The
use of high doses increases the likelihood that potentially
significant toxic effects will be identified. Findings of
adverse effects in any one species do not necessarily indicate
such effects might be generated in humans. From a conservative
risk assessment perspective however, adverse findings in
animal species are assumed to represent potential effects
in humans, unless convincing evidence of species specificity
is available.
--
Food and Agricultural Organization of the United Nations
|
Note:
This is not an exhaustive list.
When time allows more information will be added.
Bifenthrin
- Acaracide, Insecticide - CAS Numbers:
82657-04-3 (Cis); 83322-02-5 (Trans)
A chronic/carcinogenicity
study in mice
fed at doses of 0, 50, 200, 500, or 600 ppm (0, 2.5, 10, 25, or
30 mg/kg/day) in the diet for 87 weeks (males) or 92 weeks (females).
Chronic LOEL is 10 mg/kg/day based on the incidence of tremors
in both sexes. Chronic NOEL is 2.5 mg/kg/day. Carcinogenic potential
was evidenced by a statistically significant increased trend for
hemangiopericytomas in the urinary bladders
of males, a significant dose-related trend for combined
hepatocellular adenomas and carcinomas in males, and a significantly
higher incidence of combined lung adenomas and carcinomas in females.
Carcinogenicity. Using its Guidelines for Carcinogen Risk Assessment
published September 24, 1986 (51 FR 33992) the Carcinogenicity
Peer Review Committee (CPRC) has classified bifenthrin as a Group
C chemical, possible human carcinogen, based
on urinary bladder tumors in mice, but did not recommend
assignment of a cancer potency factor Q* (Q star) for a linear
quantitative cancer risk assessment, instead, the CPRC recommended
the RfD approach. Based on CPRC's recommendation that the RfD
approach be used to assess dietary cancer risk, a quantitative
linear dietary cancer risk assessment was not performed. Human
health risk concerns due to long term consumption of bifenthrin
residues are adequately addressed by the dietary risk evaluation
chronic exposure analysis using the RfD.
Ref: Federal Register: November 26, 1997.
Bifenthrin; Pesticide Tolerances. Final Rule.
http://www.fluoridealert.org/pesticides/bifenthrin.fr.nov.1997.htm
Abstract: Bifenthrin,
a synthetic pyrethroid insecticide/miticide, has been fed to male
and female Swiss Webster mice at levels of 0, 50, 200, 500, and
600 ppm in the diet for between 604 and 644 days. Tumors of the
urinary bladder were observed and initially reported as leiomyosarcomas.
Subsequently, the bladders were reviewed and the tumors showed
a pattern of both epithelioid cells and spindle cells forming
irregular vascular channels. The tumors appeared to arise from
the trigone of the bladder and, in some cases, invaded the bladder
wall. No metastases were recorded. The tumor
is usually considered rare; however, in this study, it was commonly
observed in all groups but predominantly in males.
The histogenesis of the tumor is uncertain, but from its pleomorphic
histological features, including smooth muscle and vascularity,
it is probably derived from vascular mesenchyme.
Ref: Mesenchymal
tumors of the mouse urinary bladder with vascular and smooth muscle
differentiation; by Butler WH, Cohen SH, Squire RA. Toxicol Pathol.
1997 May-Jun;25(3):268-74.
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9210258&dopt=Abstract
... In a rat teratology
study, an increased incidence of hydroureter
(without hydronephrosis) was noted in fetuses at 2 mg/kg/day
(LOEL). The NOEL was 1 mg/kg/day. EPA believes that there is sufficient
evidence for listing bifenthrin on EPCRA section 313 pursuant
to EPCRA section 313(d)(2)(B) based on the available neurological
and developmental toxicity data.
Ref:
USEPA/OPP. Support Document for the Addition of Chemicals from
Federal Insecticide, Fungicide, Rodenticide Act (FIFRA) Active
Ingredients to EPCRA Section 313. U. S. Environmental Protection
Agency, Washington, DC (1993). As cited by US EPA in: Federal
Register: January 12, 1994. Part IV. 40 CFR Part 372. Addition
of Certain Chemicals; Toxic Chemical Release Reporting; Community
Right-to-Know; Proposed Rule.
