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Adverse
Effects
ACTIVITY:
Rodenticide (diphenylamine)
CAS Name:
N-methyl-2,4-dinitro-N-(2,4,6-tribromophenyl)-6-(trifluoromethyl)benzenamine
Structure:
| Note
that both bromine and fluorine are in this pesticide. |
Reports
available from
The National Technical Information Service
(NTIS)
Order from NTIS by: phone at 1-800-553-NTIS (U.S. customers);
(703)605-6000 (other countries); fax at (703)605-6900;
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| Order
Number |
Title |
Keywords |
Source |
| NTIS/OTS0543306 |
INITIAL SUBMISSION: LETTER
FROM ELI LILLY & CO TO USEPA SUBMITTING RESULTS ON
AN ACUTE ORAL STUDY WITH M-6077 IN MONKEY WITH ATTACHMENTS
- 1992 |
ELI
LILLY & CO
M-6077
HEALTH EFFECTS
ACUTE TOXICITY
MAMMALS
MONKEYS
ORAL
GAVAGE |
EPA/OTS;
Doc #88-920005845 |
| NTIS/OTS0543309 |
INITIAL SUBMISSION: LETTER FROM
ELI LILLY & CO TO USEPA SUBMITTING RESULTS ON AN ACUTE
ORAL STUDY WITH R-O-418-78 IN RATS WITH ATTACHMENTS -
1992 |
ELI
LILLY & CO
R-O-418-78
HEALTH EFFECTS
ACUTE TOXICITY
MAMMALS
RATS
ORAL
GAVAGE |
EPA/OTS;
Doc #88-920005848 |
| NTIS/OTS0543313 |
INITIAL
SUBMISSION: LETTER FROM ELI LILLY & CO TO USEPA SUBMITTING
RESULTS ON AN ACUTE ORAL STUDY WITH R-O-21-79 IN RATS
WITH ATTACHMENTS - 1992 |
ELI
LILLY & CO
R-O-21-79
HEALTH EFFECTS
ACUTE TOXICITY
MAMMALS
RATS
ORAL
GAVAGE |
EPA/OTS;
Doc #89-920005851 |
| NTIS/OTS0543314 |
INITIAL
SUBMISSION: LETTER FROM ELI LILLY & CO TO USEPA SUBMITTING
RESULTS ON AN ACUTE ORAL STUDY WITH R-O-128-79 IN RATS
WITH ATTACHMENTS - 1992 |
ELI
LILLY & CO
R-O-128-79
HEALTH EFFECTS
ACUTE TOXICITY
MAMMALS
RATS
ORAL
GAVAGE |
EPA/OTS;
Doc #88-920005852 |
NTIS/OTS0543315
|
INITIAL SUBMISSION: LETTER FROM ELI LILLY & CO TO
USEPA SUBMITTING RESULTS ON AN ACUTE INHALATION STUDY
IN RATS WITH R-H-64-77 IN RATS WITH ATTACHMENTS - 1992 |
ELI
LILLY & CO
R-H-64-77
HEALTH EFFECTS
ACUTE TOXICITY
MAMMALS
RATS
INHALATION |
EPA/OTS;
Doc #88-920005853 |
| NTIS/OTS0543316
|
INITIAL SUBMISSON: LETTER FROM ELI LILLY & CO TO USEPA
SUBMITTING RESULTS ON AN ACUTE INHALATION STUDY WITH R-H-53-77
IN RATS WITH ATTACHMENTS - 1992 |
ELI
LILLY & CO
R-H-53-77
HEALTH EFFECTS
ACUTE TOXICITY
MAMMALS
RATS
INHALATION |
EPA/OTS;
Doc #88-920005854 |
| NTIS/OTS0543317
|
INITIAL SUBMISSION: LETTER FROM ELI LILLY & CO TO
USEPA SUBMITTING RESULTS ON AN ACUTE INHALATION STUDY
WITH R-H-52-77 IN RATS WITH ATTACHMENTS - 1992 |
ELI
LILLY & CO
R-H-52-77
HEALTH EFFECTS
ACUTE TOXICITY
MAMMALS
RATS
INHALATION |
EPA/OTS; Doc #88-920005855 |
| NTIS/OTS0543358 |
INITIAL
SUBMISSION: LETTER FROM ELI LILLY & CO TO USEPA SUBMITTING
RESULTS ON AN ACUTE ORAL STUDY WITH D-3117 IN DOGS WITH
ATTACHMENTS - 1992 |
ELI
LILLY & CO
D-3117
HEALTH EFFECTS
ACUTE TOXICITY
MAMMALS
DOGS
ORAL
GAVAGE |
EPA/OTS;
Doc #88-920005896 |
| NTIS/OTS0543359 |
INITIAL
SUBMISSION: LETTER FROM ELI LILLY & CO TO USEPA SUBMITTING
RESULTS ON AN ACUTE INHALATION STUDY WITH R-H-59-77 IN
RATS WITH ATTACHMENTS - 1992 |
ELI
LILLY & CO
R-H-59-77
HEALTH EFFECTS
ACUTE TOXICITY
MAMMALS
RATS
INHALATION |
EPA/OTS;
Doc #88-920005897
|
| NTIS/OTS0543473 |
INITAL
SUBMISSION: LETTER FROM ELI LILLY & COMPANY TO USEPA
SUBMITTING RESULTS ON COMPOUND #126714 ACUTE RABBIT ORAL
STUDY WITH ATTACHMENTS - 1992 |
ELI
LILLY & CO
COMPOUND #126714
HEALTH EFFECTS
ACUTE TOXICITY
MAMMALS
RABBITS
ORAL |
EPA/OTS;
Doc #88-920006218
|
| NTIS/OTS0543476 |
INITIAL SUBMISSION: LETTER FROM ELI LILLY & COMPANY
TO USEPA SUBMITTING RESULTS ON COMPOUND #126714 ACUTE
CAT NASOGASTRIC STUDY WITH ATTACHMENTS - 1992 |
ELI
LILLY & CO
COMPOUND #126714
HEALTH EFFECTS
ACUTE TOXICITY
MAMMALS
CATS
ORAL
GAVAGE |
EPA/OTS; Doc #88-920006221 |
| NTIS/OTS0543477
|
INITIAL SUBMISSION: LETTER FROM ELI LILLY & COMPANY
TO USEPA SUBMITTING RESULTS ON COMPOUND #126714 ACUTE
CAT NASOGASTRIC STUDY WITH ATTACHMENTS - 1992 |
ELI
LILLY & CO
COMPOUND #126714
HEALTH EFFECTS
ACUTE TOXICITY
MAMMALS
