RSS feed
  • Sodium fluoride’s effect on the male reproductive system

    From fluoridealert.org

    Date Effects Study ATSDR (2003) response to studies
    2003

    Human population study

    3-27mg/day

    objective was to study reproductive parameters in a population exposed to fluoride at doses of 3-27 mg/day compared with a group of individuals exposed to fluoride at lower doses: 2-13 mg/day.
    A significant increase in FSH (P <0.05) and a reduction of inhibin-B, free testosterone, and prolactin in serum (P <0.05) were noticed in the high fluoride group. A significant negative partial correlation was observed between urinary fluoride and serum levels of inhibin-B (r = 0.333, P = 0.028) in the low fluoride group
    . Furthermore, a significant partial correlation was observed between a chronic exposure index for fluoride and the serum concentrations of inhibin-B (r = 0.163) in the high fluoride group … The results obtained indicate that a fluoride exposue of 3-27 mg/day induces a subclinical reproductive effect that can be explained by a fluoride-induced toxic effect in both Sertoli cells and gonadotrophs.
    Environ Res 2003. Sep;93(1):20-30.

    Fluoride-induced disruption of reproductive hormones in men.

    Ortiz-Perez and Rodriguez-Martinez et al.

    Laboratorio de Toxicologia Ambiental, Facultad de Medicina, Universidad Autonoma de San Luis Potosi, San Luis Potosi, Mexico

    [As ATSDR's report has a publish date of September 2003, this study is not counted as one that ATSDR did not cite.]
    2002

    RAT

    NaF 20mg/kg/day for 29 days
    oral gavage

    exerts an adverse effect on the male reproductive system and this effect is associated with indicators of oxidative stress.

    significant diminution in the relative wet weight of the testis, prostate, and seminal vesicle

    Epididymal sperm count was decreased significantly

    Reprod Toxicol 2002 Jul;16(4):385

    Testicular toxicity in sodium fluoride treated rats: association with oxidative stress.

    Ghosh D, Das(Sarkar) S, Maiti R, Jana D, Das

    Department of Human Physiology with Community Health, Reproductive Endocrinology and Family Welfare Research Unit, Vidyasagar University, West Bengal, Midnapore, India

    Not cited by ATSDR
    2002

    Ram semen

    5 hr incubation at 381⁄4C

    0.38; 1.9; 3.8 ppm F

    The percentage of spermatozoa in ram semen with intact acrosomes and the level of spermatozoa motility decreased significantly after dilution and after 5 hr incubation at 381⁄4C. Both indices decreased significantly in the presence of NaF at concentrations ranging from 20 ugmol/L to 0.1 mol/L. The activities of androgen-dependent enzymes – acid phosphatase (ACP), lactate dehydrogenase (LDH), and gamma-glutamyl transferase (y-GT-10S) – decreased significantly when the ejaculate was treated with NaF at concentrations of 20, 100, 200 ugmol/L (0.38; 1.9; 3.8 ppm F), but they returned to the initial value of the control at 0.1 mol/L (1900 ppm F). The activity of asparate transaminase (AspAT) displayed a large increase with the increasing lower F- concentration. These changes undoubtedly affect the physiological functions of the sperm. Fluoride 2002; 35(3):153-160

    In vitro influence of sodium fluoride on ram semen quality and enzyme activities

    Zakrzewska H, Udala J, Blaszczyk B

    Dept. of Biochemistry, Agricultural University, 17 Slowackiego Street, 71-434 Szczecin, Poland

    Not cited by ATSDR
    2000

    RAT

    150 mg/L NaF in drinking water

    significant decrease of sperm count and mobility, the increase of serum and testicular lipid peroxides (LPO) contents, and the adenosine triphosphatase (ATPase) activity depression of epididymis

    GSH-Px activities in the tissues of testis and epididymis were observed in ascorbic acid and fluoride group

    Chung-Kuo Kung Kung Wei Sheng (China Public Health) 2000 Aug;16(8):697-8

    [The primary study of antagonism of selenium on fluoride-induced reproductive toxicity of male rat]

    Zhu XZ, Ying CJ, Liu SH, Yang KD, Wang QZ.

    Department of Clinic Nutrition, Tongji Hospital Tongji Medical University, Wuhan, China.

    Article in Chinese. Suggest NRC translate

    Not cited by ATSDR
    2000

    MOUSE

    100, 200 and 300 ppm NaF
    drinking water for 4 or 10 weeks

    Fertility was significantly reduced at all three concentrations by exposure for 10 weeks

    results indicate that long-term ingestion of NaF adversely affects fertility in male mice

    Full report at: http://www.fluoride-journal.com/00-33-3/333-128.pdf

    Fluoride 2000; 33(3):128-134.

    Fertility effects of sodium fluoride in male mice

    Ahmed Elbetieha•, Homa Darmani, Ahmad S Al-Hiyasat.

    Department of Applied Biological Sciences,
    Faculty of Science, Jordan University of Science and Technology, Irbid, Jordan.

    Not cited by ATSDR
    2000

    MOUSE

    NaF
    10 mg NaF/kg BW

    The reduced activity of the enzymes as well as the structural and metabolic alterations in the sperm led to a significant decrease in sperm count, and motility and live:dead ratios but an increase in abnormal sperm which ultimately lead to a poor fertility rate.

    It is concluded that fluoride has a definite effect on male reproduction and fertility.

    Environmental Sciences: an International Journal of Environmental Physiology and Toxicology. 2000; 7(1):29-38

    Reversal of fluoride-induced alteration in cauda epididymal spermatozoa and fertility impairment in male mice.

    Chinoy NJ and Sharma A

    Cited by ATSDR

    Page 167: Administration of ascorbic acid and/or calcium and cessation of sodium fluoride exposure enhanced the
    recovery of sperm function and morphology and testicular damage, as compared to no treatment, in rats
    (Chinoy et al. 1993), mice (Chinoy and Sharma 2000),

    1999

    MOUSE

    Fed a protein-deficient diet treated with NaF
    5, 10, 20 mg/kg BW for 30 days

    caused a significant decrease in protein levels in testes, cauda epididymis, and vas deferens.

    levels of cholesterol in testis and glycogen in the vas deferens were significantly enhanced as compared to controls.

    Fluoride 1999; 32(4):204-214

    Effects of protein supplementation and deficiency on fluoride-induced toxicity in reproductive organs of male mice

    NJ Chinoy and Dipti Mehta

    Reproductive Endocrinology and Toxicology Unit, Department of Zoology, School of Sciences, Gujarat University, Ahmedabad, India

    Not cited by ATSDR
    1998

    MOUSE

    NaF
    10 mg/kg BW

    significant decrease epididymis weight

    significant decline in cauda epididymal sperm motility and viability

    significant reduction in fertility rate. The cauda epididymal sperm count was also significantly reduced

    Full report at:
    http://www.fluoride-journal.com/98-31-4/314-203.htm

    Fluoride 1998; 31(4):203-216

    Amelioration of fluoride toxicity by Vitamins E and D in reproductive functions of male mice

    NJ Chinoy and A Sharma

    Reproductive Endocrinology and Toxicology Unit, UGC Department of Special Assistance and COSIST in Zoology, School of Sciences, Gujarat University, Ahmedabad 380009, India.

    Cited by ATSDR

    Page 167: Postexposure
    administration of vitamins E and/or D was also effective in the recovery of sodium-fluoride induced testicular effects in mice (Chinoy and Sharma 1998).

    1998

    MOUSE

    NaF
    10 mg/kg/day for 28 days

    RAT: NaF
    1 mg/kg/day and
    10 mg/kg/day for 28 days

    In order to contribute to the clarification the effects of NaF in animal fertility we have assessed:
    1) the effect of fluoride on spermatozoa (sperm.) motility, epididymis (Epidid.) and seminal vesicles (sem. ves.) weight and fructose (fruc.) levels in sem. ves., in mice after 28 days of treatment with 10 mg/kg/day of NaF;
    2) Effect of 1 mg/kg/day and 10 mg/kg/day (Groups F1 an F2, respectively) of NaF represted treatment for 28 days in rat on sperm. count, epidid., sem. ves. and testis weight, fruc. levels in sem. ves. and testosterone (testost.) levels.

    Conclusions: The modification of some parameters related to fertility by the repeated oral NaF intake, in rodents, suggest that NaF has potential to disturb male fertility.

    Toxicology Letters, Volume 95, Supplement 1, July 1998, Page 214

    NaF may disturb male fertility in rodents

    R. Pinto, C. Vieira, H. Mota-Filipe and B. Silva-Lima

    Lab. Pharmacology, Fac. Pharmacy, University of Lisbon, Portugal

    Not cited by ATSDR
    1997

    RAT

    10 mg NaF/kg BW
    for 30 days

    the protein profile was disturbed more in testis than in cauda epididymis, whereas phospholipids and gluthathione levels were affected more in cauda than in testis. Fluoride 1997; 30(1):41-50

    Fluoride toxicity on rat testis and cauda epididymal tissue components and its reversal

    Chinoy NJ*, Shukla S, Walimbe AS, Bhattacharya S

    * Professor and Head, Zoology Department, School of Sciences, Gujarat University, Ahmedabad, India.