Clodinafop-propargyl
-
Herbicide - CAS No. 105512-06-9
Study # 870.3700a.
Prenatal Developmental Toxicity in Rats. Maternal NOAEL = 160
mg/kg/day Maternal LOAEL > 160 mg/kg/day based on lack of effect.
Developmental NOAEL = 5 mg/kg/day Developmental LOAEL = 40 mg/kg/day
based on increased incidences of bilateral
distension and torsion of the ureters,
unilateral 14th ribs, and incomplete ossification
of the metacarpals and various cranial bones (parietals, interparietals,
occipital, and squamosal).
Ref: US EPA Pesticide Fact Sheet. Reason
for Issuance: Conditional Registration. June 6, 2000.
http://www.epa.gov/opprd001/factsheets/clodinafop.pdf
Ethalfluralin
- Herbicide - CAS No. 55283-68-6
Group
C -- Possible Human Carcinogen.
Mammary tumors (F); Suggestion of
bladder tumors (F) and kidney
tumors (M & F); Fischer 344 rats.
Ref: April
26, 2006 . Chemicals Evaluated for Carcinogenic Potential by the
Office of Pesticide Programs. From: Jess Rowland, Chief Science
Information Management Branch Health Effect Division (7509C) Office
of Pesticide Programs, USEPA.
http://www.fluorideaction.org/pesticides/pesticides.cancer.potential.2006.pdf
Flumequine
- Microbiocide - CAS No. 42835-25-6
-- PubMed Abstract:
In order to elucidate the tumor-initiating potential of flumequine
(FL) in the liver, male C3H mice were given dietary administration
of 4000 ppm FL throughout the study or for 2 weeks at the initiation
stage, and then received 2 intraperitoneal injections of D-galactosamine
(Gal) at weeks 2 and 5, with or without 500 ppm phenobarbital
(PB) in their drinking water for 13 weeks to provide tumor-promoting
effects. Hepatocellular foci were observed in 2 out of 8 and 6
out of 7 animals in the FL/PB + Gal and FL/FL + Gal groups, respectively.
In addition, in an alkaline single-cell gel electrophoresis (comet)
assay that was performed using adult, infant, or partial hepatectomized
male ddY mice to evaluate the potential of FL at 500 mg/kg or
less, to act as a DNA damaging agent.
FL induced dose-dependent DNA damage in the stomach,
colon, and urinary bladder of adult mice at 3 h but
not at 24 h after its administration. Similarly, DNA damage was
noted in the regenerating liver and the livers of infant mice
at the 3 h time point. Furthermore, in in vitro assays that were
conducted to investigate the potential of FL to inhibit
eukaryotic topoisomerase II, which is responsible for the double-strand
DNA breakage reaction as well as bacterial gyrase, inhibitory
effects of FL on topoisomerase II were high relative to the influence
on bacterial gyrase. The results of our
studies thus strongly suggest that FL has initiating potential
in the livers of mice that is attributable to its induction of
DNA strand breaks.
Ref:
Toxicol Sci 2002 Oct;69(2):317-21; Mechanistic study on flumequine
hepatocarcinogenicity focusing on DNA damage in mice; Y Kashida
et al.
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12377980&dopt=Abstract
Fluorouracil
- Former
insect Chemosterilant; now used as a pharmaceutical -
CAS No. 51-21-8
POTENTIAL
ADVERSE EFFECTS ON FETUS: Exposure in first trimester resulted
in skeletal abnormalities; hypoplasia of aorta, lungs,
thymus, and gastrointestinal tract; and
urinary tract abnormalities. Fetus exposed in third trimester
had cyanosis and clonus.
Ref:
TOXNET profile from Hazardous Substances Data Base.
http://www.fluoridealert.org/pesticides/fluorouracil.toxnet.hsdb.htm
Fluoxastrobin
- Fungicide - CAS No. 193740-76-0
-- Subchronic toxicity.
