Cotton Dust Lung

　　1. Causes of Disease

　　Byssinosis is a respiratory obstructive disease caused by inhaling plant dust such as cotton, flax, and soft hemp.

　　2. Pathogenesis

　　1. Pathogenesis

　　What exactly causes the disease in cotton dust is not yet fully clear. Many studies have shown that cotton fibers themselves are not the causative agent, but rather the plant components mixed with cotton dust, which are likely to be cotton cotyledons. However, the extracts of cotton cotyledons cannot induce the typical symptoms of cotton dust disease. At the same time, medical cotton extracts have been shown to have similar biological activity. Some chemical substances in cotton plants, such as tannins, histamine, polyphenols, methylcinnamate, 7-hydroxy-6-methoxy coumarin, and others, are also considered to be possible causative agents. Some studies focus on microbial contamination, considering Gram-negative bacteria and their endotoxins to be the causative agents of the disease. There are three hypotheses about the pathogenesis:

　　(1) Histamine Release: Early research suggested that bronchospasm caused by cotton dust exposure was due to histamine release. Researchers used cotton dust extracts and cultured human isolated lung tissue to find histamine release in the culture medium. Histamine plays an important role in bronchospasm induced by allergens during acute attacks, but it is quite different from the slow onset of bronchospasm caused by cotton dust exposure. Although histamine metabolites can be seen in the urine of cotton dust exposed workers, antihistamines cannot inhibit the reactions caused by cotton dust exposure. Therefore, histamine release is likely to be the result of general inflammatory response rather than a direct cause.

　　(2) Immunological Theory: The typical symptoms of cotton dust disease occur after a long period of exposure, which suggests that certain components in cotton dust may have antigenic effects, stimulating the body to produce specific antibodies, which may be related to the occurrence of the disease. Some studies have confirmed the existence of these specific antibodies, which may be condensed tannins, but subsequent experiments have shown that they are only non-specific protein precipitants. Research on finding specific IgG and IgE antibodies against cotton dust components has also not yielded satisfactory results. Recent studies have shown that cotton dust can activate mast cells or platelets to secrete mediators, and the inflammatory response mediated by these mediators can explain the respiratory system reactions after exposure to cotton dust.

　　(3) Endotoxin-induced inflammatory response: Many studies believe that cotton dust is contaminated with Gram-negative bacteria and their endotoxins, and the inflammatory response induced by endotoxins is the basis of cotton dust disease. Rylander heated the cotton dust extract to 80℃ for 2 hours, at which time all the bacteria had been killed, but the biological activity of the extract still existed, indicating that this biological activity is caused by endotoxins. Endotoxins can activate lung macrophages to produce biologically active substances, causing neutrophil aggregation and a series of biological reactions, thus causing acute or chronic lung inflammation. Animal inhalation experiments using Escherichia coli endotoxin and cotton dust extracts show the same histological changes, but the biological activity of dust in a humid environment does not increase, and uncontaminated cotton dust also causes cotton dust disease.

　　2. Pathology

　　Pathological examination reports are rare. From the lung gross specimens obtained from workers exposed to cotton dust who underwent surgery for other diseases, it can be seen that there may be inflammatory cell infiltration in the tracheobronchial wall, hyperplasia of mucous glands, atrophy of smooth muscle, but this change rarely extends to segmental bronchi. Centrilobular emphysema is rarely seen. Under polarized light microscopy, cotton fibers can be seen, and a few cotton dust bodies (cotton-dustbody) can be seen, which are round or elliptical with a positive iron-stained black-blue nucleus in the center, and a yellow protein coat outside. It is generally believed that they have no diagnostic significance. Some reports show that there is fibrous thickening of the alveolar wall, and in late cases, emphysema and signs of right heart hypertrophy can be seen.

　　In the late stage of cotton dust lung disease, the patient's lungs may have rales, weakened respiratory sounds, and signs of emphysema, and patients with chronic bronchitis and smokers have significant exacerbation of symptoms. There may be complications such as emphysema and pulmonary heart disease.