    Not cited by ATSDR
    1997

    GUINEA PIG

    NaF 30 mg kg-1 body weight
    30-days

    ATSDR – Page 82
    LOAEL 4.5 (mg/ kg/ day
    (decr sperm motility and viability)

    The cauda epididymal spermatozoa were highly sensitive to the effects of NaF as their structural and metabolic alterations led to marked decreases in their motility, live:dead ratio and sperm mitochondrial activity index but increases in sperm abnormalities and alterations in sperm membrane phospholipids, particularly phosphatidylinositol and phosphatidyl serine. The activities of ATPase and succinate dehydrogenase as well as glutathione levels were decreased in testis by NaF treatment, revealing disturbances in its metabolism. Med Sci Res 1997 25(2):97-100.

    Fluoride toxicity in the testis and cauda epididymis of
    guinea pig and reversal by ascorbate.

    Chinoy NJ, Patel BC, Patel DK, et al.

    Zoology Department, School of Sciences, Gujarat University, Ahmedabad, India.

    Cited by ATSDR

    ATSDR states:

    Page 179: alterations in sperm
    morphology or spermatogenesis

    See also: Pages 82 and 113

    1997

    RABBIT

    ATSDR – Page 85
    LOAEL 4.5 mg/ kg/day
    Leydig cell damage

    LOAEL 4.5 mg/ kg/ day
    Leydig cell damage

    As cited by ATSDR, page 85

    Environ Sci 5(2):79-94.1997.

    Ultrastructural studies on the leydig cells of rabbits exposed to chronic
    fluoride toxicity.

    Susheela AK, Kumar A.

    Cited by ATSDR
    1997

    GERBIL

    High fluoride (HF) pups = 2.3 ug F/g BW/day from birth to 24 days whereafter food contained 37 mg F/kg.

    Low fluoride (LF) pups: from 24 days old food contained 7 mg F/kg.

    At 16 weeks:
    Mean testes weight of High fluoride group significantly less than Low fluoride group
    A dissertation submitted to the School of Biological Sciences, University of Surrey, in fulfilment of the requirements for the Degree of Doctor of Philosophy. Guildford 1997.

    The effect of fluoride on the physiology of the pineal gland

    Jennifer Anne Luke

    Not cited by ATSDR
    1996

    Serum testosterone concentrations in patients with skeletal fluorosis

    Circulating serum testosterones in skeletal fluorosis patients were significantly lower than those of Control 1 at p < 0.01. Ref: J Toxicol Clin Toxicol 1996;34(2):183-9

    Circulating testosterone levels in skeletal fluorosis patients.

    Susheela AK, Jethanandani P.

    Fluoride and Fluorosis Research Laboratories, All India Institute of Medical Sciences, New Delhi, India.

    Cited by ATSDR

    Page 112:
    study found significantly decreased serum testosterone
    levels in 30 men diagnosed with skeletal fluorosis and in 16 men related to men with fluorosis and living in the same house as the patient (Susheela and Jethanandani 1996). The mean drinking water fluoride levels were 3.9 ppm (approximately 0.11 mg fluoride
    /kg/day), 4.5 ppm (0.13 mg fluoride
    /kg/day), and
    0.5 ppm (0.014 mg fluoride/kg/ day) in the patients with skeletal fluorosis, related men, and a control group of 26 men living in areas with low endemic fluoride levels… One limitation of this study is that the control men were younger (28.7 years) than the men with skeletal fluorosis (39.6 years) and the related men (38.7 years). In addition, the groups are small and potentially
    confounding factors are not well addressed.

    Also, pages 177, 179

    1996

    BANK VOLE

    200 micrograms F/ml drinking water for 4 months

    histopathologic changes in the germinal epithelium. Comp Biochem Physiol C Pharmacol Toxicol Endocrinol 1996 Jan;113(1):81-4

    Photoperiodic elevation of testicular zinc protects seminiferous tubules against fluoride toxicity in the bank vole (Clethrionomys glareolus).

    Krasowska A, Wlostowski T.

    Institute of Biology, Bialystok Branch of Warsaw University, Poland.

    Not cited by ATSDR
    1995

    RAT

    NaF
    10 mg/kg BW
    for 30 and 50 days

    ATSDR – Page 81
    LOAEL 4.5 mg/ kg/ day
    (decreased sperm motility and count)

    A significant reduction in electrolyte levels of sperm also occurred which would also affect their viability. The protein levels in cauda epididymal sperm suspension, vas deferens, seminal vesicle and prostate were significantly decreased after NaF administration

    The results, corroborated by earlier data from our laboratory, show that fluoride has a definite effect on male reproduction and fertility.

    Fluoride 1995; 28(2):75-86

    Amelioration of fluoride toxicity in some accessory reproductive glands and spermatozoa of rat

    Chinoy NF, Narayana MV, Dalal V, Rawat M, Patel D

    Reproductive Endocrinology and Toxicology Unit, School of Sciences, Gujarat University, Ahmedabad 380 009, India

    Cited by ATSDR
    1995

    RAT

    NaF in drinking water
    100 mg/L, and 200 mg/L for 2, 4, and 6 weeks.

    Results suggest that fluoride may have some harmful effects on the reproductive system in male rats. Fluoride 1995; 28(3):128-130

    The influence of fluoride on the content of testosterone and cholesterol in rat

    Zhao ZL, Wu NP, Gao WH

    Department of Preventive Medicine, Ningxia Medical College, 750004 China

    Not cited

    ATSDR cites in References only, not in text

    1995

    RABBIT

    10 mg NaF/kg BW/day for 20 and 23 months

    ATSDR – Page 84
    LOAEL 4.5 M mg/ kg/ day

    (structural damage of the spermatid and epididymal spermatozoa)

    The structural changes observed in the caput and cauda ductus epididymis might adversely affect the maturation of spermatozoa Int J Exp Pathol 1995 Feb;76(1):1-11

    Effects of chronic fluoride toxicity on the morphology of ductus epididymis and the maturation of spermatozoa of rabbit.

    Kumar A, Susheela AK.

    Department of Anatomy, All India Institute of Medical Sciences, New Delhi.

    Cited by ATSDR
    1994

    RAT

    NaF
    10 mg/kg BW for 50 days

    The histomorphometric studies revealed significant change in the Leydig cell diameter in correlation with the androgen levels. These results indicate that fluoride does interfere with steroidogenesis in short-term low-dose exposures in rats. Fluoride 1994; 27(1):7-12

    Effect of fluoride on rat testicular steroidogenesis

    MV Narayana and NJ Chinoy

    Zoology Department, School of Sciences, Gujarat University, Ahmedabad 380 009, Gujarat, India

    Cited by ATSDR:

    Page 112: “In contrast [to Sprando 1997], significant decreases in serum testosterone levels were observed in rats receiving daily gavage doses of 4.5 mg fluoride /kg/day as sodium fluoride for 50 days (Narayana and Chinoy 1994) and in rats exposed for 60 days to 4.5 mg fluoride /kg /day as sodium fluoride in the diet (Araibi et al. 1989).”

    1994

    RAT
    (21-24 days old)

    NaF
    10 mg/kg BW
    for 30 days

    changes resulted in a significant decrease in sperm motility and thereby fertility rate. Fluoride 1994; 27(2):67-75

    Beneficial effects of ascorbic acid and calcium on reproductive functions of sodium fluoride-treated prepubertal male rats

    Chinoy NJ, Reddy VVPC, Michael M

    Not cited by ATSDR
    1994

    RAT

    NaF
    10 mg/kg BW
    50 days

    sperm acrosomal hyaluronidase and acrosin were reduced

    low sperm motility and count

    International Journal of Fertility 39 (6) 337-346. 1994.

    Reversible effects of sodium fluoride ingestion on spermatozoa of the rat.

    Narayana MV, Chinoy NJ.

    Reproductive Endocrinology & Toxicology Unit, School of Sciences, Gujarat University, Ahmedabad, India.

    Not cited by ATSDR
    1994

    RABBIT

    10 mg NaF/kg BW daily for 18 months

    ATSDR – Page 84
    LOAEL 4.5 M mg/ kg/day
    (structural damage of the
    spermatid and epididymal spermatozoa)

    The abnormalities observed render the sperm nonfunctional and ineffective, and thus there is a possible role of fluoride in causing infertility Int J Fertil Menopausal Stud 1994 May-Jun;39(3):164-71

    Ultrastructural studies of spermiogenesis in rabbit exposed to chronic fluoride toxicity.

    Kumar A, Susheela AK

    Department of Anatomy, All India Institute of Medical Sciences, New Delhi, India.

    Cited by ATSDR
    1994

    Human spermatozoa

    The altered lysosomal enzyme activity and glutathione levels together with morphologic anomalies resulted in a significant decline in sperm motility with an effective dose of 250 mM Reprod Toxicol 1994 Mar-Apr;8(2):155-9.

    In vitro fluoride toxicity in human spermatozoa.

    Chinoy NJ, Narayana MV

    Department of Zoology, School of Sciences, Gujarat University, Ahmedabad, India.

    Not cited by ATSDR
    1992

    RAT

    F
    100- and 200 ppm in their drinking water for 6- and 16 weeks.

