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  • Fine of $50,000 + prison for refusing to export to Israel

    This was linked from Reddit today:

    http://www.bis.doc.gov/complianceandenforcement/antiboycottcompliance.htm

    “The penalties imposed for each “knowing” violation can be a fine of up to $50,000 or five times the value of the exports involved, whichever is greater, and imprisonment of up to five years. During periods when the EAR are continued in effect by an Executive Order issued pursuant to the International Emergency Economic Powers Act, the criminal penalties for each “willful” violation can be a fine of up to $50,000 and imprisonment for up to ten years.”

    Apparently it’s illegal in the US to refuse to export products to the genocidal, apartheid state of Israel.  I should have assumed, considering the deep infiltration of Zionists in our government and corporate media, but somehow this still came as a shock.

  • Sinking of S. Korean Cheosan may be a staged provocation

    Mike Rivero
    What Really Happened
    Thursday, May 27, 2010

    What can I say; here we go again!

    I hardly need to go down the list of lies used to start US wars. We have been though that over and over again.

    Nor do I need to elucidate on the many reasons why the US Government is in desperate need for yet another war with which to scare the American people into acceptance of more takes and fewer rights and freedoms.

    Anyone with half a brain realizes that the US Government, unable to gain support for an invasion of Iran, has changed gears and decided that North Korea will be the next step towards World War III.

    Here is the big lie…

    Let us start with a cloned copy of the official South Korean website detailing the sinking of the Cheosan.

    From that website we get the following picture of the remains of a torpedo dredged from the bottom of the ocean.

    The Big Lie Selling You War With North Korea 1274321650 7

    The official claim that North Korea fired this torpedo at a South Korean warship is based on the following blueprint of a North Korean torpedo claimed to be the weapon recovered from the ocean floor.

    The Big Lie Selling You War With North Korea northkoreatorpedoplans

    There are several differences between the torpedo plans and the actual torpedo recovered from the floor of the ocean. But I am going to focus on just one.

    Take a close look where the tail cone assembly (indicated by the bulkhead at the leading edge of the fins) attaches to the torpedo main hull. A major component of all modern torpedoes are the fin actuators. These are the small motors that adjust the rudder and dive planes of the torpedo in order to maintain the intended depth and course to target.

    Note that the blueprints of the North Korean torpedo show these actuators forward of the tail cone assembly, that is to say in front of the bulkhead that marks where the fin assembly attaches to the torpedo.

    The Big Lie Selling You War With North Korea ACTnorthkoreatorpedoplans

    Now let us look at the torpedo actually recovered from the bottom of the ocean near where the Cheosan was attacked.

    The Big Lie Selling You War With North Korea 1274321650 7

    Note that the recovered torpedo these actuators are built INSIDE the tail cone assembly, that is to say to the REAR of the bulkhead that marks where the fin assembly attaches to the torpedo.

    The Big Lie Selling You War With North Korea ACTin%20actualtorpedo

    And again, as seen in the official released photo of the recovered torpedo.

    The Big Lie Selling You War With North Korea ACTtorpedo

    In short, the torpedo recovered from the ocean where Cheosan was attacked is NOT the same torpedo shown in the North Korean plans. As I stated above, there are additional differences as well between the blueprints and the actual torpedo, but the actuators are the clincher.

    The torpedo recovered from the ocean where the Cheosan was sunk is not the North Korean torpedo shown in the blueprints.

