Travels of a Grain of Dust

Author: Cen Keqin, Bao Ying, Zhou Yi, Xi'an Medical College

Illustration: Cen Keqin Xi'an Medical College

Reviewer: Xiao Xinli, Associate Professor of Xi'an Jiaotong University

Hello everyone! I am a tiny particle of silica dust. Although small in size, my family is huge. We come from human mines, quarries, tunnels, quartz powder factories and glass factories. We live in this "earthly world" and are accidentally inhaled into the human body, and then we begin our journey in the human body.

I am 1 to 2 microns in diameter, look like a tetrahedron, and am mainly composed of silicon dioxide. Between breaths, the human respiratory system will strictly screen us. With 5 microns as the limit, silica dust particles with a diameter of more than 5 microns tend to adhere to the surface of the airway mucosa when passing through the upper respiratory tract of the human body, and are removed by the mucus-ciliary clearance system, and finally excreted from the body with human coughing; particles with a diameter of less than 5 microns can be inhaled into the lungs and reach the alveoli directly. Because of my slender figure, I successfully passed through the many checkpoints of the respiratory tract and entered the human body. What's important is that the smaller the particle, the stronger the pathogenicity. Tetrahedral particles like me with a size of 1 to 2 microns have the strongest pathogenicity!

Figure 1 Copyright image, no permission to reprint

Then, I will go all the way to the alveoli, where macrophages gathered in the alveolar septa or around the bronchi can devour me. My main component, silicon dioxide, interacts with water to form silicic acid. The hydroxyl groups of silicic acid form hydrogen bonds with hydrogen atoms in phospholipids or lipoproteins on the phagolysosome membrane in the macrophage, thereby changing the stability and integrity of the lysosomal membrane and causing it to rupture. After the lysosome is destroyed, a variety of hydrolases are released to cause the macrophage to disintegrate, and in this way, silica dust particles like us are released again. But the good times don't last long, and we will be devoured again by other macrophages in a free state. Repeatedly, the macrophages that engulf silica dust proliferate and aggregate locally, forming early cellular nodules .

Both collapsed macrophages and activated macrophages can release a variety of cytokines and inflammatory mediators, such as macrophage growth factor, interleukin, fibronectin, tumor necrosis factor, etc., which cause inflammatory reactions in human lung tissue, promote the proliferation of fibroblasts and the formation of collagen fibers, and thus lead to pulmonary fibrosis. In this way, we will continue to be inhaled by humans and deposited in the lungs, and then be released again after being engulfed by macrophages. The lesions in the lungs continue to progress and worsen, fibroblasts proliferate, and collagen fibers continue to increase, arranging in concentric circles or spirals, so that the initial cellular nodules gradually become fibrous silica nodules . Collagen fibers can also be further degenerated and fused, transforming into a homogeneous, translucent, frosted glass-like substance, which is the "glass degeneration" that everyone often hears. At this time, the silica nodules form typical glass nodules . Adjacent silica nodules can fuse with each other, and the center of the nodule often undergoes necrosis and liquefaction due to ischemia and hypoxia, forming silicosis cavities . Using polarized light microscopy, humans can observe silica dust particles like us in silica nodules and diseased lung tissue.

Over the years, we have caused more and more harm to the human respiratory system. Eventually, we will shrink, harden, and fibrose the human lungs, and cover them with grayish white, solid, round or oval, sandy-feeling silica nodules of varying sizes. Of course, the lesions will also affect the pleura, causing pleural thickening. Due to extensive pulmonary fibrosis, the body's resistance to tuberculosis bacteria is reduced, so patients with silicosis are prone to complications of pulmonary tuberculosis, and are also prone to secondary bacterial and viral infections, inducing respiratory failure. Late-stage patients often have obstructive emphysema, and severe coughing may also cause pulmonary bullae to rupture, causing spontaneous pneumothorax. Due to extensive damage to lung tissue, reduced capillaries, and spasm and hardening of pulmonary arterioles, the pulmonary circulation resistance increases, pulmonary hypertension, right ventricular hypertrophy and dilatation, and eventually develop into chronic cor pulmonale, and even death from right heart failure.

Figure 2 Copyright image, no permission to reprint

As a particle of silica dust, I cannot control my own body. Once I enter the human body through breathing, there is no way to press the "pause button" during this journey. Moreover, I will not be excreted by the human body and cannot be reversed. Even if people leave the silica dust working environment, I will continue to get sick in the lungs and the lung lesions will continue to develop. Humans generally develop the disease 10 to 15 years after exposure to silica dust. Although the disease progresses slowly, it will eventually lead to respiratory failure and heart failure until death. At this time, as a particle of dust, my journey in the human body will also end.

If humans don't want to have such an ending, they must find ways to stop us from starting our journey inside the human body. The key measure is prevention . First, we must attach enough importance to it, do a good job of popularizing science, and realize our harm to humans. Secondly, we must take protective measures to prevent us from being inhaled into the human body. The following measures can be taken.

•Reform production processes, reduce dust in the working environment, adopt wet operations, ventilate and remove dust, and regularly monitor the concentration of dust in the air.

•Comply with dust prevention operating procedures, wear dust-proof clothing and masks during work, and take personal protection measures.

• Regular physical examinations and chest X-rays should be conducted to detect diseases early and provide early treatment. Regular follow-up should also be conducted for those who have left dusty work.

• Strengthen tuberculosis prevention and control among workers in industrial and mining areas, vaccinate with BCG in a timely manner, and reduce the incidence of silicosis combined with tuberculosis.

• Actively engage in physical exercise, improve nutrition, enhance physical fitness, and focus on the prevention of respiratory diseases.

Although I want to be friends with humans, "fire and water don't mix". I can only give humans one sentence, please remember: "Stay away from the dust, health first!"