study 

by Timchalk et al. (1990) found that the half-life for elimination in rats is 3.6 hours and that 

virtually all of the ingested dose of triclopyr is excreted unchanged in the urine, although four 

minor metabolites are formed. In cattle, over 86 percent of the ingested dose was eliminated 

unchanged in the urine and almost all of the dose was eliminated after 24 hours (Eckerlin et 

al., 1990). Therefore, chronic exposures from contaminated mammal prey due to a single 

application of triclopyr are unlikely to cause any adverse effect. In addition, the acute dose is 

less than the chronic NOAEL for birds, so there is no basis for asserting or predicting that 

adverse effects from repeated acute exposures from multiple applications of predatory birds 

over time are plausible. 

Estimated doses using the highest application rate (10 lb/acre) are less than 0.1 of the LD50

for both triclopyr acid and triclopyr BEE, although only marginally so for triclopyr BEE 

(acute dose of 32.3 vs. 38.8 for 0.1 of the LD50). The acute dose (32.3 mg/kg) is greater 

than the bird chronic LOAEL (20 mg/kg) for decreased survival of offspring, so adverse 

affects to predatory birds are plausible from triclopyr at the highest application rate. 

Small Insectivorous Bird

Triclopyr BEE is slightly more toxic to birds in acute exposures than triclopyr acid. For 

triclopyr acid, the acute LD50 for birds in laboratory toxicity tests is 535 mg/kg and for 

triclopyr BEE the acute LD50 is 388 mg/kg. For exposure scenarios that use the typical 

application rate of 1 lb/acre, if a 10 g bird consumed contaminated insects on site shortly 

after application, assuming the highest residue rates, it would receive an acute dose of 113 

mg/kg (SERA 2003 Triclopyr, Worksheet F14b). This dose is 0.2 of the acute LD50 for 

triclopyr acid, and 0.3 of the LD50 for triclopyr BEE. Since the acute exposure scenario for 

bird is based on an LD50 rather than an acute NOAEL, the FS/SERA risk assessments base 

the level of concern on 0.1 of the LD50 (SERA 2003 Triclopyr), a factor used by EPA as a 

result of data analysis and modeling conducted by their Office of Pesticide Programs (Urban 

and Cook 1986). Therefore, the acute dose is two times greater than the level of concern 

for triclopyr acid, and three times greater than the level of concern for triclopyr BEE (but 

less than both LD50s). Adverse effects to insectivorous birds are plausible, assuming the 

highest residue rates. 

Data on degradation of herbicide residues from insects is not available, so no chronic 

exposure scenario has been developed. Residue on insects likely declines over time, but the 

extent of decline has not been quantified. However, the acute dose is five times greater 

than the chronic LOAEL for decreased survival of offspring in birds, so adverse effects to 

insectivorous birds may be expected from chronic dietary exposures. 

Estimated dose from contaminated insects, assuming the highest residue rates, at the highest 

application rate (10 lb/acre) is 1,130 mg/kg. This dose is two times greater than the LD50

for triclopyr acid and three times greater than the LD50 for triclopyr BEE. Mortality is 

expected if insectivorous birds feed exclusively within the treatment area on contaminated 

insects. 

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DRAFT 

2,4-D

Note: whether the chronic dose of 1 mg/kg is an actual NOAEL is ambiguous and it could be 

argued that it is a LOAEL. There is conflicting interpretation between EPA (USEPA, 1997) 

and the authors of the study (Serota et al., 1983) upon which the value is based. 

Small Mammal Directly Sprayed

The acute “non-lethal” dose for mammals in laboratory toxicity tests is 10 mg/kg. For, 

exposure scenarios that use the typical application rate of 1 lb/acre, if a small mammal is 

directly sprayed, and 100 percent absorption is assumed, the animal would receive an acute 

dose of 24.2 mg/kg (Project file, 2,4-D Worksheet F02a). This dose is within the range of 

doses in which mild signs of systemic toxicity are plausible, and sub-clinical signs of 

neurologic toxicity, increased thyroid weight, decreased testicular weight, decreased body 

weight gain, damage to several organs are expected (SERA, 1998, p. 3-52). 

Small Mammal Drinking Contaminated Water

The estimated dose to a small mammal from drinking water contaminated by an accidental 

spill, assuming the highest levels of contamination, is 0.664 mg/kg for acute exposure 

(Project file, 2,4-D Worksheet F05). If a small mammal consumes contaminated water over 

time, accounting for dissipation, degradation, and other processes, the animal would receive a 

chronic dose of 0.000586 mg/kg/day (Project file, 2,4-D Worksheet F07). Doses to a larger 

mammal would be even lower on a per kg body weight basis. These doses are 0.07 of the 

acute “non-lethal” dose, and 0.0006 of the chronic NOAEL, respectively. The acute dose is 

within the range of doses in which increased thyroid weight, decreased testicular weight, and 

decreased body weight gain are plausible (SERA, 1998, p. 3-52). 

At the highest application rate of 2 lb/acre, the acute dose from drinking water contaminated 

by a spill is 1.33 mg/kg (project file). This dose is 0.10 of the acute NOAEL. The acute dose 

is within the range of doses in which increased thyroid weight, decreased testicular weight, 

decreased body weight gain, sub-clinical pathology to kidney and liver, and sub-clinical signs 

of neurotoxicity are plausible (SERA, 1998, p. 3-52). 

The chronic dose (0.0017 mg/kg) is below any dose level in which effects have been noted. 

Large Herbivorous Mammal

The acute “non-lethal” dose for mammals in laboratory toxicity tests is 10 mg/kg. For 

exposure scenarios that use the typical application rate of 1 lb/acre, if a 70 kg mammal 

consumed contaminated vegetation on site shortly after application, assuming the highest 

residue rates and 100 percents of the diet contaminated, it would receive an acute dose of 

48.6 mg/kg (Project file, 2,4-D Worksheet F10). This dose is greater than the acute “nonlethal” dose. This dose is within the range of doses in which mild signs of systemic toxicity 

are plausible, and sub-clinical signs of neurologic toxicity, increased thyroid weight, 

decreased testicular weight, decreased body weight gain, damage to several organs are 

expected (SERA, 1998, p. 3-52). 

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2,4-D, cont’d.

The chronic NOAEL for mammals in laboratory toxicity tests is 1 mg/kg/day. Chronic 

exposure from the consumption of contaminated vegetation for 90 days at the treatment site, 

assuming the highest residue rates, results in a dose of 10.8 mg/kg/day (Project file, 2,4-D 

Worksheet F11a). This dose is greater than the chronic NOAEL and the chronic LOAEL (5 

mg/kg/day) for effects to kidney, blood, and liver. This dose is within the range of doses in 

which mild signs of systemic toxicity are plausible, and sub-clinical signs of neurologic 

toxicity, increased thyroid weight, decreased testicular weight, decreased body weight gain, 

damage to several organs are expected (SERA, 1998, p. 3-52). 

Estimated doses using the highest application rate (2 lbs/acre) are 97.1 mg/kg for acute doses 

and 21.5 mg/kg/day for chronic doses. The acute dose is much greater than the acute “nonlethal” dose and chronic LOAEL (5 mg/kg) for mammals (Project file, 2,4-D High Rate 

Worksheet WL Ex1). The acute dose is within the range of doses in which mild signs of 

systemic toxicity are plausible; sub-clinical signs of neurologic toxicity, increased thyroid 

weight, decreased testicular weight, decreased body weight gain, damage to several organs 

are expected; and mortality may occur (SERA, 1998, p. 3-52). The chronic dose is four 

times greater than the chronic LOAEL for effects to kidney, blood and liver. Unlike the 

case with the chronic exposure scenario involving non-selective herbicides, the acute and 

chronic exposure scenario could occur in the field. 2,4-D is selective for broadleaved weeds, 

so if 2,4-D were broadcast sprayed in foraging habitat in attempt to control broadleaved 

weeds, the forage grasses with herbicide residue would remain available to large grass-eating 

mammals. 