  • Michigan senators expected votes on HB 4961 toll privatization scam

    How the Senate stands on DRIC (Detroit-Canada bridge expansion) and  HB 4961.
    In the case of a tie, Lt. Gov Cherry would vote in favor:

    Republicans Democrats
    Supporting: None

    Leaning against: Garcia, Nofs, Pappageorge, Sanborn

    Opposing: Brown, Cassis, Cropsey, George, Jelinek

    Undecided: Allen, Bishop, Gilbert, Hardiman, Jansen, Richardville

    Not returning messages: Birkholz, Kahn, Kuipers, McManus, Patterson, Stamas, Van Woerkom

    Supporting: Anderson, Basham, Clarke (with benefit conditions for Detroiters), Jacobs, Prusi, Switalski

    Leaning toward supporting: Whitmer

    Opposing: Gleason, Olshove

    Undecided: Scott

    Not returning messages: Barcia, Brater, Cherry, Clark-Coleman, Thomas

    Declining to comment: Hunter

    Source: Gongwer interviews

  • Opsommer: Bill could create government sanctioned monopolies

    From MI Rep Paul Opsommer

    P3 LEGISLATION, DRIC BRIDGE TWO SEPARATE ISSUES SAYS OPSOMMER

    “We run the risk of creating government sanctioned monopolies if we just turn existing infrastructure over to a concessionaire who then places tolls on it.
    And if ownership is transferred to a mixed-government authority, we need to make sure those are Michigan-based governments. I do not want officials in Canada, Ohio, or Indiana setting our toll rates, exercising eminent domain, or making other decisions for our citizens.”

    Read the entire article

  • Message from MI Rep Opsommer re: HB 4961 corporate toll giveaway

    We should call this the Michigan Infrastructure Fire Sale Act (MIFS) or perhaps the Michigan Taxpayer Raping Act (M-TRAP).

    Some background on this horrible piece of proposed legislation can be found here.

    - – - – - -

    Rep Opsommer sent this message earlier today:

    No Vote Explanation for HB4961
    What is No Vote Regarding: Passage
    Date: 5/26/2010
    Time: 7:02:28 PM

    Rep. Opsommer, having reserved the right to explain his protest against the passage of the bill, made the following statement:

    “Mr. Speaker and members of the House:

    Legislative colleagues, simply put, this bill is about much more than just the DRIC. Much, much more. This is a vehicle bill that is attempting to use the DRIC as leverage for an unprecedented shift of power and authority from the legislative to the executive branch when it comes to the unilateral ability to be able to toll our citizens.

    There is no reason it has to be this way.  We should be looking at the DRIC and PPP bills separately.  That is how we have done all the other toll bridges here in Michigan. But instead, it has been a conscious decision by MDOT to wrap the DRIC bridge up into broad public-private partnership legislation that would not only allow for the DRIC but would cause the Legislature to give up its authority to statutorily authorize tolling anywhere else in the state. I don’t know if this is because the governor wants to use the bill as leverage to keep Canada happy with the DRIC, or if she simply wants to have the unilateral ability to impose tolls on taxpayers with no other checks and balances, but either way it’s wrong.

    I have a letter from the Attorney General’s office that shows that right now, today, MDOT can not toll a road or bridge or other infrastructure without legislative approval.  And you know what?  That is how it should be, and how we should keep it.

    Whether tolling is done directly by MDOT or a private contractor, you want someone who has been elected by the people determining where to use that tool.  In fact, in cases where it is being done by a private contractor who is using toll rates not just to break even but also to create profits, I would think you would want to keep voter accountability even more. If toll rates go unfairly through the roof, who are taxpayers supposed to turn too? The Legislature will be powerless at that point; it would actually be players from outside of the state who would have the final word.

    Besides taking away the tolling authority we already have, this bill is also too broad in terms of what it defines as a transportation facility.  Let me read to you the bill and how they define it:

    “A public transportation facility means any NEW, or EXISTING, DOMESTIC, or INTERNATIONAL, highway, lane, road, bridge, tunnel, overpass, ramp, interchange, ferry, airport, vehicle parking facility, vehicle transportation facility, port facility, locks facility, rail facility, intermodal or other public transit facility, or any other equipment, rolling stock, site, or facility used in the transportation of persons, goods, substances, vehicles, information, or matter of any kind, and any building, structure, parking area, appurtenance, or other property necessary or DESIRABLE for the facility”