CATS
ORAL
GAVAGE |
EPA/OTS;
Doc #88-920006222 |
|
NTIS/OTS0543478 |
INITIAL SUBMISSION: LETTER FROM ELI LILLY & COMPANY
TO USEPA SUBMITTING RESULTS ON COMPOUND #126714 ACUTE
CAT NASOGASTRIC STUDY WITH ATTACHMENTS - 1992 |
ELI
LILLY & CO
COMPOUND #126714
HEALTH EFFECTS
ACUTE TOXICITY
MAMMALS
CATS
ORAL
GAVAGE |
EPA/OTS;
Doc #88-920006223 |
| NTIS/OTS0543738 |
INITIAL
SUBMISSION: N-METHYL-2,4-
DINITRO-N-(2,4,6-TRIBROMOPHENYL)-6
-(TRIFLUOROMETHYL)-BENZENAMINE: SUBCHRONIC RAT ORAL PILOT
STUDY WITH COVER LETTER DATED 08-18-92
|
ELI
LILLY & CO
N-METHYL-2,4-DINITRO-N-
(2,4,6-TRIBROMOPHENYL)-6-
(TRIFLUOROM*
HEALTH EFFECTS
SUBCHRONIC TOXICITY
MAMMALS
RATS
ORAL
DIET
|
EPA/OTS;
Doc #88-920006666 |
| NTIS/OTS0545087 |
INITIAL
SUBMISSION: THE REVERSIBILITY OF CENTRAL NERVOUS SYSTEM
LESIONS FROM CHRONIC BROMETHALIN ADMINISTRATION WITH COVER
LETTER DATED 08-21-92 |
ELI
LILLY & CO
BROMETHALIN
HEALTH EFFECTS
CHRONIC TOXICITY
COMBINED CHRONIC TOXICITY/CARCINOGENICITY
MAMMALS
RATS
ORAL
DIET |
EPA/OTS; Doc #88-920006488 |
| NTIS/OTS0545109 |
INITIAL SUBMISSION: ACUTE BOBWHITE ORAL PILOT STUDY WITH
N-METHYL-2,4-DINITRO-N-(2,4,6-
TRIBROMOPHENYL)- 6-(TRIFLUOROMETHYL)BENZENAMINE WITH COVER
LETTER DATED 08-18-92 |
ELI
LILLY & CO
N-METHYL-2,4-DINITRO-N-
(2,4,6-TRIBROMOPHENYL)-6-
(TRIFLUOROM*
HEALTH EFFECTS
ACUTE TOXICITY
BIRDS
ORAL
GAVAGE
|
EPA/OTS;
Doc #88-920006510 |
| NTIS/OTS0545112
|
METHYL-2,4-DINITRO-N-(2,4,6-
TRIBROMOPHENYL)- 6-
(TRIFLUOROMETHYL)BENZENAMINE WITH COVER LETTER DATED 08-18-92
|
ELI
LILLY & CO
N-METHYL-2,4-DINITRO-N-
(2,4,6-TRIBROMOPHENYL)-6-
(TRIFLUOROM*
HEALTH EFFECTS
SUBCHRONIC TOXICITY
BIRDS
ORAL
GAVAGE |
EPA/OTS;
Doc #88-920006513 |
|
NTIS/OTS0545113 |
INITIAL
SUBMISSION: ACUTE BOBWHITE ORAL PILOT STUDY WITH N-METHYL-2,4-DINITRO-N-(2,4,6-
TRIBROMOPHENYL)- 6-
(TRIFLUOROMETHYL)BENZENAMINE WITH COVER LETTER DATED 08-18-92
|
ELI
LILLY & CO
N-METHYL-2,4-DINITRO-N-
(2,4,6-TRIBROMOPHENYL)-6-
(TRIFLUOROM*
HEALTH EFFECTS
ACUTE TOXICITY
BIRDS
ORAL
GAVAGE |
EPA/OTS;
Doc #88-920006514 |
| NTIS/OTS0545129 |
INITIAL SUBMISSION: ACUTE BOBWHITE ORAL TOXICITY STUDY
WITH N-METHYL-2,4-DINITRO-N-(2,4,6-
TRIBROMOPHENYL)- 6-
(TRIFLUOROMETHYL)BENZENAMINE WITH COVER LETTER DATED 08-18-92
|
ELI
LILLY & CO
N-METHYL-2,4-DINITRO-N-
(2,4,6-TRIBROMOPHENYL)-6-
(TRIFLUOROM*
HEALTH EFFECTS
ACUTE TOXICITY
BIRDS
ORAL
GAVAGE |
EPA/OTS;
Doc #88-920006530 |
|
NTIS/OTS0545133 |
INITIAL SUBMISSION: SUBCHRONIC MALLARD ORAL PILOT STUDY
WITH N-
METHYL-2,4-DINITRO-N-(2,4,6-
TRIBROMOPHENYL)- 6-(TRIFLUOROMETHYL)BENZENAMINE WITH COVER
LETTER DATED 08-18-92 |
ELI
LILLY & CO
N-METHYL-2,4-DINITRO-N-
(2,4,6-TRIBROMOPHENYL)-6-
(TRIFLUOROM*
HEALTH EFFECTS
SUBCHRONIC TOXICITY
BIRDS
ORAL
DIET |
EPA/OTS;
Doc #88-920006534 |
| NTIS/OTS0545164 |
INITIAL
SUBMISSION: 14-DAY ACUTE ORAL TOXICITY STUDY WITH BROMETHALIN
IN BOBWHITE WITH COVER LETTER DATED 08-21-92
|
ELI
LILLY & CO
BROMETHALIN
HEALTH EFFECTS
ACUTE TOXICITY
BIRDS
ORAL
GAVAGE |
EPA/OTS;
Doc #88-920006565 |
| NTIS/OTS0545167 |
INITIAL
SUBMISSION: FIVE-DAY DIETARY TOXICITY STUDY WITH BROMETHALIN
IN BOBWHITE WITH COVER LETTER DATED 08-21-92
|
ELI
LILLY & CO
BROMETHALIN
HEALTH EFFECTS
SUBCHRONIC TOXICITY
BIRDS
ORAL
DIET |
EPA/OTS; Doc #88-920006568
|
| NTIS/OTS0545168 |
INITIAL SUBMISSION: 14-DAY
ACUTE ORAL TOXICITY STUDY WITH BROMETHALIN IN BOBWHITE
WITH COVER LETTER DATED 08-21-92
|
ELI
LILLY & CO
BROMETHALIN
HEALTH EFFECTS
ACUTE TOXICITY
BIRDS
ORAL
GAVAGE |
EPA/OTS;
Doc #88-920006569 |
|
NTIS/OTS0545174 |
INITIAL SUBMISSION: FIVE-DAY
DIETARY TOXICITY STUDY WITH BROMETHALIN IN BOBWHITE WITH
COVER LETTER DATED 08-21-92 |
ELI
LILLY & CO
BROMETHALIN
HEALTH EFFECTS
SUBCHRONIC TOXICITY
BIRDS
ORAL
DIET |
EPA/OTS;
Doc #88-920006575 |
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12580294&dopt=Abstract
J Vet
Diagn Invest 2003 Jan;15(1):42-5
Thin
layer chromatography convulsant screen extended by gas chromatography-mass
spectrometry.