Medium Carnivorous Mammal

The acute “non-lethal” dose for mammals in laboratory toxicity tests is 10 mg/kg. For 

exposure scenarios that use the typical application rate of 1 lb/acre, if a 5 kg mammal 

consumed small mammal prey that has been contaminated by direct spray, assuming 100 

percent absorption for the prey, it would receive an acute dose of 2.10 mg/kg (Project file, 

2,4-D Worksheet F16a). Doses to a larger mammal would be even lower on a per kg body 

weight basis. This dose is 0.21 of the acute “non-lethal” dose, but is within the range of 

doses in which sub-clinical signs of neurologic toxicity are plausible, and increased thyroid 

weight, decreased testicular weight, decreased body weight gain, and subclinical pathology to 

kidney and liver are expected (SERA, 1998, p. 3-52). 

2,4-D does not appear to accumulate or persist in animal tissues and is eliminated fairly 

rapidly. If adverse effects from 2,4-D are to develop, they will develop relatively fast and 

will not become more severe as the duration of exposure continues (SERA, 1998, p. 3-50, 3-

51). Therefore, chronic exposures from contaminated mammal prey due to a single 

application of 2,4-D are unlikely to cause adverse effects beyond those reported above, for 

acute exposure. 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

2,4-D, cont’d.

The estimated dose (4.2 mg/kg) using the highest application rate (2 lbs/acre) is less than the 

acute “non-lethal” dose. This dose is greater than the chronic NOAEL for mammals, but 

slightly less than the chronic LOAEL (Project file, 2,4-D High Rate Worksheet WL Ex1). 

The acute dose is within the range of doses in which sub-clinical signs of neurologic toxicity 

are plausible, and increased thyroid weight, decreased testicular weight, decreased body 

weight gain, and subclinical pathology to kidney and liver are expected (SERA, 1998, p. 3-

52).

Small Herbivorous Mammal

The acute “non-lethal” dose for mammals in laboratory toxicity tests is 10 mg/kg. If a small 

mammal consumes contaminated vegetation shortly after application, assuming the highest 

residue rates, the acute dose received is 2.68 mg/kg (Project file, 2,4-D Worksheet F03). This 

dose is 0.3 of the acute “non-lethal” dose. This dose is within the range of doses in which 

sub-clinical signs of neurologic toxicity are plausible, and increased thyroid weight, 

decreased testicular weight, decreased body weight gain, and subclinical pathology to kidney 

and liver are expected (SERA, 1998, p. 3-52). 

The chronic NOAEL for mammals in laboratory toxicity tests is 1 mg/kg/day. If a small 

mammal consumes contaminated vegetation at the treatment site for 90-days, assuming 

highest residue rates, the animal would receive a chronic dose of 0.119 mg/kg/day (Project 

file, 2,4-D Worksheet F04a). This estimated dose is 0.1 of the chronic NOAEL. This dose is 

within the range of doses in which increased thyroid weight, decreased testicular weight, and 

decreased body weight gain are plausible (SERA, 1998, p. 3-52). 

Estimated doses using the highest application rate (2 lbs/acre) are less than the acute “nonlethal” dose and chronic NOAEL for mammals (Project file, 2,4-D High Rate Worksheet WL 

Ex1). The acute dose (5.36 mg/kg) is within the range of doses in which sub-clinical signs of 

neurologic toxicity are plausible, and increased thyroid weight, decreased testicular weight, 

decreased body weight gain, and subclinical pathology to kidney and liver are expected

(SERA, 1998, p. 3-52). 

Small Insectivorous Mammal

The acute “non-lethal” dose for mammals in laboratory toxicity tests is 10 mg/kg. For 

exposure scenarios that use the typical application rate of 1 lb/acre, if a small mammal 

consumes contaminated insects shortly after application, assuming the highest residue rates, 

the acute dose received is 69.4 mg/kg (Project file, 2,4-D Worksheet 14a). This dose is seven 

times greater than the acute “non-lethal” dose. This dose is within the range of doses in 

which mild signs of systemic toxicity are plausible, and sub-clinical signs of neurologic 

toxicity, increased thyroid weight, decreased testicular weight, decreased body weight gain, 

damage to several organs are expected (SERA, 1998, p. 3-52). The exposure scenario uses 

residue rates from small insects, which are substantially higher than those for large insects, 

and assumes that 100 percent of the daily diet is composed of insects that have been directly 

sprayed. For bats, in particular, the scenario is unlikely to occur in the field. It seems more 

plausible for shrews and small fossorial insectivores, however. 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

2,4-D, cont’d. 

Data on degradation of herbicide residues from insects is not available, so no chronic 

exposure scenario has been developed. Residue on insects likely declines over time, but the 

extent of decline has not been quantified. However, the acute dose is 13 times greater than

the chronic LOAEL for effects to kidney, blood, and liver. The adverse effects from chronic 

exposure are the same as those noted above for acute exposure. The exposure scenario uses 

residue rates from small insects, which are substantially higher than those for large insects, 

and assumes that 100 percent of the daily diet is composed of insects that have been directly 

sprayed. For bats, in particular, the scenario is unlikely to occur in the field. It seems more 

plausible for shrews and small fossorial insectivores, however. 

The estimated dose using the highest application rate (2 lbs/acre) is 139 mg/kg. This dose is

13 times greater than the acute “non-lethal” dose, and 27 times greater than the chronic 

LOAEL for effects to kidney, blood, and liver in mammals (Project file, 2,4-D High Rate 

Worksheet WL Ex1). The dose is within the range of doses in which frank neurological 

and/or reproductive effects, including birth defects, are expected. While this dose is above 

the LD50 for cattle (100 mg/kg), it is well below the LD50 for small mammals (1800 mg/kg) 

(SERA, 1998 2,4-D). 

Large Herbivorous Bird

Toxicity data for the effects of 2,4-D on birds is much more limited than for mammals. The 

FS/SERA risk assessment for 2,4-D contains very little information specific to birds, so the 

following discussion uses dietary LD50 for bobwhite quail and mallard (>5620 ppm) to 

calculate the toxicity index (Weed Science Society of America 2002, p. 115). Since the acute 

exposure scenario for bird is based on an LD50 rather than an acute NOAEL, 0.1 of the LD50

is used as the toxicity index. EPA uses this factor (0.1) as a result of data analysis and 

modeling conducted by their Office of Pesticide Programs (Urban and Cook, 1986). The 

acute dietary LD50 for birds in laboratory toxicity tests corresponds to 562 mg/kg. For 

exposure scenarios that use the typical application rate of 1 lb/acre, if a 4 kg bird consumed 

contaminated grass on site shortly after application, assuming the highest residue rates and 

100 percent of diet is contaminated, it would receive an acute dose of 76.0 mg/kg (Project 

file, 2,4-D Worksheet F12). The toxicity index (0.1 of the LD50) is 56.2 mg/kg. This dose is 

greater than the toxicity index, so adverse effects to grass-eating birds are plausible from 

acute dietary exposures. Unlike the case with the chronic exposure scenario involving nonselective herbicides, this acute exposure scenario very well could occur in the field. 2,4-D is 

selective for broadleaved weeds, so if 2,4-D were broadcast sprayed in foraging habitat in 

attempt to control broadleaved weeds, the forage grasses with herbicide residue would 

remain available to large grass-eating birds. 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

2,4-D, cont’d.

There is no chronic toxicity index cited in the 2,4-D risk assessment (SERA, 1998) for 

effects to birds, so the mammal chronic NOAEL will be used (birds appear to be less 

sensitive to 2,4-D than are mammals; SERA, 1998). The chronic NOAEL for mammals in 

laboratory toxicity tests is 1 mg/kg/day. Chronic exposure from the consumption of 

contaminated grass for 90 days at the treatment site, assuming the highest residue rates and 

100 percent of diet is contaminated, results in a dose of 16.9 mg/kg/day (Project file, 2,4-D 

Worksheet F13a). This estimated dose is greater than the chronic NOAEL for mammals, 

and also exceeds the chronic LOAEL for mammals (5 mg/kg/day) for effects to kidney, liver 

and blood. So adverse effects to grass-eating birds are expected from chronic dietary 

exposures. 