A subchronic toxicity feeding study with rats over 90 days demonstrated
a NOAEL of 7.3 and 18.3 mg/kg bwt/day for males and females, respectively,
based on reduced body weights and alterations
in several urinary tract-related clinical
chemistry parameters, at the higher dose levels...
Ref: Federal Register: April 23, 2003. Fluoxastrobin;
Notice of Filing a Pesticide Petition to Establish a Tolerance
for a Certain Pesticide Chemical in or on Food.
http://www.fluoridealert.org/pesticides/fluoxastrobin.fr.apr23.2003.htm
--
90-Day oral toxicity-rats. reduced
body weight gain and food intake, vacuolation in the zona fasciculate
of the adrenal cortex,
calculi in the urethra and kidney,
and histological lesions in kidney, urinary
bladder, and urethra.
Ref: Federal Register. September 16, 2005.
Fluoxastrobin; Pesticide Tolerances. Final Rule.
http://www.fluorideaction.org/pesticides/fluoxastrobin.fr.sept16.05.html
Flurprimidol
- Plant Growth Regulator - CAS No. 56425-91-3
A rat teratology study
using doses of 0, 2.5, 10, 45 or 200 mg/kg/day of flurprimidol
had a maternal toxicity NOEL of 10 mg/kg/day and a LEL of 45 mg/kg/day
based on decreased body weight gain and
food consumption. The developmental NOEL was 10 mg/kg/day and
the LEL was 45 mg/kg/day based on decreased fetal weight, increased
incidence of hydronephrosis, hydroureter
and numerous developmental
skeletal anomalies.
Ref: US EPA Pesticide Fact Sheet. February
22, 1989.
http://www.fluoridealert.org/pesticides/flurprimidol.epa.facts.1989.htm
Flusilazol
/ Flusilazole - Fungicide - CAS No. 85509-19-9
--The chronic toxicity/carcinogenicity studies in the rat, the
target organs identified were consistent with the sub-chronic
administration studies, i.e., liver and bladder. Flusilazole
was found to be oncogenic at the higher doses, causing bladder
transitional cell neoplasia in both sexes and testicular
Leydig cell adenoma in males. There is evidence
of a proliferative effect of flusilazole in the bladder transitional
epithelium, which is likely the mechanism of tumorigenesis. Therefore,
the urinary bladder tumors are considered to be caused by an epigenetic,
threshold-associated mechanism. Interference of flusilazole
with hypothalmic- pituitary-gonadal (HPG) axis is suggested as
a possible mechanism of testicular tumor induction. Evidence in
support of this theory was provided by a comparative study with
the aromatase inhibitor, ketoconazole. Flusilazole did cause a
slight reduction in both serum and testicular - testosterone and
a dose-dependent decrease in serum estradiol, but was far less
potent than ketoconazole. It would avoear reasonable to conclude
that a threshold exists for the induction by flusilazole of testicular
aienomas. The NOEL for neoplasms was 375 ppm (14.8 and 20.5 mg/kg/day
in males and females, respectively). (Page
29)
-- In mouse chronic studies, the target
organs were the liver, kidney, urinary
bladder and urethra. The incidence of hepatocellular adenomas
was increased at L 1000 ppm. Based on the combined results of
two studies, the NOEL for oncogenicity in mice is 200 ppm (36
mgrkglday) in females and 500 ppm (73.1 mg/kg/day) for males.
Since tumors occurred in excess of the MTD, and were preceded
at lower doses by histopathological change consistent with induction-related
hepatotoxicity, it is reasonable to conclude
that the induction of such tumors is related to cytotoxicity,
which demonstrates a clear threshold. (Pages
29-30)
-- Flusilazole was found to exert a clear
systemic toxicity on sub-chronic and chronic administration to
rats, mice and dogs. A similar pattern of effects was apparent
across the three species, with the liver,
urinary system and blood system targeted to varying degrees.
