-1-

United States Department ofAgriculture

Healthy Forests MakeA World of Difference

Forest ServicePacific Northwest Region

July 25, 2000

PicloramHERBICIDE INFORMATION PROFILE

This information profile is produced by theUSDA Forest Service, Pacific NorthwestRegion, for employees, forest workers, andfor the public. The profile providesinformation on forest and land managementuses, environmental and human health effects,and safety precautions for the herbicidepicloram and its formulations. A list ofdefinitions is included in Section VIII of theinformation profile.

I. BASIC INFORMATION

COMMON NAME: Picloram

CHEMICAL NAME: 4-amino-3,5,6-trichloropicolinic acid

PRODUCT NAMES: Tordon* K and Tordon*22K.

REGISTERED USE STATUS: All formulationsthat may be broadcast on soil or foliage areclassified as “Restricted Use” pesticides.Sale and use of these picloram formulationsare limited to licensed pesticide applicatorsor employees under their supervision, andonly for uses covered by the applicator’s

certification. This is due to picloram’spotential to contaminate groundwater,and its ability to damage nontarget plants,including important food crops (C&P Press1998; U.S. EPA 1988a)

FORMULATIONS: Tordon* K and Tordon*22K are the formulations of picloramcurrently available and used by the ForestService. These formulations are producedby Dow AgroSciences as a liquidcontaining the potassium salt of picloram(24.4% w/v), which is equivalent to aconcentration of 2 lbs a.e./gallon. Theremaining 75.6% of the formulationconsists of inerts including polyglycol 26-2. The U.S. EPA (1998) classifies polyglycol26-2 among Inerts of unknown toxicity (List3) that may be used in the formulation ofpesticides.

The formulation testing reported in thisprofile applies only to the Tordon* K andTordon* 22K formulations, which containonly picloram as an active herbicideingredient. Other formulated products (forexample, Tordon* 101 Mixture andTordon* RTU) contain picloram and

-2-

another herbicide. This profile does notaddress the possible effects of exposure tothe formulated herbicide mixtures.

RESIDUE ASSAY METHODS: Capillary gaschromatography with electron capture(CGCEC) detector and high performanceliquid chromatography with an ultraviolet(HPLCU) detector are both listed by U.S.EPA (1997a) as accepted methods for theanalysis of picloram in water. CGCEC is themore sensitive method, with a detectionlimit of 0.14 ppb. HPLCU has a detectionlimit of 0.3 ppm. A 1982 study found thatwater samples containing picloram atconcentrations of 10 or 50 ppb werefrequently underestimated and sometimesnot detected by private laboratories usinggas chromatography with a reporteddetection limit of 1 ppb (Norris 1982,1986). The U.S. EPA (1997a), however,indicates that concentrations of 0.350 ppbshould be detected with 99% confidence thatthe picloram concentration is greater thanzero (i.e., only a 1% chance of a falsenegative reading).

In tests submitted to the U.S. EPA, DowElanco reports detection limits of picloramin soil at 5.0 ppb and in plants at 50 ppb(DowElanco Publication a. Undated). Astudy by Tan et al. (1996) indicates that therecovery of picloram from soil samplesdecreases as the organic matter in the soilincreases (Tan et al. 1996).

II. HERBICIDE USES

REGISTERED FORESTRY, RANGELAND,RIGHT-OF-WAY USES: Tordon* K is used toprevent regrowth of woody plants inrights-of-way, such as along roads andpower lines. In forestry, Tordon* K is used

to control unwanted woody plants and toprepare sites for planting trees. Onrangelands, Tordon* 22K is used to controlnoxious weeds andwoody plants. It isalso used to controlplants on non-cropindustrial/facilitysites. Do notapply picloram onsnow or frozenground. Basal treatments can be appliedthroughout the year. Tree injection shouldnot be done during periods of heavy sapflow. OPERATIONAL DETAILS:

TARGET PLANTS: Picloram is used tocontrol broadleaf plants, brush, conifersand broad-leaf trees.

MODE OF ACTION: Picloram is apyridine herbicide that acts as a plantgrowth regulator. That is to say thatpicloram mimics naturally occurringplant auxins or hormones in a mannerthat leads to uncontrolled and abnormalplant growth, which may result in grosssigns of toxicity or death. In general,picloram is more toxic to broadleafplants than to grasses or grains.

METHOD OF APPLICATION: Bothformulations can be applied by broadcastor spot treatment as foliar (leaf) or soilspray, as basal bark treatment, or by airas broadcast spray. Tordon may not beapplied directly to water.

USE RATES: Ground rates vary accordingto local conditions and the nature of thetarget vegetation. Application rates of

-3-

0.125-1.5 lbs picloram a.e./acre arerecommended on the product label (C&PPress 1998). Theupper range ofthis applicationrate is onlyrecommended forthe control ofwoody plants andbroadleaf weeds in southern states. Elsewhere, the maximum recommendedapplication rate is 1 lb a.e./acre. Thetypical rate used in Forest Serviceprograms is about 0.5 lbs a.e./acre.

SPECIAL PRECAUTIONS: Always read all ofthe information on the product label beforeusing any pesticide. Read the label forapplication restrictions.

TIMING OF APPLICATION: Consultproduct label for precise timing ofvarious soil and foliar treatments withpicloram formulations. Do not applypicloram on snow or frozen ground.Basal treatments can be appliedthroughout the year. Tree injection shouldnot be done during periods of heavy sapflow.

DRIFT CONTROL: Do not allow carelessapplication or spray drift. Do not permitspray or spray drift to contact crops orother desirable broadleaf plants.

IV. ENVIRONMENTAL FATE

SOIL:RESIDUAL SOIL ACTIVITY: Picloram canstay active in soil for a moderately longtime, depending on the type of soil, soil

moisture andtemperature.Picloram may existat levels toxic toplants for morethan 1 year afterapplication atnormal rates. Thehalf-life of picloram in soil is reported tovary from 1 month under favorableenvironmental conditions to more than 4years in arid regions (USDA 1989). Picloram is degraded more rapidly underanaerobic than aerobic conditions and alsodegrades more rapidly at lower applicationrates (Krzyszowska et al. 1994).

ADSORPTION: Picloram chemicallyattaches to clay particles and organicmatter. If the soil contains little clay ororganic matter, picloram is easily movedby water.

PERSISTENCE AND DEGRADATION: Breakdown caused by sunlight andmicroorganisms in the soil are the mainways in which picloram degrades in theenvironment. Picloram will dissipate morequickly in warm, wet weather. Alkalineconditions, fine textured clay soils, and alow density of plant roots can increase thepersistence of picloram.

