THAT'S WHAT "COVID" IS
“A recent study of particular objects known as "nanotubes," revered for their extraordinary strength and electrical conductivity, demonstrated that such objects tend to clump within the lungs, causing suffocation.”
https://lawcat.berkeley.edu/record/1119251 Is Nanotechnology Prohibited by the Biological and Chemical Weapons Conventions
“Take the experience of researchers at DuPont, who are testing microscopic tubes of carbon, known as nanotubes, valued for their extraordinary strength and electrical conductivity.
When the researchers injected nanotubes into the lungs of rats in the summer of 2002, the animals unexpectedly began gasping for breath. Fifteen percent of them quickly died. ''It was the highest death rate we had ever seen,''
said David B. Warheit, the research leader, who began his career studying asbestos and has been testing the pulmonary effects of various chemicals for DuPont since 1984.
Early research has raised troubling issues. DuPont and others, for example, found evidence that the cells that break down foreign particles in rodent lungs have more trouble detecting and handling nanoparticles than larger particles that have long been studied by air pollution experts.
Lungs are not the only concern.
Research shows that nanoparticles deposited in the nose can make their way directly into the brain.
They can also change shape as they move from liquid solutions to the air, making it harder to draw general conclusions about their potential impact on living things. “
https://jnm.snmjournals.org/content/48/7/1039 Carbon Nanotubes: Potential Benefits and Risks of Nanotechnology in Nuclear Medicine
“Despite these potential benefits, the toxicity of CNTs (Carbon Nanotubes) is a major concern that needs to be more clearly understood and addressed. Pristine, water-insoluble CNTs have been found to be highly toxic in vitro to many different types of cells, including human keratinocytes, rat brain neuronal cells, human embryonic kidney cells, and human lung cancer cells. In addition, unmodified CNTs administered intratracheally to mice have been reported to induce the formation of lung granulomas. CNTs have also been shown to promote the aggregation of human platelets in vitro, and analogous carbon particulate matter found in the environment enhanced experimentally induced vascular thrombosis in rats.”
“[in 2015] Günter Oberdörster and co-authors published what is possibly the most comprehensive review of carbon nanotube toxicology studies to date. Focusing on inhalation of nanotubes, they document evidence of transient pulmonary inflammation, and rapid and persistent development of granulomatous lesions and interstitial fibrosis on exposure to single- and multiwalled carbon nanotubes in rodents. They cite data indicating that inhaled long and thin multiwalled carbon nanotubes can move to the lining surrounding the lungs and penetrate it, where they can potentially cause mesothelioma. Furthermore, the authors indicate that carbon nanotubes can act as a cancer promoter — with inhalation increasing the probability of developing lung cancer from exposure to other carcinogens.”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4706753/ INHALATION EXPOSURE TO CARBON NANOTUBES (CNT) AND CARBON NANOFIBERS (CNF): METHODOLOGY AND DOSIMETRY - PMC (nih.gov)
Carbon nanotubes (CNT) and carbon nanofibers (CNF) are commonly used in commerce, and applications are expected to increase in the near future (Zhao and Castranova 2011; De Volder et al. 2013). Since approximately 2004, the U.S. Environmental Protection Agency (EPA) has reviewed over 60 notices for commercialization of these materials under Section 5 of the Toxic Substances Control Act. Releases during the manufacture of these fibrous carbon nanomaterials, and during the incorporation of CNT/CNF into finished products, coupled with results from experimental animal studies showing asbestos-like effects, raised considerable human health concerns (Nowack et al. 2013).
A high dose rate and high doses may overwhelm normal defense mechanisms and thus result in significant initial pulmonary inflammation, and may also affect disposition of the administered material to secondary organs.
