Since allergic rhinitis and asthma are both type I allergic reactions, they are very similar in etiology, immunology and pathogenesis, so there are many similarities in their diagnostic tools and treatment methods. This will greatly reduce the misdiagnosis rate and improve the clinical efficacy. Anatomical and physiological basis The nasal cavity is very closely related to the bronchi and lungs, both anatomically and physiologically. The respiratory tract is defined as starting from the nostrils to the respiratory fine bronchi, which are covered with ciliated epithelial tissue. The upper and lower airways are functionally interconnected and stimulation of the nasal mucosa (e.g. nasal mucosal excitation test) can cause changes in airway reactivity. Inflammatory nasal secretions in patients with allergic rhinitis can flow into or be inhaled into the lungs via the postnasal orifice and pharynx, called postnasal drip syndrome. In particular, the unconscious flow of intranasal inflammatory secretions into the airway during sleep in the supine position is most likely an important cause of the development of allergic rhinitis into asthma (especially nocturnal asthma). Changes in breathing patterns are also one of the factors that lead to a close relationship between allergic rhinitis and asthma. Swelling of the nasal mucosa, enlargement of the turbinates and retention of secretions can lead to nasal congestion, forcing patients to change from predominantly nasal to predominantly oral breathing, so that allergens can avoid the nasal mucosal barrier and enter the lower respiratory tract directly and trigger asthma. However, there are differences between the upper and lower respiratory tracts. In the upper respiratory tract, nasal obstruction is caused by vascular congestion of the nasal mucosa or nasal polyps, whereas in the lower respiratory tract, bronchial ventilation dysfunction is mainly caused by a combination of cyclic smooth muscle contraction of the bronchi and inflammatory edema of the airway mucosa. Regarding the physical mechanisms of airflow inhalation, the physical filtration function of the upper airway, resonance, heat dissipation and moistening, keep inhaled particles larger than 5-6 microns in the nasal cavity and keep the air inhaled into the bronchi moist and close to 37°C. Dysregulation of the physical function of the upper airway can lead to changes in lower airway homeostasis. In asthmatic patients, inhalation of cold air at high flow rates due to hyperventilation by mouth can decrease FEV1 and increase airway ventilation resistance. Pathogenesis Allergic inflammation of the nasal mucosa and bronchial inflammation in asthma, for example, are usually caused by the same allergens, their pathogenesis is related to type I allergic reactions, and the pathology is allergic inflammation characterized by an increase in respiratory eosinophils. Allergic rhinitis-asthma patients’ susceptibility to allergens, or atopy, is the main factor in the development of asthma, and the main indicators of atopy in asthmatic patients are increased levels of total and specific IgE in the body. The development of allergic inflammation of the upper or lower respiratory tract in the allergic rhinitis-asthma sign is related to the type and concentration of atopic allergens to which the allergic patient is exposed. Seasonal allergens, such as grass or tree pollen can cause intermittent symptoms, i.e. intermittent/seasonal allergic rhinoconjunctivitis and/or asthma. In contrast, allergens that are present year-round, such as house dust mites, molds and animal fur are more likely to cause persistent symptoms of asthma and/or rhinitis. To some extent, allergen sensitization is related to the particle size of the allergen because pollen, which is usually about 5 microns in diameter, is very easily filtered by the upper respiratory tract barrier, so pollen allergy can lead to upper respiratory symptoms mainly when the patient develops nasal congestion and breathes through the mouth instead, which can lead to lower respiratory symptoms because the filtering function of the upper respiratory tract is bypassed. Because house dust mites, mold spores and pet allergens are small (about 1 micron in diameter), they can easily enter the lower respiratory tract and trigger asthma.