METABOLITES/DEGRADATION PRODUCTS

AND POTENTIAL ENVIRONMENTALEFFECTS: Carbon dioxide is the majorend-product of the breakdown of picloramin the soil. Carbon dioxide is a gasnormally found in the air. The relativelysmall amount of carbon dioxide producedwhen picloram degrades in soil is not likelyto be harmful to the environment.

-4-

One study regarding the breakdown ofpicloram in soil identifies two compoundsproduced in minor amounts: 4-amino-3,5-dichloro-6-hydroxy-picolinic acid and4-amino-2,3,5-trichloro-pyridine. Thesemetabolites also were found in plantsexposed to picloram. According to thestudy, the compounds are not part of themajor metabolic pathway for picloram insoil and do not accumulate in soil(DowElanco Publication b Undated).

WATER

SOLUBILITY: Picloram dissolves readily inwater.

POTENTIAL FOR LEACHING INTOGROUNDWATER: U.S. EPA characterizesthe mobility of picloram in soil asintermediate to very mobile in soils rangingin texture from clay to loam. Piclorammovement is greatest for soils with loworganic matter content, alkaline soils, andsoils that are highly permeable, sandy, orlight-textured. Under certain environmentalconditions, picloram is known to leach fromsoil into groundwater as a result ofagricultural use.

Because picloram is relatively mobile insoil, the product labels for both Tordon* K(Dow AgroSciences 1999a) and Tordon*22K (Dow AgroSciences 1999b) recommendseveral specific precautions for decreasingthe potential of groundwater contamination. These precautions are followed in all ForestService programs.

A recent study conducted by the U.S.Geologic Survey (USGS 1998) foundpicloram in 0.11-0.20% of the groundwatersurveyed. The maximum level detected was

2.2 ppb. Picloram was detected in 3% ofgroundwater samples in the Red Riverbasin covering parts of Minnesota, NorthDakota, and South Dakota, at aconcentration of less than 10 ppb (Stoner etal. 1998).

SURFACE WATERS: Picloram cancontaminate surface water through spraydrift. Moreover, picloram may have a highpotential for runoff into surface water whenconditions favor poorly draining or wetsoils that slope toward surface waters,frequently flooded areas, areas over-layingextremely shallow groundwater, areas within-field canals or ditches that drain tosurface water, areas not separated fromadjacent surface waters with vegetated filterstrips, and areas over-laying tile drainagesystems that drain to surface water(DowAgro Sciences 1999a,b).

Picloram was not detected in 3384 samplesfrom 1058 streams in major aquifersmonitored by the U.S. Geologic Survey(USGS 1998). Monitoring data indicate thatpeak concentrations of picloram in surfacewater after various methods of applicationwere 7.4-37 mg/L per lb/acre for injection,2.2 mg/L per lb/acre for broadcast groundspray, and 48-78 mg/L per lb/acre forbroadcast aerial spray (Michael and Neary1993, Table 3, p. 407).

AIR:

VOLATILIZATION: Although picloram doesnot evaporate easily, its vapors were shownto be injurious to plants. In a closedcontainer, picloram vapors damaged plantseedlings (Gentner 1964).

-5-

POTENTIAL FOR BY-PRODUCTS FROM

BURNING OF TREATED VEGETATION: Morethan 95% of picloram residue is destroyedduring burning. Brown-and-burn operationsmay result in the formation of combustionproducts of picloram, and these productsmay pose a health risk. On combustion at225EC, picloramundergoesdecarboxylation andis converted to 2,3,5-trichloro-4-aminopyridine (4A-TCP) (Bush et al.1987). 4A-TCP,which is also foundin plant and soildecomposition, is generally more toxic thanpicloram to microorganisms. There is noinformation about the toxicity of 4A-TCP tomammals.

At 900EC, picloram decomposes to carbondioxide, carbon monoxide, chlorine gas,hydrogen chloride, and ammonia. Organo-chlorines are not identified as combustionproducts of picloram (Dost 1984).

By-products from burning plants treatedwith picloram were not identified in thefield.

IV. ECOLOGICAL EFFECTS

Please refer to Section X for definitions ofecotoxicological categories.

NONTARGET TOXICITY:

SOIL MICROORGANISMS: Higher soilconcentrations of picloram result in longerpersistence of the compound. Accordingly,

at high application rates, picloram mayinhibit microbial activity (Krzyszowska etal. 1994).

At a level of 10ppm in sandy loamsoil, picloramcaused a transientdecrease innitrification after 2but not 3 weeks ofincubation and noeffect on ammoniaformation or sulfur oxidation (Tu 1994). The decrease in nitrification was relativelymild and does not portend a substantial orprolonged impact on microbial activity.

PLANTS: Picloramis highly toxic tomany nontargetplants. Mostgrasses, however,are resistant to theherbicidal effectsof picloram. Because picloram is active in soil, it canpass from soil into growing plants.Moreover, it can move from treated plants,through the roots, to nearby plants.Furthermore, irrigation water polluted withpicloram may damage or kill crop plants.

In assessing the potential effects ofherbicides on nontarget terrestrial plantspecies, the U.S. EPA developed astandardized set of plant bioassays for seedgermination, seed emergence, and post-emergence applications. The lowestreported adverse effect level for thepotassium salt of picloram is about0.000012 lbs a.e./acre, the EC25 for seedemergence in soybeans (U.S. EPA 1995).

-6-

This effect level is a factor of about 40,000below the typical application rate of 0.5 lbsa.e./acre. The highest reported NOAEL inany of the terrestrial plant bioassays is about0.062 lbs a.e./acre, for post-emergentapplication in wheat and seed germination inbarley, a factor of about 8 below the typicalapplication rate for Forest Service programs[0.5 lbs a.e./acre ÷ 0.062 lbs a.e./acre]. Consequently, although picloram is moretoxic to broadleaf plants than grains orgrasses, picloram will kill or injure numerous plant species at the typicalapplication rate of 0.5 lbs a.e./acre. Picloram treats for the control of knapweedhave been associated with transientdecreases in seven native and one exoticforb species (Rice and Toney 1996).

Picloram is also toxic to aquatic plants, bothsmall single-cell plants, commonly referredto as algae, and larger multicellular plants,commonly referred to as macrophytes. Ingeneral, single-cells plants appear to be lesssensitive than larger plants. The RED forpicloram reports a NOAEL of 13.1 ppm and an EC25 of 52.6 ppm for growthinhibition in one species of unicellular algaeexposed to the potassium salt of picloram(U.S. EPA 1995). Picloram did not affectgrowth in two species of macrophytes atconcentrations of 0.01 and 0.1 ppm butinhibited flowering at 0.1 ppm (Forsyth etal. 1997). The metabolism of picloramappears to increase toxicity to two species ofsingle-cell plants (Baarschers et al. 1988). There are no data in the literature regardingthe toxicity of picloram metabolites tomulticellular plants.

