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Rhinitis means the lining of your nose is inflamed, so it runs, blocks, itches and sets off sneezing. The allergic kind — hay fever — is a reaction to what you breathe in, such as grass pollen, dust mite, mould or animals. The non-allergic kind causes the same symptoms without an allergy, often triggered by smoke, strong smells, weather changes or certain medicines. It is very common, affecting about one in four Australians, and it is often dismissed as trivial even though a blocked nose can wreck sleep, concentration and exercise, and can make asthma much harder to control. Most people get good control with a saline rinse, a daily steroid nasal spray used with the right technique, and an antihistamine when needed. This page covers what rhinitis is, how it is diagnosed and how it is managed.
Definition
Rhinitis is inflammation of the lining of the nose, producing at least two of the following for an hour or more on most days: a runny nose, blocked nose, sneezing and itch. Allergic rhinitis — commonly called hay fever — is the form driven by an immune reaction to an inhaled allergen, and the Allergic Rhinitis and its Impact on Asthma (ARIA) guideline classifies it by whether symptoms are intermittent or persistent and by how much they interfere with sleep, daily activity, work, school and quality of life.1 Non-allergic rhinitis produces the same symptoms without allergic sensitisation, and includes irritant, hormonal, drug-induced, gustatory, occupational and idiopathic (previously "vasomotor") forms. The two frequently overlap in the same person, which is called mixed rhinitis.
Pathophysiology
In allergic rhinitis, inhaled allergen cross-links immunoglobulin E (IgE) on mast cells in the nasal mucosa. Mast cell degranulation releases histamine, tryptase, prostaglandins and leukotrienes within minutes — the early phase, responsible for sneeze, itch and watery discharge. Over the following four to eight hours, eosinophils, basophils and T-helper-2 lymphocytes are recruited to the mucosa in the late phase, which is dominated by congestion and is the part of the reaction that responds best to topical corticosteroid rather than antihistamine.2
Repeated exposure produces two effects that explain much of the clinical picture: priming, where a smaller allergen dose provokes the same response as the season progresses, and non-specific hyperresponsiveness, where the nose begins reacting to cold air, smoke, perfume and exercise — triggers that are not themselves allergens. In non-allergic rhinitis, the mechanism is largely neurogenic: sensory nerve and parasympathetic overactivity produces glandular secretion and vascular engorgement with no IgE involvement.2
The nasal airway contributes roughly half of total airway resistance, so mucosal swelling of only a few millimetres has a disproportionate effect on the work of breathing, and reliably pushes people towards mouth breathing.
Co-morbidities
Rhinitis rarely travels alone. The common associations are asthma, allergic conjunctivitis, sinusitis and chronic rhinosinusitis, nasal polyps, otitis media with effusion and eustachian tube dysfunction, obstructive sleep apnoea and snoring, atopic dermatitis and food allergy, chronic cough, dysfunctional breathing, and — in the small subgroup with aspirin-exacerbated respiratory disease — polyps and asthma together with non-steroidal anti-inflammatory drug (NSAID) sensitivity.
Prevalence
Rhinitis is the most common chronic respiratory condition in Australia. The Australian Bureau of Statistics National Health Survey found hay fever and allergic rhinitis in about one in four Australians — roughly 5 million people — making it more than twice as common as asthma.3 Prevalence peaks in the twenties and thirties, is higher in urban and inland areas with high grass-pollen loads, and is under-treated rather than over-treated: most people self-manage with intermittent antihistamines and never have their nose examined.
Causes, triggers and allergens
Perennial allergens (present year round) are house dust mite, cat and dog dander, cockroach and indoor moulds. In coastal and subtropical Queensland, high humidity keeps dust mite and mould loads high all year, so the classic "spring only" pattern is less common here than in southern Australia. Seasonal allergens are grass pollens (the dominant Australian trigger, with a long warm-season peak in Central Queensland), tree and weed pollens, and outdoor mould spores after rain.4
Non-allergic triggers include tobacco and wood smoke, bushfire smoke and dust, strong fragrances and cleaning chemicals, cold or dry air, sudden temperature change, alcohol, spicy food (gustatory rhinitis), hormonal change in pregnancy and thyroid disease, and medications — angiotensin-converting enzyme inhibitors, beta-blockers, aspirin and NSAIDs, some antihypertensives, and topical decongestants used for more than a few days.2
Occupational rhinitis deserves specific mention because it is common in the industries around Rockhampton: grain and feed dust, flour, wood dust, isocyanates in spray painting, cleaning products, laboratory animals and latex. It usually precedes occupational asthma, which makes it an early warning rather than a nuisance.
Symptoms
- Blocked nose — often alternating sides, worse lying down and worse at night.
- Runny nose — clear and watery in allergic rhinitis; thick, coloured or one-sided discharge points elsewhere.