    ATSDR – Page 112
    after 16 weeks of exposure, seminiferous tubule atrophy was observed at
    7.5 mg fluoride/kg/day and higher

    The high F intake caused several-fold increase in the F concentrations in the testes and bone as compared with control rats, both after the 6- and 16 wk exposure;

    Fifty percent of the 100- and 200 ppm F rats after 16 weeks exhibited histopathologic changes in the germinal epithelium of the testes, which resembled those in Zn-deficient rats.

    The data suggest that a deprivation of testicular Zn due to a high F intake may be directly responsible for the injury of testicular tubules.

    Comp Biochem Physiol C. 1992 Sep;103(1):31-4.

    The effect of high fluoride intake on tissue trace elements and histology of testicular tubules in the rat.

    Krasowska A, Wlostowski T.

    Institute of Biology, Bialystok Branch of Warsaw University, Poland.

    Cited by ATSDR.
    1992

    MOUSE

    NaF
    10 mg 20 mg/kg BW for 30 days.

    ATSDR – Page 81
    LOAEL: 4.5 mg/ kg/ day (decr sperm motility and count and infertility)

    significant decrease in sperm count and motility

    large numbers of deflagellated spermatozoa, with acrosomal, midpiece and tail abnormalities

    The treatment caused loss of fertility rate when normal cycling female mice were mated with treated males.

    Fluoride 1992; 25(2):71-76

    Reversible fluoride induced fertility impairment in male mice

    NJ Chinoy and E Sequeira

    Dept. of Zool., Univ. Sch. of Sciences, Gujarat Univ., Ahmedabad-380 009, India.

    Cited by ATSDR

    Page 113:
    The alterations in sperm and the infertility were reversible 30–60 days after termination of a 30-day exposure period (Chinoy and Sequeira 1992).
    Decreased sperm counts, sperm motility, and sperm viability (the ratio of live to dead sperm) have been observed in rats exposed to 2.3 mg fluoride/kg/ day and higher (Chinoy et al. 1992, 1995) and mice (Chinoy and Sequeira 1992)

    1992

    RAT

    NaF
    5 and 10 mg/kg BW/day) for 30 days

    ATSDR – Page 81
    LOAEL: 2.3 mg/ kg/ day (decreased fertility and sperm counts)

    succinate dehydrogenase activity in testis was inhibited. Similarly, adenosine triphosphatase activity and sialic acid levels in epididymides were also suppressed with more pronounced effect on cauda epididymis. Consequently, sperm motility and count were decreased leading to a significant decline in fertility by fluoride treatment. Journal of Environmental Biology 13 (1) 55-61. 1992.

    Effects of fluoride ingestion on the physiology of reproductive organs of male rats

    Chinoy NJ, Pradeep PK, Sequeira E.

    Dept. of Zool., Univ. Sch. of Sciences, Gujarat Univ., Ahmedabad-380 009, India.

    Cited by ATSDR

    Page 113:
    When exposed male rats were mated with unexposed females, decreased fertility was observed at 2.3 mg fluoride/kg/ day as sodium fluoride and higher (Chinoy and Sequeira 1992; Chinoy et al. 1992).
    Decreased sperm counts, sperm motility, and sperm viability (the ratio of live to dead sperm) have been observed in rats exposed to 2.3 mg fluoride/kg/ day and higher (Chinoy et al. 1992, 1995)

    1992

    RABBIT

    NaF
    5, 10, 20, and 50 mg/kg BW/day

    abnormal accumulation of lipids in testes.

    The increase of concentration of all lipid classes except free fatty acids in testes was directly correlated with the increase in dosage of fluoride administered.

    Fluoride 1992; 25(3):149-154

    Biochemical effects of fluoride on lipid metabolism in the reproductive organs of male rabbits

    A Shashi

    Department of Zoology, Punjabi University, Patiala, India.

    Not cited by ATSDR
    1992

    RABBIT

    NaF 5, 10, 20 and 50 mg
    via subcutaneous injections for a period of 3-1/2 months

    The testicular structural, nuclear and total proteins were significantly depleted in all test groups of animals as compared to the control. There was a significant (p < 0.001) reduction in the testicular DNA after drug administration. Indian J Pathol Microbiol. 1992 Oct;35(4):351-6.

    Testicular proteins and DNA in experimental fluorosis.

    Shashi, Kaur D.

    Department of Zoology, Punjabi University, Patiala, India.

    Not cited by ATSDR
    1991

    RAT

    chronic fluorosis was developed with drinking water containing high fluoride in male rat.

    Ultrathin sections of testes and prostate gland were observed under transmission electron microscope. The results were as follows: in the interstitial cell, microvilli on the surface of the cell decreased. Decrease or impairment of mitochrondria to various extent and distention of the smooth endoplasmic reticulum in cytoplasma were observed. Increase of lysosome, the multiform changes of mitochondria, distention and vesiculization of smooth endoplasmic reticulum and deposition of large lipid droplets appeared in some of sertoli cells of seminiferous tubule. Significant change did not appear in spermotogonium but appeared in spermatid. Spermiogenesis was blocked. There were impairment in the epithelium and interstitial tissue to some extent. The results in this experiment suggest that: interstitial cell of testes could be damaged and spermiogenesis could be blocked. J CHINA MED UNIV; 19 (5). 1991. 339-342.

    Ultrastructural observations of testes and prostate gland in rat with chronic fluorosis.

    Song K et al.

    Dep. Histoembryol.

    Article in Chinese. Suggest NRC translate

    Not cited by ATSDR
    1991

    RABBIT

    10 mg NaF/kg BW for 18 or 29 months.

    ATSDR – Page 84
    LOAEL 4.5 mg/ kg/day

    (complete cessation of spermatogenesis)

    In animals treated for 29 months, the spermatogenic cells in the seminiferous tubules were disrupted, degenerated and devoid of spermatozoa.

    Spermatogenesis ceased only in animals treated for 29 months.

    J Reprod Fertil 1991 Jul;92(2):353-60

    A study of the effect of high concentrations of fluoride on the reproductive organs of male rabbits, using light and scanning electron microscopy.

    Susheela AK, Kumar A.

    Department of Anatomy, All India Institute of Medical Sciences, New Delhi.

    Cited by ATSDR

    Page 84, 112

    1991

    RABBIT

    NaF
    20 and 40 mg/kg BW for 30 days

    Reduction in sperm motility, count, and changes in their morphology and metabolism led to the significant decline in fertility of the treated animals. Fluoride 1991; 24(1):29-39

    Effects of vitamin C and calcium on the reversibility of fluoride-induced alterations in spermatozoa of rabbits

    Chinoy NJ , Sequeira E, Narayana MV

    Department of Zoology, University School of Sciences, Gujarat University, Ahamadabad, India.

    Cited by ATSDR

    Page 167:
    Chinoy and associates have examined the effectiveness of calcium, ascorbic acid, vitamin E, and vitamin D in reversing the reproductive effects associated with oral exposure to sodium fluoride.
    Administration of ascorbic acid and/or calcium and cessation of sodium fluoride exposure enhanced the recovery of sperm function and morphology and testicular damage, as compared to no treatment, in rats
    (Chinoy et al. 1993), mice (Chinoy and Sharma 2000), and rabbits (Chinoy et al. 1991).

    1991

    RAT

    single microsose (50 ug/50 ul) NaF into vasa deferentia of Rattus norvegicus

    arrest of spermatogenesis and absence of spermatozoa in the lumina of the seminiferous tubules of the testes, which consequently led to a decline in the sperm count in the caudae epididymides.

    Scanning electron microscopy of cauda and vas deferens sperm revealed deflagellation and tail abnormalities.

    Reproductive Toxicology 1991;5(6):505-512

    Microdose vasal injection of sodium fluoide in the rat

    Chinoy NJ, Rao MV, Narayana MV, Neelakanta E

    Department of Zoology, University School of Sciences, Gujarat University, Ahamadabad, India.

    Not cited by ATSDR
    1990

    RABBIT

    NaF
    5, 10, 20 and 50
    mg/kg/day
    for 100 days

    Deficient maturation and differentiation of the spermatocytes and an increase in the amount of interstitial tissue were found in the experimental animals. In the higher dosage groups, spermatogenesis stopped and the seminiferous tubules became necrotic. Folia Morphol (Praha) 1990;38(1):63-5

    Histopathological changes in rabbit testes during experimental fluorosis.

    Shashi.

    Department of Zoology, Punjabi University, Patiala, India.

    Not cited by ATSDR
    1989

    RAT

    100 or 200 ppm NaF
    60 days

    ATSDR (2003) – Page 80
    LOAEL 4.5 mg/ kg/ day
    (50% reduction in fertility, decr in percentage of seminiferous tubules containing spermatozoa and decr testosterone levels)

    dose-related decrease in reproductive performance

    decrease in serum testosterone at 200 ppm

    ATSDR in its 1991 Toxicological profile for fluorides, hyrdogen fluoride, and fluorine, stated (page 63):
    “Male CD rats fed 5 or 10 mg fluoride/kg/day as sodium fluoride exhibited a significant increase in the thickness of the peritubular membrane of the seminiferous tubules. Both treated group also exhibited a significant decrease in the percentage of seminiferous tubules containing spermatozoa and a significant decrease in serum testosterone. As a result, there were fewer pregnancies and fewer offspring among treated animals.”

    J BIOL SCI RES; 20 (1). 1989. 19-30.