AQUATIC ANIMALS: The toxicity of picloramto aquatic animals was tested in variousspecies of trout and Daphnia magna, a small

aquatic invertebrate. Acute LC50 values formost aquatic species range from about 5 to75 ppm, with trout being more sensitive thanother aquatic species (Dow AgroSciences1998a,b; Gersich et al. 1985; Mayes et al.1987; U.S. EPA 1995). Chronic studiesusing reproductive or developmental effectsfor trout (Mayes et al. 1987) and Daphnia(Gersich et al. 1985)report no-effectlevels of 0.55 ppm(trout) and 11.8 ppm(Daphnia) andadverse effect levelsof 0.88 ppm (trout)and 18.1 ppm(Daphnia). Anearlier study(Woodward 1976)reports a much lower AEL of 0.032 ppb forchronic toxicity in trout, based on survivaland growth in young trout. As reviewed bythe U.S. EPA (1995), this study was notused by the U.S. EPA (1995) in the riskassessment on picloram because the studyinvolved exposure to picloram acid ratherthan the potassium salt of picloram, which isused in both Tordon formulations.

TERRESTRIAL ANIMALS: The toxicity ofpicloram is relatively well characterized inexperimental mammals; however, fewwildlife species have been studied. Despitethis substantial reservation, picloramappears to be relatively nontoxic toterrestrial animals. Animals exposed topicloram excrete most of the compound,unchanged, in the urine.

Acute oral LD50 values for picloram rangefrom 3000 to 5000 mg/kg body weight, andthe highest NOAEL from a chronic study is20 mg/kg/day (SERA 1999). Some

-7-

additional studies are available on birds,bees, and snails that generally support thecharacterization of picloram as relativelynontoxic to terrestrial animals. One recentfield study by Nolte and Fulbright (1997)reported no detectable effects on mammalianor avian diversity after the application ofpicloram. The 48-hour contact toxicity ofpicloram to bees is 14.5 Fg/bee (U.S. EPA1995).

A New Zealand study found a possibleassociation between sheep grazing onpastures treated with picloram and anincreased incidence of intestinal cancer. The results, however, are inconclusivebecause of the small number of sheepexposed only to picloram (Newell et al.1984)

Tordon* 22K was tested for acute oraltoxicity to birds and is considered practicallynontoxic. Moreover, the formulation didnot cause reproductive or developmentaleffects in chickens, when sprayed onfertilized eggs (U.S. EPA 1995).

THREATENED AND ENDANGERED SPECIES:Picloram applied to pastures, rangeland, orforests may be hazardous to endangeredplants. Also, picloram may be hazardous tosome endangered invertebrates if it isapplied to areas where they live. It is not,however, expected to be hazardous to otherendangered animals or birds.

V. HEALTH EFFECTS TESTING

Most of the data on potential human healtheffects from exposure to picloram arederived from the results and analyses of

animal studiesinvolving exposureto picloram.

For picloram andformulationscontainingpicloram as theonly activeingredient, the data are from studiesconducted by the manufacturer. Thesestudies were submitted to the U.S. EPA tosupport product registration but are notavailable to the general public.

ACUTE TOXICITY:

ACUTE ORAL TOXICITY: The LD50 valuesfor picloram acid and the potassium salt ofpicloram are greater than 5000 mg/kg formale rats. Female rats seem somewhatmore sensitive, with LD50 values of 4012mg/kg for picloram acid and 3536 mg/kgfor the potassium salt of picloram. Basedon these data, picloram is classified aspractically nontoxic (Category IV) for malerats and slightly toxic (Category III) forfemale rats (U.S. EPA 1995).

ACUTE DERMALTOXICITY: Dermalexposure to 2000mg/kg picloram acidor the potassium saltof picloram did notcause systemic toxicityin rabbits, based onstandard acute/singleapplication bioassayswith 14-day observation periods (U.S. EPA1995). In general, dermal LD50 values arehigher than oral LD50 values (Gaines 1969). Since the acute oral LD50 values for

-8-

picloram are 5000 mg/kg or greater, thelack of apparent toxicity at dermal doses upto 2000 mg/kg/day is to be expected, andthe studies do not have much impact on theassessment of risk for picloram.

In addition to the acute dermal studies, a 21-day dermal toxicity analysis of thepotassium salt ofpicloram wasconducted in NewZealand white rabbitsat doses of 0, 65, 217,and 650 mga.e./kg/day, 5days/week, for 3weeks. No systemic toxicity was observed(U.S. EPA 1995).

SKIN AND EYE IRRITATION SCORE: Bothpicloram acid and the potassium salt ofpicloram (the forms used by the ForestService) are classified as moderate eyeirritants (Category III) but as non-irritants tothe skin (Category IV) (U.S. EPA 1995).

ACUTE INHALATION TOXICITY: Theinhalation toxicity LC50 values of >0.035mg/L for picloram acid (Category I) and>1.63 mg/L for the potassium salt ofpicloram (Category II) are classified as highto moderate (U.S. EPA 1995).

DERMAL SENSITIZATION: The potassium salt form of picloram is considered a skinsensitizer (U.S.EPA 1995).

CHRONIC TOXICITY:These data are based on tests inlaboratory animals.U.S. EPA requires

these tests only for the active ingredientpicloram. No tests of formulations forchronic toxicity are reported. Please referto Section X for an explanation of how theNOEL (No-observed-effects level) iscalculated.

The PNW Region FEIS evaluated thequality of the testing done on picloram upto 1988. Quality considerations forindividual studies include: the dose rangesand species tested, exposure duration, andidentification of the most sensitive effect. In addition, the degree of quantitativeagreement among all tests for an effect isconsidered. Please refer to Section X for anexplanation of qualitative ratings in thissection.

SYSTEMIC TOXICITY:

REPRODUCTION/DEVELOPMENTAL:Picloram was testedfor teratogenic andreproductive effectsin rats, mice, andrabbits (U.S. EPA1992b, 1999). Thelowest-observed-adverse-effects level(LOAEL) was 500 mg/kg/day and wasassociated with developmental changes inbones (Thompson et al. 1972). Nevertheless, the LOAEL is 25 timesgreater than the systemic NOAEL of 20mg/kg/day. NOAELs for reproductiveeffects are as great as 400 mg/kg/day,which is 20 times greater than the systemicNOAEL.