It was found to be oncogenic at high dose levels in both
mice and rats, inducing bladder transitional cell neoplasia in
rats and testicular adenoma in male rats and hepatocellular
adenomas and carcinomas in mice. (Page
30)
Ref: DuPont Punch (Active ingredient: Flusilazole) and DuPont
Charisma (Active ingredients: Flusilazole and Famoxadone): Summary
of data compiled in support of a Section 18 Emergency Exemption
request for control of Asian soybean rust on soybeans. By DuPont
authors: Cosgrove T, Czochor L, Dinter A, Jemberg K, Klemens A,
Marcon A, McInnes B, Mullin L, Russell M, Ryan D, Singles S, Vanderbroeck
V. Revision No. 1: February 2, 2005.
http://www.fluorideaction.org/pesticides/flusilazole.appendix1.pdf
-- 2-Year Feeding (oncogenic)
- mouse: Systemic NOEL=3.4 mg/kg/day; Systemic LEL=27 mg/kg/day
(increased absolute and relative liver weight
and increased hepatocellular fatty change in male and females);
core grade supplementary (E.I. du Pont de Nemours & Co., Inc.,
1985d)
-- 90-Day Feeding - rat: NOEL=125
ppm (6.25 mg/kg/day); LEL=375 ppm (18.75 mg/kg/day) (bladder
hyperplasia, elevated cholesterol);
core grade minimum (E.I. du Pont de Nemours & Co., Inc.,
1983a)
-- 90-Day Feeding - dog: NOEL=25
ppm (0.625 mg/kg/day); LEL=125 ppm (3.13 mg/kg/day) (bladder
hyperplasia, elevated alanine aminotransferase/serum glutamate
pyruvate transaminase, uric acid, decreased total protein Ca albumen,
cholesterol, increased liver weight); core
grade minimum (E.I. du Pont de Nemours & Co., Inc., 1983b)
Ref: US EPA IRIS. NuStar CASRN: 85509-19-9.
Available October 6, 2003, at Toxnet.
Haloxyfop-etotyl
- Herbicide - CAS No. 87237-48-7
Reproductive Effects:
In rats, oral doses of 10 and 50 mg/kg/day
of haloxyfop-ethoxyethyl from days 6 to 16 of pregnancy reduced
the number of live offspring per litter and caused vaginal bleeding
in the mother (5). Teratogenic Effects: Oral doses of 50 mg/kg/day
of haloxyfop-ethoxyethyl in rats between days 6 and 16
of pregnancy caused developmental abnormalities
in the offspring's urogenital system and death to the fetus
(5). Oral doses of 7.5 mg/kg/day of haloxyfop-methyl given to
rats from days 6 to 15 of pregnancy caused delayed bone formation
in the offspring (6).
Ref: EXTOXNET Pesticide Information Profile
http://pmep.cce.cornell.edu/profiles/extoxnet/haloxyfop-methylparathion/haloxyfop-ext.html
Penoxsulam
- Herbicide - CAS No. 219714-96-2
-- Subchronic toxicity.
Dietary exposure to penoxsulam identified the
liver
and/or urinary tract (kidneys and
bladder) as target organs in rats, mice, and dogs following
a 4-week and 13-week administration. Effects on the liver were
reflected in increased liver weights and
hepatocellular hypertrophy, but these effects were not associated
with increases in mixed function oxidase (MFO) enzyme activity.
Effects noted in the kidneys included crystal deposition, most
likely from precipitation of penoxsulam from the urine, with resultant
irritation, inflammation, and hyperplasia of renal pelvic transitional
epithelium. Other than the crystal deposition in the kidneys,
all effects following subchronic exposure to rats appeared
to be reversible. Very high doses were associated with significant
decreases in body weight, weight gain, and feed consumption.
-- Chronic toxicity. Chronic exposure in the dog indicated that
the renal effects were not exacerbated with long-term exposure.
Following long-term exposure in rats, the
kidneys and urinary bladder were
the primary target organs. Histologic changes seen at the
end of 2 years of exposure consisted of inflammation and hyperplasia
of the renal pelvic transitional epithelium,
crystal deposition in the kidneys
and urinary bladder, and hyperplasia of the mucosa of the urinary
bladder...
