Prostate - Adverse Effects
Fluorinated and Fluoride Pesticides

A little background... The prostate is a gland of the male reproductive system. It is located in front of the rectum and just below the bladder, the organ that stores urine. The main purpose of the prostate is to produce fluid for semen, which transports sperm during the male orgasm. Ref:

The Endocrine System:

Illustration by K. Born in Our Stolen Future (1996)
by Theo Colborn, Dianne Dumanoski and JP Myers

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.

Clodinafop-propargyl - Herbicide - CAS No. 105512-06-9

Suggestive Evidence of Carcinogenic Potential. Prostate gland adenomas in male Tif:RAIf(SPF) rats at the high dose only cannot be discounted; Peroxisome Proliferator-Activated Receptor Agonism MOA for liver tumors in mice.
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.

-- Dietary treatment of rats with concentrations over 2 years resulted in initial inappetence in males and reduced body weight development in both sexes treated at 750 ppm. The main target organ of toxicity was the liver. Changes in plasma protein and lipid levels, strongly enhanced serum activities of liver enzymes, increased liver weights, and severe liver necroses were observed at dietary doses of 300 and 750 ppm in males and at 750 ppm in females. The degenerative lesions provide strong evidence that these dose levels exceeded a maximum tolerated dose (MTD). Top dose group males showed a higher incidence of prostate adenoma, while prostate hyperplasia was reduced. However, the total incidence of proliferative changes in the prostate remained unchanged indicating a progression from prostate hyperplasia to adenoma. Females treated at the same high dose had higher incidences of ovary tubular adenoma. The slightly enhanced incidences of these lesions are likely a consequence of the severe disturbance of the general metabolic balance due to excessive liver toxicity. In fact, male rats fed 750 ppm exhibited a marked increase in peroxisomal oxidation, and an increase in cytochrome P450 4A1/ A3 and 4A2 in their livers. Further, a decrease in cytochrome P450 isoenzymes including CYP 2A, CYP 3A, and male-specific CYP 2C11 was observed. The total oxidation rate of testosterone, aromatase (CYP 19A1) activity plasma estradiol concentration and plasma-- dihydrotestosterone are altered at this level of treatment. Clodinafop- propargyl is a potent peroxisome proliferator in the rat liver and this peroxisomal prolifering activity manifests itself by altering Cytochrome P450-dependent monooxygenses which are involved in steroid hormone homeostasis. The NOAEL of 10 ppm was equivalent to a mean daily dose of 0.32 mg/kg in males and 0.37 mg/kg in females. The EPA HIARC concluded that based on hepatocellular hypertrophy and kidney findings, the NOAEL was 1 ppm (0.031 in males and 0.034 in females...
8. Endocrine disruption. No special studies investigating potential estrogenic or endocrine effects of clodinafop-propargyl have been conducted. However, the standard battery of required studies has been completed. These studies include an evaluation of the potential effects on reproduction and development and an evaluation of the pathology of the endocrine organs following repeated or long-term exposure. Although prostate adenomas and ovarian adenomas were observed to be statistically increased in rats at the highest feeding level with clodinafop-propargyl, this feeding level clearly exceeded the MTD and the livers in these rats were severely compromised. These findings in the endocrine organs were considered to be secondary to the severe liver effects.
Ref: Federal Register: April 26, 2000 [Page 24471-24477]. Notice of Filing a Pesticide Petition to Establish a Tolerance for Certain Pesticide Chemicals in or on Food.

Etoxazole - Miticide, Ovicide - CAS No. 153233-91-1

Subchronic/Chronic Toxicity
-- 870.3150 90-Day Feeding Dog NOAEL = 5.33/5.42(M/F) LOAEL = 53.7/55.9 (M/F), based on clinical signs (vomiting foamy fluid and mucous stool), clinical chemistry, increased liver weights, and on centrilobular hepatocellular swelling in the liver and
acinar cell atrophy in the prostate.
Ref: US EPA Pesticide Fact Sheet. August 2002.

Fluazifop-P-butyl - Herbicide - CAS No. 79241-46-6

Reproductive Effects: In a 3-generation reproductive study in rats, effects included reductions in weight gain, fetal weight, ossification, testicular weight, spleen weight, increased prostate weight and gestational length. No Effect Level (NEL) was 1 mg/kg/day.
Target Organs: Liver, skin, kidney, eye, bone marrow, blood, reproductive system.
Ref: Material Safety Data Sheet for Fusilade DX (active indredient Fluazifop-P-Butyl). Syngenta. January 21, 2002.