CARCINOGENICITY/MUTAGENICITY:Picloram was tested for mutagenicity inseveral test systems and was analyzed for

-9-

carcinogenic activity in rats and mice. Areview and detailed evaluation of themutagenicity studies on picloram, recentlycompleted by U.S. EPA (1992b) concludesthe following:

No compelling evidence of a mutageniceffect in relevant biological systems wasuncovered. Although picloram at a singlereported dose was mutagenic in S.coelicolor, the weight of evidence from well-conducted microbial (Ames test),mammalian cell, and Drosophilamutagenicity studies tends to support theconclusion that picloram does not exhibitmutagenic activity (U.S. EPA 1992b, pp.V19 to V20).

Similarly, the Health Effects DivisionCarcinogenicity Peer Review Committee ofthe U.S. EPA Office of Pesticides reviewedthe carcinogenicity data on picloram acidand the potassium salt of picloram andclassified these agents as Group E (noevidence of carcinogenicity), based on thelack of carcinogenic activity in rats and miceexposed to picloram (U.S. EPA 1999).

OTHER POSSIBLE HEALTH EFFECTS: Thereare no data regarding potential effects on thenervous system or immune system inhumans or animals after exposure topicloram.

VI. HUMAN HEALTH EFFECTS

FOREST SERVICE EVALUATION OF HUMAN

HEALTH RISKS: The PNW Region FEIS(1988) evaluated a range of picloram healtheffects data, including some laboratorystudies cited in Section V. SERA conductedan updated risk assessment for the Forest

Service (1999) using the most recent healtheffects information and risk assessmentprocedures. Both assessments evaluate thequantitative (numerical) estimates oftoxicity and the quality of the data used tomake numerical estimates. Using differentrisk assessment procedures from those inthe PNW Region FEIS (1988), SERA(1999) rated health risk to workers and thepublic for some picloram applications in a higher risk category. Section X of thisprofile displays and discusses the riskratings from both assessments. TheMitigation Measures from the PNW RegionFEIS for herbicide applications aresufficiently protective to continue tominimize potential risks to human healthfrom Forest Service applications ofpicloram.

There are no recent studies that wouldchange the hazards of picloram identifiedby the PNW Region FEIS.

The PNW Region FEIS predicts the levelsof exposure to project workers and thepublic from typical forestry operations andfrom a large accidental spill. The risks arecompared with U.S. EPA standards ofacceptable risk for human health effects. The PNW Region FEIS identifiedmitigation measures to reduce humanexposure in all approved herbicideapplications. Also, the FEIS specifiedadditional mitigation measures to restrict oreliminate use where a specific herbicideapplication method generated a “High”risk rating.

The level of exposure to picloram that isidentified by U.S. EPA as the threshold forpotential risk of human health effects isbased on effects from repeated exposure to

-10-

picloram over a long time (chronicexposure). This level is called theReference Dose (RfD). U.S. EPA (1999)determined that picloram has much lowertoxicity in tests conducted for a single, one-time (acute) exposure than the RfD levelindicates.

The complete set of risk ratings for thePNW Region FEIS and the SERA (1999)assessments are provided in Section X.The quality of the existing data affects thereliability of the risk ratings. The PNWRegion FEIS judges the overall quality ofavailable data on picloram toxicity to be“adequate:” the studies are of sufficientquality and quantity that estimates areconsidered reliable; new studies are unlikelyto change estimates of health effects.

POTENTIAL FOR HEALTH EFFECTS TO THEPUBLIC: Forest visitors and nearby residentscould be exposed to picloram drift, tovegetation with picloram residues, and toaccidental spraying of picloram. Furthermore, they could eat food or drinkwater contaminated with picloram residue.

The PNW Region FEIS and the SERA(1999) risk assessment indicate that undernormal conditions the general public will notbe exposed to levels of picloram that exceedthe RfD. Although there are amplemonitoring data to indicate that picloram canbe transported to groundwater and surfacewater, these monitoring studies do notsuggest that typical levels of exposure willapproach the RfD.

MITIGATING MEASURES TO REDUCE

IDENTIFIED RISKS TO THE PUBLIC:Under foreseeable conditions ofapplication in National Forests of the

PacificNorthwest, thereis no exposurescenario thatsuggests that thepublic could berepeatedlyexposed topicloram levelsthat exceed theRfD. For some accidental exposuresmodeled in the SERA risk assessment,maximum one-time exposures wouldexceed the RfD established forrepeated long-term exposures.

The Forest Service considers the potentialfor public exposure when designing contactprocedures, posting and signing needs inthe Herbicide Application Plan. Currentmitigating measures including mandatorysafety responses (that is, cleaning theexposed area or the avoidance of furtherexposure) will help to reduce the possibilityof any health consequences. In addition,every effort is made to prevent publiccontact with accidental spills (emergencyspill notification system, restrict publicaccess to the spill site).

PROBABILITY OF A WORKER RECEIVING ADOSE THAT AFFECTS GENERAL HEALTH OR

REPRODUCTION: Worker exposure anddose are estimated for typical forestryapplications. Studies are availablethat measure actual worker doses ofherbicide for some typical forestryapplications. The PNW Region FEISused central estimates of exposuresfrom these studies. The SERA (1999)risk assessment used a differentmethod that accounted variability inthe study data. The differences in

-11-

methods used result in differences inqualitative risk ratings between thetwo risk assessments in somesituations.

In the PNW Region FEIS, theprobability of worker exposure to atoxic concentration of picloram forgeneral health effects is ratedNegligible for all application methods. The upper-limit worker risk estimatesin the SERA risk assessment would beclassified as Low for aerial andbackpack foliar applications, andModerate for broadcast groundapplication. The higher ratings resultfrom a scenario in which a workerwears herbicide-contaminated glovesfor one hour. The maximum exposureto picloram from this one-timeexposure would exceed the RfDestablished for repeated long-termexposures.

MITIGATING MEASURES TO REDUCEIDENTIFIED RISKS TO WORKERS: The PNWRegion FEIS does not identify specialmitigations for picloram applications toreduce worker exposure. The mitigatingmeasures that apply to all herbicideapplications were sufficient to reduceworker exposure below the identifiedthresholds of unacceptable risk to theirhealth.

ACUTE TOXICITY (POISONING): Cases of eyeand skin irritation were reported in workersexposed to picloram formulations.

LONG-TERM HUMAN HEALTH EFFECTS:There are no reported cases of long-termhealth effects in humans after exposure topicloram or its formulations.