At the highest application rate (2 lb/acre), the acute dose (152 mg/kg) is greater than the 

acute toxicity index for birds. The dose is less than the LD50, so is not likely to be lethal, but 

it is greater than 0.1 of the LD50, so sub-lethal effects may be plausible. The chronic dose 

(33.7 mg/kg/day) exceeds the chronic NOAEL and the chronic LOAEL (5 mg/kg/day) for 

effects to mammal kidney, liver, and blood. Therefore, adverse effects to grass-eating birds 

appear expected from acute and chronic dietary exposures at the typical and highest 

application rates. 

Large Fish-eating Bird

Many chemicals may be concentrated or partitioned from water into the tissues of animals in 

the water. This process is referred to as bioconcentration. The potential for bioconcentration 

of 2,4-D in fish was studied in carp and tilapia exposed to 14C-labelled 2,4-D for 0.5 to 14 

days (Wang et al., 1994, cited in SERA, 1998-2,4-D). The ranges of bioconcentration factors 

(BCF) reported in this study were 10-40 L/kg. Conversely, field studies indicate that the 

application of 2,4-D to a lake at very high application rates did not result in bioconcentration 

of the herbicide in game fish (Hoeppel and Westerdahl 1983). Due to the lack of a timeconcentration relationship in the Wang et al. study, the SERA risk assessment (SERA, 1998-

2,4-D) uses a whole-fish BCF of 25 L/kg for acute exposure chronic exposure scenarios. 

Toxicity data for the effects of 2,4-D on birds is much more limited than for mammals. The 

FS/SERA risk assessment for 2,4-D contains very little information specific to birds, so the 

following discussion uses dietary LD50 for bobwhite quail and mallard (>5620 ppm) to 

calculate the toxicity index (Weed Science Society of America 2002, p.115). Since the acute 

exposure scenario for bird is based on an LD50 rather than an acute NOAEL, 0.1 of the LD50

is used as the toxicity index. EPA uses this safety factor (0.1) as a result of data analysis and 

modeling conducted by their Office of Pesticide Programs (Urban and Cook 1986). The 

acute dietary LD50 for birds in laboratory toxicity tests corresponds to 562 mg/kg. For 

exposure scenarios that use the typical application rate of 1 lb/acre, if a predatory bird 

consumed fish from a pond contaminated by an accidental spill, assuming the highest 

concentrations in fish and highest intake on a body weight basis, it would receive an acute 

dose of 6.8 mg/kg (Project file, 2,4-D Worksheet F08). The toxicity index (0.1 of the LD50) is 

56.2 mg/kg. This dose is 0.12 of the toxicity index, so there is no basis for asserting or 

predicting that adverse effects to fish-eating birds are plausible. 

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2,4-D, cont’d.

There is no chronic toxicity index cited in the 2,4-D risk assessment (SERA, 1998) for 

effects to birds, so the mammal chronic NOAEL will be used (acute toxicities of 2,4-D to 

mammals is somewhat less than birds). The chronic NOAEL for mammals in laboratory 

toxicity tests is 1 mg/kg/day. If a predatory bird consumed fish contaminated by runoff for a 

lifetime, assuming the highest concentrations in fish and highest intake on a body weight 

basis, it would receive a chronic dose of 0.006 mg/kg/day (Project file, 2,4-D Worksheet 

F09). This estimated dose is 0.006 of the chronic NOAEL for mammals, so there is no basis 

for asserting or predicting that adverse effects to fish-eating birds are plausible. 

Estimated doses using the highest application rate (2 lb/acre) also result in exposures less 

than the acute toxicity index for birds and chronic NOAEL for mammals, so there is no basis 

for asserting or predicting that adverse effects are plausible using typical or worst-case 

exposure assumptions. 

Large Predatory Bird

Toxicity data for the effects of 2,4-D on birds is much more limited than for mammals. The 

FS/SERA risk assessment for 2,4-D contains very little information specific to birds, so the 

following discussion uses dietary LD50 for bobwhite quail and mallard (>5620 ppm) to 

calculate the toxicity index (Weed Science Society of America, 2002, p.115). Since the acute 

exposure scenario for bird is based on an LD50 rather than an acute NOAEL, 0.1 of the LD50

is used as the toxicity index. EPA uses this safety factor (0.1) as a result of data analysis and 

modeling conducted by their Office of Pesticide Programs (Urban and Cook, 1986). The 

acute dietary LD50 for birds in laboratory toxicity tests corresponds to 562 mg/kg. For 

exposure scenarios that use the typical application rate of 1 lb/acre, if a 0.6 kg bird consumed 

small mammal prey that has been contaminated by direct spray, assuming 100 percent 

absorption for the prey, it would receive an acute dose of 3.23 mg/kg (Project file, 2,4-D 

Worksheet F16b). The toxicity index (0.1 of the LD50) is 56.2 mg/kg. This dose 0.057of the 

acute toxicity index, so there is no basis for asserting or predicting that adverse effects to 

predatory birds are plausible. 

2,4-D does not appear to accumulate or persist in animal tissues and is eliminated fairly 

rapidly. If adverse effects from 2,4-D are to develop, they will develop relatively fast and 

will not become more severe as the duration of exposure continues (SERA, 1998, p. 3-50, 3-

51). Therefore, chronic exposures from contaminated mammal prey due to a single 

application of 2,4-D seem unlikely. However, the acute dose is greater than the chronic 

NOAEL, but less than the chronic LOAEL, for mammals, so adverse effects may be 

plausible. 

At the highest application rate (2 lb/acre), the estimated dose (6.46 mg/kg) is less than the 

acute toxicity index for birds, but greater than the chronic NOAEL and LOAEL for 

mammals. Therefore, adverse effects from acute doses are unlikely, but may be plausible 

from chronic exposure. 

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2,4-D, cont’d. 

Small Insectivorous Bird

Toxicity data for the effects of 2,4-D on birds is much more limited than for mammals. The 

FS/SERA risk assessment for 2,4-D contains very little information specific to birds, so the 

following discussion uses dietary LD50 for bobwhite quail and mallard (>5620 ppm) to 

calculate the toxicity index (Weed Science Society of America 2002, p.115). Since the acute 

exposure scenario for bird is based on an LD50 rather than an acute NOAEL, 0.1 of the LD50

is used as the toxicity index. EPA uses this safety factor (0.1) as a result of data analysis and 

modeling conducted by their Office of Pesticide Programs (Urban and Cook 1986). The 

acute dietary LD50 for birds in laboratory toxicity tests corresponds to 562 mg/kg. For 

exposure scenarios that use the typical application rate of 1 lb/acre, if a 10 g bird consumed 

contaminated insects on site shortly after application, assuming the highest residue rates, it 

would receive an acute dose of 113 mg/kg (Project file, 2,4-D Worksheet F14b). The toxicity 

index (0.1 of the LD50) is 56.2 mg/kg. This dose is 2 times greater than the acute toxicity 

index, so adverse effects to insectivorous birds are plausible. 

There is no chronic toxicity index cited in the 2,4-D risk assessment (SERA 1998) for effects 

to birds, so the mammal chronic NOAEL will be used (acute toxicities of 2,4-D to mammals 

is somewhat less than birds). The chronic NOAEL for mammals in laboratory toxicity tests is 

1 mg/kg/day. Data on degradation of herbicide residues from insects is not available, so no 

chronic exposure scenario has been developed. However, the acute dose is much greater 

than the chronic LOAEL for effects to mammal kidney, liver, and blood, so adverse effects 

to insectivorous birds may be expected. 

