Dust is a solid particle that can float in the air for a long time in an aerosol state (smoke, fog, dust) or in a smoky state. Production dust refers to the solid particles generated in human production activities that can float in the production environment for a longer period of time. A large amount of dust can be generated from various human production and living activities, as well as from natural fractional corrosion and gas flow. Exposure to production dust is the sole cause of pneumoconiosis, and the physical and chemical properties of production dust and its exposure characteristics and exposure are closely related to pneumoconiosis. Different dusts differ in their ability to cause fibrosis in lung tissue, and the development, regression, and prognosis of the resulting pneumoconiosis vary greatly. Dust floats in the air and the respiratory tract is the main route of invasion. As a foreign body, dust enters the respiratory tract with breathing and first causes a series of clearance reactions, causing most of the dust to be expelled from the body, while excess dust entering the lower respiratory tract and alveoli is deposited in the lungs causing pathological reactions. The effect of dust on health is the process of these physiological and pathological reactions and their results. The respiratory system has a strong foreign body removal function in terms of its structure and physiological function. 1, first of all, the curved structure of the nasal cavity and nasal hairs, as well as the pharynx, trachea direction of change and bifurcation, so that the dust particles with the respiratory airflow into the respiratory tract, due to the change in direction of the collision effect, so that the larger dust particles (> 10um) are retained in the nasal cavity and atmospheric tract. 2, with the increase in the bifurcation of the trachea and airway area, airflow speed also gradually slowed down, when the dust particles in the role of gravity can be settled in the trachea and even alveolar wall. 3, the chance of dust deposition is determined by the size and specific gravity of dust particles and the worker’s respiratory ventilation and flow rate. In general, larger dust particles are deposited in the upper respiratory tract, smaller dust particles can be deposited in the lower respiratory tract, particles with a diameter of 2 to 10 um are deposited on the tracheal wall, and dust particles with a diameter of 2 um or less can be deposited on the walls of respiratory fine bronchi and alveoli. Nearly round dust particles are easily deposited by gravity, while irregular dust particles are more often blocked in the upper airways such as the nasal cavity due to inertial collisions. A structurally normal nasal cavity has a strong dust filtering effect and can retain 30-50% of dust particles in the nasal cavity. Dust particles deposited in the respiratory tract are retained in the canal walls and cilia due to mucosal secretions. Ciliary motility of the mucosal epithelium and the cough reflex are important mechanisms for accomplishing the dust particle removal action. The regular movement of cilia in the intact bronchial mucosa epithelium allows dust particles to gradually move upward from the deeper part of the respiratory tract and to be excreted with the secretion of mucus and in the form of coughing and sputum. A significant portion of the dust particles entering the alveoli can be expelled directly with the exhaled airflow without deposition. Dust particles deposited in the alveolar wall are engulfed by macrophages to form phagosomes, which move upward to the surface of fine bronchial mucosa with ciliated epithelium through amoeboid movement, and then move to the upper respiratory tract through ciliated movement and are expelled through coughing and sputum. As can be seen above, the retention effect of the upper respiratory tract and the inertial collision and gravitational sedimentation of dust deposit in the respiratory tract, the secretion of the respiratory mucosa and the movement of the ciliated epithelium, and then the coughing and spitting are the main ways of dust discharge. Of course, unsettled dust particles can be expelled directly from the body with the exhaled airflow. In general, about 98% of the dust entering the respiratory tract can be removed by the above mechanism, and the dust particles remaining in the lungs are only 2-3% of the total amount of inhaled dust. Although only a small amount of inhaled dust can be retained in the lungs, long-term inhalation of high concentrations of respirable dust will gradually increase the amount of retained dust in the lungs. Long-term retention of dust particles in the lungs, especially mineral dust, causes fibrosis and pneumoconiosis. Second, the pathogenic effect of productive dust 1, skin, mucous membrane, upper respiratory tract irritation: long-term mucosal capillary dilation leads to mucosal hypertrophy, followed by mucosal dystrophy and atrophy, the formation of atrophic rhinitis. Hardness, sharp-edged dust particles can also mechanical direct damage to mucosal cells cause rhinitis, pharyngitis, laryngitis. Some dusts can directly damage the nasal mucosa to form ulcers and perforations. Dust scattered on the skin can block the sebaceous glands, making the skin dry and prone to secondary infections such as acne and folliculitis. Dust on the corneal stimulation and injury can cause loss of corneal sensation, corneal clouding and other changes. 2, non-specific inflammatory reaction: the stimulating effect of dust makes the mucous membrane epithelial cells proliferate and hypertrophy, mucus secretion increases, and cilia movement is weakened. Mechanical damage to the respiratory tract caused by dust also often causes secondary infection. Therefore, chronic bronchitis in dust workers is a common occupation-related disease, which is also called “dust chronic bronchitis”. The combined effect of smoking and dust can increase the incidence of chronic bronchitis. Bacterial endotoxins, proteases and tannins contained in organic dust can also cause a non-specific inflammatory response in the respiratory tract. 3. Fibrosis: Pneumoconiosis is a systemic disease caused by long-term inhalation of productive dust during occupational activities and its retention in the lungs, mainly due to diffuse fibrosis of lung tissue. The pathology is characterized by diffuse, progressive fibrotic hyperplasia of the lung tissue, causing severe impairment of respiratory function and resulting in reduced or lost work capacity. Free silica is highly cytotoxic and fibrogenic, and the fibrogenic effect of mineral dust is related to the amount of free silica in the dust. Silicosis is the most severe, fastest progressing, and most dangerous form of pneumoconiosis. The fibrogenic effect of dust is the most harmful biological effect of dust on human health. 4, carcinogenic effect: asbestos dust can cause bronchial lung cancer and mesothelioma, radioactive mineral dust can cause lung cancer, and metal dusts such as nickel and chromate are also associated with high incidence of lung cancer. Recently, the relationship between silicosis and lung cancer development has received attention, and at least some epidemiological studies support the theory that silicosis is associated with lung cancer. The relationship between welding fume and lung cancer has also been reported, and it is believed that the 6-valent chromium in welding fume may be a major factor in carcinogenesis. 5, allergenic effect: many organic dusts can cause bronchial asthma, a typical metabolic disease, such as wood dust, grain dust, chemical detergent enzymes, animal protein dust, etc. Allergic pneumonia caused by moldy hay, mushroom spores, bagasse, etc. is an immune-mediated granulomatous disease of lung tissue, such as farmers’ lung, mushroom lung, bagasse lung, etc. 6, toxic effects: inhalation of some chemical dusts, such as lead, manganese, arsenic and other toxic dusts, can cause systemic toxic reactions. 7, specific inflammatory reaction: mainly organic dust with bacteria or fungi, can cause pulmonary fungal disease, fur dust in the anthrax bacillus caused by pulmonary anthrax disease. 8, dust deposition disease Inhalation of certain inert metal dust can cause the deposition of metal dust in the lungs, such as tin, antimony, iron, etc.