Who Ya Gonna Call Before August 16 to Complain about 4G and 5G Small Cell Towers Being Installed in Front of Homes, etc.? The Senate Commerce, Science and Transportation Committee



Who Ya Gonna Call Before August 16 to Complain about 4G and 5G Small Cell Towers Being Installed in Front of Homes, etc.? The Senate Commerce, Science and Transportation Committee (Contact Info Provided).

https://www.activistpost.com/2018/08/call-before-august-16-complain-4g-5g-towers-contact-list.html

August 8, 2018

By B.N. Frank

Big Thanks to all EMF activists for providing so much information to Activist Post so we can pass it on to readers who also want to stop the widespread “Roll Out” of risky 5G technology and other Telecom Industry, FCC, and other elected officials’ nonsense.

Since 2004, The International Association of Firefighters has opposed the use of their stations as base stations for cell towers and antennas until it can be proven that this is NOT hazardous to their health. So why would any of the rest of us be okay with allowing small cell towers to be installed in front of our homes, in public rights-of-ways, and everywhere else? This violates “The Precautionary Principle.”

In addition to contacting your local, state, and federal elected officials ASAP, a list of senate committee members and their contact information is posted at the end of this article. Please contact them before August 16.

With a little luck, we can help it out. We can make this whole damn thing work out.

Here’s the deal as relayed via excerpts from an article posted by Radio + TV Business Report:

On Aug, 16 the Federal Communications Commission (FCC) has an oversight hearing which will be conducted by Senate Commerce, Science and Transportation Committee.

According to Committee Chairman John Thune (R-S.D.)

The hearing, the Committee notes, will examine policy issues before the Commission and review the FCC’s ongoing duties and activities. This includes efforts to better utilize spectrum powering our wireless economy to expanding rural broadband access, combatting robocalls, and reviewing the media landscape.

(A little more background):

For several hours on July 25, the four voting members of the FCC answered questions and, in a handful of instances, sparred with House of Representatives members who wanted assurances that the White House would not sway the Commission on its decision to send Sinclair Broadcast Group‘s intended merger with Tribune Media to an Administrative Law Judge.

Because of this, the FCC Four went to the Senate side of Capitol Hill for an oversight hearing that was conducted by Senate Commerce, Science and Transportation Committee one day later than originally planned.

On July 30, the committee announced that it would convene its hearing on August 15 at 10:15am. However, now it’s been pushed back again and will be held on August 16 at 10am at Russell Senate Office Building, Room 253.

Witness testimony, opening statements, and a live video of the hearing will be available on http://www.commerce.senate.gov.

The following list of committee members and their contact information was provided by EMF activists. Websites are not working for some officials and this has been noted next to their names. Please contact some or all of them before August 16 and let them know how you feel about all of this:

Committee on Commerce, Science, and Transportation

https://www.commerce.senate.gov/public/index.cfm/committeemembers

Contact Information for the Committee Full Committee Office
Majority: 202-224-1251
Majority Address: 512 Dirksen Senate Building; Washington DC, 20510
Minority: 202-224-0411

MAJORITY MEMBERS:

1. CHAIRMAN: Senator John Thune, South Dakota
Washington D.C. Office
United States Senate SD-511
Washington, DC 20510
Phone: (202) 224-2321
Fax: (202) 228-5429
Toll-Free: 1-866-850-3855
EMAIL FORM: https://www.thune.senate.gov/public/index.cfm/contact

2. Senator Roger Wicker Mississippi
Washington, D.C.
555 Dirksen Senate Office Building
Washington, DC 20510
Main: (202) 224-6253
Fax: (202) 228-0378
EMAIL FORM https://www.wicker.senate.gov/public/index.cfm/contact

3. Senator Roy Blunt Missouri
Washington, D.C.
260 Russell Senate Office Building
Washington, DC 20510
Phone: (202) 224-5721
EMAIL CONTACT FORM: https://www.blunt.senate.gov/public/index.cfm/contact-roy

4. Senator Ted Cruz Texas
WASHINGTON, D.C.
(202) 224-5922
404 Russell
Washington, DC 20510
EMAIL: https://www.cruz.senate.gov/?p=form&id=16

5. Senator Deb Fischer Nebraska
Washington D.C.
454 Russell Senate Office Building
Washington, DC 20510
Phone: (202) 224-6551
Fax: (202) 228-1325
EMAIL: https://www.fischer.senate.gov/public/?p=email-deb

6. Senator Jerry Moran Kansas
Washington, D.C.
Dirksen Senate Office Building
Room 521
Washington, D.C. 20510
Phone: (202) 224-6521
Fax: (202) 228-6966
https://www.moran.senate.gov/public/index.cfm/e-mail-jerry

7. Senator Dan Sullivan Alaska
WASHINGTON, D.C.
702 Hart Senate Office Building
Washington, DC 20510
Phone: (202)-224-3004
Fax: (202)-224-6501
https://www.sullivan.senate.gov/contact/email

8. Senator Dean Heller Nevada
Washington, DC
324 Hart Senate Office Building
Washington, DC 20510
Phone: 202-224-6244
Fax: 202-228-6753
https://www.heller.senate.gov/public/index.cfm/contact-form

9. Senator Jim Inhofe Oklahoma (site down)

10. Senator Mike Lee Utah (site down)

11. Senator Ron Johnson Wisconsin
328 Hart Senate Office Building
Washington, DC 20510
Phone: (202) 224-5323
Fax: (202) 228-6965
https://www.ronjohnson.senate.gov/public/index.cfm/email-the-senator