Ref: August 6, 2003. Federal Register: August
6, 2003 (Volume 68, Number 151)] [Notices] [Page 46609-46613].
Penoxsulam; Notice of Filing a Pesticide Petition To Establish
a Tolerance for a Certain Pesticide Chemical in or on Food.
http://www.fluorideaction.org/pesticides/penoxsulam.fr.aug.6.2003.htm
••
See also page 15:
June 18, 2007 - Penoxsulam.
Human Health Risk Assessment for Proposed Uses on Fish and Shellfish.
Docket: EPA-HQ-OPP-2006-0076-0004. USEPA.
http://www.fluorideaction.org/pesticides/EPA-HQ-OPP-2006-0076-0004.pdf
In subchronic and chronic feeding studies
in rats and dogs, the most sensitive target organ was the urothelium
of the urinary system. Due to limited solubility in urine,
penoxsulam (and/or its metabolites) formed
crystals/calculi, which were regularly observed in the pelvis
of the kidney and the lumen of the urinary bladder. These crystals/calculi
apparently irritated the urothelium in these organs and following
repeated dosing lead to numerous secondary effects which resulted
in significant damage to the urinary system. In various
studies, these secondary effects were manifested as altered clinical
chemistry parameters (increased blood urea nitrogen), altered
urinalyses parameters (increased urine volume, decreased urine
specific gravity), increased absolute and relative kidney weights,
gross pathological findings in the kidneys (calculi and roughened
surface), and a variety of histopathological findings in the kidney
and urinary bladder, particularly hyperplasia, inflammation and
mineralization in the pelvic epithelium of the kidney and hyperplasia
in the mucosa of the urinary bladder.
Reference: September 2004. US EPA Fact Sheet
on Penoxsulam. Page 4.
http://www.fluorideaction.org/pesticides/penoxsulam.epa.fact.sheet.2004.pdf
PFOS - PFOA
- Insecticide, EPA List 3 Inert
The toxicity profile
of PFOS is similar among rats and monkeys. Repeated exposure results
in hepatotoxicity and mortality; the dose-response curve is very
steep for mortality. This occurs in animals of all ages, although
the neonate may be more sensitive. In addition, a 2-year bioassay
in rats has shown that exposure to PFOS results in hepatocellular
adenomas and thyroid follicular cell adenomas; the hepatocellular
adenomas do not appear to be related to peroxisome proliferation.
Further work to elucidate the species differences in toxicokinetics
and in the mode of action of PFOS will increase our ability to
predict risk to humans. Epidemiologic studies
have shown an association of PFOS exposure and the incidence of
bladder cancer; further work is needed to understand this
association.
Ref:
November 21, 2002 report: Hazard Assessment of Perfluorooctane
sulfonate (PFOS) and its salts. Organisation for Economic Co-operation
and Development. ENV/JM/RD(2002)17/FINAL.
http://www.fluorideaction.org/pesticides/pfos.final.report.nov.2002.pdf
A retrospective cohort mortality study was performed on employees
at the Cottage Grove, MN
plant which produces APFO (Gilliland and Mandel,1993). At this
plant, APFO production was
limited to the Chemical Division.The cohort consisted of workers
who had been employed at the
plant for at least 6 months between January 1947 and December
1983. Death certificates of all of the workers were obtained to
determine cause of death. There was almost complete follow-up
(99.5%)of all of the study participants. ...
An update of this study was conducted to include the death experience
of employees through
1997 (Alexander,2001a). The cohort consisted of 3992 workers.