Braselton WE, Johnson M.
Animal Health Diagnostic Laboratory, College of Veterinary
Medicine, Michigan State University, East Lansing, MI 48824,
USA.
Acute onset convulsive disorders
in the canine may result from exposure to a variety of toxicants
including strychnine, insecticides, metaldehyde, zinc phosphide,
methylxanthines, drugs of abuse, bromethalin,
and the tremorgenic mycotoxins (roquefortine and penitrem
A). Although several of the above can be identified in a single
gas chromatography-mass spectrometry (GC-MS) screen most have
to be determined by separate tests. This report describes
a modification of the strychnine extraction procedure, which
allows thin layer chromatographic (TLC) identification of
strychnine, bromethalin, roquefortine,
and penitrem A in suspect baits, stomach contents or vomitus,
and extends the identification to a wide variety of drugs,
pesticides, and environmental contaminants by GC-MS. Samples
were mixed with base, extracted into CH2Cl2 and the organic
fraction back-extracted with acid. The organic fraction (neutrals)
was purified by gel permeation chromatography (GPC) and analyzed
by TLC to determine penitrem A and bromethalin.
The acidic aqueous fraction was adjusted to pH > 9 and extracted
into CH2Cl2. The resulting CH2Cl2 layer (bases) was then analyzed
by TLC to determine strychnine and roquefortine. The organic
basic and neutral fractions were recombined with a late eluting
GPC fraction and analyzed by GC-MS. Of 312 samples analyzed
by TLC from 1995 to 2001, 35 were positive for strychnine
alone, 58 were positive for both roquefortine and penitrem
A, 4 were positive for roquefortine alone, and 1 was positive
for bromethalin. None of the
samples were positive for penitrem A alone. Samples negative
by TLC were analyzed by the GC-MS extended procedure since
mid-1999, and 14 have shown positive for a wide variety of
compounds with convulsant activity.
PMID: 12580294 [PubMed - in process]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12012748&dopt=Abstract
Vet Clin
North Am Small Anim Pract 2002 Mar;32(2):469-84,
viii
Rodenticides.
Murphy
MJ.
School
of Veterinary Medicine, University of Minnesota, St. Paul,
MN 55108, USA. murph005@tc.umn.edu
Rodenticides
are second only to insecticides in the prevalence of pesticide
exposure. Hundreds of rodenticide products currently exist,
yet only a handful of them are involved in most toxicoses
of companion animals. The most commonly
reported toxicoses in the United States are those caused by
anticoagulant rodenticides, bromethalin, cholecalciferol,
strychnine, and zinc phosphide. The pathophysiologic findings,
diagnosis, and treatment of each of these five rodenticides
are discussed.
Publication
Types: Review Review, Tutorial
PMID:
12012748 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11245225&dopt=Abstract
J Chromatogr
Sci 2001 Feb;39(2):49-53
Determination
of bromethalin in commercial rodenticides found in consumer
product samples by HPLC-UV-vis spectrophotometry and HPLC-negative-ion
APCI-MS.
Mesmer
MZ, Flurer RA.
United
States Food and Drug Administration, Forensic Chemistry Center,
Cincinnati, OH 45237-3097, USA.
A small
amount of green particulate material is encountered in a consumer
complaint sample. The green particulates in the sample are
identified as a bromethalin-containing rodenticide using high-performance
liquid chromatographic (HPLC)-UV-vis spectrophotometric and
HPLC-negative-ion atmospheric pressure chemical ionization
(APCI)-mass spectrometric (MS) approaches, which are commonly
used for the detection and confirmation of bromethalin in
grain-based rodenticides. The selective and sensitive nature
of the MS detector makes it possible to determine bromethalin
without extensive sample cleanup and preconcentration. The
estimated detection limit with the UV-vis detector is 500
pg of bromethalin injected into the column. The extensive
fragmentation of the bromethalin molecule under APCI conditions
provides sufficient structural information for positive identification.
PMID:
11245225 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query_old?uid=9823589&form=6&db=m&Dopt=b
Vet
Pathol 1998
Nov;35(6):479-87
Epizootic
vacuolar myelinopathy of the central nervous system of bald
eagles (Haliaeetus leucocephalus) and American coots (Fulica
americana).
Thomas
NJ, Meteyer CU, Sileo L
Biological
Resources Division, National Wildlife Health Center, Madison,
WI, USA.
Unprecedented
mortality occurred in bald eagles (Haliaeetus leucocephalus)
at DeGray Lake, Arkansas, during the winters of 1994-1995
and 1996-1997. The first eagles were found dead during November,
soon after arrival from fall migration, and deaths continued
into January during both episodes. In total, 29 eagles died
at or near DeGray Lake in the winter of 1994-1995 and 26 died
in the winter of 1996-1997; no eagle mortality was noted during
the same months of the intervening winter or in the earlier
history of the lake. During the mortality events, sick eagles
were observed overflying perches or colliding with rock walls.
Signs of incoordination and limb paresis were also observed
in American coots (Fulica americana) during the episodes of
eagle mortality, but mortality in coots was minimal. No consistent
abnormalities were seen on gross necropsy of either species.
No microscopic findings in organs other than the central
nervous system (CNS) could explain the cause of death.
By light microscopy, all 26 eagles examined and 62/77 (81%)
coots had striking, diffuse, spongy
degeneration of the white matter of the CNS.
