Hay Fever: How to Actually Manage It

Allergic rhinitis, commonly known as hay fever, is the immune system's reaction to inhaled allergens — most often plant pollen, but also house-dust mites, animal dander, or mold spores. When the nasal mucosa of an allergic person comes into contact with the allergen, it triggers an immune-response cascade leading to classic symptoms: sneezing, watery nasal discharge, itching, and nasal congestion, often accompanied by itchy, red eyes.

Although it's often treated as a seasonal nuisance rather than a serious health problem, its impact on sleep quality, concentration, work or school performance, and overall well-being during periods of severe symptoms is well documented. In some people, untreated or poorly controlled hay fever also contributes to the development or worsening of asthma — both conditions involve the same continuous mucous membrane of the airways.

This article focuses on the general approach to treating hay fever — the mechanism of symptoms, the main drug classes, and where allergen immunotherapy fits into the overall treatment plan. Separately, in our article on quercetin and allergic rhinitis, we cover specific data on that flavonoid as a potential treatment supplement — here we focus on the approach based on standard, best-studied methods.

Allergic rhinitis practically splits into two groups with different courses and different treatment approaches. Seasonal hay fever is triggered by the pollen of specific plants — trees in early spring, grasses in late spring and summer, weeds in autumn — and its intensity changes throughout the year according to the local pollen calendar, which allows for partly predicting periods of severe symptoms and starting treatment in advance. Year-round rhinitis is triggered by allergens present in the environment throughout the year — house-dust mites, pet dander, mold spores in damp rooms — and manifests as a relatively constant level of discomfort without clear seasonality.

Diagnosis largely relies on a characteristic clinical picture — recurring symptoms linked to a specific time of year or exposure — but confirming the specific allergen requires additional testing. Skin prick tests are most commonly used, applying small amounts of allergen extracts to the skin of the forearm and observing a wheal-and-flare reaction after about 15-20 minutes, or a blood test for specific IgE antibodies directed against particular allergens.

Accurately identifying the specific allergen has practical value beyond mere curiosity — it allows exposure-reduction efforts to be targeted, and when considering allergen immunotherapy it's essential, since the desensitizing vaccine must contain exactly the allergen (or group of allergens) the person actually reacts to.

Histamine is one of the main mediators released during an allergic reaction, responsible for itching, sneezing, and watery nasal discharge, which is why drugs blocking its receptors (antihistamines) have for decades been the mainstay of symptomatic treatment. Older first-generation antihistamines (e.g., diphenhydramine) cross the blood-brain barrier and cause significant sedation and reduced concentration, making them a worse choice during the day, especially when driving or working tasks requiring focus. Second-generation drugs (e.g., cetirizine, loratadine, fexofenadine) have much less sedative effect while retaining efficacy and are today's standard choice among oral medications.

A separate class is intranasal antihistamines (e.g., azelastine), applied directly to the nasal mucosa, acting faster than the oral form (often within 15-30 minutes) and with even lower risk of systemic side effects, since they act mainly locally. They tend to be underrated compared to better-known tablets, despite well-documented effectiveness.

Intranasal corticosteroids (e.g., mometasone, fluticasone, budesonide sprays) act directly on the inflammation of the nasal mucosa, reducing the production of inflammatory mediators over a much broader range than antihistamines alone, which only block the action of histamine. This explains why in the ARIA (Allergic Rhinitis and its Impact on Asthma) guidelines, intranasal corticosteroids, alone or combined with intranasal antihistamines, are recommended as first-line treatment for moderate and severe symptoms, rather than a fallback option for cases resistant to standard oral drugs.

Unlike antihistamines and intranasal steroids, which ease symptoms only for as long as they're used, allergen immunotherapy (desensitization) is currently the only available method that can permanently change the immune system's response to a given allergen. It involves regularly administering gradually increasing doses of the allergen — subcutaneously (SCIT, as injections at a doctor's office) or sublingually (SLIT, as tablets or drops taken independently at home) — usually over 3-5 years, which gradually "teaches" the immune system tolerance.

Hay fever is often dismissed because it rarely endangers life — but that's not the same as a low cost to uncontrolled symptoms spread over several months a year, year after year. The good news is that the treatment options available today — from well-chosen intranasal medications to allergen immunotherapy — can genuinely and durably improve quality of life for most people with allergic rhinitis, as long as treatment is matched to symptom severity rather than limited to one, randomly chosen tablet from the pharmacy.