    Effect of high fluoride on the reproductive performance of the male rat.

    Araibi AA, Yousif WH, Al-Dewachi OS.

    Cited by ATSDR
    1989

    MOUSE

    NaF
    10 mg 20 mg/kg BW
    for 30 days.

    NaF treatment caused severe disorganization and denudation of germinal epithelial cells of seminiferous tubules with absence of sperm in the lumina.

    epithelial cell nuclear pyknosis and absence of luminal sperm were observed.

    Reprod Toxicol 1989;3(4):261-7

    Effects of fluoride on the histoarchitecture of reproductive organs of the male mouse.

    Chinoy NJ, Sequeira E.

    Not cited by ATSDR
    1989

    MOUSE

    NaF
    10 mg 20 mg/kg BW
    for 30 days.

    testis succinic dehydrogenase levels decreased, in the epididmides sialic acid and ATPase levels decreased; in the vas deferens glycogen levels increased, seminal vesicles fructose levels increased in the prostate glands, acid phosphatase and total protein levels increased. Fluoride 1989; 22(1):78-85

    Fluoride induced biochemical changes in reproductive organs of male mice

    Chinoy NJ, Sequeira E.

    Not cited by ATSDR
    1987

    MOUSE

    NaF
    10, 20, 40 mg/kg
    Different assays were used

    Incidence of micronucleus and sperm abnormality increased with dose.

    … Of all the assay results in the present study, the sperm abnormality was highest …

    Caryologia 1987, 40:1-2; 79-87

    Genotoxic effect of an environmental pollutant, sodium flouride, in mammalian in vivo test system

    Pati PC and Bhunya SP

    Laboratory of Genetic Toxicology, Department of Zoology, Utkal University, Vani Vihar, Bhubaneswar, India

    Not cited.

    ATSDR only cited chromosome aberrations in mouse bone

    1985

    RAT

    5 ppm F

    A lowering in the production of testosterone was thought to be due to Perfluorochemicals exposure. A series of tests using sodium fluoride exposure to rats were performed. “The results provide unequivocal evidence that 250 uM fluoride inhibits testosterone secretion by rat testes perfused in vitro… The present observation of deleterious effects by 250 uM fluoride (5 ppm) emphasizes the sensitivity of steroidogenesis to fluoride.” 3rd International Congress of Andrology, Boston,
    Massachusetts.
    J Androl 6:59 (1985)

    Reproductive toxicology of fluoride

    Chubb C

    University of Texas Health Science Center, Dallas, Texas 75235.

    Not cited

    ATSDR cites in References only, not in text

    1984

    RAT

    NaF
    5.0 mg/kg and
    20.0 mg/kg

    NaF at 5.0 mg/kg
    glutathione-S-transferase activity increased 4-fold in the testis


    NaF at 20.0 mg/kg
    decrease in lipid peroxidation in
    testes
    Toxicol Lett 1984 May;21(2):167-72

    Alterations in drug metabolising enzymes and lipid peroxidation in different rat tissues by fluoride.

    Soni MG, Kachole MS, Pawar SS.

    Biochem. Div., Dept. Chem., Marathwada Univ., Aurangabad 431004, India.

    Not cited by ATSDR
    1983

    RAT

    A marked fall (P < 0.01) in the testosterone production was recorded at a fluoride concentration of 100 ppm and testosterone synthesis was maximally inhibited (P < 0.01) at 200 ppm. There was a noticeable, though marginal, inhibition in testosterone synthesis even at 10 ppm fluoride concentration… The fluoride ions which diffuse into the cells inhibit steroidogenesis… IRCS Med. Sci. 11, 813-814 (1983)

    In vitro inhibition of testosterone synthesis in the presence of fluoride ions

    Kanwar KC, Vig PS, Kalla NR

    Department of Biophysics, Panjab University, Chandigarh, India.

    Not cited by ATSDR
    1983

    Chicken

    NaF
    600 ppm

    98 days old to 158 days of age

    NaF (150, 300 or 600 ppm) were added to the basal ration of Hisex male and female chickens (98 days old)… (until 158 days of age)… initiation of spermatogenesis was delayed in the testes of the 600 ppm group and giant spermatid cells were observed. Breed variation in the response of chicken to the added level of F- was suggested. FLUORIDE; 16 (1). 1983. 37-43.

    Effect of high fluoride intake on chicken performance, ovulation, spermatogenesis and bone fluoride content.

    MEHDI A WR, AL-SOUDI KA, AL-JIBOORI N AJ,
    AL-HITI MK

    Dep. Vet. Physiol. Anim. Sci., Baghdad Univ., Coll. Agric., Baghdad, Iraq.

    Not cited by ATSDR
    1982

    MOUSE

    Inbred mice, fed a low-F- diet, 0.263 | .028 ppm F-, were given drinking water containing 0, 1, 5, 10, 50, 100 or 200 ppm F- for 3-6 wk

    Cytological studies on bone marrow cell chromosomes and spermatocytes showed that 1-200 ppm F- (as NaF) was able to induce chromosomal changes in a dose-dependent manner. The frequency of the induced chromosomal damage was significantly higher in each treatment than in the controls. The abnormalities included translocations, dicentrics, ring chromosomes, and bridges plus fragments, or fragments by themselves. There was a significant correlation between the amount of F- in the body ash and the frequency of chromosomal abnormalities. FLUORIDE; 15 (3). 1982. 110-118

    Cytological effects of sodium fluoride on mice.

    Mohamed AH
    Chandler ME

    Dept. of Biology and School of Medicine, University of Missouri, Kansas City

    Not cited

    ATSDR cites in References only, not in text

    1981

    MOUSE

    cytochemical alterations in Leidig cells and in the basal parts of the Sertoli cells Fluoride 1981; 14(4):182-191

    Fluorosis: geographical pathology and some experimental findings

    AA Zahvoronkov and LS Strochkova

    Institute of Human Morphology, Moscow, USSR

    Not cited by ATSDR
    1981

    RAT

    The effects of fluoride (F-) administration were studied on 2 groups of weanling male Wistar rats, a control fed a basal diet containing 0.09 mg% F- and the other fed a diet containing 50 mg% F- for 30 days… The amount of F- accumulated in brain, heart, thymus, kidney, testes, adrenal and femur of the F–fed group was significantly higher than those of controls. J TOKYO MED COLL; 39 (3). 1981. 441-460.

    Hygienic study on fluoride: 4. Physiological effects of fluoride on rat.

    TOMOMATSU T

    Dep. Biochem., Tokyo Med. Coll.

    Not cited by ATSDR
    1980

    MOUSE

    NaF
    500 and 1000 ppm
    in drinking water for 3 months

    lack of maturation and differtiation of spermatocytes

    spermatogenesis had stopped and seminiferous tubules became necrotic.

    Fluoride 1980; 13(4):160-162

    Histological Finding of Mice Testes Following Fluoride Ingestion

    Kour K, Singh J.

    Department of Anatomy, Government Medical College, Srinagar, Kashmir, India

    Not cited.

    Cited by ATSDR in its References but not in the text

    1978

    Human spermatozoa

    Adenylate cyclase from ejaculated human spermatozoa was inhibited by fluoride J Reprod Fertil 1978 May;53(1):59-61

    Inhibitors of adenylate cyclase from ejaculated human spermatozoa.

    Haesungcharern A, Chulavatnatol M.

    Not cited by ATSDR
    1978

    RAT (immature)

    NaF

    increased frequency of occurrence of various seminiferous tubules containing spermatids

    The mechanism of action of NaF may be hypothetical, but it probably consists of direct action on the seminiferous epithelium level.

    Andrologia 1978 May-Jun;10(3):223-33

    The influence of human menopausal gonadotropin, natrium fluoride and cyproterone acetate on the spermatogenesis in immature rats.

    Kula K.

    Not cited by ATSDR
    1978

    MOUSE

    Impaired spermatogenesis Iraqi Journal of Veterinary Medicine 1978:2,103-135

    Effect of high fluoride intake on reproductive system of the male mice

    Ridha M, Al-Jiboori N, Mehdi AW

    Not cited by ATSDR
    1977

    Human males suffering from fluorosis

    Compared to healthy controls, testosterone content proved to be decreased and FSH content elevated in patients with fluorosis Probl Endokrinol (Mosk) 1977 Jul-Aug;23(4):104-7

    [Effect of inorganic fluorine compounds on the functional state of the pituitary-testis system]

    Tokar’ VI, Savchenko ON.

    Article in Russian. Suggest NRC translate

    Not cited by ATSDR
    1977

    RAT

    NaF

    androgen-binding protein (ABP) synthesis is inhibited at 0 degrees C or in the presence of cycloheximide, puromycin or sodium fluoride.

    Immature (17-25-day-old rat) testes showed a higher rate of ABP synthesis per 100 mg tissue than adult rat testes during ‘baseline’ conditions

    Mol Cell Endocrinol 1977 Oct;8(4):335-46

    In vitro synthesis of rat testicular androgen-binding protein (ABP).

    Ritzen EM, Hagenas L, Ploen L, French FS, Hansson V.

    Not cited by ATSDR
    1976

    RAT

    The enzyme of the spermatozoa from the cauda epididymidis was more sensitive to inhibition by ouabain and fluoride J Reprod Fertil 1976 Sep;48(1):91-7

    Changes in surface ATPase of rat spermatozoa in transit from the caput to the cauda epididymidis.