Vacuolation
occurred in all myelinated CNS tissue, including the cerebellar
folia and medulla oblongata, but was most prominent in the
optic tectum.
In the spinal cord, vacuoles were concentrated near the gray
matter, and occasional swollen axons were seen. Vacuoles were
uniformly present in optic nerves but were not evident in
the retina or peripheral or autonomic nerves. Cellular inflammatory
response to the lesion was distinctly lacking. Vacuoles were
8-50 microns in diameter and occurred individually, in clusters,
or in rows. In sections stained by luxol fast blue/periodic
acid-Schiff stain, the vacuoles were delimited and transected
by myelin strands. Transmission electron microscopy revealed
intramyelinic vacuoles formed in the myelin sheaths by splitting
of one or more myelin lamellae at the intraperiodic line.
This lesion is characteristic of toxicity
from hexachlorophene, triethyltin, bromethalin,
isonicotinic acid hydrazide, and certain exotic plant toxins;
however, despite exhaustive testing, no etiology was determined
for the DeGray Lake mortality events. This
is the first report of vacuolar myelinopathy
associated with spontaneous mortality in wild birds.
PMID:
9823589, UI: 99040923
Source:
1996 ANNUAL MEETING OF THE NORTH AMERICAN CONGRESS OF CLINICAL
TOXICOLOGY, PORTLAND, OREGON, USA, OCTOBER 10-15, 1996. JOURNAL
OF TOXICOLOGY CLINICAL TOXICOLOGY; 34 (5). 1996.
572-573.
POSSIBLE
BROMETHALIN-INDUCED TOXICITY IN A HUMAN A CASE REPORT
BULLER G, HEARD J, GORMAN S
BIOSIS COPYRIGHT: BIOL ABS. RRM MEETING ABSTRACT MEETING POSTER
HUMAN MALE ADULT PATIENT BROMETHALIN RODENTICIDES NEUROTOXINS
VENGEANCE TOXICOLOGY RAT POISON NEUROLOGIC SYMPTOMS SEIZURE
MUSCLE TREMORS NERVOUS SYSTEM DISEASE TOXICITY MUSCLE DISEASE
Prevention
and Control of Wildlife Damage. 1994.
Hygnstrom,
S.E., R.M. Timm, and G.E. Larson.
Univ.
Nebraska Cooperative Extension, USDA Animal Damage Control,
and Great Plains Agric. Council.
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1632057&dopt=Abstract
Vet Pathol
1992 Mar;29(2):139-44
Neuropathologic
findings of bromethalin toxicosis in the cat.
Dorman
DC, Zachary JF, Buck WB.
Department
of Veterinary Biosciences, College of Veterinary Medicine,
University of Illinois, Urbana.
Ten random
source male domestic shorthair cats, 2 to 6 years old and
3.0-4.4 kg body weight, were each given a single oral dose
(1.5 mg/kg) of bromethalin (cat Nos. 1-5) or bait vehicle
carrier (cat Nos. 6-10). Bromethalin-dosed cats developed
a toxic syndrome characterized by ataxia, focal motor seizures,
vocalization, decerebrate posture, decreased conscious proprioception,
recumbency, depression, and semicoma. Bromethalin-dosed cats
were euthanatized if seizure activity or hindlimb paralysis
developed. Survival times were 48 hours (cat No. 1), 89 hours
(cat No. 2), 90 hours (cat No. 3), and 97 hours (cat No. 4).
Control cats (cat Nos. 6-10) and one bromethalin-dosed cat
(cat No. 5) were euthanatized on day 20 after dosing. Spongy
change (edema--characterized by the
formation of vacuoles in extracellular spaces and myelin lamellae),
hypertrophied fibrous astrocytes, and hypertrophied oligodendrocytes
were observed in the white matter of the cerebrum,
cerebellum, brain stem, spinal cord, and optic nerve of all
bromethalin-dosed cats. Spongy change occasionally extended
into contiguous cerebellar Purkinje cell layer and cerebral
cortical gray matter. The severity of lesions varied
among cats but was most pronounced in cat No. 5 (480 hours
after dosing). A leukocytic inflammatory response, gitter
cell (macrophage) response, or axonal degeneration was not
observed in the vacuolated areas. Ultrastructural findings
included separation of myelin lamellae at the interperiod
lines with the formation of intramyelinic vacuoles (intramyelinic
edema), rupture and coalescence of intramyelinic vacuoles
into larger extracellular spaces (spongy change), and pronounced
cytosolic edema of astrocytes and oligodendroglial cells.
PMID:
1632057 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1539906&dopt=Abstract
Am J Vet
Res 1992 Jan;53(1):138-42
Effects
of an extract of Gingko biloba on bromethalin-induced cerebral
lipid peroxidation and edema in rats.
Dorman
DC, Cote LM, Buck WB.
Department
of Veterinary Biosciences, College of Veterinary Medicine,
University of Illinois, Urbana 61801.
The effects
of administration of a commercially available extract of Gingko
biloba (EGB) on bromethalin-induced
brain lipid peroxidation and cerebral edema in adult
male Sprague-Dawley rats was determined. Gingko biloba extract
was given (100 mg/kg) by gavage immediately after bromethalin
(1.0 mg/kg) administration. Rats were euthanatized at 24 hours
after dosing. Brain lipid peroxidation
was determined by measurement of brain
malonaldehyde-thiobarbituric acid chromophore (MDA-TBA) concentration,
brain sodium concentration, and brain
water content. Treatment of bromethalin-dosed rats (10/group)
with EGB was associated with a statistically significant (P
less than 0.05) decrease in clinical sign severity, compared
with bromethalin-dosed saline solution-treated rats. All rats
given bromethalin and saline solution developed clinical signs
of toxicosis including CNS depression, hind limb weakness,
ataxia, paralysis, and coma. Some rats given bromethalin and
EGB developed clinical signs, however, none developed hind
limb paralysis. The brain MDA-TBA
concentration (2.4 +/- 0.5 delta MDA-TBA concentration/mg
of protein), percentage of water in brain
tissue (80.3 +/- 0.30%), and brain
sodium concentration (6.68 +/- 0.21 mg/g of dry weight) were
significantly increased in rats given bromethalin and saline
solution, compared with control rats given saline solution
(1.0 +/- 0.1 delta MDA-TBA concentration/mg of protein; 78.1
+/- 0.33% water in brain tissue;
4.83 +/- 0.30 mg of brain Na+/g
of dry weight) and rats given bromethalin and EGB (1.6 +/-
0.2 delta MDA-TBA concentration/mg of protein; 79.3 +/- 0.31%
water in brain tissue; 5.37 +/-
0.34 mg of brain Na+/g of dry
weight). (ABSTRACT TRUNCATED AT 250 WORDS)
PMID:
1539906
[PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2017873&dopt=Abstract
Vet Hum
Toxicol 1991 Feb;33(1):9-11
Electroencephalographic
changes associated with bromethalin toxicosis in the dog.