At the highest application rate (2 lb/acre), the estimated dose (226 mg/kg) is much greater 

than the acute toxicity index for birds and chronic LOAEL for effects to mammal kidney, 

liver, and blood. Therefore, adverse effects to insectivorous birds are expected from acute 

and chronic dietary exposures at the typical and highest application rates. 

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APPENDIX 1 

Estimated doses for each exposure scenario for 12 herbicides. 

The upper estimate used for this analysis includes worst-case assumptions such as 

highest residue rates, highest food intake, etc. 

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Chlorsulfuron / Typical Application Rate 

Only the Upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 1.36E+00 1.36E+00 1.36E+00 F02a 

 bee, 100% absorption 8.98E+00 8.98E+00 8.98E+00 F02b 

Contaminated vegetation 

small mammal 7.00E-02 7.00E-02 1.50E-01 F03 

large mammal 9.63E-01 9.63E-01 2.72E+00 F10 

large bird 1.51E+00 1.51E+00 4.26E+00 F12 

Contaminated water 

small mammal, spill 1.11E-02 2.22E-03 1.11E-01 F05 

Contaminated insects 

small mammal 1.30E+00 1.30E+00 3.89E+00 F14a 

small bird 2.11E+00 2.11E+00 6.32E+00 F14b 

Contaminated prey 

predatory mammal (small mammal) 1.17E-01 1.17E-01 1.17E-01 F16a 

predatory bird (small mammal) 1.81E-01 1.81E-01 1.81E-01 F16b 

predatory bird (fish) 1.97E-02 1.97E-03 2.95E-01 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 2.95E-03 1.47E-03 1.26E-02 F04a 

large mammal, on site 1.22E-01 4.05E-02 1.14E+00 F11a 

large bird, on site 1.90E-01 6.34E-02 1.79E+00 F13a 

Contaminated water 

small mammal 4.92E-06 8.20E-07 7.38E-06 F07 

Contaminated fish 

predatory bird 4.03E-05 3.36E-06 9.07E-05 F09 

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Chlorsulfuron / Highest Application Rate 

Only upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals. 

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet

Acute/Accidental Exposures 

Direct spray 

small animal, 100% absorption 6.06E+00 6.06E+00 6.06E+00 F02a 

bee, 100% absorption 4.01E+01 4.01E+01 4.01E+01 F02b 

Contaminated vegetation 

small mammal 3.13E-01 3.13E-01 6.70E-01 F03 

large mammal 4.30E+00 4.30E+00 1.21E+01 F10 

large bird 6.73E+00 6.73E+00 1.90E+01 F12 

Contaminated water 

small mammal, spill 4.95E-02 9.89E-03 4.95E-01 F05 

Contaminated insects 

small mammal 5.78E+00 5.78E+00 1.73E+01 F14a 

small bird 9.40E+00 9.40E+00 2.82E+01 F14b 

Contaminated prey 

predatory mammal (small mammal) 5.25E-01 5.25E-01 5.25E-01 F16a 

predatory bird (small mammal) 8.08E-01 8.08E-01 8.08E-01 F16b 

predatory bird (fish) 8.79E-02 8.79E-03 1.32E+00 F08 

Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 1.32E-02 6.58E-03 5.64E-02 F04a 

large mammal, on site 5.43E-01 1.81E-01 5.11E+00 F11a 

large bird, on site 8.50E-01 2.83E-01 8.00E+00 F13a 

Contaminated water 

small mammal 2.20E-05 3.66E-06 3.29E-05 F07 

Contaminated fish 

predatory bird 1.80E-04 1.50E-05 4.05E-04 F09 

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Clopyralid / Typical Application Rate 

Only upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet

Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 8.49E+00 8.49E+00 8.49E+00 F02a 

 bee, 100% absorption 5.61E+01 5.61E+01 5.61E+01 F02b 

Contaminated vegetation 

small mammal 4.38E-01 4.38E-01 9.38E-01 F03 

large mammal 6.02E+00 6.02E+00 1.70E+01 F10 

large bird 9.42E+00 9.42E+00 2.66E+01 F12 

Contaminated water 

small mammal, spill 4.65E-01 1.11E-01 2.33E+00 F05 

Contaminated insects 

small mammal 8.10E+00 8.10E+00 2.43E+01 F14a 

small bird 1.32E+01 1.32E+01 3.95E+01 F14b 

Contaminated prey 

predatory mammal (small mammal) 7.34E-01 7.34E-01 7.34E-01 F16a 

predatory bird (small mammal) 1.13E+00 1.13E+00 1.13E+00 F16b 

predatory bird (fish) 3.18E-01 3.79E-02 2.38E+00 F08 

Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 1.77E-02 7.04E-03 9.87E-02 F04a 

large mammal, on site 7.29E-01 1.94E-01 8.95E+00 F11a 

large bird, on site 1.14E+00 3.03E-01 1.40E+01 F13a 

Contaminated water 

small mammal 3.59E-04 5.12E-05 6.66E-04 F07 

Contaminated fish 

predatory bird 2.45E-04 1.75E-05 6.83E-04 F09 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Clopyralid / Highest Application Rate 

Only upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 1.21E+01 1.21E+01 1.21E+01 F02a 

 bee, 100% absorption 8.01E+01 8.01E+01 8.01E+01 F02b 

Contaminated vegetation 

small mammal 6.25E-01 6.25E-01 1.34E+00 F03 

large mammal 8.60E+00 8.60E+00 2.43E+01 F10 

large bird 1.35E+01 1.35E+01 3.80E+01 F12 

Contaminated water 

small mammal, spill 6.65E-01 1.58E-01 3.32E+00 F05 

Contaminated insects 

small mammal 1.16E+01 1.16E+01 3.47E+01 F14a 

small bird 1.88E+01 1.88E+01 5.64E+01 F14b 

Contaminated prey 

predatory mammal (small mammal) 1.05E+00 1.05E+00 1.05E+00 F16a 

predatory bird (small mammal) 1.62E+00 1.62E+00 1.62E+00 F16b 

predatory bird (fish) 4.54E-01 5.41E-02 3.41E+00 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 2.52E-02 1.01E-02 1.41E-01 F04a 

large mammal, on site 1.04E+00 2.77E-01 1.28E+01 F11a 

large bird, on site 1.63E+00 4.33E-01 2.00E+01 F13a 

Contaminated water 

small mammal 5.12E-04 7.32E-05 9.52E-04 F07 

Contaminated fish 

predatory bird 3.50E-04 2.50E-05 9.75E-04 F09 

115
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Dicamba / Typical Application Rate 

Only upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 7.27E+00 7.27E+00 7.27E+00 F02a 

 larger mammal, 100% absoption 1.69E+00 1.69E+00 1.69E+00 F02c 

 bee, 100% absorption 4.81E+01 4.81E+01 4.81E+01 F02b 

Contaminated vegetation 

small mammal 3.75E-01 3.75E-01 8.04E-01 F03 

large mammal 5.16E+00 5.16E+00 1.46E+01 F10 

large bird 8.08E+00 8.08E+00 2.28E+01 F12 

Contaminated water 

small mammal, spill 1.55E-01 2.22E-02 1.33E+00 F05 

Contaminated insects 

small mammal 6.94E+00 6.94E+00 2.08E+01 F14a 

small bird 1.13E+01 1.13E+01 3.38E+01 F14b 

Contaminated prey 

predatory mammal (small mammal) 6.29E-01 6.29E-01 6.29E-01 F16a 

predatory bird (small mammal) 9.70E-01 9.70E-01 9.70E-01 F16b 

predatory bird (fish) 6.99E-02 5.00E-03 8.99E-01 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 5.41E-03 2.70E-03 2.32E-02 F04a 

large mammal, on site 2.23E-01 7.44E-02 2.10E+00 F11a 

large bird, on site 3.49E-01 1.16E-01 3.29E+00 F13a 

Contaminated water 

small mammal 4.39E-07 2.20E-07 1.32E-06 F07 

Contaminated fish 

predatory bird 1.98E-07 4.95E-08 8.91E-07 F09 

116
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Dicamba / Highest Application Rate 

