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dinoseb (Premerge, Dinitro) Herbicide Profile 4/87

                                      dinoseb
      CHEMICAL NAME:      2-sec-butyl-4,6-dinitrophenol (56)
      TRADE NAME(S):      Premerge, Vertac Dinitro Weed Killer, Dynamyte 3,
                          Dow General Weed Killer, Dow Selective Weed Killer
                          (58).
      FORMULATION(S):     Premerge 3 Dinitro Amine Herbicide, Vertac Dinitro
                          Weed Killer, Dynamyte 3 (all formulated as the
                          alkanolamine salt of dinoseb and contain the
                          equivalent of 0.36 kg (3 lb) of dinoseb per l
                          (gal); Dow General Weed Killer, 0.6 kg/l (5 lb
                          dinoseb/gal) as the free phenol; Dow Selective Weed
                          Killer, 0.12 kg (1 lb) ammonium salt of dinoseb/l
                          (gal); various formulations alone or in
                          combinations with other weed killers such as
                          naptalam are available from formulators (58).
      TYPE:               Nitrophenolic herbicide
      BASIC PRODUCER(S):  Tifa Ltd.                    Vertac Chemical Corp.
                          Tifa Squiare                 5100 Poplar
                          50 Division Ave.             Memphis, TN 38137
                          Millington, NJ 07946
      STATUS:             Restricted use.  On October 7, 1986, the EPA
                          issued an emergency suspension and cancellation
                          that prohibits the sale, distribution, and use of
                          all dinoseb products.  This action was taken
                          and based primarily on evidence that dinoseb
                          exposure poses a risk of birth defects, male
                          sterility, and acute toxicity to agricultural
                          workers.  This order became effective immediately
                          on the above date.
     ***********************************************************************
                             *** NOTICE ***
                                             April 22, 1987
                              DINOSEB
What is the Status Nationally?
     The EPA ordered an emergency suspension of all registered
products containing dinoseb or any of its salts on October 14, 1986.
This action prohibited all sale, distribution, and use of dinoseb
products.  Also at the same time, EPA issued an intent to cancel the
registrations of all pesticide products containing dinoseb and to deny
all pending applications for any product containing dinoseb.
     The decision to suspend dinoseb was related to new data
submitted to EPA.  The new data, the EPA administrator said, showed
that:
          1.  Dinoseb is a developmental toxicant in laboratory
               animals.
          2.  Dinoseb affects the reproductive system of male
               laboratory animals.
          3.  Acute toxicity of dinoseb is achieved through exposure
               to relatively low doses by both the oral and dermal
               routes when compared with other pesticides.
          4.  The use of dinoseb also poses hazards to wildlife.
     Recently, the EPA has allowed three states (Washington, Idaho
and Oregon) to use dinoseb as a result of hearings.  These hearings
were primarily requested by processors (the Agriculture Department
requested hearings for Oregon) and demonstrated new benefit data,
or that the EPA underestimated the economic situation as a result of
the suspension of dinoseb.
What is the Status in New York?
     All pesticide formulations containing dinoseb are suspended.
No one can sell, distribute, transport, or use pesticide formulations
containing dinoseb.  The Department of Environmental Conservation
(DEC) has quarantined most suppliers and applicators possessing
dinoseb products.
     Dr. Robin Bellinder and the Chemicals-Pesticides Program
submitted an emergency exemption, Section 18 request, on March
20, 1987 to the DEC for the use of dinoseb to control broadleaf weeds
in peas and beans (snap, dry, and lima).  The request is still at DEC
and and has not been formally sent to EPA.
What About Reimbursement and Disposal?
     Procedures for requesting indemnification (compensation) and
disposal for pesticide products containing dinoseb products were
published in the April 15, 1987 Federal Register (enclosed).
     The right of indemnification extends to "any person" who has
suffered economic loss as well as those who owned products at the
time of suspension.  Indemnification claims for dinoseb products
must be filed with the EPA no later than July 14, 1987.  Follow their
procedures in the Federal Register Notice ( please note that form(s)
must be obtained and filled out, so don't wait until the last minute).
