Occupational asthma

Introduction to occupational asthma Occupational asthma (occupationalasthma) refers to asthma caused by exposure to asthmatic substances in the occupational environment. Its incidence is closely related to the degree of industrial development. In addition, the incidence is related to the nature of the asthma, such as long-term exposure. Among workers with tonic isocyanate, the incidence of occupational asthma is about 5% to 10%, and among workers who are in the detergent industry and have been in contact with proteolytic enzymes for a long time, the incidence rate is 50% or higher. With the development of industry, the incidence of occupational asthma in China is also increasing year by year. The specific bronchial provocation test is the most diagnostic method for diagnosing occupational asthma and screening for occupational asthma. Avoid contact with allergens is treatment. The most important measure of occupational asthma. basic knowledge The proportion of illness: 0.007%-0.009% Susceptible people: no specific population Mode of infection: non-infectious Complications: pneumothorax mediastinal emphysema

Occupational asthma cause

(1) Causes of the disease

Internal cause

It has been found that occupational asthma practitioners engaged in high molecular weight allergen-related industries generally have atopy physique, and studies have shown that they are associated with the patient's genes. These people are more likely to develop asthma after exposure to asthma. The original substance easily enters the body, and the B lymphocyte reactivity is abnormally increased. After contacting the allergen, a specific IgE is generated to form a sensitized state, and when the occupational allergen re-enters the body, it is easy to induce an allergic reaction and an asthma attack.

2. Causes

The causes of occupational asthma are divided into high molecular weight biological substances and low molecular weight chemical substances, most of which are occupational asthmatic substances, and a few are irritants. Currently, there are more than 250 kinds of asthmatic factors recorded in the book. There are still many suspicious factors yet to be determined.

(1) Plants: grain dust, flour, soybeans, castor beans, coffee beans, tea leaves, tobacco leaves, vegetable gum, cottonseed, linseed, etc.

(2) Animal body composition and its excrement: laboratory animals, birds, eggs, milk, crabs, shrimps, etc.

(3) Insects: household dust mites, glutinous rice, poultry mites, silkworms, crickets, bees, etc.

(4) Enzymes: papain, succinylase, trypsin, pepsin, trypsin, fungal amylase, and the like.

(5) Vegetable gum: gum arabic, tragacanth, carrageenan, etc.

(6) Isocyanates: such as toluene diisocyanate (TDI), methylene diphenyl diisocyanate, hexamethylene diisocyanate, and the like.

(7) Phthalic anhydrides such as phthalic anhydride, trimellitic anhydride, triphenyl hexacarboxyhydride and the like.

(8) Drugs: such as penicillin, cephalosporin, spiramycin, tetracycline, piperazine citrate and the like.

(9) Wood dust: wood dust such as mahogany, cedar, maple, oak and other wood.

(10) Metals: such as platinum, nickel, chromium, cobalt, and the like.

(11) Others: rosin, formaldehyde, ethylenediamine, ammonium thioglycolate, etc.

Among them, 1 to 5 are high molecular weight biological substances, and 6 to 11 are low molecular weight compounds. At present, the scope of occupational asthma in China is defined as isocyanates, phthalic anhydrides, amines, platinum complex salts and sisal.

According to the difference of asthmatic factors, occupational asthma can be divided into high molecular weight allergen prototype and low molecular weight allergic prototype. According to the pathophysiological mechanism, it can be divided into immune-mediated and non-immune-mediated, immune-mediated The patient's onset has an incubation period, which can be divided into two types: IgE-mediated and non-IgE-mediated. The former is mostly induced by high molecular weight allergens and a few low molecular weight allergens. The latter is only found in low molecular weight allergens. Originally induced occupational asthma, non-immune-mediated patients have no incubation period for asthma attacks, and inflammation of the airway can be caused by direct stimulation of asthma, and can also stimulate mast cells, smooth muscle cells or nerve fibers through the pharmacological action of asthma. Indirectly caused by.

(two) pathogenesis

The pathogenesis of occupational asthma is quite complex, with both immunological and non-immune mechanisms.

1. Immune mechanism: induced by occupational allergens, IgE-mediated allergic reaction is one of the main pathogenesis of occupational asthma, including rapid-onset allergic reactions and delayed-onset allergic reactions, the former mainly through Mast cells release inflammatory cytokines, which manifests as asthma attacks occurring within a few minutes after entering the workplace, and begins to weaken after 1 hour. The latter is mainly caused by eosinophils, and monocytes release soluble factors to cause airway contraction. In order to develop an asthma attack several hours after inhalation of sensitization, occupational asthma caused by some low molecular weight allergens is a non-IgE-dependent immune mechanism.

2. Non-immune mechanisms: Many occupational asthmatic factors can cause reflex bronchoconstriction, such as S02, acid smoke, ammonia, etc., which directly stimulate the airway, causing the release of inflammatory mediators and neuropeptides and inflammation of the airways. The sensitivity of airway nerve reflex is enhanced and it is easy to cause asthma attacks. Some occupational allergens such as TDI can directly act on lung tissue, promote the release of factors such as substance P and histamine releasing factor, or block -receptor. The body reduces cAMP levels and causes bronchospasm.