POTENTIAL FOR ADVERSE HEALTH

EFFECTS FROM INERT INGREDIENTS

CONTAINED IN THE FORMULATED

PRODUCT: The manufacturer identifiedsome inert chemicals in picloramformulations. Both of the Tordonformulations contain Polyglycol 26-2 [CASNo. 069029-39-6] (C&P Press 1998). Thiscompound is classified by the U.S. EPA(1998) as a List 3 inert. Other inerts in theformulations were not identified to thepublic.

The identity of all inert ingredients inpicloram formulations were disclosed to theU.S. EPA. The U.S. EPA classifies allinerts into one of four categories, called"Lists". List 1 contains chemicals ofknown toxic concern. List 2 containschemicals of suspected toxic concern whichare high priority for testing. List 4 containschemicals of known nontoxic character,generally recognized as safe to humans. Allother chemicals are classified on List 3:Inerts of unknown toxicity. U.S. EPA didnot find enough information available onthe toxic properties of List 3 chemicals toclassify them on Lists 1, 2, or 4. All inertingredients used in Tordon formulations areclassified by the U.S. EPA on List 3 orList 4.

HEALTH EFFECTS ASSOCIATED WITHCONTAMINANTS: Almost no chemicalmanufacturing process yields a totally pureproduct. The available toxicity studies onpicloram were conducted with the technicalgrade product. Consequently, if toxicimpurities are present in the technical gradeproduct, they are likely to be accounted forby the toxicity studies on the technicalgrade product.

-12-

On the other hand, any amount of acarcinogen in an otherwise noncarcinogenicmixture may pose a carcinogenic risk. Thisis the situation with picloram. Technicalgrade picloram contains hexachlorobenzene. Nominal or averageconcentrations of hexachlorobenzene are 8ppm, and the maximum concentration is 50ppm (U.S. EPA 1997b). The U.S. EPAclassifies hexachlorobenzene as a probablehuman carcinogen for which the data areadequate to consider risk quantitatively.

Accidental exposure scenarios for workersand members of the general public result inshort-term exposures to hexachlorobenzenethat are above the background dose of0.000001 mg/kg/day. The highest doseestimate is about 0.02 mg/kg, the upperrange of exposure for a worker wearingcontaminated gloves for 1 hour. Formembers of the general public, the highestdose estimate is about 0.006 mg/kg and isassociated with the short-term consumptionof contaminated fish. The highest chronicexposure scenario for members of thegeneral public is 0.00000035 mg/kg/day,associated with the consumption ofcontaminated fish by subsistencepopulations.

Based on the standard assumptions used inForest Service risk assessments, thecontamination of picloram withhexachlorobenzene does not appear topresent a substantial cancer risk. Administratively, the Forest Service hasadopted a substantial cancer risk level of onein one-million (1÷1,000,000) as a triggerthat would require special steps to mitigateexposure or restrict and possibly eliminateuse. All cancer risks associated withhexachlorobenzene in picloram are below

one in one-million.

HEALTH EFFECTS ASSOCIATED WITH

OTHER FORMULATIONS: Someformulations contain picloram mixed withthe herbicides 2,4-D or triclopyr.Information Profiles for 2,4-D or Triclopyrdescribe the properties and potential effectsof exposure to these herbicide ingredients.

None of the profiles on individualherbicides fully describe the potential forhealth or environmental effects fromexposure to formulations containingmultiple herbicides. There may be greaterconcern for mixtures of picloram and 2,4-D. Tordon 202c, a commercialformulation of picloram and 2,4-D, isassociated with adverse reproductive effectsin mice (Blakley et al. 1989a,b,c).

Additional information about the propertiesof these formulations and their potentialeffects on human health and theenvironment will be prepared before theformulations are used in the PNW Region.

SOCIETAL PERCEPTIONS: Public opinionabout herbicide use, in general, rangesfrom a perception that herbicides arecompletely safe, to a perception that theyare very hazardous. A full range of opinionis available in the PNW Region FEIS. Thisprofile provides workers and the generalpublic with information that may be usefulin assessing the hazards associated with theuse of picloram in PNW Region NationalForests.

-13-

VII. SAFETY PRECAUTIONS

SIGNAL WORDS AND DEFINITIONS:All of the following are taken from productlabels and material safety data sheets (DowAgroSciences 1998a,b, 1999a,b).

PRECAUTIONARY STATEMENTS (Tordon* Kand Tordon* 22K): Causes moderate eyeirritation. Avoid contact with eyes orclothing. Prolonged or frequent repeatedskin contact may cause allergic skinreactions in someindividuals.

PERSONALPROTECTIVEEQUIPMENT (PPE)(Tordon* K andTordon* 22K):Applicators andother handlers must wear: long-sleeved shirtand long pants, waterproof gloves, shoesand socks.

USER SAFETY RECOMMENDATIONS(Tordon* K and Tordon* 22K). Usersshould: wash hands before eating, drinkingchewing gum, using tobacco or using thetoilet; remove clothing immediately ifpesticide gets inside, then wash thoroughlyand put on clean clothing; remove PPEimmediately after handling this product;wash the outside of gloves before removing;and as soon as possible, wash thoroughlyand change into clean clothing.

FIRST AID (Tordon* K and Tordon* 22K):

EYES: Irrigate with flowing waterimmediately and continuously for 15minutes. Consult medical personnel.

SKIN: Wash off in flowing water orshower.

INGESTION: If swallowed, seek medicalattention. Do not induce vomiting unlessdirected to do so by medical personnel.

INHALATION: Remove to fresh air if effectsoccur. Consult a physician.

NOTE TO PHYSICIAN: If burn is present,treat as any thermal burn, afterdecontamination. No specific antidote. Supportive care. Treatment based onjudgment of the physician in response toreactions of the patient.

HANDLING STORAGE AND DISPOSAL(Tordon* K andTordon* 22K): Keepout of reach ofchildren. Do notcontaminate food,feed, or water bystorage or disposal. Pesticide wastes are toxic. Wastesresulting from the use of this product maybe disposed of on site or at an approvedwaste disposal facility. See product labelfor additional clean-up instructions.

EMERGENCY (SPILL) HAZARDS ANDPROCEDURES (Tordon* K and Tordon*22K): Absorb in inert material such as drysand. In case of large spills, dike area tocontain product. Call Dow AgroSciences at800-992-5994.

VIII. DEFINITIONS

Absorption -- The process by which achemical passes through the body membranes

-14-

and enters the bloodstream. The main routesby which toxic agents are absorbed are thegastrointestinal tract, lungs, and skin.

Acute toxicity – The amount of a substance as asingle dose to cause poisoning in a test animal.

Acute exposure -- A single exposure ormultiple exposure occurring within a short time(24 hours or less).

Adverse-effect level (AEL) -- Signs of toxicitythat must be detected by invasive methods,external monitoring devices, or prolongedsystematic observations.

a.e. – Acid equivalents.

