A Fibrous Disease: Iron, Asbestos and the Spike Protein


First: The word "asbestos", first used in the 1600s, ultimately derives from the Ancient Greek ἄσβεστος, meaning "unquenchable" or "inextinguishable".

Fiber-related disease has provided much of the impetus for fiber research in recent years. Asbestos has been the fiber type most commonly associated with disease. The name “asbestos” is a commercial term applied to the fibrous forms of several minerals that have been used for similar purposes and includes chrysotile, amosite, crocidolite, and the fibrous forms of tremolite, anthophyllite, and actinolite. The three primary diseases associated with asbestos exposure are asbestosis, the result of inflammation and collagen formation in lung tissue; lung cancer; and mesothelioma, an otherwise rare form of cancer associated with the lining surrounding the lungs. A current theory describing the toxicity of fibers indicates that fiber dose, fiber dimension, and fiber durability in lung fluid are the three primary factors determining fiber toxicity.

The dose, or number of fibers deposited in the lungs, is clearly an important factor in determining the likelihood of disease. Both fiber diameter and length are important in the deposition of fibers in the lungs and how long they are likely to remain in the lungs. The graphic indicates some of the factors that determine fiber deposition and removal in the lungs. Fiber length is thought to be important because the macrophages that normally remove particles from the lungs cannot engulf fibers having lengths greater than the macrophage diameter.

Thus, longer fibers are more likely to remain in the lungs for an extended period of time. The macrophages die in the process of trying to engulf the fibers and release inflammatory cytokines and other chemicals into the lung. This and other cellular interactions with the fibers appear to trigger the collagen buildup in the lungs known as fibrosis or asbestosis and, over a longer period, produce cancer as well. Fiber diameter is also important because fiber aerodynamic behavior indicates that only small diameter fibers are likely to reach into and deposit in the airways of the lungs. The smaller the fiber diameter, the greater its likelihood of reaching the gas exchange regions. Finally, fibers that dissolve in lung fluid in a matter of weeks or months, such as certain glass fibers, appear to be somewhat less toxic than more insoluble fibers. The surface properties of fibers are also thought to have an effect on toxicity. Asbestos is one of the most widely studied toxic materials and there have been many symposia dedicated to and reviews of its behavior in humans and animals.

It is important to note that overlaps between mesothelioma have been observed. What is most interesting is that, as one article states, THE ONLY DIFFERENCE IS EXPOSURE TO ASBESTOS.

Let us consider this. Yes, this is true. However, there IS THE EXPOSURE TO THE SPIKE PROTEIN. Which, appears to be a “fibrous particulate” in and of itself. Especially in the sense that is seems to be very difficult to degrade, precisely like asbestos.


Among others, a common finding in the lung parenchyma of asbestos-exposed patients is anthracosis. This has been observed in COVID. In a study of 8 patients that died of COVID Anthracosis, common in elderly persons as a result of chronic carbon accumulation, was present in the lungs and pulmonary hilar lymph nodes in all cases.


I believe the spike protein acts as a fibrous pathological particulate, just like asbestos, silicon carbide and carbon nanotubes.

COVID-19 cases show diffuse pauci-inflammatory microvessel endothelial damage in the brain and other organs including the skin from the endocytosis of circulating viral spike protein that induces C5b-9, caspase-3 and cytokine production that is associated with a microencephalopathy. This encephalopathy is marked, in part, by neuronal dysfunction, evidenced by increased nNOS and NMDAR2 plus the reduction of key neuronal proteins that include MFSD2a and SHIP1. 2) Injection of the S1 full length spike subunit into the tail vein of mice, but not the S2 subunit or truncated S1 subunit, induces an equivalent microvascular encephalopathy that shares with the human COVID-19 brain disease the endocytosis of the S1 subunit in ACE2+ endothelia, caspase 3, C5b-9, TNFα, and IL6 activation, and the over-expression of nNOS and much reduced expression of MFSD2a.

The observed injury parallels that caused by asbestos.


The locally altered homeostasis of iron produced by the reaction to asbestos fibers and the presence of the potentially reversible iron reservoir of the iron-containing proteins have a central role in the asbestos toxicity mechanism as responsible for increased iron-mediated Reactive Oxygen Species (ROS) production. We can speculate that the iron we found in the black granules of anthracosis mostly originates from inhaled environmental particles.

However, remember, we are most likely dealing with systemic fibrosis, not just fibrosis in organs related to INHALATION.

Referenced/Related Papers

Endothelial cell damage is the central part of COVID-19 and a mouse model induced by injection of the S1 subunit of the spike protein


Asbestos-induced Endothelial Cell Activation and Injury: Demonstration of Fiber Phagocytosis and Oxidant-dependent Toxicity


Study Says Carbon Nanotubes as Dangerous as Asbestos


Mesothelioma and COVID-19: 3 Similarities Between Two Deadly Diseases


Measurement of Fibers


Conformational Changes of the Receptor Binding Domain of SARS-CoV-2 Spike Protein and Prediction of a B-Cell Antigenic Epitope Using Structural Data


Pathology and Pathogenesis of SARS-CoV-2 Associated with Fatal Coronavirus Disease, United States


Differential protein folding and chemical changes in lung tissues exposed to asbestos or particulates