There are three factors involved in the development of this disease: (a) Genetic factors People with a family history of allergic reactions are susceptible to this disease. Most of the patients’ families have a history of asthma, urticaria or drug allergy. Previously, this patient was called an atopic individual, whose body has a higher ability to produce IgE antibodies than normal. However, in recent years, some authors have found no significant difference in the incidence between twins and the general population. (ii) Nasal mucosal susceptibility Susceptibility arises from frequent stimulation by antigenic substances, but the degree of susceptibility depends on the number of mast cells and basophils in the nasal mucosal tissue and the ability to release chemical mediators. It has been confirmed that the number of these cells in the nasal mucosa of patients with allergic rhinitis is not only higher than normal, but also has a strong ability to release chemical mediators. (C) Antigenic substances The antigenic substances that stimulate the body to produce IgE antibodies are called allergens. The allergenic substance re-enters the nasal mucosa and combines with the corresponding IgE to cause a metamorphic reaction. The allergens that cause this disease are divided into two categories according to the way they enter the body: inhalation and food: 1. Inhalation allergens are inhaled into the nasal cavity through breathing. These allergens are mostly suspended in the air. (1) Pollen Not all plant pollen can cause disease. Only those pollen with high pollen volume, wide vegetation area, strong allergenicity and spread by wind are most likely to become allergens. Due to differences in vegetation species, allergenic pollen varies from region to region. Such as northern Europe to birch and ladder grass pollen; North America is dominated by ragweed; Japan is dominated by cedar pollen; China’s vast territory, allergic pollen in various regions are not consistent, the northern region to wild artemisia pollen, but in the north and south of the river are found ragweed, should be taken seriously. In recent years, it is believed that with the continuous development of industrialization, the concentration of sulfur dioxide and other harmful substances in the air has increased, which can cause the protein structure of the pollen surface suspended in the air to mutate, so that the original pollen without allergenicity also has a strong allergenicity. This may be one of the main reasons for the significant increase in incidence. There is significant seasonality in both the types and levels of pollen in the air, with spring and summer/autumn being the peaks of pollen dispersal. (2) Fungi are extremely widespread in nature and are found mainly in soil and decaying organic matter. Its mycelium and spores are allergenic, but the spores are stronger. Spores can be widely spread by wind, and the number in the air is sometimes higher than pollen, and higher in rural than urban areas. The most common species of fungi are Aspergillus, Alternaria, Penicillium, Aspergillus and Saccharomyces. Among them, Aspergillus and Streptomyces have significant seasonality, and their spores in the air in the number of peak in the summer. Indoor high temperature and darkness and humidity is conducive to fungal growth. Indoor ornamental flower pots in the soil often become a good place for fungal growth. (3) House dust mites belong to the phylum Arthropoda, the spider family. Adult mites are generally 300-500μm in size and are found in all corners of the house, including the dust in mattresses, pillows and sofa cushions. The excrement, eggs, debris and disintegrated limbs of mites can be allergens. (4) Animal dander Animal dander is one of the strongest allergens. Susceptible individuals can be sensitized if they have long-term contact with the animal in question. After sensitization, even a small amount of dander can trigger nasal symptoms. The animal dander that causes respiratory allergic reactions mainly comes from animals in close contact with people, such as domestic pets (ornamental dogs, cats), domestic dogs, cattle, horses and sheep. The authors have met a pathology laboratory technician, every contact with experimental animals guinea pigs will have sneezing episodes, followed by a lot of clear snot, and mild asthma. (5) Feathers Feathers in poultry, bedding, pillows and clothing, and feathers shed by domestic ornamental birds can be allergens. (6) House dust is one of the common allergens that cause perennial rhinitis. Its composition is quite complex, a hodgepodge of substances, including animal, plant and chemical substances. 2. Ingestive allergens are allergens that enter the body from the digestive tract and cause nasal symptoms. The way in which the period acts on the nasal mucosa is very complex and still not very clear. Milk, eggs, fish and shrimp, meat, fruits, and even certain vegetables can become allergens. The pathogenesis of allergic rhinitis is actually a type I allergic reaction that occurs in the nasal mucosa. Allergens enter the body through the respiratory tract, are processed by macrophages, and stimulate B lymphocytes to become plasma cells, which produce specific IgE antibodies. It has been proved that the specific IgE antibodies in the nasal mucosa mainly come from the tonsils, and the IgE reaches the nasal mucosa through the blood and attaches to the cell membrane of mast cells and basophils in the nasal mucosa with its Fc segment, making the nasal mucosa in a sensitized state. When the allergenic material enters the nasal mucosa again, the Fab segment of the bad egg IgE antibody binds and bridges the adjacent IgE, resulting in the mutation of the cell membrane structure of mast cells and basophils, releasing a variety of chemical mediators, mainly histamine, kinins, leukotrienes, eosinophil chemotactic factors, pro-cleavage adenosine, platelet activating factor, pentraxin and so on. These mediators, through their respective receptors in the vascular wall of the nasal mucosa, glands and nerve endings, cause dilation of small blood vessels, increased vascular permeability, increased exudation, inflammatory cell infiltration (mainly eosinophils), tissue edema, and increased excitability of nerve endings. The above pathological changes can lead to the corresponding clinical symptoms and signs.