Dorman
DC, Parker AJ, Buck WB.
Department
of Veterinary Biosciences, College of Veterinary Medicine,
University of Illinois, Urbana 61801.
Electroencephalogram
(EEG) recordings were obtained before and during the clinical
syndrome induced by a bromethalin rodenticide given to dogs.
Nine dogs given 6.25 mg bromethalin/kg po developed clinical
signs and EEG abnormalities 15 to 58 h postdosing. Predominant
abnormal EEG changes included spike and spike-and-wave EEG
patterns (66%), high voltage slow wave (HVSA, 50-150 microV,
1-6 Hz) activity (44%) photoconvulsive or photoparoxysmal
irritative responses (44%), and marked voltage depression
(dominant activity less than 10 microV) in all leads (33%).
PMID:
2017873 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2094433&dopt=Abstract
J Vet
Diagn Invest 1990 Apr;2(2):123-8
Diagnosis
of bromethalin toxicosis in the dog.
Dorman
DC, Simon J, Harlin KA, Buck WB.
Department
of Veterinary Biosciences, College of Veterinary Medicine,
University of Illinois, Urbana 61801.
Dogs given
a single oral dose of bromethalin at 6.25 mg/kg developed
a toxic syndrome characterized by hyperexcitability, tremors,
seizures, depression, and death within 15-63 hours after bromethalin
administration. Gross lesions included mild cerebral edema
(2/5) and mild pulmonary congestion (2/5). Histologic
lesions included diffuse white matter spongiosis (5/5),
mild microgliosis (3/5), optic nerve
vacuolization (3/5), mild thickening of Bowman's capsule
(2/5), and occasional splenic megakaryocytes (2/5). Ultramicroscopic
examination of midbrain stem
revealed occasional swollen axons, intramyelinic vacuolization,
and myelin splitting at the intraperiod line. Bromethalin
was detected in kidney, liver, fat, and brain tissues,
using gas chromatography with electron capture detection.
Photodegradation of extracted bromethalin may limit accurate
quantification of tissue residues.
PMID:
2094433 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=search&db=PubMed&term=bromethalin%5bAll%20Fields%5d
Vet Clin
North Am Small Anim Pract 1990
Mar;20(2):339-52
Toxicology
of selected pesticides, drugs, and chemicals. Anticoagulant,
cholecalciferol, and bromethalin-based
rodenticides.
Dorman
DC.
Department
of Veterinary Biosciences, University of Illinois, Urbana-Champaign
College of Veterinary Medicine.
The control
of rodent pests is a continuing goal of mankind. To this end,
a multitude of rodenticides have been produced, each designed
to kill rodents by exerting their toxic effects on various
body systems. As examples, veterinarians have had to manage
companion animal poisonings due to anticoagulant, sodium fluoroacetate
(compound 1080), thallium, barium carbonate, and zinc phosphide-based
rodenticides. Many of these rodenticides
were introduced because of their anticipated safety in relation
to nontarget species; unfortunately, this has not been the
case. Veterinarians must attempt to identify the specific
rodenticide involved in poisoning cases. Therapeutic success
in these poisonings is often more dependent upon symptomatic
and supportive care rather than the use of antidotal therapy.
Publication
Types: Review Review, Tutorial
PMID:
2156370 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2741313&dopt=Abstract
Vet Hum
Toxicol 1989 Jun;31(3):239-40
No
Abstract available
A suspected
case of bromethalin toxicity in a domestic cat.
Martin
T, Johnson B.
California
Veterinary Diagnostic Laboratory System, University of California,
Davis 95616.
PMID:
2741313 [PubMed - indexed for MEDLINE]
Fundam
Appl Toxicol 1988 Nov;11(4):664-72
The
toxicity and mechanism of action of bromethalin: a new single-feeding
rodenticide.
van
Lier RB, Cherry LD.
Toxicology
Division, Lilly Research Laboratories,
Greenfield, Indiana 46140.
Bromethalin is a new rodenticide for the control of commensal
rodents. Doses in excess of the LD50
(2 mg/kg in rats) will cause death within 8–12 hr
and it is preceded by one to three episodes of clonic convulsions
with death usually due to respiratory arrest. Multiple low
doses or sublethal intoxication yields hind leg weakness and
loss of tactile sensation in rodents.
Histopathology of the brain and spinal cord of these animals
revealed a spongy degeneration of the white matter which was
shown upon ultramicroscopic examination to be intramyelenic
edema. No inflammation or cellular destruction of neuronal
tissue was noted. LD50 values ranged
from 1.8 mg/kg in the cat to approximately 13 mg/kg in rabbits.
The only apparent nonsusceptible species was the guinea pig
which could tolerate doses in excess of 1000 mg/kg without
effect. Identification of the desmethyl metabolite was demonstrated
in the blood and liver of treated animals by comparison of
chromatographic retention times to that of a reference standard,
but direct mass spectral identification was unsuccessful in
part due to the low dose which could be administered. Therefore,
the metabolism of bromethalin was studied by indirect means.
Animals were pretreated with three inducers of microsomal
drug metabolism: phenobarbital, 3-methylcholanthrene (3MC),
and Aroclor 1254 (Aroclor) and one inhibitor, SKF-525A. Pretreated
mice or rats were given an LD50 dose of bromethalin or the
desmethyl analog and the percentage of surviving animals was
determined. Phenobarbital and SKF-525A were protective when
bromethalin was given, but SKF-525A increased lethality when
the desmethyl analog was administered. Aroclor and 3MC both
promoted lethality. It was concluded that SKF-525A could block
the conversion of bromethalin to the desmethyl analog and
beyond but each of the inducers promoted conversion of bromethalin
to the desmethyl analog. Induction of subsequent pathways
also must have occurred so that the net level of the desmethyl
metabolite was higher than control when Aroclor and 3MC were
given but lower than control when phenobarbital was given.
