The nose as the airway gatekeeper, is responsible for filtering, humidifying and warming air (10,000 litres daily). Rhinitis is inflammation of the nasal lining with clinically symptoms includes nasal running, sneezing, itching, rhinorrhoea and obstruction. Allergy by IgE-mediated mast cell degranulation is common reason od rhinitis and is common allergic disorders. Allergen avoidance is remarkably effective in AR patients and immunotherapy is important absolute treatment of AR, but there are some challenges to this treatment (7–9). AR is common disease in children and affects up to 50% of the pediatric population worldwide. The AR medications (seasonal and perennial) have an impact on the quality of life. Available treatments of AR include anti-histamines, intranasal corticosteroids, immunotherapy, and anti-leukotrienes. The anti-histamine drugs are first-line therapy for AR, and first-generation anti-histamines are associated with adverse effects (such as sedation) that are caused by the lack of H1 receptor selectivity and the drug penetration into the central nervous system. Therefore, the second-generation anti-histamine drugs were developed with less frequent adverse effects. The intranasal corticosteroid drugs can be absorbed through airway and may have effect on hypothalamic-pituitary-adrenal axis suppression. Montelukast as an antagonist of the leukotriene receptor, which binds to the cysteinyl leukotriene receptor 1 with high affinity (10–12). AR group that were challenged with cold air conditions had increased histamine level compared to the AR group in normal air conditions and it was showed that decreased temperature and cold weather can stimulate histamine releasing and clinical output of allergic reaction in the influenced tissue, especially mucosal and sub-mucosal tissue of airways. Therefore, for control of these problems, anti- histamine drug therapy is needed and recommended.
AR has 10–40% prevalence in the world, which affects many aspects of life and, is an ongoing problem in the public health field. Cold weather is associated with the development of AR, especially for male children and extreme cold temperature is strong trigger of AR in children. On the other hand, it was estimated that 48–74% of the population is affected by heat waves all the world in 2100. Therefore, identifying the AR risk factors is important (13, 14).
There are clinical, epidemiological and biological evidences that propose cold air affects to respiratory symptoms and AR (15). Cold weather and inhalation of dry air causes respiratory symptoms in the general population. Cold sensitivity in asthma was further confirmed in clinical provocation studies and during exercise tests in cold weather. Wintertime cold temperature is associated with increased exacerbations of asthma. Furthermore, decreased temperature increases symptoms of AR that may have a negative impact on the everyday life quality of people with AR. The AR in combination with asthma increases cold weather-related breath shortness even more than asthma alone. On the other hand, nasal mucosa drying could lead to hyperosmolality and bronchoconstriction (16, 17). In this study, cold air and decreased temperature leaded to increased nasal rubbing in AR mice and sneezing was increased in the AR mice that were kept in dry air condition. In the cold conditions, mucosal tissue of nasal and upper airways are irritated and the blood circulation may be changed, therefore, lead to clinical symptoms and nasal rubbing. In the dry air conditions, the mucosal tissue lost humidity and elasticity that may lead to irritation of local nerves and presents clinical symptoms in sneezing form. LTB4 and LTC4 levels as main leukotriene and important inflammatory factors, were increased in the AR group mice that were challenged by warm air conditions compared to the AR group without any challenge. Increased temperature may be trigger of the inflammatory factors, especially leukotriene producing pathways such as lipo-oxygenase cycle.
Increased airway temperature by hot humid air triggers immediate and transient bronchoconstriction. These changes are sensed by the transient receptor potential vanilloid type 1 receptor (TRPV1) that is also expressed in the sensory nerve fibers innervating the pharynx, larynx and upper airways. TRPV is a family of ion-channels containing 6 trans-membrane domains that form non-selective, non-voltage-gated cationic channels and TRPV1-4 are activated in a different temperature range (18, 19). Some infections such as Linguatula serrata can change expression of some related molecules and immune responses that should be noted (20, 21). Total IgE and IL-4 levels had no significant changes in AR-C, AR-W, AR-H and AR-D groups compared the AR group. The genes of MUC5a and HRH1 were highly expressed in AR mice that were in cold air conditions compared with the AR mice that were in standard air conditions. Moreover, the CysLT1R gene was highly expressed in AR mice that were in warm air conditions compared with the AR mice that were in standard air conditions. Therefore, warm air conditions not only have effect of leukotriene producing, but also on the increases leukotriene receptor expression. Also, cold air conditions not only increases histamine releasing, but also increases histamine receptor expression. MUC5a gene increasing showed that cold temperature could increase mucus production and secretion that leads to mucus hypersecretion and nasal obstruction. At least. It was observed that, air temperature and humidity had effect on AR pathophysiology and can change clinical in molecular pattern of AR. Therefore, weather conditions can be important factor in control and treatment of AR and has influence on the future appearance of AR.