Pulmonary exposure to SWCNT resulted in a rapid but transient inflammatory and injury response, as evidenced by increased levels of bronchoalveolar lavage fluid (BALF) neutrophils, lactate dehydrogenase (LDH) activity, and protein. Granulomas, predominantly in the terminal bronchioles, were reported 1 wk postexposure and persisted through 3 mo postexposure. A 15% rise in mortality rate within 1 d postexposure was noted and attributed to physical blockage of conducting airways by large SWCNT agglomerates. Lam et al. (2004) also reported rapid and persistent granulomas in mice after IT instillation of mice to very high doses of SWCNT (0.1–0.5 mg of SWCNT/mouse).
Mangum et al. (2006) exposed rats by pharyngeal aspiration to purified SWCNT (0.5 mg/rat; 2.6% Co and 1.7% Mo) suspended in 1% Pluronic. Data showed no apparent inflammatory responses. However, cell proliferation and platelet-derived growth factor (PDGF) protein levels were significantly increased 1 d postexposure and significant interstitial fibrosis was noted at 21 d postexposure. Shvedova et al. (2005) exposed mice by pharyngeal aspiration to purified SWCNT (10–40 µg/mouse). A rapid and transient inflammation and pulmonary damage were noted. In addition, granulomatous lesions and interstitial fibrosis within 7 d postexposure, which lasted through the 59-d course of the study, were observed. Granulomas were associated with the deposition of agglomerates in the terminal bronchioles and proximal alveoli, while interstitial fibrosis was associated with deposition of more dispersed SWCNT structures in the distal alveoli.
Murray et al. (2012) compared the potency of SWCNT to crocidolite asbestos after aspiration in mice. At 1 and 7 d postexposure,
SWCNT (40 µg/mouse) were significantly more potent in inducing transforming growth factor (TGF)-beta, a fibrogenic factor, than asbestos (120 µg/mouse). (!!!!!)
In addition, SWCNT were substantially more potent in inducing alveolar interstitial fibrosis as evidenced by lung collagen and alveolar wall connective tissue thickness than asbestos at 28 d postexposure. Shvedova et al. (2014) confirmed the greater fibrotic potency of SWCNT compared to asbestos at 1 year after aspiration in mice.
Recently, Shvedova et al. (2013) presented data suggesting that SWCNT may act as a cancer promoter.
However, lung tumor growth was significantly greater in mice preexposed to SWCNT as measured by the following: (1) 5-fold increase in lung weight, (2) 2.5-fold elevation in the number of visible tumors, and (3) 3-fold rise in the area of metastatic nodules. Data indicated that this tumor promotion was associated with SWCNT-induced upregulation of granulocyte myeloid-derived suppressor cells, which would depress antitumor immunity. This may be viewed as an important hypothesis-forming study.
In summary, pulmonary exposure of mice to SWCNT induced granulomatous lesions associated with deposition of micrometer-sized agglomerates as well as rapid and progressive interstitial fibrosis associated with migration of smaller SWCNT structures into the alveolar septa.
Li et al. (2007a) compared the pulmonary response of mice exposed to purified MWCNT by IT instillation versus inhalation.
Intratracheal instillation produced inflammation and severe destruction of alveolar structures, while inhalation predominately resulted in moderate pathology consisting of alveolar wall thickening and cell proliferation but general alveolar structure was retained. This study demonstrated significant differences in the type and degree of pulmonary responses to MWCNT in mice between bolus-type IT instillation and inhalation, with higher doses deposited in lung by inhalation resulting in only moderate effects compared to severe lesions induced by instillation of lower doses. (!!!!!)
A recent investigation indicated that MWCNT act as a strong promoter of lung tumors (Sargent et al. 2014). MWCNT produced a marked rise in tumor incidence in mice treated with the initiator chemical (initiator alone having a 50% incidence, while the initiator plus MWCNT group displayed a 90% incidence). In addition, MWCNT increased multiplicity (number of tumors/lung) compared to the inducer alone from 1.4 to 3.3 tumors/lung, with tumors being significantly larger in the initiator plus MWCNT group compared to initiator alone. Pathological analysis indicated that tumors were both bronchoalveolar adenomas and bronchoalveolar adenocarcinomas, with significantly more malignant tumors in the initiator plus MWCNT mice. This study is the first to demonstrate lung cancer promotion after inhalation of MWCNT.