    My colleagues, that is more than a mouthful.  It is literally anything that is not permanently nailed down in this state, and even then includes some of those things as well.  This is supposed to be a transportation bill?  Really? And it includes such things under the definition as a catchall phrase such as “matter of any kind”?  They should define it the other way, what are the things MDOT couldn’t define as a public transportation facility?  I’m not sure to be honest.  And to be clear, under their definition for all these things it includes not just new but also existing.  It includes domestic and out of state and international.  When it comes to condemnation, it also includes property not just necessary for the project, but also just merely desirable for the facility.  That even includes commercial uses like gas stations, restaurants, hotels, convention centers, and other things that would fall under the definition of being merely “desirable”.  So when a taxpayer has his or her private property taken away, and given to another private entity so that they can make a profit off of it, we can expect that the property may be taken away for a Speedway, or a McDonalds, or a Red Roof Inn, or a Kellogg Center type project that could all be part of any various toll bridge or toll road mixed projects.  Under the current bill these companies would not even have to pay property taxes.

    My colleagues, when such a project gets plunked down in your back yard, if the Senate doesn’t stop it, you will have absolutely NO formal vote on that project.  You will have to tell your constituents that it is out of your hands.  Now, some people may like that.  I know where they have passed legislation like this in other states that the consultants actually sell that as a feature, that the legislature gets left of the hook. Well, Michigan legislators are better than that, and there is no way we should be allowing for that here.

    Simply put, this takes away too much power from the legislature, power and oversight that it already has, and then also substantially broadens the power of what MDOT can do with that authority at the same time. And the real question is, what does that have to do with the DRIC?  Why not run bills like we have for the Blue Water bridge? The answer is quite simply that we could, and the only reason we aren’t is because the DRIC is being used as leverage to try to pass a bill that in its current form of robbing legislative power would have NO chance, a 0% chance, of passing out of this body on its own. No chance at all.

    And why are we being pressured into feeling like we have to do this today?  Being pressured from sources from outside of Michigan? If it wasn’t for the fact that the main potential investor in all of this, the Ontario pension fund OMERS, was recently granted expanded powers by the Canadian government to provide investment management services I am not sure we would even be here. So when tolls are being paid in Michigan, tolls not just to break even mind you but also for profit, Michigan drivers could end up paying toll rates set to ensure that OMERS pensioners makes a high rate of return. We shouldn’t be making decisions on tolling Michigan taxpayers based off of the financial needs and a quest by a Canadian pension fund, the whole reason for the supposed $550 million dollar “loan” they are offering us in the first place, a loan that will have to be repaid by, you guessed it, Michigan tolling.

    And now, there are reports that Ohio is getting involved, and has introduced a resolution supporting the DRIC.  Ohio?  Ohio is now going to tell us who MDOT should be allowed to toll?  Maybe we should also ask Indiana or Wisconsin what they think before we pass this bill as well. Maybe we should also check with Mexico to see where they want the NAFTA superhighway to go? At the end of the day, whose law is this anyway?  Well it is ours, or at least it should be.  Maybe some of you  just contracted out our legislative authority and laws as well.

    To conclude, if we pass laws in Michigan that give MDOT unilateral tolling power in our state it should be because that is what the Michigan Legislature feels is right, not because of pressure from other states or countries.  And it should also not allow for “instrumentalities of government” from other countries and states to be able enter into contracts that could potentially determine the tolling rates and eminent domain location decisions taking place in Michigan.  Under this bill, new governmental authorities will be created, authorities that will be defined as an instrumentality of government that in some cases will include people from outside of this state.  The bill says that ownership of a project can in vested into these new creations. They will be the ones entering into the contracts.  People will be making decisions that don’t even live here and may not be citizens of our country, let alone our state.  These facilities should not just be publicly owned, but owned by the MICHIGAN public. Texas has put a moratorium on these based on their experience with Mexico for a reason, a moratorium that apparently we have not learned from or listened to.  For some reasons we appear to be in a race instead to be like California, which has little oversight and whose history on these projects is replete with problems. Even there, their law is nowhere near as broad as what has just passed out of the House.