Only upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 4.85E+01 4.85E+01 4.85E+01 F02a 

 larger mammal, 100% absorption 1.12E+01 1.12E+01 1.12E+01 F02c 

 bee, 100% absorption 3.21E+02 3.21E+02 3.21E+02 F02b 

Contaminated vegetation 

small mammal 2.50E+00 2.50E+00 5.36E+00 F03 

large mammal 3.44E+01 3.44E+01 9.71E+01 F10 

large bird 5.38E+01 5.38E+01 1.52E+02 F12 

Contaminated water 

small mammal, spill 1.03E+00 1.48E-01 8.87E+00 F05 

Contaminated insects 

small mammal 4.63E+01 4.63E+01 1.39E+02 F14a 

small bird 7.52E+01 7.52E+01 2.26E+02 F14b 

Contaminated prey 

predatory mammal (small mammal) 4.20E+00 4.20E+00 4.20E+00 F16a 

predatory bird (small mammal) 6.46E+00 6.46E+00 6.46E+00 F16b 

predatory bird (fish) 4.66E-01 3.33E-02 6.00E+00 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 3.60E-02 1.80E-02 1.54E-01 F04a 

large mammal, on site 1.49E+00 4.96E-01 1.40E+01 F11a 

large bird, on site 2.33E+00 7.76E-01 2.19E+01 F13a 

Contaminated water 

small mammal 2.93E-06 1.46E-06 8.78E-06 F07 

Contaminated fish 

predatory bird 1.32E-06 3.30E-07 5.94E-06 F09 

117
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Glyphosate / Typical Application Rate 

Only upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 4.85E+01 4.85E+01 4.85E+01 F02a 

 bee, 100% absorption 3.21E+02 3.21E+02 3.21E+02 F02b 

Contaminated vegetation 

small mammal 8.57E-01 8.57E-01 2.11E+00 F03 

large mammal 3.44E+01 3.44E+01 9.71E+01 F10 

large bird 5.38E+01 5.38E+01 1.52E+02 F12 

Contaminated water 

small mammal, spill 2.66E+00 1.06E+00 5.32E+00 F05 

Contaminated insects 

small mammal 4.63E+01 4.63E+01 1.39E+02 F14a 

small bird 8.E+01 7.52E+01 2.26E+02 F14b 

Contaminated prey 

predatory mammal (small mammal) 4.20E+00 4.20E+00 4.20E+00 F16a 

predatory bird (small mammal) 6.46E+00 6.46E+00 6.46E+00 F16b 

predatory bird (fish) 9.45E-01 1.89E-01 2.83E+00 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 4.69E-02 2.35E-02 2.31E-01 F04a 

large mammal, on site 5.65E+00 1.88E+00 5.32E+01 F11a 

large bird, on site 8.84E+00 2.95E+00 8.32E+01 F13a 

Contaminated water 

small mammal 2.93E-04 2.93E-05 2.34E-03 F07 

Contaminated fish 

predatory bird 1.04E-04 5.20E-06 1.25E-03 F09 

118
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Glyphosate / Highest Application Rate 

Only upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 1.70E+02 1.70E+02 1.70E+02 F02a 

 bee, 100% absorption 1.12E+03 1.12E+03 1.12E+03 F02b 

Contaminated vegetation 

small mammal 3.00E+00 3.00E+00 7.38E+00 F03 

large mammal 1.20E+02 1.20E+02 3.40E+02 F10 

large bird 1.88E+02 1.88E+02 5.32E+02 F12 

Contaminated water 

small mammal, spill 9.31E+00 3.72E+00 1.86E+01 F05 

Contaminated insects 

small mammal 1.62E+02 1.62E+02 4.86E+02 F14a 

small bird 3.E+02 2.63E+02 7.90E+02 F14b 

Contaminated prey 

predatory mammal (small mammal) 1.47E+01 1.47E+01 1.47E+01 F16a 

predatory bird (small mammal) 2.26E+01 2.26E+01 2.26E+01 F16b 

predatory bird (fish) 3.31E+00 6.61E-01 9.92E+00 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 1.64E-01 8.21E-02 8.07E-01 F04a 

large mammal, on site 1.98E+01 6.59E+00 1.86E+02 F11a 

large bird, on site 3.09E+01 1.03E+01 2.91E+02 F13a 

Contaminated water 

small mammal 1.02E-03 1.02E-04 8.20E-03 F07 

Contaminated fish 

predatory bird 3.64E-04 1.82E-05 4.37E-03 F09 

119
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Imazapic / Typical Application Rate 

Only upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 2.42E+00 2.42E+00 2.42E+00 F02a 

 bee, 100% absorption 1.60E+01 1.60E+01 1.60E+01 F02b 

Contaminated vegetation 

small mammal 1.25E-01 1.25E-01 2.68E-01 F03 

large mammal 1.72E+00 1.72E+00 4.86E+00 F10 

large bird 2.69E+00 2.69E+00 7.60E+00 F12 

Contaminated water 

small mammal, spill 2.42E+00 2.42E+00 2.42E+00 F05 

Contaminated insects 

small mammal 2.31E+00 2.31E+00 6.94E+00 F14a 

small bird 3.76E+00 3.76E+00 1.13E+01 F14b 

Contaminated prey 

predatory mammal (small mammal) 2.10E-01 2.10E-01 2.10E-01 F16a 

predatory bird (small mammal) 3.23E-01 3.23E-01 3.23E-01 F16b 

predatory bird (fish) 1.67E-02 5.00E-03 7.49E-02 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 8.02E-04 1.20E-04 1.02E-02 F04a 

large mammal, on site 3.31E-02 3.31E-03 9.29E-01 F11a 

large bird, on site 5.18E-02 5.18E-03 1.45E+00 F13a 

Contaminated water 

small mammal 2.93E-07 1.46E-07 4.39E-07 F07 

Contaminated fish 

predatory bird 2.20E-08 5.50E-09 4.95E-08 F09 

120
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Imazapic / Highest Application Rate 

Only upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 4.36E+00 4.36E+00 4.36E+00 F02a 

 bee, 100% absorption 2.89E+01 2.89E+01 2.89E+01 F02b 

Contaminated vegetation 

small mammal 2.25E-01 2.25E-01 4.82E-01 F03 

large mammal 3.10E+00 3.10E+00 8.74E+00 F10 

large bird 4.85E+00 4.85E+00 1.37E+01 F12 

Contaminated water 

small mammal, spill 4.21E-01 2.53E-01 1.26E+00 F05 

Contaminated insects 

small mammal 4.16E+00 4.16E+00 1.25E+01 F14a 

small bird 6.77E+00 6.77E+00 2.03E+01 F14b 

Contaminated prey 

predatory mammal (small mammal) 3.78E-01 3.78E-01 3.78E-01 F16a 

predatory bird (small mammal) 5.82E-01 5.82E-01 5.82E-01 F16b 

predatory bird (fish) 3.16E-02 9.49E-03 1.42E-01 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 1.44E-03 2.16E-04 1.84E-02 F04a 

large mammal, on site 5.95E-02 5.95E-03 1.67E+00 F11a 

large bird, on site 9.32E-02 9.32E-03 2.62E+00 F13a 

Contaminated water 

small mammal 5.27E-07 2.64E-07 7.91E-07 F07 

Contaminated fish 

predatory bird 3.96E-08 9.90E-09 8.91E-08 F09 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Imazapyr / Typical Application Rate