In general, available studies indicate that pulmonary exposure of mice or rats to MWCNT induce granulomas and interstitial fibrosis. Evidence also indicates that MWCNT deposited in the lung migrate to the pleura and diaphragm.
Only three studies evaluating responses following exposures to CNF have been reported, two mouse aspiration studies and a 13-wk rat inhalation study.
In summary, pharyngeal aspiration of CNF in mice (high bolus dose) resulted in interstitial fibrosis.
RESPONSES TO INTRAPERITONEAL INJECTION OF MWCNT In summary, intracavitary high bolus injection of MWCNT in mice and rats induces mesothelioma.
SYSTEMIC CARDIOVASCULAR AND NEUROLOGICAL RESPONSES TO PULMONARY EXPOSURE TO CNT Inhalation of MWCNT resulted in a depression of the responsiveness of coronary arterioles to dilators 24 h postexposure (Stapleton et al. 2011). Further, pharyngeal aspiration of MWCNT produced an induction of mRNA for certain inflammatory mediators and markers of blood–brain barrier damage in the olfactory bulb, frontal cortex, midbrain and hippocampus 24 h postexposure (Sriram et al. 2009).
A recent MWCNT inhalation study in rats reported 24 h after a 5-h inhalation to 5 mg/m3 pulmonary inflammation and translocation to systemic organs (Stapleton et al. 2012). Data also showed an impairment of endothelium-dependent dilation in cardiac coronary arterioles, which was not resolved yet by 7 d postexposure, revealing the potential of inhaled MWCNT not only to induce pulmonary inflammatory effects but also to produce serious extrapulmonary effects after a short-term exposure to a high concentration of 5 mg/m3, resulting in an estimated lung burden of 13 µg/rat.
Translocation of CNT to Systemic Sites Translocation of ip MWCNT from the abdominal cavity to the lung was reported by Liang et al. (2010).
However, the study by Stapleton et al. (2012) found low levels of systemic translocation of inhaled MWCNT into liver, kidneys, and heart. DeLorme et al. (2012) also observed rare events of translocated CNF in brain, heart, liver, kidneys, spleen, intestinal tract and mediastinal lymph nodes, but no histopathological changes were seen. Mercer et al. (2013b) documented translocation of MWCNT to the lymphatics, liver, kidneys, heart, and brain after inhalation of MWCNT (lung burden of 28 µg/mouse).
Systemic Inflammation Erdely et al. (2009) reported that aspiration of SWCNT or MWCNT induced a significant increase in blood neutrophils and mRNA expression and protein levels for certain inflammatory markers in blood at 4 h postexposure, but not at later times.
Kido et al. (2014) interpreted their finding of increased mRNA expression of inflammatory cytokines in splenic macrophages after 3 mo of inhalation exposure of rats to MWCNT as indicators of systemic inflammation. Translocated MWCNT were noted in spleen of exposed rats, and both splenic macrophages and T-lymphocytes displayed increased expression of cytokines/chemokines including interleukin (IL)-2, suggesting a potential impact on antitumor activities and general immunosurveillance.
Neurogenic Signals In summary, although a few studies reported cardiovascular responses after pulmonary exposure to CNT, the results are far from complete. Dose and time-course relationships for a variety of cardiovascular endpoints need to be determined. Mechanisms by which pulmonary particles induce cardiovascular responses require elucidation. Although MWCNT have been observed in cardiovascular tissue after pulmonary exposure, it is unclear whether this tissue burden is sufficient to explain cardiovascular reactions observed.