    Chulavatnatol M, Yindepit S.

    Not cited by ATSDR
    1972

    Patient with endemic fluorosis

    bilateral calcification of the vas deferens Fluoride 1972; 5(2):86-88

    Cacification of the vas deferens in a patient with endemic fluorosis
    Case report

    SPS Teotia and M Teotia

    Not cited by ATSDR
    Note:
    Kanwar et al. (1983) stated, “degeneration of the seminiferous tubules at high doses of fluoride intake was reported in 1934″ by Phillips PH and Lamb AR, Arch. Pathol. 17, 169.

    ATSDR cites a 1933 study by Phillips and Lamb in its References:
    Phillips PH, Lamb AR, Hart EB, et al. 1933. Studies on fluorine in the nutrition of the rat: II. Its influence on reproduction. Am J Physiol 106:356-364.

  • The best, and worst, laundry detergents with 1,4-dioxane contamination

    Saturday, May 22, 2010 by: Ethan A. Huff

    (NaturalNews) One of the major issues being tackled by consumer watchdog groups this year is the presence of 1,4-dioxane, a synthetic petrochemical carcinogen, in consumer products. Since hair care products, cleaning formulas and laundry detergents are all susceptible to containing this toxic chemical byproduct, which is not listed on product labels, David Steinman from the Green Patriot Working Group (GPWG) began a study in 2007 to see which consumer products are the worst offenders. This year, his organization along with the Organic Consumers Association (OCA), released the results of a portion of the study conducted last year on laundry detergents.

    When cleaning products and detergents are processed using ethoxylation, a cheap technique that lessens the severity of the harsher ingredients, 1,4-dioxane is created. Since it is considered a byproduct of ethylene oxide reacting with other ingredients, 1,4-dioxane is technically considered a contaminant and thus does not have to be included on product labeling. As a result, consumers are largely unaware of its presence in major household products.

    For the study, Steinman evaluated 20 different laundry detergents from both conventional and “natural” brands. Evoxa, an independent, third-party laboratory that is highly respected for its rigorous methods and high standards, conducted all product testing. The results are as follows:

    Conventional brands:
    1. Tide (P&G) – 55 parts per million (ppm)
    2. Ivory Snow Gentle (P&G) – 31 ppm
    3. Tide Free (P&G) – 29 ppm
    4. Purex (Dial Corp.) – 25 ppm
    5. Gain 2X Ultra (P&G) – 21 ppm
    6. Cheer BrightClean Detergent (P&G) – 20 ppm
    7. Era 2X Ultra (P&G) – 14 ppm
    8. Arm & Hammer (Church & Dwight Co.) – 5.0 ppm
    9. Wisk 2X Ultra (Sun Products Corp.) – 3.9 ppm
    10. Woolite Complete Detergent (Reckitt Benckiser) – 1.3 ppm
    11. All laundry detergent (Unilever) – 0.6 ppm
    12. Dreft powdered detergent (P&G) – non-detectable (ND)
    13. Sun Burst (Sun Products Corp.) – ND

    “Natural” brands:
    1. Planet Ultra Liquid laundry detergent – 6.1 ppm
    2. Mrs. Meyers laundry detergent – 1.5 ppm
    3. Clorox Green Works Natural laundry detergent – ND
    4. Ecos laundry detergent (Earth Friendly Products) – ND
    5. Life Tree Laundry Liquid – ND
    6. Method Squeaky Green laundry detergent – ND
    7. Seventh Generation Free & Clear laundry detergent – ND

    Of the products detected, P&G products came up the highest in 1,4-dioxane levels, as did most of the conventional brands. Of the natural brands tested, only two were found to contain 1,4-dioxane, and in levels far below the average conventional brand. While not all available brands were tested, it is clear from the results that consumers need to be wary of most conventional brands. They also must perform due diligence in verifying that their “natural” brand of choice is truly free of 1,4-dioxane as well.

    The 1,4-dioxane found in laundry detergent is particularly harmful in the fact that the chemical binds easily to water and remains there. Even after water containing the chemical has been purified and filtered, low levels have been detected, indicating that it is not easily removed from water. Numerous water supplies across the country have been found to be tainted with 1,4-dioxane.

    Of the 80,000 known chemicals, only 200 are tested by the EPA; 1,4-dioxane is not one of the ones tested. Average aggregate exposure to 1,4-dioxane is unknown since it is found in numerous consumer care products. Because it is a known carcinogen that is implicated in causing cancer, liver disease and other serious problems, it is important to avoid it whenever possible.

    OCA has prepared a Personal Care and Cleaning Products Safety Guide outlining which consumer products are safe and free of 1,4-dioxane and which ones are not. Categories include dishwashing soap, hand soap, all-purpose soap, laundry detergents, household cleaners, body washes and shampoos, conditioners, facial cleansers, lotions, sunscreens and deodorants.

  • Scientists Find ‘Baffling’ Link between Autism and Vinyl Flooring

    Swedish children who live in homes with vinyl floors are more likely to have autism, according to a new study, but what’s behind the link is unclear

    By Marla Cone and Environmental Health News

    Is vinyl bad for baby? Young children with vinyl flooring in their rooms had a higher rate of autism than those who didn’t, according to a recent study.
    FLICKR/VETCW3

    Children who live in homes with vinyl floors, which can emit chemicals called phthalates, are more likely to have autism, according to research by Swedish and U.S. scientists published Monday.

    The study of Swedish children is among the first to find an apparent connection between an environmental chemical and autism.

    The scientists were surprised by their finding, calling it “far from conclusive.” Because their research was not designed to focus on autism, they recommend further study of larger numbers of children to see whether the link can be confirmed.

    Bernard Weiss, a professor of environmental medicine at University of Rochester and a co-author of the study, said the connection between vinyl flooring and autism “turned up virtually by accident.” He called it “intriguing and baffling at the same time.”

    Experts suspect that genetic and environmental factors combine to cause autism, a neurodevelopmental disorder that has increased dramatically in children over the past 20 years.

    In the new study, Swedish families were asked questions about flooring as part of research investigating allergies and indoor air pollutants. Phthalates, used to make soft plastic, have in previous studies been connected to allergies and asthma.

    The study was based on surveys that asked a variety of questions related to the indoor environment. Of the study’s 4,779 children between the ages of 6 and 8, 72 had autism, including 60 boys.

    The researchers found four environmental factors associated with autism: vinyl flooring, the mother’s smoking, family economic problems and condensation on windows, which indicates poor ventilation.

    Infants or toddlers who lived in bedrooms with vinyl, or PVC, floors were twice as likely to have autism five years later, in 2005, than those with wood or linoleum flooring.

    “A greater proportion of children with autism spectrum disorder were reported to have PVC as flooring material in the child’s and the parent’s bedroom in 2000 compared to children without autism spectrum disorder,” the scientists wrote in the journal Neurotoxicology. “Furthermore, children with autism spectrum disorder were reported to live in homes with more condensation on the inside of the windows, which…may be seen as an indicator for deficient ventilation.”

    Children in the study also were twice as likely to have autism if their mothers smoked cigarettes. The autistic children also were more likely to have asthma.

    The lead investigator was Carl-Gustav Bornehag of Karlstad University in Sweden, who in 2004 found a high rate of asthma and allergies among children living in households with dust containing phthalates.
    The scientists reported that they do not know if asthma and autism are related, or whether phthalates contributed to the risk of autism by some other mechanism, such as disruption of hormones. Phthalates in animal tests interfere with male hormones and sexual development.

    “The data are far from conclusive. They are puzzling, even baffling, and not readily explicable at this time,” the scientists wrote in their study. “However, because they are among the few clues that have emerged about possible environmental contributions to autistic disorders, we believe that they should be weighed carefully and warrant further study.”

    Several scientists who did not participate in the study cautioned that it has too many limitations to draw conclusions, but they suggested that new studies be designed to look for a connection between autism and indoor air pollutants.

    Dr. Philip Landrigan, a pediatrician who is director of the Children’s Environmental Health Center at Mount Sinai School of Medicine, called the results “intriguing, but in my mind preliminary because they are based on very small numbers.” Landrigan said he has “no doubt that environmental exposures are involved in causation of autism,” but he suspects the most significant exposures occur not in childhood, but early in pregnancy, “when the basic architecture of the brain is still being established.”

    The researchers relied on questionnaires and did not measure any chemicals in the homes, which limits the reliability of the findings because they do not know for certain that the children were exposed to phthalates. Previous studies have found that phthalates are common in household dust.

    Phthalates are used as softeners in plastic for vinyl flooring as well as other building materials, toys and medical equipment. The chemicals have become increasing controversial in recent years, with Congress last year banning their use in children’s products.

    The American Chemistry Council, representing chemical companies producing phthalates, said in a statement Monday that the new study does not prove a link between the chemicals and autism. “No other means for assessing these children existed except for the questionnaire and the parent’s responses, making this finding rather insignificant,” said Chris Bryant, the group’s managing director. Autism, he said, “was not systematically analyzed, but just happened to be a question asked five years into the study.”