12. Senator Shelley Moore Capito West Virginia

13. Senator Cory Gardner Colorado
Washington, D.C.
354 Russell
Senate Office Building
Washington, DC 20510
P: (202) 224-5941
F: (202) 224-6524
https://www.gardner.senate.gov/contact-cory/email-cory

14. Senator Todd Young Indiana (site down)

MINORITY MEMBERS:

1. Ranking Member Bill Nelson Florida
WASHINGTON, DC OFFICE
United States Senate
716 Senate Hart Office Building
Washington, DC 20510
Phone: 202-224-5274
Fax: 202-228-2183
https://www.billnelson.senate.gov/contact-bill

2. Senator Maria Cantwell Washington
Washington, DC
511 Hart Senate Office Building
Washington, DC 20510
Phone: (202) 224-3441
Fax: (202) 228-0514
https://www.cantwell.senate.gov/contact/email

3. Senator Amy Klobuchar Minnesota
Washington, DC
302 Hart Senate Office Building
Washington, DC 20510
phone: 202-224-3244
fax: 202-228-2186
https://www.klobuchar.senate.gov/public/index.cfm/email-amy

4. Senator Richard Blumenthal Connecticut
https://www.blumenthal.senate.gov/contact
Washington D.C.
706 Hart Senate Office Bldg.
Washington, DC, 20510
tel (202) 224-2823
fax (202) 224-9673

5. Senator Brian Schatz Hawaii
722 HART SENATE OFFICE BUILDING
WASHINGTON, DC 20510
PHONE: (202) 224-3934
FAX: (202) 228-1153
https://www.schatz.senate.gov/contact

6. Senator Ed Markey Massachusetts
Washington, D.C.
255 Dirksen Senate Office Building
Washington, D.C. 20510
202-224-2742
https://www.markey.senate.gov/contact

7. Senator Tom Udall New Mexico
Washington/Capitol Hill
531 Hart Senate Office Building
Washington DC, 20510
(202) 224-6621
https://www.tomudall.senate.gov/contact/email-tom

8. Senator Gary Peters Michigan
Hart Senate Office Building
Suite 724
Washington, DC 20510
(202) 224-6221
https://www.peters.senate.gov/contact/email-gary

9. Senator Tammy Baldwin Wisconsin (site down)

10. Senator Tammy Duckworth Illinois (site down)

11. Senator Maggie Hassan New Hampshire (site down)

12. Senator Catherine Cortez Masto Nevada (site down)

13. Senator Jon Tester Montana (site down)

There is no end to what we can do together. There is no end.

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Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly. In fact, “high LDL-C may be protective is in accordance with the finding that LDL-C is lower than normal in patients with acute myocardial infarction”.



Cardiovascular medicine
Research
Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review
http://bmjopen.bmj.com/content/6/6/e010401.full?sid=cfb00014-f0a8-407d-ae71-a3278160ca49

Uffe Ravnskov1, David M Diamond2, Rokura Hama3, Tomohito Hamazaki4, Björn Hammarskjöld5, Niamh Hynes6, Malcolm Kendrick7, Peter H Langsjoen8, Aseem Malhotra9, Luca Mascitelli10, Kilmer S McCully11, Yoichi Ogushi12, Harumi Okuyama13, Paul J Rosch14, Tore Schersten15, Sherif Sultan6, Ralf Sundberg16
Author affiliations
Abstract

Objective It is well known that total cholesterol becomes less of a risk factor or not at all for all-cause and cardiovascular (CV) mortality with increasing age, but as little is known as to whether low-density lipoprotein cholesterol (LDL-C), one component of total cholesterol, is associated with mortality in the elderly, we decided to investigate this issue.

Setting, participants and outcome measures We sought PubMed for cohort studies, where LDL-C had been investigated as a risk factor for all-cause and/or CV mortality in individuals ≥60 years from the general population.

Results We identified 19 cohort studies including 30 cohorts with a total of 68 094 elderly people, where all-cause mortality was recorded in 28 cohorts and CV mortality in 9 cohorts. Inverse association between all-cause mortality and LDL-C was seen in 16 cohorts (in 14 with statistical significance) representing 92% of the number of participants, where this association was recorded. In the rest, no association was found. In two cohorts, CV mortality was highest in the lowest LDL-C quartile and with statistical significance; in seven cohorts, no association was found.

Conclusions High LDL-C is inversely associated with mortality in most people over 60 years. This finding is inconsistent with the cholesterol hypothesis (ie, that cholesterol, particularly LDL-C, is inherently atherogenic). Since elderly people with high LDL-C live as long or longer than those with low LDL-C, our analysis provides reason to question the validity of the cholesterol hypothesis. Moreover, our study provides the rationale for a re-evaluation of guidelines recommending pharmacological reduction of LDL-C in the elderly as a component of cardiovascular disease prevention strategies.

This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

http://dx.doi.org/10.1136/bmjopen-2015-010401
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Strengths and limitations of this study

This is the first systematic review of cohort studies where low-density lipoprotein cholesterol (LDL-C) has been analysed as a risk factor for all-cause and/or cardiovascular mortality in elderly people.

Lack of an association or an inverse association between LDL-C and mortality was present in all studies.