Occupational asthma prevention

For patients with occupational asthma, focusing on early detection and early diagnosis, in the case of normal lung function and clear pathogenic factors, timely escape from the original working environment can fully recover, affecting prognosis factors in occupational asthma patients, including contact time, from The age of the disease, the degree of atopic physical condition, the degree of lung damage and the level of airway responsiveness, etc., when the patient has irreversible airway obstruction and forms chronic obstructive pulmonary disease or other complications, the prognosis is poor.

Occupational asthma complications Complications Pneumothorax mediastinal emphysema

Occupational asthma can be complicated by pneumothorax, mediastinal emphysema, mucus fistula embolism, etc. are the most common complications.

Occupational asthma symptoms common symptoms chest tightness wheezing

Typical occupational asthma manifests as coughing, wheezing, chest tightness or accompanied by rhinitis, conjunctivitis, etc. during work or after work. Symptoms are closely related to the working environment, and are triggered by high molecular weight occupational asthma. Asthmatic asthma reaction, which is characterized by asthma symptoms when the patient enters the working environment, and the symptoms are relieved quickly after leaving the scene. It has contact with the working environment - asthma attack - separation from the working environment - asthma relief - re-sex recurrence characteristics, induced by low molecular weight asthma Occupational asthma is characterized by a delayed asthmatic response, which occurs sometime after work and is therefore easily overlooked or misdiagnosed.

Occupational asthma check

Specific IgE detection uses common allergens and specific allergen complexes for skin tests to understand whether a patient has atopic physique and to help determine whether a patient is sensitive to a specific occupational allergen, using radioactive allergens The original adsorption test (RAST) or ELISA can detect IgE antibodies against occupational allergens in the serum of patients, which are more sensitive but less specific.

Pulmonary function

Pulmonary function for occupational asthma indicators include PEF, FEV1 (forced expiratory volume in one second), etc. Continuous observation of PEF has a certain significance in the diagnosis of occupational asthma, requiring patients to measure once every 2 hours regardless of work or rest. For several weeks, it can help determine whether airway obstruction caused by asthma is work-related. This method is sensitive, but not specific enough.

2. Non-specific bronchial provocation test

Continuous non-specific bronchial provocation test with formylcholine or histamine can confirm whether the patient has airway hyperresponsiveness and help to determine the relationship between changes in airway responsiveness and the working environment. When the patient goes to work for more than 2 weeks, If the reaction is negative, the diagnosis of occupational asthma can be ruled out even if there are related symptoms. If the patient is negative after a period of time off the job, occupational asthma cannot be excluded.

3. Specific bronchial provocation test

It is currently believed that the specific bronchial provocation test is a gold indicator for the diagnosis of occupational asthma. The test has certain risks. Professionals need to operate and prepare rescue measures. The whole test takes several days to complete. On the first day, the bronchiectasis is stopped. For the determination of basic lung function, the difference of FEV1 should not exceed 10%; on the second day, after inhaling the soluble aerosol, the lung function of the patient was measured as a control; on the third day, the patient was exposed to the allergen, and the contact time was based on the allergen. Depending on the nature and dosage, it can vary from 1 to 10 min. For high molecular weight allergens, FEV1 is measured once every 10 minutes, and the sensitizer dose is increased once every 20 minutes. The test can be completed on the same day for low molecular weight allergens. Because it induces mostly delayed allergic reactions, it takes several days to increase the dose slowly. FEV1 is measured once every 10 minutes within 1 hour, then every 2 minutes, every 30 minutes, then 8 hours, once every hour. FEV1 decreased by 20% as a positive reaction.

Diagnosis of occupational asthma

Diagnostic points

There is no uniform standard for the diagnosis of occupational asthma. First, we must establish a diagnosis of asthma, and then further determine the relationship between asthma attacks and occupations, and find out the asthma, mainly the following points.

1. Defining the diagnosis of asthma: According to the diagnostic criteria of asthma, the diagnosis can be confirmed based on the medical history, clinical manifestations, signs at the onset of symptoms, and laboratory tests such as pulmonary function tests.

2. Defining the relationship between asthma and occupation: Careful inquiry about the patient's current medical history and past history, generally get clues, suspected of asthma in the following cases, such as the patient's previous history of no asthma, new materials in contact with new work or work After the onset of asthma; the patient has a thirst in the working environment; colleagues working in the same environment have similar episodes; asthma attacks are related to the work environment, and symptoms are relieved after work or transfer.

3. Looking for occupational asthma: Through specific laboratory tests such as specific skin tests, serological tests and specific bronchial provocation tests can help find occupational asthmatic factors. Currently, specific bronchial provocation tests are considered Screening for the most diagnostic value of occupational asthma.

Should pay attention to the identification of industrial bronchitis, cardiogenic asthma, bronchial mucus obstruction.

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