    The industry group has said flooring emits “extremely low” levels of phthalates. Because the compounds are heavy molecules with low volatility, they do not tend to evaporate, and wear and tear that might release particles into dust is slight, they said.

    Vinyl flooring is commonplace in Sweden, where only about 1 percent of homes have carpeted floors. But it is uncommon in U.S. bedrooms, so it may not be related to autism among American children. However, carpeting contains other contaminants, including pesticides and brominated flame retardants, which have been found to harm brain development in animal tests.

    The scientists said their new finding “suggests that studies of other chemical contaminants with endocrine disruptor properties might yield useful insights into the genesis of” autism.

    Previously, three studies in California have found a connection between children’s exposure to household or agricultural pesticides and autism.

    Rates of autism in California have increased seven-fold since 1990, a recent study found. Because genetics do not change that quickly, scientists suspect that chemical pollutants are probably playing a role. But there have been few studies attempting to pinpoint which chemicals, or combination of chemicals.

    This article originally ran at Environmental Health News, a news source published by Environmental Health Sciences, a nonprofit media company.

  • Fluorocarbons – Charles Kettering, and “Dental Caries”

    With as much toxic exposure as we get in modern society, I will give credit where credit is due.  There are many good scientists working tirelessly to protect people from environmental hazards.  Many toxins (lead in gasoline for example) have been eliminated due to efforts by researchers like those at Kettering Laboratory.  However, there are dark forces at work in water fluoridation policy.

    “Pablum, a popular infant food prepared from bone meal [*], formerly contained as much as 18 ppm. When this amount of fluoride was found to be excessive -it produced mottled teeth- manufacturers reduced the fluoride content of Pablum to between 1.33 and 2.12 ppm”

    We don’t need poison chemicals in the baby food then, and we still don’t need it.  in ANY amount. Find me one physician who says there is a biological need for fluoride in the body.  I know of none.  It is not an essential nutrient and causes a range of diseases.

    Fluoride and mercury are still 2 of the “old standby” toxins used to brain damage children, reduce fertility and population.  The long term effects are well-understood which is why it’s used. You can still walk into the grocery store and buy fluoridated “baby water.”

    There is the public story about preventing cavities, and then the real story behind water fluoridation.  And that is the one you probably haven’t heard, but it’s the one you need to know, to protect yourself and your family.

    From fluoride-history.de

    see also:

    http://www.eh.uc.edu/allweb/history/history.htm

    http://www.libraries.wright.edu/special/manuscripts/ms262.html

    http://www.runet.edu/~wkovarik/papers/kettering.html



    Until they became famous for the “Freon” type refrigerants, the names of Charles Kettering and Thomas Midgley were widely known for their leaded gasoline battle. Tetraethyl lead was first prepared in Europe, in 1859, as a pure compound and during the slow development in European Universities there was no hint that once it would become very important commercially (Seyferth D.: “The rise and fall of tetraethyllead”, Organometallics 22 (2003) 2346 and 5154).

    “After leaded gasoline entered the market in 1923-24, a fatal refinery accident drew news media attention to the poisonous nature of the full strength additive and the potential public health risk from fuel containing the dilute additive. Public health scientists insisted that alternatives existed, but industry in general and GM in particular vehemently insisted that tetraethyl lead was the only additive that could be used … When five men died in a New Jersey refinery in October, 1924, a storm of protest and scientific dispute surrounded General Motors, Standard Oil of New Jersey, and E. I. Du Pont de Nemours Corp., the three principal developers of leaded gasoline. G.M. and Standard together  had formed the Ethyl Gasoline Corp., and Du Pont participated as one-third owner of G.M. and as the largest tetraethyl lead manufacturer … ” (http://www.runet.edu/~wkovarik/papers/kettering.html)

    The same team that so successfully fought the leaded gasoline battle of the 1920´s, Charles Franklin Kettering, director of General Motors research, Thomas Midgley, his assistant, originator of the idea to use tetraethyl lead as an antiknocking agent, and their “toxicologist” Robert Kehoe, created another, not less important issue in the 1930´s: fluorocarbons used as refrigerants, propellants and fire extinguishers.

    Again, Kettering presented the technical devices for the project, a refrigerator, a refrigerant dehumidifying apparatus, an (automatically controlled) air conditioner, an air conditioner for an automobile:

    Charles F. KETTERING, assignor to Frigidaire Corporation, Dayton, Ohio: “Refrigerating apparatus”, US Patent 1,886,339; filed Dec. 31, 1928; patented Nov. 1, 1932

    Charles Frank KETTERING, assignor to Frigidaire Corporation, Dayton, Ohio: “Refrigerating apparatus”, US Patent 1,955,192; filed Dec. 30, 1931; patented Apr. 17, 1934

    Charles F. KETTERING, assignor to Frigidaire Corporation, Dayton, Ohio: “Refrigeration”, US Patent 1,978,463; filed Jan. 28, 1933; patented Oct. 30, 1934

    Charles F. KETTERING, assignor to General Motors Corporation, Dayton, Ohio: “Refrigerating apparatus”, US Patent 2,093,968; filed Dec. 24, 1934; patented Sept. 21, 1937

    Charles F. KETTERING, assignor, by mesne assignments, to General Motors Corporation: “Refrigerating apparatus”, US Patent 2,130,092; filed Dec. 30, 1931, renewed April 28, 1937; patented Sept. 13, 1938

    Charles F. KETTERING, assignor to General Motors Corporation, Dayton, Ohio: “Refrigerating apparatus”, filed March 28, 1936; patented Sept. 13, 1938

    Charles Franklin KETTERING, assignor to General Motors Corporation, Dayton, Ohio: “Refrigerating apparatus”, US Patent 2,294,036; filed Dec. 29, 1938; patented Aug. 25, 1942


    Interestingly, when Midgley developed the “Freon”-type fluorocarbons in 1930, related compounds had already been made elsewhere by a very similar procedure. The manufacture of “fluoroform” (trifluoromethane) was patented by the pharmaceutical company Valentiner and Schwarz, of Leipzig- Plagwitz, Germany, in 1899: German Patents DE 105,916 (filed Jan. 5, 1899), DE 106,513 (Feb. 26, 1899), and U.S. Patent 643,835 (filed May 4, 1899). The inventors reacted silver fluoride with iodoform in the presence of chloroform (i.e. by substitution of another halogen by fluoride derived from a heavy metal fluoride). Next came Methyl fluoride to be  used as a “cold producer or refrigerating agent”: Walter LACHMANN, of Hamburg, Germany: “Method of producing low temperatures by means of methyl-fluoride”, British Patent GB 717; filed in the U.K. on Jan. 9, 1912; pat. Oct. 10, 1912.


    1930

    In 1930, Thomas Midgley, in cooperation with Albert Leon Henne and Robert Reed McNary, developed the Freons, as a substitute for the toxic gaseous refrigerants (ammonia, butane, methyl chloride (or bromide), sulfur dioxide) in use at that time. ”The pioneer work on organic fluorides of F. Swarts has been used as a basis for the manufacture of dichlorodifluoromethane.” Even toxicity tests had been performed, probably to prevent any unwanted discussions: “Robert A. Kehoe made a preliminary investigation of the toxic properties of dichlorodifluoromethane from which it was evident that this compound was remarkably non-toxic(Midgley & Henne: Ind. Eng. Chem. 22 (May 1930) 542)

    Thomas MIDGLEY, Albert L. HENNE, Robert R. McNARY, assignors to Frigidaire Corporation: “Heat transfer”, US Patent 1,833,847; filed Feb. 8, 1930; patented Nov. 24, 1931; also German Patents (DE) 623,322; filed Feb. 9, 1930, publ. Nov. 28, 1935; and 630,838; filed Feb. 9, 1930; publ. May 14,1936

    Thomas MIDGLEY, Albert L. HENNE, Robert R. McNARY, assignors to Frigidaire Corporation, Dayton, Ohio: “Manufacture of aliphatic fluoro compounds”, US Patent 1,930,129; filed April 5, 1930; patented Oct. 10, 1933; also German Patent (DE) 573,534 on the separation of certain aliphatic fluoro compounds; filed July 2, 1930; publ. March 16, 1933

    Francis R. BICHOWSKY, assignor, by mesne assignments, to General Motors Corporation: “Self propelling fire extinguishing charge containing a double halogen hydrocarbon compound”, US Patent 2,021,981; filed June 23, 1930; patented Nov. 26, 1935

    Thomas MIDGLEY, assignor to Frigidaire Corporation, Dayton, Ohio: “Process of preventing fire by nontoxic substances”, US Patent 1,926,395; filed July 31, 1930; patented Sept. 12, 1933

    Thomas MIDGLEY, Albert L. HENNE, Robert R. McNARY, assignors to Frigidaire Corporation, Dayton, Ohio: “Process of preventing fire by nontoxic substances”, US Patent 1,926,396; filed July 31, 1930; patented Sept. 12, 1933

    I. G. Farbenindustrie Aktiengesellschaft of Frankfurt, Germany: “Manufacture of methane derivatives containing chlorine and fluorine”, British Patent GB 370,356; priority Dec. 12, 1930 in Germany, filed in GB on Dec. 11, 1931; granted April 7, 1932


