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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.
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Sinking of S. Korean Cheosan may be a staged provocation
Mike Rivero
What Really Happened
Thursday, May 27, 2010What 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 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.

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.

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

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.

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

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.
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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
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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.” -
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 PMRep. 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.
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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.
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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 gavageexerts 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 weeksFertility 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 BWThe 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 dayscaused 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 BWsignificant 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.htmFluoride 1998; 31(4):203-216
Amelioration of fluoride toxicity by Vitamins E and D in reproductive functions of male miceNJ 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 daysRAT: NaF
1 mg/kg/day and
10 mg/kg/day for 28 daysIn 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 daysthe 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 reversalChinoy 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-daysATSDR – 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 spermatogenesisSee also: Pages 82 and 113
1997 RABBIT
ATSDR – Page 85
LOAEL 4.5 mg/ kg/day
Leydig cell damageLOAEL 4.5 mg/ kg/ day
Leydig cell damageAs 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 groupA 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 daysATSDR – 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 daysThe 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 dayschanges 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 dayssperm 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 higherThe 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 daysATSDR – 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/dayabnormal 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 monthsThe 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 daysReduction 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 rabbitsChinoy 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 daysDeficient 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 daysATSDR (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 usedIncidence 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/kgNaF 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 testesToxicol 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 ppm98 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 MKDep. 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 MEDept. 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 monthslack 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 reportSPS 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 Representation – turning 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.”
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