    I am also concerned that this bill will hamstring our local governments from being able to build roads.  In other states, like California, local government has had to first pay a penalty in order to build something simply because others might consider it as competition.  Can you imagine, paying someone else for the right to build on your own land? We are being sold that this is a panacea, that there is no risk to Michigan, and yet the bill passed today is nowhere near strong enough in ensuring that local governments won’t have to pay penalties like this in order to build in their own backyard or face injunctions to stop expansion or construction that is underway.

    This version of the bill is the wrong way to go, and I vote resoundingly NO.

  • CSI mind control programming

    I’ll tell you who the anti-american traitors are, it’s the actors in this propaganda piece-of-shit TV show.

    These hollywood goblins should chug a big glass of fluorosilicic acid if they think it’s so great.  That’s the chemical they’re putting in our water to brain damage and sterilize us.  When you participate in this mind control psyop you’re guilty of giving those little boys osteoscarcoma (bone cancer). skeletal and dental fluorosis, reduced fertility, brain damage, and many other health problems.

    This propaganda is disgusting and evil.   CSI actors, if you’re reading this, please just go kill yourselves.  You hurt little kids for money and you do not deserve to live.

    And here is more scientific proof than you ever wanted that fluoride is toxic, especially to children.

  • 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.

  • Toll privatization scheme in Michigan HB 4961 amounts to a tax paid directly to private corporations, without representation

    Update (May 26/ 2010 7pm) This bill has passed the house, 56-51 and is going to the Senate.

    Michigan House Bill 4961 [pdf] boils down to Taxation without Representationturning the State’s right to levy taxes over to private international corporations, essentially ceding sovereignty over critial infrastructure.  The corporations will be able to levy highway tolls without oversight or regulation on US citizens, should this bill pass.

    At an absolute minimum it allows the creation of a single high occupancy toll lane.   After the next repaving of an entire highway, tolls can be collected on all lanes.

    Now that the financial elite have tanked our economy, they’re trying to buy up our infrastructure and property using their international corporations that operate above the law.

    Some important exerpts from the bill:

    … to abolish the office of state  highway commissioner and the commissioner’s advisory board and to transfer their powers and duties…

    TO PROVIDE FOR PUBLIC-PRIVATE  TRANSPORTATION FACILITIES; TO AUTHORIZE PUBLIC-PRIVATE AGREEMENTS RELATING TO … TOLLING, OPERATING, OR  MAINTAINING A PUBLIC-PRIVATE TRANSPORTATION FACILITY

    [allow private corporation to tax the use of public "transportation facilities" ... but what constitutes a transportation facility?]

    “TRANSPORTATION FACILITY” MEANS ANY NEW OR EXISTING  HIGHWAY, ROAD, BRIDGE, TUNNEL, OVERPASS, RAMP, INTERCHANGE, FERRY,  AIRPORT, VEHICLE PARKING FACILITY, VEHICLE TRANSPORTATION FACILITY,  PORT FACILITY, LOCKS FACILITY, RAIL FACILITY, INTERMODAL OR OTHER  PUBLIC TRANSIT FACILITY, OR ANY OTHER EQUIPMENT, ROLLING STOCK,  SITE, OR FACILITY USED IN THE TRANSPORTATION OF PERSONS, GOODS,  SUBSTANCES, VEHICLES, …

    [Wait for it, wait ....]

    INFORMATION, OR MATTER OF ANY KIND

    [data cables are included in "transportation facilities?!"  This bill would allow sale and private taxation of network (internet/data) infrastructure as a "transportation facility" based on "congestion."  Data cables are already leased by big cable/telcos so what does this mean for them?]