    1931

    Albert L. HENNE, assignor, by mesne assignments, to General Motors Corporation: “Dehydration of antimony trifluoride and manufacture of fluorinated aliphatic compounds”, US Patent 2,082,161; filed Jan. 30, 1931; renewed Oct. 16, 1935; patented June 1, 1937

    Albert L. HENNE, assignor, by mesne assignments, to General Motors Corporation: “Fluorination of aliphatic compounds”, US Patent 1,973,069; filed Jan. 30, 1931; patented Sept. 11, 1934 (silicon tetrafluoride + antimony chloride as catalysts for partial fluorination of carbon tetrachloride)

    Albert L. HENNE, assignor by mesne assignments, to General Motors Corporation: “Fluoriation in the presence of chlorine as a catalyst”, US Patent 1,990,692; filed Jan. 30, 1031; patented Feb. 12, 1935

    Albert L. HENNE, assignor, by mesne assignments, to General Motors Corporation: “Manufacture of fluorated aliphatic compounds”, US Patent 2,007,198; filed Jan. 30, 1931; patented July 9, 1935

    Albert L. HENNE, assignor, by mesne assignments, to General Motors Corporation: “Method of manufacturing halo-fluoro hydrocarbons”, US Patent 1,978,840; filed Jan. 30, 1931; renewed Sept. 9, 1933; patented Oct. 30, 1934

    Thomas MIDGLEY, Albert L. HENNE, Robert Reed McNARY, assignors, by mesne assignments, to General Motors Corporation: “Manufacture of halo-fluoro derivative of aliphatic hydrocarbons”, US Patent 2,007,208; filed Feb. 24, 1931; patented July 9, 1935

    Thomas MIDGLEY, Albert L. HENNE, assignors to Frigidaire Corporation, Dayton, Ohio:  “Preparation of aliphatic halo-fluoro compounds”, US Patent 2,013,062; filed Feb. 26, 1931; patented Sept. 3, 1935

    Thomas MIDGLEY, Albert L. HENNE, Robert R. McNARY, assignors, by mesne assignments, to General Motors Corporation: “Manufacture of Antimony trifluoride”, US Patent 2,024,008; filed Feb. 26, 1931; patented Dec. 10, 1935

    Albert L. HENNE, assignor, by mesne assignments, to General Motors Corporation: ”Manufacture of pentavalent antimony compounds”, US Patent 1,984,480; filed June 5, 1931; renewed Jan. 9, 1934; patented Dec. 18, 1934

    Albert L. HENNE, assignor, by mesne assignments, to General Motors Corporation: “Fluoration of aliphatic halides”, US Patent 2,013,050; filed June 26, 1931; renewed May 10, 1934; patented Sept. 3, 1935

    Thomas MIDGLEY, Albert L. HENNE, Robert R. McNARY, assignors, by mesne assignments, to General Motors Corporation: “Heat transfer and refrigeration”, US Patent 1,968,049; original application Feb. 8, 1930, divided and this application filed Nov. 19, 1931; patented July 31, 1934

    Thomas MIDGLEY, assignor, by mesne assignments, to General Motors Corporation: “Process of testing for halogens”, US Patent 1,990,706; filed Dec. 21,1931; patented Feb. 12, 1935

    Werner URSUM: “Füllungen für Feuerlöscher”, German Patent DE 587,932; filed July 1, 1931; pat. Nov. 10, 1933


    1932

    In 1932, it was reported that dichlorodifluoromethane decomposes when passing through a flame (e.g. in an outbreak of fire in a kitchen whereby the refrigerant may be released from the refrigerator) and thereby delivers hydrogen fluoride and hydrogen chloride. Midgley and Henne (Ind. Eng. Chem. 24 (June 1932) 641) were quick to claim: “It is demonstrated that even under the worst possible circumstances life is not endangered.” A footnote in their report (page 644) says: “Experiments conducted by R. A. Kehoe at Cincinnati demonstrate that hydrogen fluoride is not more toxic than hydrogen chloride and hence that these two may be considered together” (a claim contradictory to experiments performed earlier by other researchers).


    1934

    Thomas MIDGLEY, Albert L. HENNE, Robert R. McNARY, assignors, by mesne assignments to General Motors Corporation, Dayton, Ohio: “Heat transfer and refrigeration”, US Patent 1,968,050; original application filed Nov. 19, 1931; divided and this application filed April 30, 1934; patented July 31, 1934

    Thomas MIDGLEY, Albert L. HENNE, Robert R. McNARY, assignors to General Motors Corporation, Dayton, Ohio: “Heat transfer and refrigeration”, US Patent 2,104,882; original application Nov. 19, 1931; divided and this application filed May 1, 1934


    HF Toxicity experiments in animals, carried out at the Kettering Laboratory in Cincinnati and reported in 1934 and 1935 by Willard Machle, Frederick Thamann, Karl Kitzmiller, Jacob Cholak, and Eugene W. Scott, were supported in part by Kinetic Chemicals Inc., a subsidiary of E. I. Du Pont de Nemours & Company, manufacturer of the Freons (J. Ind. Hyg. Toxicol. 16 (March 1934) 129; 17 (Sept. 1935) 223; 17 (Sept. 1935) 230).


    1935

    Albert L. HENNE, assignor to General Motors: “Halide detector”, US Patent 2,136,741; filed Feb. 9, 1935; patented Nov. 15, 1938

    “Freon is used not only in household and larger mechanical refrigerating units in cold storage for perishable products but also in the air-conditioning field of buildings, mines, railroad passenger cars, etc. Approximately 1,700 tons of acid spar were used in the manufacture of the new refrigerants in the first ten months of 1935, since which time there has been a noteworthy increase. The Kinetic Chemicals Inc., a Du Pont subsidiary, Wilmington, Delaware, controls and manufactures the ´Freons´ and many of the refrigerator manufacturers are offering equipment containing these gases, particularly Freon.” (Paul Hatmaker, Hubert W. Davis: “The fluorspar industry of the United States with special reference to the Illinois-Kentucky District”, State Geological Survey, Bulletin No. 59, Urbana, Il., 1938, p.82).


    1936

    Willard Machle of the Kettering Institute examined the “Normal urinary fluorine excretion and the problem of mottled enamel” (Dental Cosmos 78 (1936) 612).


    1937

    Midgley was awarded the Perkin Medal of the Society of Chemical Industry on January 8, 1937, at a joint meeting of the American Section of the Society of Chemical Industry and the New York Section of the American Chemical Society at the Chemists´ Club, New York (Ind Eng. Chem. 29 (1937) 239). In his talk “From the Periodic Table to Production” (p. 241), Midgley remarked: “C. F. Kettering was a primary factor. Without his guiding genius, faith, patience, and financial support it is likely that neither Ethyl gasoline nor the Freon refrigerants would be in existence today.

    Also in 1937 the idea of another public relations stroke originated in certain dental circles: dental researchers would be asked for a summary on their research efforts relative to the causes and control of dental caries; these summaries could be published in a monograph (J.W. Gies to R.W. Bunting, March 28, 1940; in the R. W. Bunting papers, Bentley Historical Library, University of Michigan). Charles F. Kettering became a counselor in an “Advisory Committee on Research in Dental Caries” of the American Dental Association.


    1938

    Letters, i.e. requests for summaries,  were sent to almost 200 dental researchers in 25 countries from the “Advisory Committee on Research in Dental Caries” of the American Dental Association´s Research Commission, detailing in the letter-head the participation of the famous Charles F. Kettering of General Motors.

    Thomas MIDGLEY, Albert L. HENNE, assignors, by mesne assignments, to Kinetic Chemicals, Wilmington, Delaware: “Fluorination process”, US Patent 2,192,143; filed May 7, 1938; patented Feb. 27, 1940


    1939

    The compilation of the dental research summaries was published by the ”Advisory Committe on Research in Dental Caries of the Research Commission of the American Dental Association” under the title of “Dental Caries“.

    Machle, Scott and Treon, of the Kettering Institute, published the “normal urinary fluorine excretion and the fluorine content of food and water” (Am. J. Hygiene 29 (1939) 139)


    1940

    A review of “Dental Caries”, which Russell W. Bunting called a “World Almanac of Dental Errors(R.W. Bunting to J.W. Gies, June 22, 1940; in the R.W.Bunting papers, Bentley Historical Library, University of Michigan), stated: ”A noteworthy departure from committees dealing with technical matters was the inclusion of Mr. C. F. Kettering, well known as an engineer and industrial manager. The inclusion of a layman of such ability brings a freshness of viewpoint from one well  trained in scientific method and gifted with exceptional organizing ability” (J. Am. Dent. Assoc. 27 (Jan. 1940) 117).

    Machle and E. E. Evans, of the Kettering Institute, examined the “Exposure to fluorine in industry” (J. Ind. Hyg. Toxicol. 22 (June 1940) 213)


    1941

    After another set of letters was sent world-wide to dental researchers, the second edition of “Dental Caries” was published by the same Committe that compiled the 1939 version.