     Disposal information can be found on page of 12357 of the
Federal Register notice.  The EPA is encouraging registrants and
suppliers to take back suspended or canceled dinoseb products.
     For more information regarding dinoseb, please contact the
Chemicals-Pesticides Program.
      *********************************************************************
      PRINCIPAL USES:  The phenol form (Vertac General Weed Killer) is
      used as a general contact herbicide in orchards, vineyards, forage
      legumes, and for killing potato vines and desiccating seed crops to
      facilitate harvest.  The ammonium salt (Vertac Selective) is used as a
      selective contact herbicide in alfalfa, clover, birdsfoot trefoil,
      onions, garlic, peas, and small grains.  Alkanolamine salts such as
      Premerge 3 are applied to kill germinating seeds contained in the upper
      soil surface layers in preemergence treatments and also in early
      postemergence and directed sprays in numerous crops.  Drexel Dynamyte 3
      for use on lentils (56).
      APPLICATION METHOD(S): Preplant, preemergence, postemergence and directed
      postemergence applications possible depending upon weed problem, crop,
      and dinoseb formulation (58).
                                   I.  EFFICACY
      Important Weeds Controlled: Effective on most small annual seedlings,
      broadleaves (8b).
           Spraying is most effective at relatively high temperatures.  Control
      should last from between 3-6 weeks (8b).
                             II.  PHYSICAL PROPERTIES
      MOLECULAR FORMULA:  C10 H12 N2 O5 (62)
      MOLECULAR WEIGHT:   240.2 (62)
      PHYSICAL STATE:     Orange solid (pure compound); orange-brown solid
                          (technical product, 95-98% pure) (62).
      ODOR:               Pungent odor (pure compound) (58)
      MELTING POINT:      38-42 C (pure compound); 30-40 C (technical
                          product) (62).
      BOILING POINT:      Not determined.  Flash point 177 C (pure compound)
                          (58).
      VAPOR PRESSURE:     1 mmHg at 151.1 C; 20 mmHg at 217.3 C (pure
                          compound) (58).
      SOLUBILITY:         0.0052 g/100g water at 25 C (pure compound) (58).
                          III.  HEALTH HAZARD INFORMATION
      OSHA STANDARD:  NA
      NIOSH RECOMMENDED LIMIT:  NA
      ACGIH RECOMMENDED LIMIT:  NA
      TOXICOLOGY
           A.  ACUTE TOXICITY
               DERMAL:  Staining of skin and minor irritation by very small
                        amounts.  Rapid absorption - The dinoseb LD50 value for
                        guinea pigs is in the range of 100 to 200 mg/kg.  The
                        LD50 value for skin adsorption in rabbits of 3 dinoseb
                        formulations are:  170 mg/kg for Premerge 3 Dinitro
                        Amine Herbicide, 75 mg/kg for Dow General Weed Killer,
                        and 212 mg/kg for Dow Selective Weed Killer (58).
               ORAL:    LD50 = 58 mg/kg (rat) (58).
               INHALATION:  Dusts may be irritating and may cause serious
                            illness (58).
               EYES:    Mild to moderate irritation expected (58).
           B.  SUBACUTE AND CHRONIC TOXICITY:
           Fed to rats for 5 to 13 days as 0.05% of diet; caused rapid
      emaciation, slight kidney and liver effects, and death (58).
           Rats - 6 months:
                0.01% in diet - no effects.
                0.02% in diet - growth depression without mortality.
           In a  91-day dog study there was no effect at 100 ppm in the diet
      which is approximately 4 mg/kg per day (58).
           In 180-day feeding trials rats receiving 100 mg/kg diet suffered
      no ill effect (62).
                        IV.  ENVIRONMENTAL  CONSIDERATIONS
      Behavior In Or On Soils
      1.  Adsorption and leaching characteristics in basic soil types:
            Dinoseb is not tightly adsorbed on most agricultural soils.  It
            can leach in porous, sandy soils; but experiments have shown
            that for normal temperature zone rainfall and infiltration
            rates, it should not be leached from the top foot of soil by
            rainfall in the first year after application, during which time
            it is subjected to soil microbial degradation.