    … INCLUDING THE SALE OF REVENUE BONDS …

    [turn the business holdings into a fiat financial market; enable fractional lending based on expected future revenue, destabilizing the business]

    “INSTRUMENTALITY OF GOVERNMENT” MEANS A LEGAL PUBLIC  ENTITY CREATED OR EMPOWERED TO CARRY OUT FUNCTIONS COMMONLY CARRIED  OUT BY UNITS OF GOVERNMENT

    THE AGREEMENT SHALL PROVIDE THAT THE OWNERSHIP  OF A TRANSPORTATION FACILITY WITHIN THIS STATE SHALL BE VESTED IN  AN INSTRUMENTALITY OF GOVERNMENT AND THAT TITLE TO THE  TRANSPORTATION FACILITY SHALL NOT BE ENCUMBERED

    [the corporation will have complete "unencumbered" control]

    NO PROVISION OF A  PUBLIC-PRIVATE AGREEMENT SHALL ALLOW THE PUBLIC TO BE DEPRIVED OF  THE USE AND BENEFIT OF A TRANSPORTATION FACILITY EXCEPT AS  NECESSARY TO IMPLEMENT TOLLS OR OTHER CHARGES

    [the corporation has the authority to deny access if you don't pay the toll]

    A TOLL MAY BE  IMPOSED ON A HIGHWAY ONLY IF IMPOSED FOR THE USE OF NEW HIGHWAYS,  OR THE USE OF EXPANDED HIGHWAY CAPACITY BEYOND HIGHWAY CAPACITY IN  PLACE ON THE EFFECTIVE DATE OF THE AMENDATORY ACT THAT ADDED THIS  SECTION.

    [tolls may be levied for any expansion or heavy traffic (?)]

    TOLLS AND OTHER CHARGES IMPOSED FOR THE USE OF A  TRANSPORTATION FACILITY ARE NOT SUBJECT TO REGULATION BY ANY OTHER  GOVERNMENTAL AGENCY.

    [the tolling will not be regulated by the government]

    NOTHING IN THIS SECTION SHALL BE CONSTRUED TO  ALLOW THE CONVERSION OF ANY NONTOLL OR NONUSER-FEE LANES EXISTING  ON THE EFFECTIVE DATE … WITH THE EXCEPTION OF A HIGH-OCCUPANCY VEHICLE LANE THAT MAY BE OPERATED AS A HIGH-OCCUPANCY  TOLL LANE FOR VEHICLES NOT OTHERWISE MEETING THE REQUIREMENTS FOR  USE OF THAT LANE.

    At a minimum, if this passes, the corporation(s) will create high occupancy toll lanes.  Initially this allows them to just take one lane and turn it into a private toll lane.  If we let this pass, how easy will it be to expand it to 2 “managed lanes,” or 3, or the whole highway?

    When the highway needs repaving, will the private company dictate who gets the contracts? And how do we select which private company gets to take control in the first place? Well, anything goes according to this:

    ANY COMPETITIVE SELECTION PROCESS THAT THE DEPARTMENT  DETERMINES TO BE APPROPRIATE OR REASONABLE …  USING A COMPETITIVE  SELECTION PROCESS WHEN TO THE EXTENT PRACTICABLE

    ….

    INFORMATION SUBMITTED UNDER SUCH A  PROMISE OF CONFIDENTIALITY SHALL NOT BE SUBJECT TO DISCLOSURE UNDER  THE FREEDOM OF INFORMATION ACT

    [The bidding process will be competative to the extent that the government determines is "reasonable," but you'll never know because whatever we say is "private negotiations" will be exempt from FOIA requests]

    A newer version of the bill (pdf) has been released that is substantially the same but provides for “public hearings” to receive user input; amounting to no real oversight or accountability.

    THE COMMISSION SHALL CONDUCT A PUBLIC HEARING AT LEAST ONCE EVERY 5 YEARS TO RECEIVE PUBLIC COMMENT AND INPUT WITH REGARD TO THEN EXISTING PUBLIC TRANSPORTATION FACILITIES ….