Arid – A terrestrial region lacking moisture, ora climate in which the rainfall is not sufficient tosupport the growth of trees or woody plants.

Assay -- A kind of test (noun); to test (verb).

Basal treatment – Application method bywhich herbicide is applied to the stem of a plantjust above the soil.

Bioconcentration factor -- The concentration ofa compound in an aquatic organism divided bythe concentration in the ambient water of theorganism.

Broadleaf weed -- A nonwoody dicotyledonousplant with wide bladed leaves designated as apest species in gardens, farms, or forests.

Carcinogen -- A chemical capable of inducingcancer.

Chronic exposure -- Long-term exposurestudies often used to determine the carcinogenicpotential of chemicals. These studies areusually performed in rats, mice, or dogs andextend over the average lifetime of the species(for a rat, exposure is 2 years).

Contaminants -- Impurities present in acommercial grade chemical.

Degraded -- Broken down or destroyed.

Dermal -- Pertaining to the skin.

Drift -- That portion of a sprayed chemicalthat is moved by wind off a target site.

EC25 – The concentration of a chemical that isestimated to cause a toxic effect in 25% of thetreated subjects.

Formulation -- A commercial preparation of achemical including any inerts or contaminants.

Half-life – For compounds that are eliminatedby first-order kinetics, the time required for theconcentration of the chemical to decrease byone half.

Herbicide -- A chemical used to control,suppress, or kill plants, or to severely interrupttheir normal growth processes.

Inerts -- Adjuvants or additives in commercialformulations of glyphosate that are not readilyactive with the other components of themixture.

Invertebrate -- An animal that does not have aspine (backbone).

LC50 – The concentration of a chemicalcalculated to kill 50% of test animals.

LD50 – The dose of a chemical calculated tokill 50% of test animals.

Leach – To dissolve out by the action of water

Lowest-observed-adverse-effect level(LOAEL) -- The lowest dose of a chemical ina study, or group of studies, that producesstatistically or biologically significant increasesin frequency or severity of adverse effects

-15-

between the exposed population and itsappropriate control.

Margin of safety (MOS) -- The ratio betweenan effect or no effect level in an animal and theestimated human dose.

Metabolite -- A compound formed as a result ofthe metabolism or biochemical change ofanother compound.

mg/kg -- A common way of expressing dose:milligram of a toxic agent per kilogram of bodyweight.

Microorganisms -- A generic term for allorganisms consisting only of a single cell, suchas bacteria, viruses, and fungi.

Mutagenicity -- The ability to cause geneticdamage (that is damage to DNA or RNA). Mutations can lead to birth defects,miscarriages, or cancer.

Nontarget -- Any plant or animal that atreatment inadvertently or unavoidably harms.

No-observed-adverse-effect level (NOAEL) --The dose of a chemical at which no statisticallyor biologically significant increases in frequencyor severity of adverse effects were observedbetween the exposed population and itsappropriate control. Effects may be produced atthis dose, but they are not considered to beadverse.

No-observed-effect level (NOEL) -- The doseof a chemical at which no treatment-relatedeffects were observed.

Persistence – The tendency of an appliedpesticide to remain in the environment.

ppb -- An abbreviation for parts per billion. Equivalent to µg/L for concentrations in waterand to µg/kg for concentrations in soil or othernon-aqueous media.

ppm -- An abbreviation for parts per million. Equivalent to mg/L for concentrations in waterand to mg/kg for concentrations in soil or othernon-aqueous media.

Reproductive effects -- Adverse effects on thereproductive system that may result fromexposure to a chemical or biological agent.

RfD -- A daily dose that is not expected tocause adverse human health effects over alifetime of exposure. These values are derivedby the U.S. EPA.

Systemic toxicity -- Effects that requireabsorption and distribution of a toxic agent to asite distant from its entry point at which pointeffects are produced. Systemic effects are theobverse of local effects.

Teratogen – A compound that causes birthdefects.

Toxicity -- The inherent ability of an agent toaffect living organisms adversely.

Uncertainty Factor (UF) -- A factor used inoperationally deriving the RfD and similarvalues from experimental data. UFs areintended to account for (1) the variation insensitivity among members of the humanpopulation; (2) the uncertainty in extrapolatinganimal data to the case of humans; (3) theuncertainty in extrapolating from data obtainedin a study that is less than lifetime exposure;and (4) the uncertainty in using LOAEL datarather than NOAEL data. Usually each ofthese factors is set equal to 10.

-16-

IX. Information Sources

For generalinformation onherbicide use by theForest Service, referto the PNW RegionTreatment MethodsProfile forHerbicides.

The principal sources of information andfindings in this profile are the PNW RegionFEIS (USDA/FS 1988) and a more recentrisk assessment on picloram prepared for theForest Service (SERA 1999).

The PNW Region asked the parties to theMediated Agreement for ManagingCompeting and Unwanted Vegetation RODto submit any significant new informationon picloram to be evaluated for this Profilerevision. NCAP (Northwest Coalition forAlternatives to Pesticides) providedreferences to one article (Cox, 1998) andtwo web sites (Stoner, 1998) and (USGS, 1998).The three references were evaluated in boththe SERA risk assessment (SERA1999) andin relevant topic sections of this Profile.

Baarschers WH; Donnelly JG; Heitland HS. 1988. Microbial toxicity of triclopyr andrelated herbicides. Tox. Assess. 3 (2):127-136.

Blakley PM; Kim JS; Firneisz GD. 1989a. Effects of paternal subacute exposure toTordon 202c on fetal growth anddevelopment in CD-1 mice. Teratology. 39(3): 237-241.

Blakley PM; Kim JS; Firneisz GD. 1989b. Effects of preconceptional and gestationalexposure to Tordon 202c on fetal growthand development in CD-1 mice. Teratology. 39(6): 547-553.

Blakley PM; Kim JS; Firneisz GD. 1989c. Effects of gestational exposure to Tordon202c on fetal growth and development inCD-1 mice. J Toxicol Environ Health. 28(3): 309-316.

Bush PB; Neary DG; McMahon CK,Taylor, Jr. JW. 1987. Suitability ofhardwoods trated with phenoxy andpyridine herbicides for use as firewood. Arch. Environ. Contam. Toxicol. 16:333-341.

C&P Press (Chemical and PharmaceuticalPress). 1998. EPR II for Windows. Electronic Pesticide Reference.

Cox C. 1998. Picloram. Journal ofPesticide Reform. 18 (1):13-20.

Dost FN. 1984. Combustion ofherbicides. Unpublished report forBonneville Power Administration, U.S.Department of Energy.