We may not have included studies where an evaluation of LDL-C as a risk factor for mortality was performed but where it was not mentioned in the title or in the abstract.

We may have overlooked relevant studies because we have only searched PubMed.

Minor errors may be present because some of the authors may not have adjusted LDL-C by appropriate risk factors.

Some of the participants with high LDL-C may have started statin treatment during the observation period and, in this way, may have added a longer life to the group with high LDL-C and some of them may have started with a diet able to influence the risk of mortality.

We may have overlooked a small number of relevant studies because we only searched papers in English.

Introduction
Rationale

For decades, the mainstream view has been that an elevated level of total cholesterol (TC) is a primary cause of atherosclerosis and cardiovascular disease (CVD). There are several contradictions to this view, however. No study of unselected people has found an association between TC and degree of atherosclerosis.1 Moreover, in most of the Japanese epidemiological studies, high TC is not a risk factor for stroke, and further, there is an inverse association between TC and all-cause mortality, irrespective of age and sex.2

In a recent meta-analysis performed by the Prospective Studies Collaboration, there was an association between TC and CV mortality in all ages and in both sexes.3 However, even in this analysis, the risk decreased with increasing age and became minimal after the age of 80 years. Since atherosclerosis and CVD are mainly diseases of the elderly, the cholesterol hypothesis predicts that the association between CV mortality and TC should be at least as strong in the elderly as in young people. There may be a confounding influence in these studies, however, because TC includes high-density lipoprotein cholestrol (HDL-C), and multiple studies have shown that a high level of HDL-C is associated with a lower risk of CVD.
Objectives

We examined the literature assessing low-density lipoprotein cholesterol (LDL-C) as a risk factor for mortality in elderly people. Since the definition of CVD varies considerably in the scientific literature, we have chosen to focus on the association between LDL-C and all-cause and CVD mortality, because mortality has the least risk of bias among all outcome measures. If Goldstein and Brown’s recent statement that LDL-C is ‘the essential causative agent’ of CVD4 is correct, then we should find that LDL-C is a strong risk factor for mortality in elderly people.


Methods
Search strategy

UR and RS searched PubMed independently from initial to 17 December 2015. The following keywords were used: ‘lipoprotein AND (old OR elderly) AND mortality NOT animal NOT trial’. We also retrieved the references in the publications so as not to miss any relevant studies. The search was limited to studies in English.
Inclusion and exclusion criteria

All included studies should meet the following criteria: the study should be a cohort study of people aged 60 years or older selected randomly from the general population, or a study where the authors had found no significant differences between the participants and the source population’s demographic characteristics. The studies should include an initial assessment of LDL-C levels, the length of the observation time and information about all-cause and/or cardiovascular mortality at the end of follow-up. The studies should also include information about the association between LDL-C and all-cause and/or CVD mortality. We excluded studies that did not represent the general population (eg, case–control studies; case reports; studies that included patients only); studies where data about elderly people were not given separately, and studies without multivariate correction for the association between LDL-C and all-cause and/or CV mortality. We accepted studies where the authors had excluded patients with serious diseases or individuals who had died during the first year.
Study selection, data items and extraction

Studies where the title or abstract indicated that they might include LDL-C data of elderly people, were read in full, and the relevant data were extracted by at least three of the authors, for example, year of publication, total number of participants, sex, length of observation time, exclusion criteria, LDL-C measured at the start and the association between initial LDL-C and risk of all-cause and/or at follow-up. When more than one adjusted HR was reported, the HR with the most fully adjusted model was selected.

Quality assessment

The design of the study satisfies almost all points of reliability and validity according to the Newcastle Ottawa Scale as regards selection, comparability and exposure.5 Thus, all studies represented elderly people only; ascertainness of exposure (eg, measurement of LDL-C) was present in all studies, and outcome was unknown at the start. It can be questioned if all of the studies represented the general population because, as shown below, in some of them various types of disease groups were excluded.

Results
Study selection

Our search gave 2894 hits. We excluded 160 studies, which were not in English, and 2452 studies because, judged from the abstract, it was obvious that they were irrelevant.

The rest of the papers were read in full; 263 of these studies were excluded for the following reasons: (1) the participants did not represent the general population; (2) LDL-C was not measured at the start; (3) follow-up information was not given for the elderly separately; or (4) no information was present about mortality during the observation period (figure 1). One of the studies6 was excluded because it included the same individuals as in a previous study.7
Figure 1

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Figure 1

Flow Chart. CV, cardiovascular; LDL-C, low-density lipoprotein cholesterol.
Study characteristics

The remaining 19 studies including 30 cohorts with a total of 68 094 participants met the inclusion criteria (figure 1). All-cause mortality was recorded in 28 cohorts. In 16 of these cohorts (representing 92% of the individuals), the association was inverse and with statistical significance in 14; in 1 of the cohorts, the association was mirror-J-formed with the lowest risk in the highest quartile; in the rest of the papers, no association was found. CV mortality was recorded in nine cohorts; in one of them, the association was almost U-shaped with the lowest risk in the highest quartile (curvilinear fit: p=0.001); in one of them, the association was mirror-J-formed and also with the lowest risk in the highest quartile (curvilinear fit: p=0.03); in the other seven cohorts, no association was found (table 1).