      2.  Microbial breakdown:  There is no buildup in soil and microbial
            breakdown has been demonstrated.
      3.  Loss from photodecomposition and/or volatilization:  Some losses
            via steam distillation under specific conditions of soil
            acidity, high temperatures, and surface soil moisture.
      4.  Resultant average persistence of phytotoxicity at recommended
            rates:  Two to 4-weeks under average conditions of use (58).
      Toxicological Properties
      1.  General toxicity to wildlife and fish:
           a.  Toxicity to fish - dinoseb is highly toxic to fish.  After 24
               hr of exposure, goldfish showed no effect at 0.1 ppm; but at
               0.4 ppm, all died.  Since dinoseb is not used in aquatic
               areas, there is little or no practical hazard to fish as long
               as direct contamination of lakes and streams is avoided.
           b.  Five-day dietary studies with dinoseb show that it is
               moderately toxic to birds.  The LC50 of dinoseb to ring-necked
               pheasant is 515 ppm and to Japanese quail is 409 ppm.
           c.  Under actual use conditions, the practical hazard of dinoseb
               to birds and other wildlife is very low.  Since dinoseb is a
               potent contact herbicide, vegetation is neither attractive nor
               palatable to wildlife soon after treatment.  Residues on
               treated vegetation degrade quite rapidly and are very low by
               about 3 weeks after spraying.  No proven cases of injury to
               birds or other wildlife have occurred during wide-scale
               commercial use of dinoseb for over 20 years.
                                     References
      Toxicological studies on laboratory animals, certain
           alkyldinitrophenols used in agriculture.  The Dow Chemical Co.,
           Midland, Michigan.
      Dinitrophenol -- toxicological information and suggestions regarding
           treatment for persons swallowing herbicides containing
           dinitrophenol.  The Dow Chemical Company, Midland, Michigan (58).
                      V.  EMERGENCY AND FIRST AID PROCEDURES
           The chemical information provided below has been condensed
      from original source documents, primarily from "Recognition and
      Management of Pesticide Poisonings", 3rd ed. by Donald P.  Morgan,
      which have been footnoted.  This information has been provided in
      this form for your convenience and general guidance only.  In
      specific cases, further consultation and reference may be required
      and is recommended.  This information is not intended as a sub-
      stitute for a more exhaustive review of the literature nor for the
      judgement of a physician or other trained professional.
           If poisoning is suspected, do not wait for symptoms to develop.
      Contact a physician, the nearest hospital, or the nearest Poison
      Control Center.
      FREQUENT SYMPTOMS AND SIGNS OF POISONING:
           YELLOW STAINING of skin and hair often signify contact with a
      nitrophenolic chemical.  Staining of the sclerae and urine indicate
      absorption of potentially toxic amounts.  PROFUSE SWEATING, HEADACHE,
      THIRST, MALAISE, and LASSITUDE are the common early symptoms of
      poisoning.  WARM, FLUSHED SKIN, TACHYCARDIA, and FEVER characterize a
      serious degree of poisoning.  APPREHENSION, restlessness, anxiety,
      manic behavior, or unconsciousness reflect severe cerebral injury.
      CONVULSIONS occur in the most severe poisonings.  Cyanosis, tachypnea
      and dyspnea result from stimulation of metabolism, pyrexia, and tissue
      anoxia.  Weight loss occurs in persons chronically poisoned at low
      dosages (25).
           SKIN CONTACT:  Wash contaminated skin and hair promptly with soap
      and water, or with water alone if soap is not available (25).
           INGESTION:  Induce vomiting by giving an emetic and repeat until
      vomit is clear.  Then give two teaspoonfuls of baking soda in a glass
      of water.  Send for a physician immediately (58).
           INHALATION:  If any illness occurs due to inhalation of dust or
      spray mists, remove the person to fresh air and call a physician (58).
           EYE CONTACT:  Flush chemical from eyes with copious amounts of
      clean water (25).