    Lyle D. GOODHUE, William N. SULLIVAN, assignors to Claude A. Wickard, as Secretary of Agriculture of United States of America, and his successors in office: “Method of applying parasiticides”, US Patent 2,321,023; filed July 29, 1941; patented June 8, 1943


    1942

    Tests with hydrogen chloride published in 1942 led to the conclusion that “hydrogen chloride has nearly the same immediate toxic action as hydrogen fluoride, but produces less serious residual effects than this compound.” The organs of animals “surviving exposure to hydrogen fluoride showed more frequent and more severe pathological changes than those of animals exposed to hydrogen chloride. The concentration level which appeared safe for long exposure was also much lower in the case of hydrogen fluoride” (J. Ind. Hyg. Toxicol. 24 (Oct. 1942) 222).

    In the meantime, the aerosol propellants had also gained importance for military purposes:

    Excerpt from Chapter 2, “Historical background”, in Paul A. SANDERS, of E. I. Du Pont de Nemours & Company, “Principles of Aerosol Technology“, Van Nostrand Reinhold Company, New York, etc., 1970:

    “One of the most important developments in the aerosol field occurred during World War II. During an investigation to find a way of combating the insects which caused disease among overseas troops, Goodhue and Sullivan, of the Department of Agriculture, developed a portable aerosol dispenser which used “Freon” 12 fluorocarbon as the propellant … From July 1942, when the requirement was 10,000 containers per day, until the end of the war, one company alone, Westinghouse Corporation, supplied over 30,000,000 aerosols to the Armed Forces. Other companies engaged in supplying aerosols for the military included Regal Chemical Company, Brooklyn, New York; Airsol Inc., Neodesha, Kansas; and Bridgeport Brass Company, Bridgeport, Connecticut. Immediately after the war, Westinghouse Corporation dropped out of the aerosol field, but the others continued to produce aerosol products.”

    Being active in fluoride research, the Kettering Institute was also approached by Mead Johnson and Company, manufacturer of “Pablum” infant food (J. Ind. Hyg. Toxicol. 24 (Sept. 1942) 199; 25 (March 1943) 112):

    “Pablum, a popular infant food prepared from bone meal [*], formerly contained as much as 18 ppm. When this amount of fluoride was found to be excessive -it produced mottled teeth- manufacturers reduced the fluoride content of Pablum to between 1.33 and 2.12 ppm” (George Walbott, Albert L. Burgstahler, Lewis McKinney: “Fluoridation the great dilemma”, Lawrence, Kansas, 1978, p. 39). Mead Johnson replaced the veal bone ash by tricalcium phosphate (George Waldbott: Am. J. Clin. Nutr. 13 (Dec. 1963) 393).

    * Lambert D. JOHNSON, Nathan F. TRUE, Barry H. ENGEL, assignors to Mead Johnson and Company: “Food product and method”, US Patent 1,990,329; filed May 8, 1933; patented Feb. 5, 1935


    1943

    J. F. Treon, Instructor in toxicology, Kettering Laboratory of Applied Physiology, Cincinnati, Ohio, became one of the many people (besides Hodge, Voegtlin, Stokinger …) to supervise research programs for the “Manhattan District” (the project for the construction of the first atomic bomb). In this project fluorocarbons played a major role as coolants and lubricants. “The toxicity of these substances was tested by an experimental program similar to that used by the Toxicology Division of the U. S. Public Health Laboratories.” … “These compounds were found to be moderately toxic to animals upon inhalation, but some of the intermediate products formed in the production of these compounds were found to be toxic to animals in concentrations varying from 70 – 500 parts per million parts of air. The animals exposed to toxic concentrations of these intermediate products of the fluorocarbons died apparently as a result of respiratory failure” (from: HREX Archives, “Manhattan District History, Book I – General, Volume 7 “Medical Program”, printed Dec. 31, 1946; reproduced at the National Archives).

    Meanwhile, Albert L. Henne was under contract for the National Defense Research Committee (from July 1, 1942 to June 30, 1943) to find new ways for the synthesis of fluorinated hydrocarbons. However, “the procedures proved insufficient and too lengthy, and were abandoned when it was realized that better results were claimed at Purdue (i.e. Purdue Research Foundation, -> McBee), and when direct fluorination was adopted for large scale production” (from: National Defense Research Committee of the Office of Scientific Research and Development, “Final Report on Fluorocarbons and Related Compounds”, Report OSRD No. 1792, Sept. 10, 1943; “cleared” upon F.O.I.A. request on Sept. 18, 2001).


    1946

    Harold Simmons Booth et al. describe the use of Freon 12 (dichlorodifluoromethane) for the manufacture of dry uranium tetrafluoride of high purity (J. am. chem. Soc. 68 (1946) 169). The publication of this paper “was delayed for war-time security reasons” as the editor notes in a footnote. Other methods for the preparation of this compound (which was essential for the Manhattan Project for the production of uranium hexafluoride) “yield products containing water and hydrogen fluoride from which it is difficult to separate uranium tetrafluoride without some decomposition.” Freon 12 was found to react quantitatively with uranium trioxide to produce pure anhydrous uranium tetrafluoride at elevated temperatures.


    1961

    A book by Kettering Lab scientist E. J. Largent, “Fluorosis. The health aspects of fluorine compounds”, Ohio State University Press, 1961, was expressly designed, as indicated on its jacket, to ”aid industry in law suits arising from fluoride damage.”

  • EPA Says Breathing Is Deadly, But Radioactive Drinking Water Is Good For Us

    Environmental Protection Agency: Gas that humans exhale is a threat to public health, yet uranium and arsenic poisoned water is perfectly nutritious

    EPA Says Breathing Is Deadly, But Radioactive Drinking Water Is Good For Us 081209top2

    Paul Joseph Watson
    Prison Planet.com
    Tuesday, December 8, 2009

    While the EPA declares the gas that we exhale to be a deadly poison, as protesters at Copenhagen decry the suffering of polar bears as their population figures increase to record levels, and as delegates in the Danish capital warn of the dastardly peril of cows farting, a New York Times report confirming that U.S. drinking water contains dangerous levels of arsenic, uranium and other radioactive substances barely gets noticed.

    Furthermore, the new study shows that the Environmental Protection Agency knew that water systems all over the United States were contaminated with dangerous levels of numerous toxic substances, yet failed to punish the vast majority of water authorities involved.

    Since the environmental movement was completely hijacked by globalists hell bent on world government and devastating carbon taxes, real environmental problems have been swept aside as the contrived scam of man-made global warming swallows up all the attention.

    Our drinking water is contaminated with toxic waste, our food supply is poisoned by genetically modified garbage, and our consumer products are laced with cancer-causing chemicals, but who cares right? Surely all this pales in comparison to the effort to stop the world warming by a percentage of a degree over the next 100 years?

    More than 20 percent of the nation’s water treatment systems have violated key provisions of the Safe Drinking Water Act over the last five years, according to a New York Times analysis of federal data.

    That law requires communities to deliver safe tap water to local residents. But since 2004, the water provided to more than 49 million people has contained illegal concentrations of chemicals like arsenic or radioactive substances like uranium, as well as dangerous bacteria often found in sewage.

    But unlike the mammoth threat posed by the life-giving gas carbon dioxide, which the EPA yesterday classified as a health threat to the same humans that exhale it, the Environmental Protection Agency is noticeably less concerned about the fact that our water is filled with contaminants that are “linked to millions of instances of illness within the United States each year.”

    Indeed, records show that fewer than 6 percent of the water systems that broke the law were ever punished or fined by the EPA.

    “In some instances, drinking water violations were one-time events, and probably posed little risk. But for hundreds of other systems, illegal contamination persisted for years, records show,” according to the article.

    The Senate Environment and Public Works committee will question a high-ranking E.P.A. official about why they allowed water companies to continue such contamination without punishment at a hearing today.

    According to the study, not only were water systems contaminated with radioactive substances like uranium as well as arsenic, but they were also found to contain cancer-causing solvents and illegal amounts of bacteria.

    “The amount of radium detected in drinking water was 2,000 percent higher than the legal limit,” adds the report. Radium is described as “extremely radioactive” and has a half-life of 1602 years. People exposed to radium suffer serious health effects including sores, anemia and bone cancer. The use of radium in paints as late as the 1950’s was eventually halted after many deaths were attributed to exposure to the chemical.

    True to form, the NY Times chooses to characterize water which contains deadly radioactive chemicals as “dirty” in its headline!

    Millions in U.S. Drink Dirty Water, Records Show – oh its just a bit of dirt you know! Cancer-causing radioactive toxins and poisonous arsenic – its just a little dirty!

    “The problem, say current and former government officials, is that enforcing the Safe Drinking Water Act has not been a federal priority,” reports the Times, adding that current and former EPA officials who attempted to make the agency enforce the drinking water law were targeted.

    “I proposed drinking water cases, but they got shut down so fast that I’ve pretty much stopped even looking at the violations,” said one longtime E.P.A. enforcement official who, like others, requested anonymity for fear of reprisals. “The top people want big headlines and million-dollar settlements. That’s not drinking-water cases.”

    So there you have it – according to the EPA – breathing is a threat to human health – but drinking water laced with arsenic, cancerous carcinogens, and radioactive chemicals is perfectly nutritious!

    So pour a fresh glass of toxic tap water, drink up and say cheers to the fact that the government really cares about our health and the real environmental issues – before you drop dead.

  • Mercury vapor from dental amalgam results in toxic accumulation in body tissues

    A great demonstration of mercury vapor being released from dental amalgam (silver) fillings.

  • How Mercury Causes Brain Neuron Degeneration – University of Calgary