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Table 1

Association between LDL-C and all-cause mortality and CVD mortality, respectively, in 19 studies including 30 cohorts with 68 094 individuals from the general population above the age of 60 years
Risk of bias across studies

One explanation for the increased risk of mortality among people with low cholesterol is that serious diseases may lower cholesterol soon before death occurs. Evidence to support this hypothesis may be obtained from 10 of the studies in which no exclusions were made for individuals with terminal illnesses. However, in four of the studies, participants with a terminal illness or who had died during the first observation year were excluded. In one of those studies,8 LDL-C was not associated with all-cause mortality; in the three others,16 ,20 ,24 which included more than 70% of the total number of participants in our review, LDL-C was inversely associated with all-cause mortality and with statistical significance. Thus, there is little support for the hypothesis that our analysis is biased by end of life changes in LDL-C levels.

It is also potentially relevant that all studies did not correct for the same risk factors, and some of them did not inform the reader about which risk factors they corrected for. However, taking all studies together, 50 different risk factors were corrected for in the Cox analyses (table 2).

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Table 2

Factors corrected for in the multifactorial analyses of each study

It is worth considering that some of the participants with high LDL-C may have started statin treatment during the observation period. Such treatment may have increased the lifespan for the group with high LDL-C. However, any beneficial effects of statins on mortality would have been minimal because most statin trials have had little effect on CVD and all-cause mortality, with a maximum reduction of mortality of two percentage points. It is therefore relevant that the 4-year mortality among those with the highest LDL-C in the included cohorts was up to 36% lower than among those with the lowest LDL-C. Furthermore, in the largest study20 that included about two-thirds of the total number of participants in our study, the risk was lower among those with the highest LDL-C than among those on statin treatment.

It is also possible that those with the highest LDL-C were put on a different diet than those with low LDL-C. However, this potential bias in mortality outcomes could have gone in both directions. Some of the individuals with high LDL-C may have followed the official dietary guidelines and exchanged saturated fat with vegetable oils rich in linoleic acid. In a recent study, the authors reported that among participants who were older than 65 at baseline, a 30 mg/dL decrease in serum cholesterol was associated with a higher risk of death (HR 1.35, 95% CI 1.18 to 1.54).26 If applied to the general population, this finding suggests that the conventional dietary treatment for high cholesterol with vegetable oil replacing saturated fat may actually increase mortality in those individuals with high LDL-C. Thus, the lack of an association between LDL-C and mortality may have been even stronger than reported since the dietary intervention may have been counterproductive.

Finally, it is potentially relevant that we limited our literature search to PubMed. In preliminary searches with PubMed, OVID and EMBASE, we identified 17 relevant studies in PubMed, but only 2 in OVID and EMBASE, and these 2 studies were found in PubMed as well. Therefore, it is highly unlikely that there are studies with findings with divergent results from those we have reported here, as all of them reported either no association or an inverse association between LDL-C and mortality.
Discussion

Assessments of the association between serum cholesterol and mortality have been studied for decades, and extensive research has shown a weak association between total cholesterol and mortality in the elderly; several studies have even shown an inverse association. It is therefore surprising that there is an absence of a review of the literature on mortality and levels of LDL-C, which is routinely referred to as a causal agent in producing CVD4 and is a target of pharmacological treatment of CVD.

Our literature review has revealed either a lack of an association or an inverse association between LDL-C and mortality among people older than 60 years. In almost 80% of the total number of individuals, LDL-C was inversely associated with all-cause mortality and with statistical significance.

These findings provide a paradoxical contradiction to the cholesterol hypothesis. As atherosclerosis starts mainly in middle-aged people and becomes more pronounced with increasing age, the cholesterol hypothesis would predict that there should be a cumulative atherosclerotic burden, which would be expressed as greater CVD and all-cause mortality, in elderly people with high LDL-C levels.

Our results raise several relevant questions for future research. Why is high TC a risk factor for CVD in the young and middle-aged, but not in elderly people? Why does a subset of elderly people with high LDL-C live longer than people with low LDL-C? If high LDL-C is potentially beneficial for the elderly, then why does cholesterol-lowering treatment lower the risk of cardiovascular mortality? In the following we have tried to address some of these questions.
Inverse causation

A common argument to explain why low lipid values are associated with an increased mortality is inverse causation, meaning that serious diseases cause low cholesterol. However, this is not a likely explanation, because in five of the studies in table 1 terminal disease and mortality during the first years of observation were excluded. In spite of that, three of them showed that the highest mortality was seen among those with the lowest initial LDL-C with statistical significance.18 ,20 ,24
Is high LDL-C beneficial?

One hypothesis to address the inverse association between LDL-C and mortality is that low LDL-C increases susceptibility to fatal diseases. Support for this hypothesis is provided by animal and laboratory experiments from more than a dozen research groups which have shown that LDL binds to and inactivates a broad range of microorganisms and their toxic products.27 Diseases caused or aggravated by microorganisms may therefore occur more often in people with low cholesterol, as observed in many studies.28 In a meta-analysis of 19 cohort studies, for instance, performed by the National Heart, Lung and Blood Institute and including 68 406 deaths, TC was inversely associated with mortality from respiratory and gastrointestinal diseases, most of which are of an infectious origin.29 It is unlikely that these diseases caused the low TC, because the associations remained after the exclusion of deaths occurring during the first 5 years. In a study by Iribarren et al, more than 100 000 healthy individuals were followed for 15 years. At follow-up, those whose initial cholesterol level was lowest at the start had been hospitalised significantly more often because of an infectious disease that occurred later during the 15-year follow-up period.30 This study provides strong evidence that low cholesterol, recorded at a time when these people were healthy, could not have been caused by a disease they had not yet encountered.