DowAgroSciences. 1998a. Material DataSafety Sheet: Tordon* K. Product Code87096, MSDS: 000380. DowAgroSciences LLC, Indianapolis, IN.

DowAgroSciences. 1998b. Material DataSafety Sheet: Tordon* 22K. Product Code87116, MSDS: 000380. Dow Agro-Sciences LLC, Indianapolis, IN.

Dow AgroSciences 1999a. SpecimenLabel: Tordon* K. Revised 02-12-99

-17-

Dow AgroSciences 1999b Specimen Label:Tordon* 22K. Revised 02-12-99 DOWELANCO PUBLICATIONS:

a. Picloram Technical Information Guide. Undated.

b. Mullison WR. Undated. AToxicological and EnvironmentalReview of Picloram.

Durkin PR; Rubin L; Withey J; Meylan W. 1995. Methods of assessing dermalabsorption with emphasis on uptake fromcontaminated vegetation. Toxicol. Indust.Health. 11(1): 63-79.

Forsyth DJ; Martin PA; Shaw GG. 1997. Effects of herbicides on two submersedaquatic macrophytes, Potamogeton pectinatusL. and Myriophyllum sibiricum Komarov, in aprairie wetland. Environ. Pollut. 95(2):259-268.

Gaines TB. 1969. Acute toxicity ofpesticides. Tox. Appl. Pharamacol. 14: 515-534.

Gentner WA. 1964. Herbicidal Activity ofVapors of 4-amino-3,5,6-trichloro-picolinicAcid. Weeds. 12: 239-240

Gersich FM; Hopkins DL; Milazzo DP. 1985. Acute and chronic toxicity of technicalpicloram (4-amino-3,5,6- trichloropicolinicacid) to Daphnia magna Straus. Bull EnvironContam Toxicol. 35 (1):121-6.

Grier N. 1999. Letter to Leslie Rubin,USDA from Norma Grier, NorthwestCoalition for Alternatives to Pesticides,dated December 17, 1999.

Krzyszowska AJ; Allen RD; Vance GF. 1994. Assessment of the fate of twoherbicides in a Wyoming rangeland soil:column studies. J. Environ. Qual. 23(5):1051-1058.

Mayes MA; Hopkins DL; Dill DC. 1987. Toxicity of picloram (4-amino-3,5,6-trichloropicolinic acid) to life stages of therainbow trout. Bull. Environ. Contam.Toxicol. 38(4): 653-660.

Landry T; Johnson K; Cieszlak F; et al. 1986. Picloram: A Two-year DietaryChronic Toxicity-oncogenicity Study inFischer 344 Rats. Unpublished studyprepared by Dow Chemical U.S.A. 243 p. MRID 00132705. (Cited in U.S. EPA1992a, 1999).

Mayes MA; Hopkins DL; Dill DC. 1987. Toxicity of picloram (4-amino-3,5,6-trichloropicolinic acid) to life stages of therainbow trout. Bulletin of EnvironmentalContamination and Toxicology. 38 (4):653-660.

Michael JL; Neary DG. 1993. Herbicidedissipation studies in southern forestecosystems. Environ. Toxicol. Chem. 12(3): 405-410.

Newell KW; Ross AD; Renner RM. 1984. Phenoxy and Picolinic Acid Herbicides andSmall Intestinal Adenocarcinoma in Sheep. Lancet. December 8, 1984: 1301-1305.

Nolte KR; Fulbright TE. 1997. Plant, smallmammal, and avian diversity followingcontrol of honey mesquite. J. Range Manag. 50(2): 205-212.

-18-

Norris LA. 1982. Accuracy and Precision ofAnalyses for 2,4-D and Picloram in Water byContract Laboratories. Unpublished reportfor Pacific Northwest Forest and RangeExperiment Station, Forest Service, U.S.Department of Agriculture.

Norris LA. 1986. Accuracy and Precision ofAnalyses for 2,4-D and Picloram in Water byContract Laboratories. Weed science. 34(3):485-489.

Rice PM; Toney JC. 1996. Plant populationresponses to broadcast herbicide applicationsfor spotted knapweed control. Down toEarth. 51(2):14-19.

SERA (Syracuse Environmental ResearchAssociates, Inc.). 1999. Picloram (Tordon Kand Tordon 22K): Final Report. Prepared bySERA, Inc., Fayetteville, NY underUSDA/FS Contract No. 53-3187-5-12.

Stoner JD; Lorenz DL; Goldstein RM;Brigham ME; Cowdery TK. 1998. WaterQuality in the Red River of the North Basin,Minnesota, North Dakota, and South Dakota,1992-95. U.S. Geological Survey Circular1169. Update 4/12/98.http://water.usgs.gov/pubs/circ1169

Tan LK; Humphries D; Yeung PYP; FlorenceLZ. 1996. Determinations of clopyralid,picloram, and silvex at low concentration insoils by calcium hydroxide-water extraction and gas chromatographymeasurement. J. Agricult. Food Chem. 44(4): 1135-1143.

Thompson OJ; Emerson JL; Strebing RJ;Gerbig CG; Robinson VB. 1972. Teratologyand postnatal studies on 4-amino-3,5,6-trichloropicolinic acid (picloram) in the rat. Food Cosmet. Toxicol. 10: 797-803.

Tu CM. 1994. Effects of herbicides andfumigants on microbial activities in soil. Bulletin of Environmental Contaminationand Toxicology. 53 (1):12-17.

USDA Forest Service (United StatesDepartment of Agriculture Forest Service). 1988. Managing Competing and UnwantedVegetation, Final Environmental ImpactStatement. Pacific Northwest Region.

USDA Forest Service (United StatesDepartment of Agriculture Forest Service). 1989. Pesticide Background Statements. Volume I. Herbicides. AgricultureHandbook No. 663.

U.S. EPA (United States EnvironmentalProtection Agency). 1988a. Guidance forthe Reregistration of Pesticide ProductsContaining Picloram as the ActiveIngredients. U.S. EPA, OPTS,Washington, DC. EPA Publication No.540/RS-88-132.

U.S. EPA (United States EnvironmentalProtection Agency). 1988b. PicloramHealth Advisory. U.S. EPA, ODW,Washington, DC.

U.S. EPA (United States EnvironmentalProtection Agency). 1992a. Integrated RiskInformation System, Picloram. Rev. 5/1/92.www.epa.gov/ngispgm3/iris/subst/0256.htm

U.S. EPA (United States EnvironmentalProtection Agency). 1992b. Drinking watercriteria document for picloram. UnitedStates Environmental Protection Agency. Health and Ecological Criteria Division.