      NOTES TO PHYSICIAN:
      1.   IN EVENT OF SYSTEMIC POISONING:
           A.  REDUCE ELEVATED BODY TEMPERATURE BY PHYSICAL MEANS.
               Administer sponge baths and cover victim with low-temperature
               blankets.  In fully conscious patients, administer cold,
               sugar-containing liquids by mouth as tolerated.
           B.  Administer OXYGEN continuously by mask to minimize tissue
               anoxia.
           C.  Unless there are manifestations of cerebral edema, administer
               INTRAVENOUS FLUIDS at maximum tolerated rates to enhance
               urinary excretion of toxicant and to support physiologic
               mechanisms for heat loss.  IN the presence of CEREBRAL EDEMA,
               intravenous FLUIDS must be administered very CAUTIOUSLY to
               avoid increasing the cerebral injury.  Monitor fluid balance,
               blood electrolytes and sugar, adjusting IV infusions to
               stabilize electrolyte concentrations.  Follow urine contents
               of albumin and cells.  Follow serum alkaline phosphatase, GOT,
               and LDH to evaluate liver injury.
           D.  Administer SEDATIVES, if necessary, to control apprehension,
               excitement, and/or convulsions.  Although not previously used
               in this type of poisoning, DIAZEPAM (Valium) should help:
               adult dose, 5-10 mg slowly IV, or IM (deep); child's dose, 0.1
               mg/kg.  Repeat every 2-4 hours as needed.  Amobarbital or
               pentobarbital may be needed.  Dose in adults:  200 mg, IM or
               slowly IV, every 4-6 hours; child's dose:  up to 5 mg/g.
               CAUTION:  Be prepared to counteract respiratory depression and
                         hypotension which may follow administration of
                         anticonvulsants and sedatives.
      2.   If toxicant has been INGESTED, evacuate the stomach and intestine.
           A.  If victim is alert and respiration is not depressed, give
               SYRUP OF IPECAC, followed by 1-2 glasses of water, to induce
               vomiting (adults 12 years and older:  30 ml; children under
               12:  15 ml).
               CAUTION:  OBSERVE victim closely AFTER administering IPECAC.
                         If consciousness level declines, or if vomiting has
                         not occurred in 15 minutes, immediately INTUBATE,
                         ASPIRATE, and LAVAGE the stomach.
               Following emesis, have victim drink a suspension of 30-50 gm
               ACTIVATED CHARCOAL in 3-4 ounces of water to bind toxicant
               remaining in the gastrointestinal tract.
           B.  IF VICITM IS NOT FULLY ALERT, empty the stomach immediately by
               INTUBATION, ASPIRATION, and LAVAGE, using isotonic saline or
               5% sodium bicarbonate.  Because these pesticides are usually
               dissolved in petroleum distillates, emesis and intubation of
               the stomach involve serious risk that solvent will be
               aspirated, leading to chemical pneumonitis.  For this reason:
               (a)  If victim is unconsciousa or obtunded and factilities are
                    at hand, insert an ENDOTRACHEAL TUBE (cuffed, if
                    available) prior to gastric intubation.
               (b)  Keep victim's HEAD BELOW LEVEL OF THE STOMACH and turned
                    to the left, during intubation and lavage (Trendelenburg,
                    or left lateral decubitus, with head of table tipped
                    downward).
               (c)  ASPIRATE PHARYNX as regularly as possible to remove
                    gagged or vomited stomach contents.
               (d)  After aspiration of gastric contents and washing of
                    stomach, instill 30-50 gm of ACTIVATED CHARCOAL in 3-4
                    ounces of water through the stomach tube to limit
                    absorption of remaining toxicant.  Do NOT instill cream,
                    milk, or other materials containing vegetable or animal
                    fats, as these are likely to enhance absorption.
           C.  If bowel movement has not occurred in 4 hours, and if patient
               is fully conscious, give SODIUM SULFATE as a cathartic:  0.25
               mg/kg body weight in 1-6 ounces of water.  Magnesium sulfate
               and citrate are equally suitable unless renal function is
               impaired; retention of magnesium may depress CNS function and
               alter myocardial irritabiity.