Another explanation for an inverse association between LDL-C and mortality is that high cholesterol, and therefore high LDL-C, may protect against cancer. The reason may be that many cancer types are caused by viruses.31 Nine cohort studies including more than 140 000 individuals followed for 10–30 years have found an inverse association between cancer and TC measured at the start of the study, even after excluding deaths that occurred during the first 4 years.32 Furthermore, cholesterol-lowering experiments on rodents have resulted in cancer,33 and in several case–control studies of patients with cancer and controls matched for age and sex, significantly more patients with cancer have been on cholesterol-lowering treatment.32 In agreement with these findings, cancer mortality is significantly lower in individuals with familial hypercholesterolaemia.34

That high LDL-C may be protective is in accordance with the finding that LDL-C is lower than normal in patients with acute myocardial infarction. This has been documented repeatedly without a reasonable explanation.35–37 In one of the studies,37 the authors concluded that LDL-C evidently should be lowered even more, but at a follow-up 3 years later mortality was twice as high among those whose LDL-C had been lowered the most compared with those whose cholesterol was unchanged or lowered only a little. If high LDL-C were the cause, the effect should have been the opposite.
Conclusions

Our review provides the first comprehensive analysis of the literature about the association between LDL-C and mortality in the elderly. Since the main goal of prevention of disease is prolongation of life, all-cause mortality is the most important outcome, and is also the most easily defined outcome and least subject to bias. The cholesterol hypothesis predicts that LDL-C will be associated with increased all-cause and CV mortality. Our review has shown either a lack of an association or an inverse association between LDL-C and both all-cause and CV mortality. The cholesterol hypothesis seems to be in conflict with most of Bradford Hill’s criteria for causation, because of its lack of consistency, biological gradient and coherence. Our review provides the basis for more research about the cause of atherosclerosis and CVD and also for a re-evaluation of the guidelines for cardiovascular prevention, in particular because the benefits from statin treatment have been exaggerated.38–40
Acknowledgments

The study has been supported by a grant from Western Vascular Institute.
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ALERT: Emergency at US nuclear plant after “massive” fire and multiple explosions — “All of a sudden we heard this loud boom and the whole ground started shaking” — “Intense Flames… Heavy Black Smoke… Chaos” — 100s of fire personnel called in — “We ask that the public stay away from the area” (VIDEOS)


http://enenews.com/alert-emergency-nuclear-plant-after-massive-fire-multiple-explosions-all-sudden-heard-loud-boom-ground-started-shaking-videos?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+ENENews+%28Energy+News%29

U.S. Nuclear Regulatory Commission, Mar 7, 2016 (emphasis added): [Oconee Nuclear Station, SC] EMERGENCY DECLARATION DUE TO FIRE/EXPLOSION IN THE MAIN TRANSFORMER… At 1520 EST, the licensee declared a Notification of Unusual Event… personnel were applying additional foam to prevent a re-flash… Offsite assistance was requested with three local fire departments… At 1658 EST, the licensee declared an Alert [when] the fire damaged an overhead power line that supplies emergency power to all three units at Oconee.

WHNS transcript, Mar 7, 2016: People fishing on the lake… reported hearing a loud boom and seeing black smoke, and then steam… Witnesses say there were two explosions… This afternoon [was] chaos… Fire crews [were] all on scene at the Oconee nuclear plant after a massive electrical fire… Fire Official: “It’s also in very close proximity to the buildings… I know they worked on… preventing the transformer from impinging on any of the other structures”… People in the area were very concerned when they saw heavy black smokeWitness: “All of a sudden we heard this loud boom and the whole ground started shaking.”… It’s a scary situation… [An official] said it was a very rare problem.

Loudspeaker at Oconee Nuclear Station: “Attention all site personnel… This is an emergency message… An unusual event has been declared for Unit 1… TSC – OSC [Technical Support Center – Onsite Operational Support Center] activation is necessary and the TSC – OSC has not yet been activated. Activate the TSC – OSC — I repeat, activate the TSC – OSC.”

WYFF, Mar 7, 2016: Scott Batson, site vice president [said] the intense flames and smoke came from oil burning… Batson said because a cable burned in the fire fell and caused other equipment to be affected, which led to the “unusual event” to be upgraded to an alert.

FOX Carolina, Mar 7, 2016: Hundreds of fire personnel sprang into action after a fire started at the Oconee Nuclear Plant.

WSPA transcript, Mar 7, 2016: Nearby Resident:I freaked out – you see a fire, smoke at a a power plant”… Fire Chief: “When you’re responding to a call, and you can see it when you leave the station like that, it really kind of gets your adrenaline going.”

Oconee County Emergency Management, Mar 7, 2016: “We ask that the public stay away from the area as emergency personnel and Duke Energy staff work.”

Greenville News, Mar 6, 2016: The alert was necessary because the problem could have affected operations of the plant itself… The transformer is 25 to 30 feet from the turbine building that serves Unit 1 and about 100 yards from the reactor building

WLOS, Mar 6, 2016: A transformer burst into flames at an Upstate nuclear power station…. Officials did ask the public to stay away from the area… The fire chief also said crews are continuing to work with on-site personnel to ensure… there is no further extension.