Only upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet 

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 1.09E+01 1.09E+01 1.09E+01 F02a 

 bee, 100% absorption 7.21E+01 7.21E+01 7.21E+01

Contaminated vegetation 

small mammal 5.63E-01 5.63E-01 1.21E+00 F03 

large mammal 7.74E+00 7.74E+00 2.19E+01 F10 

large bird 1.21E+01 1.21E+01 3.42E+01 F12 

Contaminated water 

small mammal, spill 5.98E-01 2.99E-01 1.22E+00 F05 

Contaminated insects 

small mammal 1.04E+01 1.04E+01 3.12E+01 F14a 

small bird 1.69E+01 1.69E+01 5.08E+01 F14b 

Contaminated prey 

predatory mammal (small mammal) 9.44E-01 9.44E-01 9.44E-01 F16a 

predatory bird (small mammal) 1.45E+00 1.45E+00 1.45E+00 F16b 

predatory bird (fish) 2.04E-01 5.11E-02 6.25E-01 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 2.13E-02 6.66E-03 1.17E-01 F04a 

large mammal, on site 8.80E-01 1.83E-01 1.06E+01 F11a 

large bird, on site 1.38E+00 2.87E-01 1.65E+01 F13a 

Contaminated water 

small mammal 6.59E-06 6.59E-07 6.59E-05 F07 

Contaminated fish 

predatory bird 2.25E-06 1.13E-07 3.38E-05 F09 

122
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Imazapyr / Highest Application Rate

Only upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 3.03E+01 3.03E+01 3.03E+01 F02a 

 bee, 100% absorption 2.E-01 2.E-01 2.E-01 F02b 

Contaminated vegetation 

small mammal 1.56E+00 1.56E+00 3.35E+00 F03 

large mammal 2.15E+01 2.15E+01 6.07E+01 F10 

large bird 3.37E+01 3.37E+01 9.50E+01 F12 

Contaminated water 

small mammal, spill 1.66E+00 8.31E-01 3.39E+00 F05 

Contaminated insects 

small mammal 2.89E+01 2.89E+01 8.67E+01 F14a 

small bird 4.70E+01 4.70E+01 1.41E+02 F14b 

Contaminated prey 

predatory mammal (small mammal) 2.62E+00 2.62E+00 2.62E+00 F16a 

predatory bird (small mammal) 4.04E+00 4.04E+00 4.04E+00 F16b 

predatory bird (fish) 5.68E-01 1.42E-01 1.73E+00 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 5.92E-02 1.85E-02 3.24E-01 F04a 

large mammal, on site 2.44E+00 5.09E-01 2.93E+01 F11a 

large bird, on site 3.83E+00 7.97E-01 4.59E+01 F13a 

Contaminated water 

small mammal 1.83E-05 1.83E-06 1.83E-04 F07 

Contaminated fish 

predatory bird 6.25E-06 3.13E-07 9.38E-05 F09 

123
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Metsulfuron methyl / Typical Application Rate 

Only upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet 

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 7.27E-01 7.27E-01 7.27E-01 F02a 

 bee, 100% absorption 4.81E+00 4.81E+00 4.81E+00 F02b 

Contaminated vegetation 

small mammal 3.75E-02 3.75E-02 8.04E-02 F03 

large mammal 5.16E-01 5.16E-01 1.46E+00 F10 

large bird 8.08E-01 8.08E-01 2.28E+00 F12 

Contaminated water 

small mammal, spill 1.11E-02 1.11E-03 4.43E-02 F05 

Contaminated insects 

small mammal 6.94E-01 6.94E-01 2.08E+00 F14a 

small bird 1.13E+00 1.13E+00 3.38E+00 F14b 

Contaminated prey 

predatory mammal (small mammal) 6.29E-02 6.29E-02 6.29E-02 F16a 

predatory bird (small mammal) 9.70E-02 9.70E-02 9.70E-02 F16b 

predatory bird (fish) 1.59E-03 7.95E-05 9.54E-03 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 1.58E-03 7.89E-04 6.76E-03 F04a 

large mammal, on site 6.51E-02 2.17E-02 6.13E-01 F11a 

large bird, on site 1.02E-01 3.40E-02 9.60E-01 F13a 

Contaminated water 

small mammal 8.78E-07 4.39E-07 1.76E-06 F07 

Contaminated fish 

predatory bird 1.27E-06 3.17E-07 3.80E-06 F09 

124
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Metsulfuron methyl / Highest Application Rate 

Only upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet 

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 3.64E+00 3.64E+00 3.64E+00 F02a 

 bee, 100% absorption 2.40E+01 2.40E+01 2.40E+01 F02b 

Contaminated vegetation 

small mammal 1.88E-01 1.88E-01 4.02E-01 F03 

large mammal 2.58E+00 2.58E+00 7.28E+00 F10 

large bird 4.04E+00 4.04E+00 1.14E+01 F12 

Contaminated water 

small mammal, spill 5.54E-02 5.54E-03 2.22E-01 F05 

Contaminated insects 

small mammal 3.47E+00 3.47E+00 1.04E+01 F14a 

small bird 5.64E+00 5.64E+00 1.69E+01 F14b 

Contaminated prey 

predatory mammal (small mammal) 3.15E-01 3.15E-01 3.15E-01 F16a 

predatory bird (small mammal) 4.85E-01 4.85E-01 4.85E-01 F16b 

predatory bird (fish) 7.95E-03 3.97E-04 4.77E-02 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 7.89E-03 3.95E-03 3.38E-02 F04a 

large mammal, on site 3.26E-01 1.09E-01 3.07E+00 F11a 

large bird, on site 5.10E-01 1.70E-01 4.80E+00 F13a 

Contaminated water 

small mammal 4.39E-06 2.20E-06 8.78E-06 F07 

Contaminated fish 

predatory bird 6.33E-06 1.58E-06 1.90E-05 F09 

125
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Picloram / Typical Application Rate 

Only upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet 

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 2.E-01 2.E-01 2.E-01 F02a 

 bee, 100% absorption 6.E-02 6.E-02 6.E-02 F02b 

Contaminated vegetation 

small mammal 1.E-02 1.E-02 3.E-02 F03 

large mammal 2.E-01 2.E-01 5.E-01 F10 

large bird 6.E-03 6.E-03 2.E-02 F12 

Contaminated water 

small mammal, spill 5.E-03 1.E-03 3.E-02 F05 

Contaminated insects 

small mammal 2.38E-01 2.38E-01 7.14E-01 F14a 

small bird 9.E-03 9.E-03 3.E-02 F14b 

Contaminated prey 

predatory mammal (small mammal) 2.16E-02 2.16E-02 2.16E-02 F16a 

predatory bird (small mammal) 7.54E-04 7.54E-04 7.54E-04 F16b 

predatory bird (fish) 7.E-05 1.E-05 6.E-04 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 8.E-04 4.E-04 3.E-03 F04a 

large mammal, on site 3.E-02 1.E-02 3.E-01 F11a 

large bird, on site 5.E-02 2.E-02 5.E-01 F13a 

Contaminated water 

small mammal 7.E-06 7.E-07 3.E-05 F07 

Contaminated fish 

predatory bird 5.E-06 3.E-07 3.E-05 F09 

126
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Picloram / Highest Application Rate 

Only upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 2.42E+01 2.42E+01 2.42E+01 F02a 

 bee, 100% absorption 1.60E+02 1.60E+02 1.60E+02 F02b 

Contaminated vegetation 

small mammal 1.25E+00 1.25E+00 2.68E+00 F03 

large mammal 1.72E+01 1.72E+01 4.86E+01 F10 

large bird 2.69E+01 2.69E+01 7.60E+01 F12 

Contaminated water 

small mammal, spill 4.43E-01 1.33E-01 2.53E+00 F05 

Contaminated insects 

small mammal 2.31E+01 2.31E+01 6.94E+01 F14a 

small bird 3.76E+01 3.76E+01 1.13E+02 F14b 

Contaminated prey 

predatory mammal (small mammal) 2.10E+00 2.10E+00 2.10E+00 F16a 

predatory bird (small mammal) 3.23E+00 3.23E+00 3.23E+00 F16b 

predatory bird (fish) 3.03E-01 4.54E-02 2.60E+00 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 1.60E-02 8.01E-03 6.87E-02 F04a 

large mammal, on site 6.61E-01 2.20E-01 6.22E+00 F11a 

large bird, on site 1.04E+00 3.45E-01 9.74E+00 F13a 

Contaminated water 

small mammal 1.46E-04 1.46E-05 5.86E-04 F07 

Contaminated fish 

predatory bird 1.00E-04 5.00E-06 6.00E-04 F09 

127
Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Sethoxydim / Typical Application Rate 