Summary In general, pulmonary exposure of rats or mice by IT instillation, pharyngeal aspiration, or inhalation of SWCNT or MWCNT and CNF results in transient inflammation and lung damage. Granulomatous lesions and interstitial fibrosis, which are of rapid onset and persistent in nature, have also been a common occurrence.
Evaluation of Carcinogenicity and Toxicity The International Agency for Research on Cancer (IARC) convened a Monograph meeting in October 2014, to evaluate—among other compounds—evidence for labeling CNT with respect to carcinogenicity (Grosse et al. 2014). Based on the data of mesothelioma induction by MWCNT-7 in several studies in mice and rats, the Working Group concluded that there is sufficient evidence of carcinogenicity for MWCNT in animals, limited evidence for two other types of MWCNT, and inadequate evidence for SWCNT. Given that there was inadequate evidence in humans and sufficient evidence in two animal species, MWCNT-7 were classified as “possibly carcinogenic to humans” (Group 2B), and other MWCNT and SWCNT as “not classifiable as to their carcinogenicity to humans” (Group 3). Thus, the IARC Working Group acknowledged that differences in biological activities between distinct MWCNT need to be considered for carcinogen classification, given also that mechanistic evidence for carcinogenicity is not strong for any specific CNT. Since the IARC (2014) carcinogenicity classification for MWCNT is presently based on bolus-type ip injection studies in rodents, the outcome of a 2-yr multidose rat inhalation study with MWCNT-7 with respect to their carcinogenicity will be crucial for a final classification of these MWCNT as either a Group 1 or Group 2A or 2B carcinogen. The 2-yr inhalation study has been completed, and results will be published in the near future (Fukushima et al. personal communication). - [See: https://outraged.substack.com/p/bombshell-studies “We were able to show that the selected carbon nanotubes had mechanistic potency to induce tumors, comparable to that of asbestos fibers.”]
In 2013, the National Institute for Occupational Safety and Health recommended an occupational exposure limit of 1 µg/m3 – a thousand times lower than what manufacturers and distributers were using at the time. (https://www.cheaptubes.com/wp-content/uploads/2015/03/Carbon-Nanotubes-MSDS.pdf)
https://chemsec.org/new-chemicals-on-the-sin-list-challenge-the-global-supply-chain/
ChemSec announced the addition of carbon nanotubes to the SIN (‘Substitute It Now’) list1. Carbon nanotubes were added as an entire material class that “should be restricted or banned in the EU.”
The SIN List now includes carbon nanotubes, one of the more well-studied nanomaterials. First engineered in the 1990s, they are used to make durable, lightweight materials, for electrical conductivity, as a super black pigment and for water purification, among other uses.
“Several studies have shown that carbon nanotubes cause lung cancer. The small tubes induce inflammation in a somewhat similar way to asbestos. Reprotoxic properties have also been observed. Up until now, the debate about the safety of nano has focused on the fact that more research is needed. However, here is a perfect example of where there is enough science to say that these materials should not be used”, says Dr. Lennquist.
https://chemsec.org/nano-might-be-really-small-but-the-consequences-might-not-be/
These materials [nano] are being used in a growing number of applications and enormous resources are being put into innovation, but so little into safety and regulation.
So what do we know? If you have a toxic chemical – it will also be toxic in its nano form. The level of toxicity can vary, as well as the mode of action.
For example, nano-particles can be very difficult to dissolve, as they stick to surfaces and are thus difficult to dose correctly. If you put them in an aquarium that contains test organisms and organic material, molecules such as proteins immediately coat the particles. The coated particles can again have different properties from the non-coated nano-particles.
However, new and more accurate tests for nano have been developed lately.
Legally, nano falls under REACH, but how REACH should tackle these materials is still under much debate. So far, ECHA and member states have been unsuccessful in their attempts to get additional data from registrants of chemicals in nano form with the motivation that the nano form may have different properties from the bulk form. The board of appeal has always overruled such requests on the grounds of lack of definitions. The definitions and characterisation further add to this being such a complex issue.