From last month: ALERT: Fire/explosion at North Carolina nuclear plant (VIDEO)

 

I check the news every day for radiation news, nuke problems, etc.  How the hell can anyone protect themselves, when it takes a week to show up in the news?

ENENews: uncontrollable fission of the melted nuclear fuel assemblies continue somewhere under the remains of the station…



TV: “Truly unsettling” discovery at Fukushima… problem “far greater than previously thought” — Boss reveals 600 tons of fuel melted, can’t find it — Top Official: “Nobody really knows where fuel is”… We may never be able to get it and just leave wherever — “Uncontrollable fission” is continuing under site (VIDEO)
http://enenews.com/tv-unsettling-discovery-fukushima-problem-greater-previously-thought-plant-chief-reveals-600-tons-nuclear-fuel-melted-location-mystery-top-official-really-fuel-never-be-able-wind-leaving-molten?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+ENENews+%28Energy+News%29
Published: June 2nd, 2016 at 1:18 am ET
By ENENews

ABC Australia, May 24, 2016 (emphasis added): [ABC’s Mark Willacy] has been invited on a tour of [Fukushima Daiichi]… What Willacy discovers is truly unsettling… retrieving hundreds of tonnes of melted nuclear fuel turns out to be far greater than previously thought.

ABC Australia transcript excerpts, May 24, 2016:

Willacy: Tonight we go on a journey into the heart of this ongoing crisis… and we reveal the frightening enormity of the clean-up… and how dangerous it still is.
Gregory Jaczko, former Chairman of the US Nuclear Regulatory Commission: This really is unchartered territory. Nobody really knows where the fuel is… There’s no playbook – they’re making this up as they go along.
Willacy: The man in charge of decontaminating and decommissioning the Fukushima plant, Naohiro Masuda. Has anything like this ever been attempted before?
Masuda: There has never been an accident at a nuclear plant like the one at Fukushima where three reactors had meltdowns. We are currently working on a timetable to decommission the reactors over the next 30 to 40 years.
Naoto Kan, Former Prime Minister: I think it will take longer… This is a major accident, which has never happened anywhere in the world… 40 years is an optimistic view.
Willacy: We are heading to the buildings housing the melted reactors… Tepco is worried about possible nuclear terrorism, and won’t allow us to film certain security sites.
Masuda: This is a job we’ve never done and there is no textbook.
Willacy: [At Reactor 3 there was an] explosion right after the nuclear fuel melted… What happened inside [Reactor 2] no-one really knows… [Reactor 1] is where probably the worst meltdown occurred. They don’t know where the nuclear fuel is.
Masuda: We haven’t actually seen where the melted fuel fell, so it’s important to find it as soon as possible.
Willacy: For the first time, Foreign Correspondent can reveal just how vast the amount of melted nuclear fuel is, the three molten blobs that lie somewhere deep within each of these buildings.
Masuda: It’s estimated that 200 tonnes of debris lies within each unit… 600 tonnes of melted debris fuel and a mixture of concrete and other metals are likely to be here.
Willacy: The most daunting task, one the nuclear industry has never faced, is getting the melted fuel out. TEPCO admits the technology it needs hasn’t been invented.
Jaczko: It may be possible that we’re never able to remove the fuel. You may just wind up having to leave it there and somehow entomb it as it is. I mean that’s certainly a possibility. There is no playbook, they’re making this up as they go along.
Kan: If all the reactors had had a meltdown, there was a risk that half or all of Japan could have been destroyed… the accident took us to the brink of destruction.
Jaczko: You have to now accept that in all nuclear power plants… there’s a chance you can have this kind of a very catastrophic accident… that’s the reality of nuclear power.

ABC Australia, May 24, 2016: Fukushima clean-up chief still hunting for 600 tonnes of melted radioactive fuel… [TEPCO] has revealed that 600 tonnes of reactor fuel melted during the disaster, and that the exact location of the highly radioactive blobs remains a mystery… [C]hief of decommissioning at Fukushima, Naohiro Masuda, said the company hoped to… begin removing it from 2021… “But unfortunately, we don’t know exactly where (the fuel) is” [said Masuda]. [Gregory Jaczko, Chairman of the US NRC] at the time of the meltdowns at Fukushima doubts the fuel can be retrieved… “Nobody really knows where the fuel is… It may be possible that we’re never able to remove the fuel. You may just have to wind up leaving it there and somehow entomb it as it is.”… For the first time, TEPCO has revealed just how much of the mostly uranium fuel melted down… [Masuda said] “about 600 tonnes of melted debris fuel and a mixture of concrete and other metals are likely to be there.”

RT, May 24, 2016: 600 tons of melted radioactive Fukushima fuel still not found, clean-up chief reveals… [The fuel] burnt through the respective reactor pressure vessels, concentrating somewhere on the lower levels of the station… fuel from Reactor 1 poured out completely… the exact location of the highly radioactive “runaway” fuel remains mystery for TEPCO. The absolutely uncontrollable fission of the melted nuclear fuel assemblies continue somewhere under the remains of the station… [TEPCO’s] plan for Fukushima nuclear power plant implies a 30-40 year period… Yet experts doubt the present state of technology is sufficient to deal with the unprecedented technical task.