Only upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 7.27E+00 7.27E+00 7.27E+00 F02a 

bee, 100% absorption 4.81E+01 4.81E+01 4.81E+01 F02b 

Contaminated vegetation 

small mammal 3.75E-01 3.75E-01 8.04E-01 F03 

large mammal 5.16E+00 5.16E+00 1.46E+01 F10 

large bird 8.08E+00 8.08E+00 2.28E+01 F12 

Contaminated water 

small mammal, spill 3.99E-01 6.21E-02 9.97E-01 F05 

Contaminated insects 

small mammal 6.94E+00 6.94E+00 2.08E+01 F14a 

small bird 1.13E+01 1.13E+01 3.38E+01 F14b 

Contaminated prey 

predatory mammal (small mammal) 6.29E-01 6.29E-01 6.29E-01 F16a 

predatory bird (small mammal) 9.70E-01 9.70E-01 9.70E-01 F16b 

predatory bird (fish) 9.81E-01 7.63E-02 3.68E+00 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 1.80E-03 9.02E-04 7.73E-03 F04a 

large mammal, on site 7.44E-02 2.48E-02 7.01E-01 F11a 

large bird, on site 1.17E-01 3.88E-02 1.10E+00 F13a 

Contaminated water 

small mammal 3.51E-05 8.78E-07 5.27E-05 F07 

Contaminated fish 

predatory bird 5.04E-04 6.30E-06 1.13E-03 F09 

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DRAFT 

Sethoxydim/ Highest Application Rate 

Only upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 9.09E+00 9.09E+00 9.09E+00 F02a 

 bee, 100% absorption 6.01E+01 6.01E+01 6.01E+01 F02b 

Contaminated vegetation 

small mammal 4.69E-01 4.69E-01 1.00E+00 F03 

large mammal 6.45E+00 6.45E+00 1.82E+01 F10 

large bird 1.01E+01 1.01E+01 2.85E+01 F12 

Contaminated water 

small mammal, spill 3.99E-01 6.21E-02 9.97E-01 F05 

Contaminated insects 

small mammal 8.67E+00 8.67E+00 2.60E+01 F14a 

small bird 1.41E+01 1.41E+01 4.23E+01 F14b 

Contaminated prey 

predatory mammal (small mammal) 7.87E-01 7.87E-01 7.87E-01 F16a 

predatory bird (small mammal) 1.21E+00 1.21E+00 1.21E+00 F16b 

predatory bird (fish) 9.81E-01 7.63E-02 3.68E+00 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 2.25E-03 1.13E-03 9.66E-03 F04a 

large mammal, on site 9.30E-02 3.10E-02 8.76E-01 F11a 

large bird, on site 1.46E-01 4.86E-02 1.37E+00 F13a 

Contaminated water 

small mammal 4.39E-05 1.10E-06 6.59E-05 F07 

Contaminated fish 

predatory bird 6.30E-04 7.88E-06 1.42E-03 F09 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Sulfometuron methyl / Typical Application Rate 

Only upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 1.09E+00 1.09E+00 1.09E+00 F02a 

 bee, 100% absorption 7.21E+00 7.21E+00 7.21E+00 F02b 

Contaminated vegetation 

small mammal 5.63E-02 5.63E-02 1.21E-01 F03 

large mammal 7.74E-01 7.74E-01 2.19E+00 F10 

large bird 1.21E+00 1.21E+00 3.42E+00 F12 

Contaminated water 

small mammal, spill 4.43E-02 1.44E-02 1.22E-01 F05 

Contaminated insects 

small mammal 1.04E+00 1.04E+00 3.12E+00 F14a 

small bird 1.69E+00 1.69E+00 5.08E+00 F14b 

Contaminated prey 

predatory mammal (small mammal) 9.44E-02 9.44E-02 9.44E-02 F16a 

predatory bird (small mammal) 1.45E-01 1.45E-01 1.45E-01 F16b 

predatory bird (fish) 1.06E-01 1.72E-02 4.37E-01 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 9.00E-04 4.50E-04 3.86E-03 F04a 

large mammal, on site 3.71E-02 1.24E-02 3.50E-01 F11a 

large bird, on site 5.81E-02 1.94E-02 5.47E-01 F13a 

Contaminated water 

small mammal 2.64E-07 6.59E-08 4.61E-07 F07 

Contaminated fish 

predatory bird 1.08E-06 1.35E-07 2.84E-06 F09 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Sulfometuron methyl / Highest Application Rate 

Only upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 9.21E+00 9.21E+00 9.21E+00 F02a 

 bee, 100% absorption 6.09E+01 6.09E+01 6.09E+01 F02b 

Contaminated vegetation 

small mammal 4.75E-01 4.75E-01 1.02E+00 F03 

large mammal 6.54E+00 6.54E+00 1.85E+01 F10 

large bird 1.02E+01 1.02E+01 2.89E+01 F12 

Contaminated water 

small mammal, spill 3.74E-01 1.22E-01 1.03E+00 F05 

Contaminated insects 

small mammal 8.79E+00 8.79E+00 2.64E+01 F14a 

small bird 1.43E+01 1.43E+01 4.29E+01 F14b 

Contaminated prey 

predatory mammal (small mammal) 7.97E-01 7.97E-01 7.97E-01 F16a 

predatory bird (small mammal) 1.23E+00 1.23E+00 1.23E+00 F16b 

predatory bird (fish) 8.95E-01 1.45E-01 3.69E+00 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 7.60E-03 3.80E-03 3.26E-02 F04a 

large mammal, on site 3.14E-01 1.05E-01 2.95E+00 F11a 

large bird, on site 4.91E-01 1.64E-01 4.62E+00 F13a 

Contaminated water 

small mammal 2.23E-06 5.56E-07 3.89E-06 F07 

Contaminated fish 

predatory bird 9.12E-06 1.14E-06 2.39E-05 F09 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Triclopyr acid / Typical Application Rate 

Only upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 2.42E+01 2.42E+01 2.42E+01 F02a 

 bee, 100% absorption 1.60E+02 1.60E+02 1.60E+02 F02b 

Contaminated vegetation 

small mammal 3.30E-01 3.30E-01 4.95E-01 F03 

large mammal 1.72E+01 1.72E+01 4.86E+01 F10 

large bird 2.69E+01 2.69E+01 7.60E+01 F12 

Contaminated water 

small mammal, spill 5.32E-01 3.32E-01 2.66E+00 F05 

Contaminated insects 

small mammal 2.31E+01 2.31E+01 6.94E+01 F14a 

small bird 3.76E+01 3.76E+01 1.13E+02 F14b 

Contaminated prey 

predatory mammal (small mammal) 2.10E+00 2.10E+00 2.10E+00 F16a 

predatory bird (small mammal) 3.23E+00 3.23E+00 3.23E+00 F16b 

predatory bird (fish) 3.02E-01 9.42E-02 2.26E+00 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 1.62E-02 6.20E-03 6.52E-02 F04a 

large mammal, on site 2.52E+00 6.46E-01 3.20E+01 F11a 

large bird, on site 3.95E+00 1.01E+00 5.01E+01 F13a 

Contaminated water 

small mammal 4.39E-03 1.17E-03 7.32E-03 F07 

Contaminated fish 

predatory bird 2.49E-03 3.32E-04 6.23E-03 F09 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Triclopyr acid / Highest Application Rate 