U.S. EPA (United States EnvironmentalProtection Agency). 1995. Reregistration

-19-

Eligibility Decision (RED): Picloram. Prevention, Pesticides, and ToxicSubstances, EPA 738-R95-019. August1995.

U.S. EPA (U.S. Environmental ProtectionAgency). 1997a. EMMI: EnvironmentalMonitoring Methods Index. EPA Databaseof Analytical Methods for RegulatedSubstances. CD-ROM Version developedby Enviro Dynamics, Inc. GovernmentInstitutes, Rockville MS 20850.

U.S. EPA (United States EnvironmentalProtection Agency). 1997b.Hexachlorobenzene: IRIS Entry. Lastupdate 3/1/97. http://www.epa.gov/iris/subst/ 0347.htm.

U.S. EPA (U.S. Environmental ProtectionAgency). 1998. Lists of Inert PesticideIngredients. Http://www.epa.gov/opprd001/ inerts/lists.html. UpdatedAugurs 7, 1998.

U.S. EPA (United States EnvironmentalProtection Agency). 1999. Picloram;Time-Limited Pesticide Tolerances. FederalRegister. 64(2):418-425.

USGS (U.S. Geological Survey). 1998. Dataon Pesticides in Surface and Ground Water ofthe United States., Results of the NationalWater Quality Assessment Program(NAWQA). Revised Oct. 23, 1998. Http://wwwdwatcm.wr.usgs.gov/cppt/pns_data/data.html.

Woodward DF. 1976. Toxicity of theherbicides dinoseb and picloram to cutthroatand lake trout. J. Fish. Res. Board Canada. 33: 1671-1676.

X. Toxicity and Risk Categories

ESTIMATES OF HEALTH RISK TO THE

PUBLIC AND TO WORKERS FROM FOREST

SERVICE OPERATIONS: The FEIS predictslevels of human exposure (dose) for projectworkers and for the public, for both atypical field project and for a large acci-dental spill. These dose levels arecompared with the highest dose level inanimal tests that showed no effect (NOEL). This level of exposure is referred to as theMargin of Safety or Margin of Exposureapproach. The SERA (1999) riskassessment used a conceptually similarapproach in which the estimated level ofexposure is divided by some estimate ofacceptable exposure. Both the FEIS andthe SERA (1999) assessment also expressrisk qualitatively. In the FEIS, the risk isranked from "Negligible" to "High" basedon the margin between the expected humandose and the highest NOEL "no effect"dose. A "High" risk rating means that thehighest NOEL dose is not more than 10times larger than predicted human doseunder the specified conditions. A"Moderate" risk rating means that thehighest NOEL dose is between 10 and 100times larger than the expected human dose.

As illustrated in the following tables, thequalitative expression of risk for both workers and the general public isreasonably consistent between the FEIS andthe updated SERA (1999) risk assessments. The PNW Region determined that no newinformation summarized in this profile orin SERA (1999) would change the public orworker mitigations in the 1988 FEIS,which were based on potential humanhealth risks.

-20-

Estimated Health Risks To ProjectWorkersa.

ScenarioRisk Category

Typical Lower Upper

Directedgroundb

Negligible Negligible Negligible/Low

Broadcastgroundsprayc

Negligible Negligible Negligible/Moderate

Aerial Negligible Negligible Negligible/Low

a From PNW FEIS and SERA 1999. Where riskclassification differ in the two assessments, theclassification from SERA is presented in italics.b Backpack, cut surface, and streamlinec Boomspray

Estimated Health Risks To The Publica.

ScenarioRisk Category

Typical Lower Upper

AccidentalSprayb

Negligible Negligible Negligible/Moderate

Dermal,vegetation c

Negligible/Low

Negligible Negligible/Moderate

Contamin-ated fruit d

Negligible Negligible Low

Contamin-ated waterd

Negligible Negligible Low/Negligible

Contamin-ated fish d

Negligible Negligible Negligible

a From PNW FEIS and SERA 1999. Where riskclassification differ in the two assessments, theclassification from SERA is presented in italics.b PNW is based on spray drift. SERA 1999assessment is based on direct spray.d PNW based on deposition data. SERA 1999 basedon Durkin et al.(1995).d PNW is based on short-term exposures. SERA1999 assessment is based on longer-term exposures.

ECOTOXICOLOGICAL CATEGORIES

Mammalian (Acute Oral):

mg/kg Risk Category

<10 very highly toxic

10-50 highly toxic

51-500 moderately toxic

501-2000 slightly toxic

>2000 practically non toxic

Avian (Acute Oral):

mg/kg Risk Category

<10 very highly toxic

10-50 highly toxic

51-500 moderately toxic

501-2000 slightly toxic

>2000 practically non toxic

Avian (Dietary):

mg/kg Risk Category

<50 very highly toxic

50-500 highly toxic

501-1000 moderately toxic

1001-5000 slightly toxic

>5000 practically non toxic

Aquatic:

ppm Risk Category

<0.1 very highly toxic

0.1-1 highly toxic

>1-10 moderately toxic

>10-100 slightly toxic

>100 practically non toxic

-21-

TABLES OF CATEGORIES OF TOXICITY

Human Hazards

Route of Administration

Risk Category Signal Word Oral (mg/kg) Dermal(mg/kg)

Inhalation(mg/kg)

I DANGER -- Poison 0-50 0-200 0-0.2

II WARNING >50-500 >200-2000 >0.2-2.0

III CAUTION >500-5000 >2000-20,000

>2.0-20

IV NONE >5000 >20,000 >20

Hazard

Category Eye Irritation Skin Irritation

I corrosive: corneal opacity not reversible within7 days corrosive

II corneal opacity reversible within 7 days;irritation persisting for 7 days severe irritation at 72 hours

III no corneal opacity;irritation reversible within 7 days moderate irritation at 72 hours

IV no irritation mild or slight irritation at 72 hours

Category of Quality of Health Effects Data

Inadequate: Inadequate information available for evaluating toxicity. There were too fewstudies of sufficient quality to yield useful or reliable information.

Marginal-Inadequate:

Some useful information exists for evaluating toxicity. There were studies ofmarginal quality that provided useful information, but studies were inconsistentand some contained flaws. It is likely that new studies would change estimates ofhealth effects.

Marginal: Marginal but useful information available for evaluating toxicity. There werestudies of adequate quality, and results did not vary greatly, but more informationwould increase reliability. Although new studies may change estimates of healtheffects, the results are considered moderately reliable.

Adequate: Adequate information is available. Studies are of sufficient quality and quantitythat estimates of human health are considered reliable. New studies are unlikelyto change estimates of health effects.