Watch ABC Australia’s broadcast here

ENENews: “100% death rate of baby seals on California coast — ‘None have survived'”


100% death rate of baby seals on California coast — “None have survived” — “Many are starving, suffering from shortage of food in Pacific Ocean” — “Extremely thin… all sorts of illnesses, infections” — “Milkless moms immediately abandoning pups” — TV: “The problem is getting worse” (VIDEOS)

Health Ranger: “California to throw adults in JAIL if they refuse government-mandated vaccines”


California to throw adults in JAIL if they refuse government-mandated vaccines

SB792
 (NaturalNews) In case you haven’t noticed, there’s an incremental push right now by the controlling elite to force vaccinations on all Americans, both young and old. And this agenda is gaining considerable traction in California, where legislators are now moving forward with plans to force childhood vaccines on all adults who work in daycare centers, both private and public.

Senate Bill 792, also known as the “Day care facilities: immunizations: exemptions” act, was presented quietly alongside SB 277, which eliminates personal, philosophical and religious vaccine exemptions for children who attend both private and public schools in the Golden State. The bill, as recently heard by the California Assembly Human Services Committee, reads as follows:

This bill, commencing September 1, 2016, would prohibit a day care center or a family day care home from employing any person who has not been immunized against influenza, pertussis, and measles.

If passed, SB 792 would represent the first adult vaccine mandate in the U.S. that disallows exemptions for personal reasons, and that threatens criminal penalties for those who fail or refuse to comply. Here’s how Vaccine Impact describes SB 792:

SB 792, would eliminate an adult’s right to exempt themselves from one, some, or all vaccines, a risk-laden medical procedure.


This bill would make California the first state to require mandated vaccinations for all childcare workers, including all private and public school early childhood education programs (Headstart, Private preK and preschools), family daycares, and daycare centers.

SB 792 represents medical violence against adults

An affront to both medical and religious liberty, SB 792 appears to be the wave of the future in New America, where the perceived health of the “herd” is now more important than the health of the individual. Never before in the history of the United States have legislators pushed this hard to literally force vaccine injections on the public under duress.

But why do they feel the need to do this if vaccines really work and are truly safe as claimed? The answer is that vaccines aren’t safe and effective, and more people than ever are acknowledging this truth and opting out of the “requirements” of the system through vaccine exemptions, hence the rush to eliminate these exemptions as quickly as possible, starting with California.

“This bill eliminates medical autonomy, crushes religious freedom, undermines personal freedom, and burdens quality providers with a non-optional series of medical interventions in the form of mandated vaccines that are not even 100% effective,” adds Vaccine Impact.

Contact California legislators and say NO to SB 792

As of this writing, SB 792 awaits a hearing by California’s Committee on Appropriations, having recently passed through the Assembly Human Services Committee with a 6-1 vote. The official vote tally reveals that the following members of this committee voted in FAVOR of passing SB 792:

Ian C. Calderon
Kansen Chu
Patty Lopez
Brian Maienschein
Mark Stone
Tony Thurmond

You can contact the above individuals here and let them know how you feel about their betrayal of medical freedom in California.

You can also contact the individual members of the Committee on Appropriations and tell them to vote AGAINST SB 792 by visiting: pro.assembly.ca.gov

If Americans sit idly by while corrupt legislators pass incremental bills like SB 277 and SB 792, it will only be a matter of time before even stricter bills come along mandating vaccinations for additional groups of people, until eventually everyone is forced into being vaccinated by the state for the benefit of “public health.”

“Laws like these are forging a burden of responsibility that is collectively shared by everyone,” writes Joshua Krause for GlobalResearch.ca.

“It won’t be long before they try to force vaccines on every adult and child in California. And if they pull it off there, legislators in other states will try to see if they can use the sheepish tyranny of majority rule to force vaccines on their citizens as well.”

Sources:

experimentalvaccines.org

vaccineimpact.com

globalresearch.ca

leginfo.legislature.ca.gov

apro.assembly.ca.gov

ENENews: Scientists: West Coast bird die-off “is biggest ever recorded” — Stomachs completely empty — “Staggering… Alarming… Unheard of… Never seen anything like it” — “Unprecedented in size, scope, duration” — “Deaths could reach many hundreds of thousands” — “A host of other freakish phenomena”


Scientists: West Coast bird die-off “is biggest ever recorded” — Stomachs completely empty — “Staggering… Alarming… Unheard of… Never seen anything like it” — “Unprecedented in size, scope, duration” — “Deaths could reach many hundreds of thousands” — “A host of other freakish phenomena” (VIDEO)

Published: February 4th, 2016 at 9:41 am ET
By ENENews
http://enenews.com/scientists-west-coast-bird-die-biggest-recorded-staggering-unheard-never-anything-like-unprecedented-size-scope-duration-worst-case-scenario-deaths-could-reach-many-hundreds-thousands-host?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+ENENews+%28Energy+News%29


http://www.adn.com/article/20160129/scientists-think-gulf-alaska-seabird-die-biggest-ever-recorded
Alaska Dispatch News, Jan 29, 2016 (emphasis added): Scientists think Gulf of Alaska seabird die-off is biggest ever recorded… The mass of dead seabirds that have washed up on Alaska beaches in past months is unprecedented in size, scope and duration, a federal biologist said… The staggering die-off… is a signal that something is awry in the Gulf of Alaska, said Heather Renner, supervisory wildlife biologist at the Alaska Maritime National Wildlife Refuge… It coincides with widespread deaths of other marine animals, from whales in the Gulf of Alaska to sea lions in California… Common murres and whales… are not the only Gulf of Alaska marine animals to fall victim to ailments… Kachemak Bay saw an eight-fold increase in sea otter deaths… Sea stars in Kachemak Bay in 2015 were found stricken with a wasting disease similar.