Mechanistic studies showed that bromethalin
is rapidly converted to the desmethyl analog which is an extremely
potent uncoupler of oxidative phosphorylation. It was theorized
that if this occurs in the central nervous system, a fluid
imbalance may ensue due to insufficient ATP. Fluid
buildup in the cranium was determined by measuring cerebrospinal
fluid pressure (CSFP), brain and spinal cord moisture, and
cation concentrations. These studies
demonstrated that rats had mean CSFP of 251 ± 23 mm
water 24 hr after being treated with 1 mg/kg bromethalin compared
to a control value of 68 ± 5 mm water. Pressures
could be reduced within 1 to 2 hr by infusion of an osmotic
diuretic such as mannitol or urea; however, CSFP would rise
again when the infusion was stopped. CSFP returned to normal
values within 7 days after a single dose of 1 mg/kg bromethalin.
Subcutaneous injections of dexamethasone hastened reduction
of CSF pressure.
PMID:
3229590 [PubMed - indexed for MEDLINE]
FULL REPORT AVAILABLE AT http://www.fluorideaction.org/pesticides/bromethalin.1988.full.pdf
Proceedings
of the Thirteenth Vertebrate Pest Conference 1988;13:64-69.
Status
of bromethalin outside the United States.
Spaulding,
S.R. (a) and H. Spannring (b)
(a)
Ciba-Geigy Animal Health/Hygiene, Basel, Switzerland
(b) Ciba-Geigy Agricultural Research Centre, St. Aubin, Switzerland
Bromethalin
has been extensively researched over the past decade in the
United States, Switzerland, England, Denmark, and France.
United States EPA registrations were received in 1982 and
commercial pelleted formulations containing 0.01% bromethalin
were developed and introduced in the USA by Ralston Purina
(ASSAULT) in 1985 and Velsicol (VENGEANCE) in 1986. Ciba-Geigy
is currently developing new formulations under the tradename
DORATID® for use outside the United States. Bromethalin
acute toxicity and 14-day subchronic studies are reviewed
and data from recently completed 90-day subchronic studies
required for registration outside the US are presented. Pharmacodyamic
studies have shown that bromethalin acts as an uncoupler of
oxidative phosphorylation, thus interrupting the vital production
of ATP necessary to maintain essential metabolic functions.
Laboratory and field trial data are presented from Switzerland,
France, England, and Denmark that indicate the effectiveness
of new bromethalin formulations against anticoagulant resistant
and susceptible rodents. A comparative rodenticide pen testing
system is described from which test results confirm bromethalin's
quick action and feed consumption efficiency when compared
to second-generation anticoagulants.
Excerpt:
The search for a novel rodenticide with a mode of action different
from anticoagulants began in the mid-1970s when leads from
a fungicide screening program at Lilly Research Laboratories
indicated the rodenticidal potential of a group of compounds
classified as dipheylamines. After several years of screening
and structure-activity relation tests, bromethalin was identified
as the compound with the greatest biological potential. At
the 1979 British Crop Protection Conference, Dreikorn (1979)
presented the first biological results from laboratory tests
with white rats and mice...
Marketing rights were subsequently licensed by Eli Lilly to
Ralston Purina and Velsicol in the United States and Ciba-Geigy
for all countries outside the United States...
American
Chemical Society. 1984, 45-63.
The
Discovery and Development of Bromethalin, an Acute Rodenticide
with a Unique Mode of Action.
Dreikom,B.,O'Dorherty,
GO.
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6666021&dopt=Abstract
Vet Med
Nauki 1983;20(8):72-80
[Toxic
action and
deratization effect of acute rodenticide]
[Article
in Bulgarian]
Kesiakova
S, Nikiforov I.
Tested
was the toxic action and the deratization effect of the new
acutely acting rodenticide EL614
[bromethalin] recently introduced into deratization
practice. The experiments were carried out with laboratory
rats and pigs as well as with the rats found in a swine breeding
complex. Studied were the morphologic and histopathologic
changes in the internal organs of rats that had swallowed
baits carrying the preparation in various concentration. It
was found that LD50 for rats up to the 24th hour after swallowing
the poison was 4.13 mg/kg, and it was 1.78 mg/kg at the 48t
hour, and 1.32 mg/kg at the 72nd hour. Intoxication and death
set in as the result of impaired function of almost all organs,
which was explained by the lipidotropic action of the preparation.
Particularly severe were the lesions (hemodynamic and degenerative)
in the brain. In field trials the baits contained EL614
in concentration of 0.005 per cent, showed a low deratization
effect the first day after setting them. In this case the
effect could be explained by the stress developing among the
rodent population. The same baits in amounts surpassing 300-400
g caused intoxication and death in pigs of 20 kg live weight.
PMID:
6666021 [PubMed - indexed for MEDLINE]
Proc. Vertebr.
Pest Conf. 1982;10:10-16.
Bromethalin
- a promising new rodenticide.
Jackson,
W.B., S.R. Spaulding, R.B.L. van Lier, and B.A. Dreikorn.
Unpubl. report
submitted to EPA by Eli Lilly Co. 1981.
A
secondary toxicity study in beagle dogs maintained for two
weeks on diets derived from bromethalin
(EL-614, Compound 126814) treated rodents.
van
Lier, R.B.L.
| Bromethalin
Bibiography Citation [p 163-164] in US EPA Reregistration
Eligibility Decision (RED) Rodenticide Cluster.
EPA738-R-98-007. July 1998. |
| MRID
* |
Study |
Citation
to study in RED |
| |
(Unpublished
study received Oct 29,
1981 under 1471-121; submitted
by Elanco Products Co., Div.
of Eli Lilly and Co., Indianapolis, Ind.; CDL: 246173-M)
|
- |
| 42733503
|
Holmes,
C.; Swigert, J. (1993)
Bromethalin: A 48-Hour Flow-Through Acute Toxicity Test with
the Cladoceran (Daphnia magna): Final Report: Lab Project
Number: 199A-101. Unpublished study prepared by Wildlife
International Ltd. 46 p. |
Acute
Toxicity to Freshwater Invertebrates p 66
Ecological Effects, Invertebrate Toxicity, p 147 |
| 00026524
|
Van Lier,
R.B.L.; Arthur, B.H.; Ansley, A.D.; et al. (1979)
Acute Hazard Evaluation of Compound
126714 Including Dermal, Ocular, and Inhalation Testing:
Study Nos. B-D-59-77, B-D-74-77, B-E-75-77, R-H-50-77, R-H-52-77,
R-H-53-77, R-H-58-77, R-H-59-77, R-H-64-77. (Unpublished study
received Dec 13, 1979 under 1471-EX-72; submitted by
Elanco Products Co., Div. of Eli Lily and Co., Indianapolis,
Ind.; CDL:241521-G) |
Toxicology:
p 148
Acute Oral Toxicity - Rat;
Acute Dermal Toxicity - Rabbit/Ratp;
Acute Inhalation Toxicity - Rat;
Primary Eye Irritation - Rabbit;
Primary Dermal Irritation - Rabbit; |
| 41653001
|
Rock,
G.; Sites, D.; Van Lier, R. (1990)
A Guinea Pig Sensitization Study with
Bromethalin (Compound 12671): Lab Project Number: GOO390.