The eligibility requirement was
increased to 1 year of employment at the Cottage Grove plant,
and the exposure categories were
changed to be more specific. Workers were placed into 3 exposure
groups based on job history
information: definite PFOA exposure (n =492, jobs where cell generation,
drying, shipping and
packaging of PFOA occurred throughout the history of the plant);
probable PFOA exposure (n = 1685, other chemical division jobs
where exposure to PFOA was possible but with lower or
transient exposures); and not exposed to fluorochemicals (n =1815,primarily
non-chemical
division jobs). In this new cohort, 607 deaths were identified:
46 of these deaths were in the PFOA exposure group, 267 in the
probable exposure group, and 294 in the non-exposed group. When
all employees were compared to the state mortality rates, SMRs
were less than 1 or only slightly higher for all of the causes
of death analyzed. None of the SMRs were statistically significant
at p =.05. The highest SMR reported was
for bladder cancer (SMR =1.31,95%CI =0.42 – 3.05)).
Five deaths were observed (3.83 expected).
Ref:
April
10, 2003: Preliminary
Risk Assessment of the Developmental Toxicity associated with
Exposure to Perfluorooctanoic Acid and its Salts. US
EPA Office of Pollution Prevention and Toxics. 63 pages.
Sodium
fluorosilicate
(Sodium Hexafluorosilicate) - Insecticiide;
Wood Preservative; EPA List 3 Inert - CAS No. 16893-85-9
-- Mice orally given
sodium hexafluorosilicate (70 mg/kg; 0.37 mmol/kg) exhibited toxic
effects in the peripheral nerves, sensation, and in behavior.
In rats, an oral dose (248 mg/kg; 1.32 mmol/kg) administered intermittently
for one month produced toxic effects in the
kidney, ureter, and/or bladder,
as well as musculoskeletal and biochemical effects
(RTECS, 1997). Using guinea pigs, inhalation experiments (13-55
mg/m 3 [1.7-7.2 ppm] sodium hexafluorosilicate in air for ¥6 hours)
resulted in pulmonary irritation;
the lowest concentration that caused death was 33 mg/m 3 (4.3
ppm) (Patty, 1963; cited by HSDB, 2000b).
-- Rats, oral; 248 mg/ kg (1.32 mmol/ kg) for 30 days intermittent;
Toxic effects in the kidney, ureter,
and/ or bladder
(other changes in urine composition) were observed. Musculoskeletal
(other changes) and biochemical (enzyme inhibition, induction,
or changes in blood or tissue [phosphatases] levels) effects were
seen. RTECS* (1997)
-- Rats, 70 mg/ kg (LD Lo ; 0.37 mmol/ kg); Fatty liver degeneration
and other changes in the liver and toxic
effects in the kidney,
ureter, and bladder primarily changes in glomeruli were
observed. RTECS* (1997)
Ref: Review of Toxicological Literature.
October 2001. Sodium Hexafluorosilicate [CASRN 16893-85-9] and
Fluorosilicic Acid [CASRN 16961-83-4]. Prepared for Scott Masten,
Ph.D. National Institute of Environmental Health Sciences P.O.
Box 12233 Research Triangle Park, North Carolina 27709. Contract
No. N01-ES-65402. Submitted by Karen E. Haneke, M.S. (Principal
Investigator) Bonnie L. Carson, M.S. (Co-Principal Investigator)
Integrated Laboratory Systems P.O. Box 13501 Research Triangle
Park, North Carolina 27709.
http://www.fluoridealert.org/pesticides/fluorosilicates.nih.2001.pdf
Transfluthrin
- Insecticide - CAS
No. 118712-89-3
-- The target organs
were the liver (rat,
mouse and dog) and kidney
(rat). There was evidence of
liver hypertrophy in the rat from 250 mg kg d (28 study) and after
administration for 90 d at 500 ppm (equivalent to 40 mg kg d),
in the dog from 350 ppm (equivalent to 14 mg kg d) after 90 d
administration and from 30 ppm (equivalent to1 mg kg d) after
1 yr and in the mouse, from 1000 pppm (equivalent to 280 mg kg
d) after 2 yr administration. Increased kidney weights, proximal
tubule degeneration and regenertion and increases in protein in
the urine were observed in male rats from 50 ppm and in females
from 500 ppm. Similar pathological findings were seen after
2 yr dietary administration with focal hyperplasia
in the urinary bladder in both sexes at 2000 ppm in the
rat and hepatocyte hypertrophy at 1000 ppm in the mouse. In the
rat, increases in fluoride content of teeth
and bone were observed from 50 ppm in oral studies and
at 200 mg m3 following inhalation exposure in 90 d studies.