http://www.adn.com/article/20160129/scientists-think-gulf-alaska-seabird-die-biggest-ever-recorded
Heather Renner, Alaska Maritime National Wildlife Refuge: “We are in the midst of perhaps the largest murre die-off ever recorded”… [In Homer] the beaches are “littered” with murre carcasses… A breeding colony in the Barren Islands that is usually teeming in late summer with adult murres tending their young was deserted this year… “nobody was home… In more than three decades of monitoring murres in the Barrens, we’ve never had complete reproduction failure before“… Similar failures occurred at some other nesting colonies.

http://www.nprb.org/assets/amss/images/uploads/files/2016_AMSS_Poster_Sessions.pdf
USGS (pdf), Jan 2016: During March through September 2015, at least 25 seabird mortality events were reported across Alaska… The primary avian species reported included common and thick-billed murres, black-legged kittiwakes, horned and tufted puffins, glaucous-winged gulls, and sooty and short-tailed shearwaters… Some of these avian mortalities were concurrent with whale, pinniped, sea otter, and fish mortalities…

Marine Science Symposium – LIVEBLOG – Thursday

Alaska Public Radio, Jan 28, 2016: [T]his event will likely be the largest and most widespread on record. And seeing the starving birds dying far inland apparently searching for food is “nearly unheard of,” said USFWS’s Heather Renner.

Dead murres wash up on Haines’ beach

KHNS, Jan 15, 2016: “We’re seeing the effects of this throughout the food web,” [Rob Kaler U.S. Fish & Wildlife Service biologist] says… The murres’ stomachs are completely empty, Kaler says… Not only is the bird die-off unsettling, the implications are scary, [bird expert Pam Randles] says. “Our salmon eat that stuff and who knows what else is dying off, or starving, or having trouble?” Norm Hughes has been commercial salmon fishing in Alaska for more than 30 years. He says last season saw skinnier fish – up to 20 percent smaller… “there’s less fish”…

http://edition.cnn.com/2016/01/21/us/alaska-bird-die-off/
CNN, Jan 22, 2016: “We have never found close to 8,000 birds on a 1-mile long beach before,” [seabird biologist David Irons] said… “It is an order of magnitude larger than any records that I am aware of… Seabird biologists say seabirds are indicators of the health of the ecosystem. Now they’re dying and that is telling us something… this is bigger than I’ve ever seen.”

APRN, Jan 28, 2016: Scientists say murre die-off comparable to Exxon Valdez spill… Heather Renner with USFWS says it is already one of the largest die-offs in history and, unlike when the tanker went aground, not many people have gone out to remote beaches to survey for dead seabirds… “there’s dead murres on the ground everywhere, and it’s hard not to notice them.”

http://www.economist.com/news/united-states/21689605-thousands-seabirds-are-washing-up-dead-alaskas-shores-murre-mystery
The Economist, Jan 30, 2016: [Probably hundreds] of thousands of these birds have drifted in dead… last summer they failed to raise chicks. And they have been dying in large numbers along the Pacific coast, from California to Alaska… “Whole systems are out of whack,” says Heather Renner… Old-timers in Homer have never experienced anything like this. And they are perplexed by a host of other freakish phenomena…

KTOO, Jan 28, 2016: “[T]here’s dead murres on the ground everywhere, and it’s hard not to notice them.”… The reason for the dead birds is still a mystery… “I think it suggests something more related to the food web structure,” said Renner.

http://homertribune.com/2016/01/murre-deaths-lead-to-more-questions/
Homer Tribune, Jan 2016: Irons found an estimated 7,800 dead murres on a one-mile stretch of beach… he had never seen anything like that. Similar reports came in from other areas… “The really frustrating question of why they are starving to death”… said Heather Renner… [M]urres abandoned their breeding attempts mid-season at many colonies in the Gulf of Alaska, something very uncommon.

http://news.discovery.com/animals/massive-bird-die-off-puzzles-alaska-scientists-1602031.htm

LiveScience, Feb 3, 2016: Massive Bird Die-Off Puzzles Alaska Scientists — Dead common murres have washed ashore in Alaska in alarming numbers … leaving scientists concerned and confused… [The birds] have nothing in their stomachs… [S]imilar events affected seabird populations in Washington, Oregon and California.

http://www.cbc.ca/news/canada/north/alaskan-scientist-thinks-murre-die-off-related-to-algal-blooms-1.3424246

CBC News, Jan 28, 2016: Bruce Wright, a senior scientist Aleutian Pribilof Islands Association… estimates up to 200,000 Alaskan murres could die. With a population he puts at more than two million, Wright said the species should recover, as long as the food base comes back.

http://www.nytimes.com/2016/01/19/science/what-does-it-mean-when-animals-suffer-a-vast-die-off.html
New York Times, Jan 18, 2016: Animals Die in Large Numbers, and Researchers Scratch Their Heads… The latest victims are common murres… this die-off has surprised experts, because it has been going on for around a year and it covers such a vast area… “I still don’t think we’ve seen the worst,” said [John F. Piatt, USGS seabird expert], who… speculated that if the worst happened, the deaths could reach into the many hundreds of thousands.

Watch CNN’s broadcast here:
http://edition.cnn.com/2016/01/21/us/alaska-bird-die-off/