　　The characteristic symptoms of cotton dust disease are chest tightness or chest束缚感(chesttightness), although workers may describe this symptom in different ways, such as chest tightness, shortness of breath, chest oppression, and chest coldness, but all describe the same feeling. The above symptoms mainly appear after 2-3 hours of work on the first day of returning to work after holidays or weekends, and are different from occupational asthma, which occurs immediately after work. It may be accompanied by mild dry cough. This symptom may persist for many years without change. If the patient continues to be exposed to cotton dust, they may suddenly find that the symptoms worsen, not only dry cough, chest tightness, and shortness of breath after returning to work on the first day of rest, but also other symptoms during the workweek. The cough may worsen, and sputum may be produced. The symptoms may persist without disappearance, and the patient may gradually develop dyspnea. In the early stage, the patient often has no positive signs in the lung examination. In the late stage, the patient may have rales, weakened respiratory sounds, and signs of emphysema. Patients with chronic bronchitis and smokers have significant exacerbation of symptoms. Patients with emphysema and pulmonary heart disease may also be combined.

　　Prevention first of all is to reduce the dust in the working environment. The national standard of China stipulates that the maximum allowable concentration of free silicon dioxide dust in the air of the workshop is 1.5mg/m3, which contains 50% to 80% free silicon dioxide dust. Strengthen the management of the industry, establish strict health supervision and environmental monitoring systems. Establish and improve dust prevention institutions, including regular dust monitoring systems, and evaluate the effectiveness of dust prevention measures. Start with technical measures, pay attention to process reform, and fundamentally eliminate the generation of dust in the production process and process. Strengthen publicity and education, formulate health cleaning systems, and achieve civilized production. Conduct pre-employment and regular physical examinations, regularly take chest X-rays, and also regularly follow up those who have left the dust work. Those with upper respiratory tract diseases, bronchopulmonary diseases, especially those with pulmonary tuberculosis, cardiovascular diseases, and cannot engage in this kind of work. Strengthen personal protection, pay attention to personal hygiene, carry out physical exercise, pay attention to nutrition, etc.

　　Cotton dust lung disease patients may have concurrent bacterial infections, with an increase in blood leukocytes.

　　Pulmonary function changes: Cotton dust workers may experience acute pulmonary ventilation function decline during working days, that is, the pulmonary ventilation function decreases before and after the shift, and the symptoms of chest tightness are similar. The acute ventilation function decline is also obvious on the first day of work after rest on holidays or weekends, and then gradually subsides, and is related to the severity of the symptoms. This acute change can be relieved by bronchodilators. It is generally believed that FEV1 is a relatively reliable and easy-to-use indicator for measuring acute changes in pulmonary ventilation function. Other indicators such as indirect maximal breathing capacity (indirect maximal breathing capacity, IMBC), PEFR, CV (closing volume), CC (closing capacity) have also been studied, but these indicators have a large variability and are not very stable. How much the decline in FEV1 after the shift has clinical significance is currently controversial. The Chinese diagnosis criteria for cotton dust disease stipulate that a decline of more than 10% in FEV1 after the shift has diagnostic significance. Some people analyzed the decline in FEV1 after the shift in 22 cases with symptoms of cotton dust disease, among whom 16 cases were greater than 10%, 3 cases were between 5% and 10%, and 3 cases were less than 5%.

　　Currently, the focus of research on lung function damage is whether cotton dust exposure causes permanent respiratory function damage. Theoretically, the decline in acute lung ventilation function is based on pathological conditions of respiratory tract inflammation and bronchial smooth muscle spasm. Long-term and repeated acute reactions will eventually lead to chronic damage to respiratory function, and most studies have proven this point. Some researchers surveyed 1,323 workers with more than 3 years of work experience in 4 cotton spinning factories, with 135 non-cotton dust contact managers as controls. The definition of lung function abnormalities is FVC below 80% of the predicted value or FEV1 below 70% of the predicted value. The study found that 5% of the workers exposed to dust had lung function abnormalities, while the control group had only 0.7%. There is a correlation between lung function damage and working experience (r=0.945). Workers with more than 15 years of work experience accounted for 14.3% of lung function abnormalities, and those with more than 20 years accounted for 16.6%. In a survey of 851 workers exposed to dust in a cotton spinning factory, 190 had typical 'Monday' symptoms, and 18.4% of the workers had chronic lung function damage (FEV1 less than 80% of the predicted value), while only 2 (1.7%) out of the 135 in the control group did, smoking can exacerbate the impact of cotton dust on respiratory function.

　　What foods are good for cotton dust lung disease patients:It is advisable to have a light diet, eat more vegetables and fruits, reasonably match the diet, and pay attention to sufficient nutrition.

　　No special treatment, patients with stage 1 cotton dust disease can be transferred to work with lower dust concentration or without contact with cotton dust, and patients with stage 2 cotton dust disease should be transferred away from work with cotton, hemp, and other dust. For those with obvious symptoms, bronchodilators and antihistamines can be administered.