-- Carcinogenicity. There is an increased incidence of
urinary blader papillomas and carcinomas (at a very low
incidence) in males and females at 2000 ppm in mice
(females only) at 1000 ppm. Both types of tumour are considered
to arise via a non genotoxic mechanism. Studies
using rat hepatocytes showed that transfluthrin
does not cause cell proliferation but acts as a weak promotor
with a NOEL of 5 ppm.
Ref: Evaluation on: Transfluthrin Use as
a Public Hygiene Insecticide. September 1997. Prepared by: the
UK Health and Safety Executive, Biocides & Pesticides Assessment
Unit, Magdalen House, Stanley Precinct, Bootle, Merseyside L20
3QZ. Available from: Department for Environment, Food and Rural
Affairs, Pesticides Safety Directorate, Mallard House, Kings Pool,
3 Peasholme Green, York YO1 7PX. UK. Also at http://www.pesticides.gov.uk/citizen/evaluations/165_confirm-box.htm
• Note: This was transcribed
from the copy available on the web. While one can easily read
this report on the web, the report is inaccessible, or locked,
to any attempt to copy it. Any errors are mine. EC.
Trifloxysulfuron-sodium
- Herbicide - CAS No. 199119-58-9
Chronic toxicity dogs
NOAEL: 51.1/45.3 mg/kg/day (M/F) LOAEL: 123/121 mg/kg/day (M/F):
M = gray- white foci in lungs, fibrous thickening
of lung pleura, equivocal decreased body weight gain; F
= equivocal increased incidence and severity of
chronic urinary bladder inflammation.
Ref:
Federal Register: September 17, 2003 (Volume 68, Number 180)]
Rules and Regulations. Trifloxysulfuron; Pesticide Tolerance.
Final Rule.
http://www.fluorideaction.org/pesticides/trifloxysulfuron.fr.sept.03.htm
Trifluralin
- Herbicide - CAS No. 1582-09-8
Group
C -- Possible Human Carcinogen. Thyroid
(follicular celladenomas & carcinomas); Neoplasms of the renal
pelvis (M);
Benign urinary bladder tumors (F);
Fischer 344 rats.
Ref: April
26, 2006 . Chemicals Evaluated for Carcinogenic Potential by the
Office of Pesticide Programs. From: Jess Rowland, Chief Science
Information Management Branch Health Effect Division (7509C) Office
of Pesticide Programs, USEPA.
http://www.fluorideaction.org/pesticides/pesticides.cancer.potential.2006.pdf
Long term toxicity and carcinogenicity (Annex IIA, point 5.5).
Carcinogenicity. Evidence
of carcinogenic potential in Fischer 344 rat,
(tumour formation in various tissues, i.e.
kidney, urinary bladder, thyroid,
Leydig cell). The mechanism of tumour formation is not identified.
R40. (page 46)
Ref: March 14, 2005. European
Food Safety Authority: Conclusion regarding the
peer review of the pesticide risk assessment of the active substance
trifluralin. EFSA Scientific Report (2005) 28, 1-77.
http://www.fluoridealert.org/pesticides/trifluralin.eu.long.2005.pdf
EPA has classified
trifluralin as a Group C (possible human) carcinogen. Classification
is based on the induction of urinary tract
tumors (renal pelvis carcinomas and urinary
bladder papillomas) and thyroid tumors (adenomas/carcinomas
combined) in one rat study.
Ref: March 2000.
Public Health Assessment Cenex Supply and Marketing, Inc. Quincy,
Washington. CERCLIS # WAD058619255. Draft for Public Comment..
Prepared by: Washington State Department of Health Under Cooperative
Agreement with the Agency for Toxic Substances and Disease Registry.
Also available at
http://www.doh.wa.gov/ehp/oehas/Cenex%20PHA%20Draft%20Public%20Review.pdf
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