      3.   DO NOT administer atropine, aspirin, or other antipyretics to
           control fever.  Animal tests indicate that aspirin enhances,
           rather than reduces, the toxicity of nitrophenolic and
           nitrocresolic compounds.
      4.   During convalescence, administer high-calorie, high-vitamin diet
           to facilitate repletion of body fat and carbohydrate.
      5.   Discourage subsequent contact with the toxicant for at least 4
           weeks, to allow full restoration of normal metabolic processes.
      6.   HEMODIALYSIS and HEMOPERFUSION may be considered in severe
           poisonings by aromatic nitro-compounds, although most phenols are
           extensively bound to plasma proteins.  EXCHANGE TRANSFUSION is
           another option in poisonings characterized by impaired renal
           function.  So long as renal and liver functions are intact, these
           compounds are efficiently excreted (25).
                        VI.  FIRE AND EXPLOSION INFORMATION
           Premerge 3 Dinitro Amine Herbicide - flammable (flash point
             29.4 C, TCC)
           Dow General Weed Killer - flammable (flash point 15.6 C TCC)
           Dow Selective Weed Killer - flammable (flash point 18.9 C TCC) (58)
                                VII.  COMPATIBILITY
           Premerge 3 - compatible with hard water.
           Dow General Weed Killer - forms loose emulsions in all types of
             water; needs mechanical agitation.
           Dow Selective Weed Killer - compatible with hard water.
           Formulations are noncorrosive to equipment if cleaned after use (58)
                            VIII.  PROTECTIVE MEASURES
      STORAGE AND HANDLING:  Do not get in eyes, on skin, or on clothing.  Do
      not take internally.  Wash thoroughly with soap and water after
      handling and before eating or smoking.  Avoid breathing spray mist or
      vapors.  Do not store near heat or open flame.  This product is toxic
      to fish and wildlife.  Birds and other wildlife in treated areas may be
      killed.  Keep out of lakes, streams, or ponds.  Do not apply where
      run-off is likely to occur.  Do not apply when weather conditions favor
      drift from areas treated (40b).
      PROTECTIVE CLOTHING:  Wear suitable protective equipment such as
      chemical workers goggles, rubber or plastic gloves and rubber or
      plastic apron while pouring and transferring the concentrated product
      and at other times when contact is likely.  Wear protective clothing
      such as long sleeved shirt and long legged pants or coveralls while
      mixing or spraying.  Do not wear contaminated clothing or shoes (40b).
      PROTECTIVE EQUIPMENT:  To avoid breathing spray mist, wear a mask or
      respirator of a type recommended by NIOSH or MSHA.  Keep respirator
      clean.  Wash throughly and change cartridge as necessary (40b).
                       IX.  PROCEDURES FOR SPILLS AND LEAKS
                     IN CASE OF EMERGENCY, CALL, DAY OR NIGHT
                                  (800) 424-9300
                      PESTICIDE TEAM SAFETY NETWORK/CHEMTREC
                               X.  LITERATURE CITED
       8b. Thomson, W.T.  1981.  Agricultural chemicals - book 2:
               herbicides.  Revised ed.  Thomson Publications, Fresno, CA.
               274 pp.
      25.  Morgan, D.P.  1982.  Recognition and management of pesticide
               poisonings, 3rd ed.  U.S. Environmental Protection Agency,
               Washington, DC.  120 pp.
      40b. The Dow Chemical Company.  1980.  Specimen label:  Premerge 3.
               Midland, MI.
      56.  Farm Chemicals Handbook, 70th ed.  1984.  R. T. Meister, G. L.
               Berg, C. Sine, S. Meister, and J. Poplyk, eds.  Meister
               Publishing Co., Willoughby, OH.
      58.  Weed Science Society of America, Herbicide Handbook Committee.
               1983.  Herbicide handbook of the weed science society of
               America, 5th ed.  Weed Science Society of America, Champaign,
               IL.  515 pp.
      62.  The Pesticide Manual:  A World Compendium, 7th ed.  1983.  C.R.
               Worthing, ed.  The British Crop Protection Council, Croydon,
               England.  695 pp.
      4/29/87