Unpublished study prepared by Lilly
Research Labs. 39 p. |
Acute
Toxicity Values of Technical Bromethalin - Dermal Sensitization;
p 14
Toxicology
Dermal Sensitization - Guinea Pig, p 148. |
| 00101543 |
Cochrane,
R.; Kehr, C.; Van Lier, R.; et al. (1982)
The Toxicity of Bromethalin (EL-614,
Compound 126714) to Hen Chickens in a 24-day Acute Oral Delayed
Neurotoxicity Study: Study A00981. (Unpublished study
received Apr 29, 1982 under 1471-121; submitted by Elanco
Products Co., Div. of Eli Lilly and Co., Indianapolis,
IN; CDL:247447-B) |
An
acute delayed neurotoxicity study was conducted in the hen.
White rock strain hen (30 animals) were initially dosed
with bromethalin in PEG-400 at 9 mg/kg and redosed on day
3 with 15 mg/kg. Observation was for 24 days. Bromethalin
did not produce acute delayed neurotoxicity in the hen.
p 14
Toxicology
Acute Delayed Neurotoxicity - Hen, p 148
|
| 43582102
|
Monnot,
G. (1987) 13-Week
Oral Toxicity Study in the Rat: Bromethalin (CGA 175156):
Lab Project Number: 610209: 601326-D. Unpublished study prepared
by Hazleton-Institut Francais de Toxicologie.
277 p. |
Bromethalin
Subchronic Toxicity, p 22
Sprague Dawley rats (10/sex/group) received daily gavage
doses of 0 (25% polyethylene glycol in H O), 5, 25, or 125
micrograms/kg/day (ug/kg/day) of bromethalin technical for
13 2 weeks. Parameters evaluated included daily observation,
weekly body weight and food consumption, ophthalmoscopy,
clinical pathology, necropsy, organ weights, and histopathology.
The NOEL is 25 µg/kg/day. The LOEL
is 125 µg/kg/day, based on spongy degeneration (leukoencephalomyelopathy)
observed in most of the central white fiber tracts of the
brain, cerebellum, pons, brain stem, and thoracic spinal
cord of both sexes and optic nerves of males. There
were no effects on mortality, clinical chemistry, ophthalmoscopy,
body weight, food consumption, clinical pathology and histopathology
of other tissues.
Toxicology
- 90-Day Feeding - Rodent, p 148 |
| 43582101
|
Monnot,
G. (1987) 13-Week
Oral Toxicity Study in the Beagle Dog: Bromethalin (CGA 175156):
Lab Project Number: 610203: 601325-D. Unpublished study prepared
by Hazleton-Institut Francais de Toxicologie.
273 p. |
Bromethalin
Subchronic Toxicity
In a second 90-day study, groups of 4 male and 4 female
beagle dogs were orally dosed by gavage for 90 days at levels
of 0, 5, 25, 125, or 200 ug/kg/day with bromethalin technical.
Observations included daily clinical evaluations, ophthalmoscopy,
body weight, food consumption, clinical pathology evaluations
at weeks 6 and 13, necropsy, organ weights and histopathology.
The NOEL is 25 µg/kg/day. The LOEL
is 125 µg/kg/day based on spongy degeneration observed in
nervous tissue components (cervical, thoracic, and lumbar
spinal cord, brain stem, right and left optic nerves, frontal
and median brain, pons, and cerebellum) in both sexes of
dogs. At the high dose, 3 male dogs displayed the
following neurotoxic signs before death or being sacrificed
moribund: salivation and hypoactivity, followed by trembling,
myoclonia, hyperesthesia, groaning, and decubitus.
Other measured parameters were considered comparable between
control and treated dogs of both sexes. The above two subchronic
toxicity studies in rats and beagle dogs are not guideline-type
subchronic neurotoxicity studies. However, these studies
will satisfy the data requirements for a 90-day neurotoxicity
screening battery because a NOEL and a LOEL was established
in both studies. p 22-23
Toxicology,
p 148
90-Day Feeding - Non-rodent;
90-Day Neurotoxicity - Mammal |
| 42793101
|
Ponnock,
K. (1993)
An Acute Neurotoxicity Study of Bromethalin in the Rat Via
Oral Gavage Administration: Lab Project Number: 92-3807.
Unpublished study prepared by Bio/dynamics,
Inc. 334 p. |
Acute
Toxicity, p 15
An acute neurotoxicity study was conducted in rats. Male
and female Sprague-Dawley CD rats were orally gavaged with
bromethalin in mineral oil at doses of 0, 0.8, 1.5 or 3
mg/kg. The NOEL was greater than 3 mg/kg (HDT) and the LOEL
was not determined in this study. Although this study was
classified as unacceptable, the study can be upgraded if
the registrant can provide the following data: the rationale
of vehicle choice and volume used, the stability of test
material in mineral oil, the rationale for choice of testing
time on dosing day, and body temperature measurements. Body
temperature is a measurement that should have been taken,
given the mechanism of action of bromethalin
(uncoupler of oxidative phosphorylation) (MRID 42793101).
However, a new study will not be required since adequate
information is available to determine an acute NOEL for
bromethalin neurotoxicity. p 15
Toxicology,
p 148 - 90-Day Neurotoxicity - Mammal |
| 00086731 |
Miller,
B.J.; Van Lier, R.B.L.; Owen, N.V.; et al. (1981)
A Teratology Study with Bromethalin
(EL-614, 126714) in the Wistar Rat: Study R02181. (Unpublished
study received Oct 29, 1981 under 1471-121; submitted by Elanco
Products Co., Div. of Eli Lilly and Co., Indianapolis,
Ind.; CDL:246172-I) |
Developmental
Toxicity, p 30-31
A developmental
toxicity study was conducted with Harlan Wistar rats (25
rats/group). Rats were orally gavaged on gestation days
6 through 15 at a dosing volume of 5 ml/kg with 0 (vehicle,
PEG-200), 0.1, 0.3, or 0.5 mg/kg/day bromethalin technical.