Only upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 2.42E+02 2.42E+02 2.42E+02 F02a 

 bee, 100% absorption 1.60E+03 1.60E+03 1.60E+03 F02b 

Contaminated vegetation 

small mammal 3.30E+00 3.30E+00 4.95E+00 F03 

large mammal 1.72E+02 1.72E+02 4.86E+02 F10 

large bird 2.69E+02 2.69E+02 7.60E+02 F12 

Contaminated water 

small mammal, spill 5.32E+00 3.32E+00 2.66E+01 F05 

Contaminated insects 

small mammal 2.31E+02 2.31E+02 6.94E+02 F14a 

small bird 3.76E+02 3.76E+02 1.13E+03 F14b 

Contaminated prey 

predatory mammal (small mammal) 2.10E+01 2.10E+01 2.10E+01 F16a 

predatory bird (small mammal) 3.23E+01 3.23E+01 3.23E+01 F16b 

predatory bird (fish) 3.02E+00 9.42E-01 2.26E+01 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 1.62E-01 6.20E-02 6.52E-01 F04a 

large mammal, on site 2.52E+01 6.46E+00 3.20E+02 F11a 

large bird, on site 3.95E+01 1.01E+01 5.01E+02 F13a 

Contaminated water 

small mammal 4.39E-02 1.17E-02 7.32E-02 F07 

Contaminated fish 

predatory bird 2.49E-02 3.32E-03 6.23E-02 F09 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Triclopyr BEE / Typical Application Rate 

Only upper exposure estimates are used in this document.

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 2.42E+01 2.42E+01 2.42E+01 F02a 

 bee, 100% absorption 1.60E+02 1.60E+02 1.60E+02 F02b 

Contaminated vegetation 

small mammal 3.30E-01 3.30E-01 4.95E-01 F03 

large mammal 1.72E+01 1.72E+01 4.86E+01 F10 

large bird 2.69E+01 2.69E+01 7.60E+01 F12 

Contaminated water 

small mammal, spill 5.32E-01 3.32E-01 2.66E+00 F05 

Contaminated insects 

small mammal 2.31E+01 2.31E+01 6.94E+01 F14a 

small bird 3.76E+01 3.76E+01 1.13E+02 F14b 

Contaminated prey 

predatory mammal (small mammal) 2.10E+00 2.10E+00 2.10E+00 F16a 

predatory bird (small mammal) 3.23E+00 3.23E+00 3.23E+00 F16b 

predatory bird (fish) 3.02E-01 9.42E-02 2.26E+00 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 1.62E-02 6.20E-03 6.52E-02 F04a 

large mammal, on site 2.52E+00 6.46E-01 3.20E+01 F11a 

large bird, on site 3.95E+00 1.01E+00 5.01E+01 F13a 

Contaminated water 

small mammal 4.39E-03 1.17E-03 7.32E-03 F07 

Contaminated fish 

predatory bird 2.49E-03 3.32E-04 6.23E-03 F09 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

Triclopyr BEE / Highest Application Rate 

Only upper exposure estimates are used in this document.

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 2.42E+02 2.42E+02 2.42E+02 F02a 

 bee, 100% absorption 1.60E+03 1.60E+03 1.60E+03 F02b 

Contaminated vegetation 

small mammal 3.30E+00 3.30E+00 4.95E+00 F03 

large mammal 1.72E+02 1.72E+02 4.86E+02 F10 

large bird 2.69E+02 2.69E+02 7.60E+02 F12 

Contaminated water 

small mammal, spill 5.32E+00 3.32E+00 2.66E+01 F05 

Contaminated insects 

small mammal 2.31E+02 2.31E+02 6.94E+02 F14a 

small bird 3.76E+02 3.76E+02 1.13E+03 F14b 

Contaminated prey 

predatory mammal (small mammal) 2.10E+01 2.10E+01 2.10E+01 F16a 

predatory bird (small mammal) 3.23E+01 3.23E+01 3.23E+01 F16b 

predatory bird (fish) 3.02E+00 9.42E-01 2.26E+01 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 1.62E-01 6.20E-02 6.52E-01 F04a 

large mammal, on site 2.52E+01 6.46E+00 3.20E+02 F11a 

large bird, on site 3.95E+01 1.01E+01 5.01E+02 F13a 

Contaminated water 

small mammal 4.39E-02 1.17E-02 7.32E-02 F07 

Contaminated fish 

predatory bird 2.49E-02 3.32E-03 6.23E-02 F09 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

2,4-D / Typical Application Rate 

Only upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet 

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 2.42E+01 2.42E+01 2.42E+01 F02a 

 bee, 100% absorption 1.60E+02 1.60E+02 1.60E+02 F02b 

Contaminated vegetation 

small mammal 1.25E+00 1.25E+00 2.68E+00 F03 

large mammal 1.72E+01 1.72E+01 4.86E+01 F10 

large bird 2.69E+01 2.69E+01 7.60E+01 F12 

Contaminated water 

small mammal, spill 6.64E-01 6.64E-01 6.64E-01 F05 

Contaminated insects 

small mammal 2.31E+01 2.31E+01 6.94E+01 F14a 

small bird 3.76E+01 3.76E+01 1.13E+02 F14b 

Contaminated prey 

predatory mammal (small mammal) 2.10E+00 2.10E+00 2.10E+00 F16a 

predatory bird (small mammal) 3.23E+00 3.23E+00 3.23E+00 F16b 

predatory bird (fish) 4.53E+00 2.27E+00 6.80E+00 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 2.77E-02 1.39E-02 1.19E-01 F04a 

large mammal, on site 1.14E+00 3.81E-01 1.08E+01 F11a 

large bird, on site 1.79E+00 5.97E-01 1.69E+01 F13a 

Contaminated water 

small mammal 2.93E-04 1.46E-04 5.86E-04 F07 

Contaminated fish 

predatory bird 2.00E-03 5.00E-04 6.00E-03 F09 

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Preventing and Managing Invasive Plants Final Environmental Impact Statement April 2005 

DRAFT 

2,4-D / Highest Application Rate 

Only upper exposure estimates are used in this document. 

Worksheet G01 (modified): Summary of Exposure Scenarios for Terrestrial Animals

Scenario Dose (mg/kg/day) 

Typical Lower Upper Worksheet

 Acute/Accidental Exposures 

Direct spray 

 small animal, 100% absorption 4.85E+01 4.85E+01 4.85E+01 F02a 

 bee, 100% absorption 3.21E+02 3.21E+02 3.21E+02 F02b 

Contaminated vegetation 

small mammal 2.50E+00 2.50E+00 5.36E+00 F03 

large mammal 3.44E+01 3.44E+01 9.71E+01 F10 

large bird 5.38E+01 5.38E+01 1.52E+02 F12 

Contaminated water 

small mammal, spill 1.33E+00 1.33E+00 1.33E+00 F05 

Contaminated insects 

small mammal 4.63E+01 4.63E+01 1.39E+02 F14a 

small bird 7.52E+01 7.52E+01 2.26E+02 F14b 

Contaminated prey 

predatory mammal (small mammal) 4.20E+00 4.20E+00 4.20E+00 F16a 

predatory bird (small mammal) 6.46E+00 6.46E+00 6.46E+00 F16b 

predatory bird (fish) 9.07E+00 4.53E+00 1.36E+01 F08 

 Longer-term Exposures 

Contaminated vegetation 

small mammal, on site 5.55E-02 2.77E-02 2.38E-01 F04a 

large mammal, on site 2.29E+00 7.63E-01 2.15E+01 F11a 

large bird, on site 3.58E+00 1.19E+00 3.37E+01 F13a 

Contaminated water 

small mammal 5.86E-04 2.93E-04 1.17E-03 F07 

Contaminated fish 

predatory bird 4.00E-03 1.00E-03 1.20E-02 F09 

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DRAFT 

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