The definitions of nano and registration requirements for nano forms have been discussed in depth by the ECHA and others for many years. In November 2018, however, a REACH annex was agreed that will come into force in 2020 and will clarify aspects such as characterization, registration requirements and test methods.
At ChemSec, we are frustrated by the fact that uncertainty is so often used to slow down the regulation of chemicals. One can always find uncertainties, and thereby delay decisions.
When it comes to nano materials there is definitely no lack of uncertainty. But instead of being paralysed by the things we do not know, we should act on the things we do know – and we must take a precautionary approach. I believe three things are urgently needed:
There needs to be transparency on nano. Production, processes, volumes and products should be registered.
Specific safety data should be required for nano forms, with realistic testing of hazardous properties for human health and the environment.
In the case of the few nano forms that have been around for a long time, for which data exists showing they are of high concern, they should be regulated ASAP.
There are many types of carbon nanotubes. They can be single-walled, double-walled, multiwalled, long, short or tangled. The difficulty with characterisation and identifying what is “one” nanomaterial is very challenging from a regulatory perspective. Studies of hazardous properties are conducted on one specific form, possibly even from a specific production batch. Can we use that data to say anything about other forms?
In the case of carcinogenicity, which is an important reason for the SIN Listing, evidence of carcinogenicity exists for some forms of multiwalled carbon nanotubes. But in addition to this, for a number of other forms, evidence of lung inflammation and other mechanisms associated with cancer exist.
Shifting the perspective, we could not find good reason to exclude any form from being a suspected carcinogen. Environmental persistence seems to be shared by all forms, while toxicity for reproduction has mainly been seen for single-walled carbon nanotubes.
You can read our full response to the critique in Nature Nanotechnology in the same scientific journal here. It is written together with assistant professor Steffen Foss Hansen from DTU, who coordinated the scientific work behind the SIN Listing of carbon nanotubes.
https://www.nature.com/articles/s41565-020-0692-7.epdf?sharing_token=JGfLkzP7HmNQWL2v9SCT7NRgN0jAjWel9jnR3ZoTv0Nr-nG1MCFIeIr0a8NK7SnlOUsdbYjQTWyrqAigxgZojabbQrBe0kIOFEjxSCelYCggDbFDBaNs2TpkUCX5JqGE6PY0Fmt0-1FMpSTr2_lHl8hItqd6DDxluJI8WrFwufw%3D SIN List criticism based on misunderstandings | Nature Nanotechnology
First, the SIN List is not based on risk assessment, but hazard identification.
The inherent hazard endpoints used to evaluate whether substances are SVHCs are carcinogenicity, toxicity to reproduction and environmental persistence.
We evaluated evidence for carcinogenicity of single-walled CNTs (SWCNTs), double-walled CNTs (DWCNTs) and multiwalled CNTs (MWCNTs), referring to the review by the International Agency for Research on Cancer (IARC) and we highlighted that the results of genotoxicity studies in vivo and in vitro were positive for both SWCNTs and MWCNTs. We, furthermore, highlighted that lung inflammation, granuloma formation and fibrosis were observed in rats and mice exposed to SWCNTs, DWCNTs or MWCNTs by inhalation, intratracheal instillation or pharyngeal aspiration in the studies reviewed by IARC. As noted by Kuempel et al., both of these findings are significant as genotoxicity and persistent inflammation are considered key events in the development of lung cancer and mesothelioma from exposure to poorly-soluble and fibres, including CNTs. Since the review by the IARC, additional studies on a variety of different types of MWCNTs, for example by Rittinghausen et al. and Sakamoto et al., have been published that support the evidence of MWCNT carcinogenicity after intraperitoneal injection in rats.
I see from Skywater Technology that DARPA is involved in development of Carbon Nanotube. It seems the DoD is running our country.
Thank you for this excellent research.