Surviving dams were sacrificed on gestation day 20, necropsied
and reproductive findings were recorded. The
NOEL for developmental toxicity is 0.5 mg/kg/day (HDT).
There were no compound-related external, visceral or skeletal
effects in bromethalin-treated fetuses in comparison to
controls on either a litter or fetal basis.
The
NOEL for maternal toxicity is 0.3 mg/kg/day and the LOEL
is 0.5 mg/kg/day. Several effects occurred at the 0.5 mg/kg/day
including four deaths during gestation (gestation days 12,
16, 17, and 17). Three high-dose females revealed upper
respiratory tract infections which was regarded as secondary
due to physiological stress from treatment. Additionally,
in 10 of the 25 high-dose females, including the four which
died, clinical signs consisting of hind leg weakness and
decreased muscle tone were seen. Other
observations included poor grooming, weakness, ventral soiling,
chromodacryorrhea, decreased respiration, labored respiration,
hypothermia, hind leg paralysis, prostration and dehydration.
During
the dosing period, high-dose dams
had a 30.2% decrease in weight gain in comparison to controls.
During the post dosing period, weight gain in the high-dose
females was decreased by only 11.7% in comparison to controls.
Due to the substantial decreased weight gain during the
dosing period, the high-dose females experienced a 13.9%
decrease in weight gain for the entire gestation period
in comparison to controls. These decreased weight gains
are considered to be treatment-related. Food consumption
was decreased by 8.7% in high-dose animals in the post dosing
period in comparison to controls. The observed decrease
in weight gain during the post dosing period may be because
of decreased food consumption. The food consumption was
comparable between controls and treated groups, including
the high-dose group at other times.
Toxicology,
p 148 - Developmental Toxicity - Rabbit |
*
MRID = Master Record Identification (number).
US EPA's system of recording and tracking studies submitted. |
Bromethalin
Bibliography (p 162) for
US EPA. Reregistration
Eligibility Decision (RED) Rodenticide Cluster. EPA738-R-98-007.
July 1998. |
| MRID
* |
- |
| 42333401 |
Rose,
J. (1992) Product
Identity and Disclosure of Ingredients; Description of Beginning
Materials and Manufacturing Process: Bromethalin. Unpublished
study prepared by Purina Mills, Inc.
55 p. |
| 42403001 |
Rose,
J. (1992) Product
Identity and Disclosure of Ingredients and Discussion of the
Formation of Impurities: Bromethalin. Unpublished study
prepared by Purina Mills, Inc.
15 p. |
| 42333401
|
Rose,
J. (1992) Product
Identity and Disclosure of Ingredients; Description of Beginning
Materials and Manufacturing Process: Bromethalin. Unpublished
study prepared by Purina Mills, Inc.
55 p. |
| 42403001
|
Rose,
J. (1992) Product
Identity and Disclosure of Ingredients and Discussion of the
Formation of Impurities: Bromethalin. Unpublished study
prepared by Purina Mills, Inc.
15 p. |
| 00086718
|
Koenig,
D.K.; Loh, A.; Wilson, J.T.; et al. (1981)
Test Article Characterization of Bromethalin:
Technical Lot B31-72C-18R. (Unpublished study received
Oct 29, 1981 under 1471-121; submitted by Elanco
Products Co., Div. of Eli Lilly and Co., Indianapolis,
Ind.; CDL:246169-F) |
| 41599601
|
Davis,
M. (1990) Physical
Characterization of Bromethalin: Final Report: Lab
Project Number: SC900029.
Unpublished study prepared by Battelle.
13 p. |
| 41599603
|
Davis,
M. (1990) Determination
of the n-Octanol/Water Partition Coefficient of Bromethalin:
Lab Project Number: SC900030. Unpublished study prepared by
Battelle. 35 p. |
| 00086741
|
Cochrane,
R.L.; Kehr, C.C.; Van Lier, R.B.L.; et al. (1981)
The Toxicity of Bromethalin (EL-614,
Compound 126714) to Bobwhite in a 14-day Acute Oral Study:
Study A008-80. (Unpublished study received Oct 29, 1981 under
1471-121; submitted by Elanco Products
Co., Div. of Eli Lilly and Co., Indianapolis, Ind.;
CDL: 246173-C) |
| 00086745 |
Kehr,
C.C.; Van Lier, R.B.L.; Jordan, W.H.; et al. (1981)
The Toxicity of Bromethalin (EL-614,
Compound 126714) to Bobwhite in a Five-day Dietary Study:
Study A007-80. (Unpublished study received Oct 29, 1981 under
1471-121; submitted by Elanco Products
Co., Div. of Eli Lilly and Co., Indianapolis, Ind.;
CDL: 246173-G) |
| 42733501
|
Conner,
B.; Holmes, C.; Swigert, J. (1993)
Bromethalin: A 96-Hour Flow-Through
Acute Toxicity Test with the Bluegill (Lepomis macrochirus):
Final Report: Lab Project Number: 199A-102. Unpublished study
prepared by Wildlife International Ltd.
43 p. |
| 42733502
|
Conner,
B.; Holmes, C.; Swigert, J. (1993)
Bromethalin: A 96-Hour Flow-Through
Acute Toxicity Test with the Rainbow Trout (Oncorhynchus
mykiss): Final Report: Lab Project Number: 199A-103. Unpublished
study prepared by Wildlife International
Ltd. 45 p. |
| 00086751
|
Kehr,
C.C.; Van Lier, R.B.L.; Brannon, D.R.; et al. (1981)
The Toxicity of Bromethalin (EL-614,
Compound 126714) to Bluegills in a 96-hour Static Test:
Study F151-80. (Unpublished study
received Oct 29, 1981
under 1471-121; submitted by Elanco
Products Co., Div. of Eli Lilly and Co., Indianapolis,
Ind.; CDL: 246173-M) |
*
MRID = Master Record Identification (number).
US EPA's system of recording and tracking studies submitted. |
Return
to Bromethalin Index page
|