    After the next repaving, all highway lanes can be turned into toll lanes.   Signing this bill will inevitably turn our Michigan highways into private revenue streams for multinational corporations, not to mention ports, rail, and network infrastructure.  This is infrastructure we’ve already paid to build, and need to maintain ourselves in order to sustain the local economy by hiring local workers and companies.

    People from Michigan, it is absolutely critical that we reject this bill.  We can not let them hand our infrastructure over to international corporations as many other states have.  In the long run Michigan will lose on this deal in a big way.

    They mean business and will do whatever is necessary including paying off our elected officials.  Call your representatives and let them know we’re watching!

    - – - – - – - – - – - – -

    From MI Rep Paul Opsommer:

    OUT-OF-STATE MEDDLING WORSENS HB 4961

    May 24, 2010

    State Rep. Paul Opsommer today criticized Canadian and Ohio officials for pushing legislation that would allow the Michigan Department of Transportation to toll virtually anywhere in Michigan.

    “At the end of the day, whose law is this anyway?” asked Opsommer, R-Dewitt. “Canada’s understandable need to be part of border discussions is now being eclipsed by their off-base efforts to support the Ontario pension fund, and now we have resolutions being introduced involving the Ohio Legislature as well. If we pass laws in Michigan that give MDOT unilateral tolling power in our state it should be because that is what the Michigan Legislature feels is right, not because of pressure from other states or countries.”

    Opsommer made his comments in response to a recent news story that officials in Ohio are advocating for their resolution SR 223 in support of the Detroit River International Crossing. The bill in Michigan that would allow for that, HB 4961, would also give new power to MDOT at the expense of the Legislature. HB 4961 is also criticized for allowing “instrumentalities of government” from other countries and states to enter into contracts that could potentially determine the tolling rates and eminent domain decisions taking place in Michigan.

    “It has been a conscious decision by MDOT to wrap the DRIC bridge up into broad public-private partnership legislation that would not only allow for the DRIC but would cause the Legislature to give up its authority to statutorily authorize tolling anywhere else in the state,” Opsommer said. “I don’t know if this is because the governor wants to use the bill as leverage to keep Canada happy with the DRIC, or if she simply wants to have the unilateral ability to impose tolls on taxpayers with no other checks and balances, but either way it’s wrong.”

    The Ambassador Bridge, Blue-Water Bridge and all other tolled facilities in Michigan received their tolling authority through stand alone bills authorized by the Legislature. Opsommer cited a recent letter from the attorney general’s office that concurs that MDOT currently only has the ability to toll where the Legislature has given its formal approval.

    “Whether tolling is done directly by MDOT or a private contractor, you want someone who has been elected by the people determining where to use that tool,” Opsommer said. “In cases where it is being done by a private contractor who is using toll rates not just to break even but also to create profits, I would think you would want to keep voter accountability even more. If toll rates go unfairly through the roof, who are taxpayers supposed to turn too? The Legislature will be powerless at that point; it would actually be players from outside of the state who would have the final word.”

    Opsommer also pointed to international pressure from Canada as having an unfair influence on the process.

    “If it wasn’t for the fact that the main potential investor in all of this, the Ontario pension fund OMERS, was recently granted expanded powers by the Canadian government to provide investment management services I am not sure we would even be here,” Opsommer said. “We shouldn’t be making decisions on tolling Michigan taxpayers based off of the financial needs and a quest for high returns by a Canadian pension fund. The DRIC and HB 4961 should be treated as two entirely separate issues.”

    The National Motorists Association has endorsed a substitute version of HB 4961 that would ensure the Michigan Legislature still retained its tolling authority over MDOT and other instrumentalities of government from outside of the state.

    “It is essential to not pass any version which does not provide for specific legislative approval for any public-private partnership that will involve direct tolling for the users,” said Jim Walker of the National Motorist’s Association. “Should the H-6 unfortunately pass in the House, I hope the Senate will have the courage to fix this issue.”