PFOA - Insecticide, US EPA List 3 Inert

Perfluorooctanoic acid (PFOA) has been found at low levels (10 to 100 parts per billion) in sera of the general population and at higher levels in occupationally exposed workers. Although PFOA has been reported to be a promoter of rodent hepatocarcinogenesis and to alter reproductive hormones in humans and rodents, there is little information on human health effects associated with PFOA exposure. The present study examined the relationship between PFOA and mortality using a retrospective cohort mortality design. The cohort consisted of 2788 male and 749 female workers employed between 1947 and 1983 at a plant that produced PFOA. The all-causes standardized mortality ratio was .75 (95% confidence interval [CI], .56 to .99) for women and .77 (95% CI, .69 to .86) for men. Among men the cardiovascular standardized mortality rate was .68 (95% CI, .58 to .80) and the all-gastrointestinal diseases was .57 (95% CI, .29 to .99). There was no significantly increased cause-specific standardized mortality ratio for either men or women. Ten years of employment in exposed jobs was associated with a 3.3-fold increase (95% CI, 1.02 to 10.6) in prostate cancer mortality compared to no employment in PFOA production. There were only six prostate cancer deaths overall and four among the exposed workers; thus, the results must be interpreted cautiously. If prostate cancer mortality is related to PFOA, PFOA may increase prostate cancer mortality by altering reproductive hormones in male workers.
Ref: 1993. J Occup Med Sep;35(9):950-4. Mortality among employees of a perfluorooctanoic acid production plant; by Gilliland FD, Mandel JS.
Division of Environmental and Occupational Health, School of Public Health, University of Minnesota, Minneapolis.

Abstract excerpt: Perfluorooctanoate (PFOA) and perfluorooctane sulfonate (PFOS) are synthetic surfactants used in Japan. An epidemiological study of workers exposed to PFOA revealed a significant increase in prostate cancer mortality. A cross-sectional study of PFOA-exposed workers showed that PFOA perturbs sex hormone homeostasis. We analyzed their concentrations in surface water samples collected from all over Japan by LC/MS with a solid phase extraction method... Systematic searches of Yodo and Kanzaki Rivers revealed two highly contaminated sites, a public-water-disposal site for PFOA and an airport for PFOS. The former was estimated to release 18 kg of PFOA/d. PFOA in drinking water in Osaka city [40 (1.07) ng/L] was significantly higher than in other areas. The present study confirms that recognizable amounts of PFOA are released in the Osaka area and that people are exposed to PFOA through drinking water ingestion.
Ref: 2004. J Occup Health. Jan;46(1):49-59. Perfluorooctanoate and perfluorooctane sulfonate concentrations in surface water in Japan; by Saito N, Harada K, Inoue K, Sasaki K, Yoshinaga T, Koizumi A.

Sulfentrazone - Herbicide - CAS No. 122836-35-5

Reproduction and fertility effects (rat) Nonguideline - [870.3800] Parental/Systemic NOAEL = 20 mg/kg/day LOAEL = 51 mg/kg/ day (F1 females) based on decrease in pre-mating body weight gain (10%) Offspring and Reproductive NOAEL = 16 mg/kg/ day LOAEL = 40 mg/kg/ day based on reduced gestation day 20 fetal weights; decreased postnatal day 0, 4 and 7 pup weights; decreased pup survival; delayed vaginal patency; reduced epididymal, prostate, and testicular weights Additional information supports the conclusions reached in the 2- generation reproduction study in rats
Ref: Federal Register: September 24, 2003. Sulfentrazone; Pesticide Tolerances. Final Rule.

Tetraconazole - Fungicide - CAS No. 112281-77-3

Chronic & Carcinogenicity Studies. There were small and flaccid testes with reduced spermatogenesis, absence of spermatozoa in epididymides, and small and flaccid prostate and seminal vesicles with reduced secretion at 800 and 1250 ppm, and interstitial cell hyperplasia and prominent multinucleate spermatids in the testes at 1250 ppm. (page 5)
Ref: August 2005 - Evaluation of Tetraconazole in the product Domark 40ME Fungicide. Australian Pesticides and Veterinary Medicines Authority.

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