- Sneezing in bouts, and itch of the nose, palate, throat or ears.
- Post-nasal drip, throat clearing and chronic cough.
- Reduced sense of smell — usually partial and fluctuating in rhinitis; complete or progressive loss suggests polyps.
- Eye symptoms — itch, redness and watering, in up to three-quarters of people with allergic rhinitis.
- Tiredness, poor concentration and disturbed sleep, which are frequently the most disabling features and the ones patients least often connect to their nose.
Allergic and non-allergic patterns
Itch, sneeze and eye involvement point strongly to an allergic mechanism. A predominantly runny or blocked nose without itch, starting after the age of thirty-five, triggered by weather change, smells and irritants rather than by exposure to animals or pollen, points to non-allergic rhinitis. Onset in childhood with a family history of asthma or eczema favours allergy.2
How severity is judged
ARIA grades rhinitis as intermittent (fewer than four days a week or fewer than four consecutive weeks) or persistent, and as mild or moderate–severe depending on whether sleep, daily activity, sport, work or school are affected.1 The severity that matters clinically is functional, not the number of sneezes: a blocked nose that fragments sleep every night is moderate–severe rhinitis even if daytime symptoms are modest.
Symptoms that are not rhinitis
Diagnosis
Why diagnosis matters
Two reasons. First, rhinitis is the commonest reason asthma stays poorly controlled despite correct inhaler use — the upper and lower airway behave as one organ, and treating only the chest leaves half the problem untouched.5 Second, "sinus" is the label most people and many clinicians reach for, which sends patients towards repeated antibiotics for a condition that is inflammatory and needs a topical anti-inflammatory instead.
How is it diagnosed?
Clinically, from the history and an examination of the nose. The pattern of symptoms, their timing against exposures, the response to previous treatment and the presence of atopic disease elsewhere carry most of the diagnostic weight. Examination with an otoscope or nasal speculum looks for pale, swollen turbinates, clear secretions, septal deviation, crusting and — importantly — visible polyps.2
Allergy testing
Testing identifies which allergen, not whether there is disease: a positive test without matching symptoms is sensitisation, not allergy. Skin prick testing is first-line, gives results in fifteen minutes and is more sensitive than blood testing; antihistamines must be stopped for several days beforehand. Allergen-specific IgE blood testing is used when skin testing is not possible — extensive eczema, antihistamines that cannot be stopped, or a history of anaphylaxis. Total IgE and unvalidated IgG "food intolerance" panels have no role.4
When imaging is and is not needed
Plain sinus X-rays are obsolete. Computed tomography (CT) of the sinuses is not indicated for uncomplicated rhinitis; it is reserved for suspected chronic rhinosinusitis unresponsive to treatment, suspected complications, one-sided disease, or surgical planning — and incidental mucosal thickening on a CT ordered for another reason is a very common source of over-diagnosis.6
Investigations for related conditions
- Spirometry with reversibility testing in anyone with cough, wheeze, chest tightness or exercise limitation — asthma is present in around a quarter of people with allergic rhinitis and is often unrecognised.5
- Nasal endoscopy by an ear, nose and throat surgeon where polyps, one-sided disease or treatment failure is suspected.6
- Sleep study where snoring, witnessed apnoeas or unrefreshing sleep suggest obstructive sleep apnoea.
- Peak nasal inspiratory flow — a simple, cheap, repeatable measure of nasal patency, useful for tracking treatment response objectively.
Management
Management and goals
The goal is a nose that is clear enough to breathe through, sleep through and exercise with — not a symptom-free nose in every pollen season. Realistic targets are: sleeping through the night without blockage, no interference with sport or work, minimal need for rescue antihistamine, and control of any associated asthma and eye symptoms. Treatment is judged over weeks, not days.
Treatment options
| Treatment | What it does best | Notes |
|---|---|---|
| Saline rinse or spray | Clears allergen, mucus and crust; improves symptoms and helps other sprays reach the mucosa | Cheap, safe, no interactions; use before medicated sprays7 |
| Intranasal corticosteroid (INCS) | Blockage, discharge, sneeze, itch and eye symptoms — the most effective single treatment for persistent or moderate–severe rhinitis | Needs daily use; full benefit takes 1–2 weeks8 |
| Oral non-sedating antihistamine | Sneeze, itch, runny nose, eye symptoms; works within an hour | Poor effect on blockage; useful as add-on or for intermittent symptoms8 |
| Combination INCS plus intranasal antihistamine | Moderate–severe or inadequately controlled rhinitis | Faster and more effective than either alone8 |
| Intranasal antihistamine alone | Rapid, as-needed relief | Onset within 15–30 minutes; bitter taste is the usual complaint |
| Leukotriene receptor antagonist | Occasional adjunct where asthma coexists | Less effective than INCS; neuropsychiatric warning applies9 |
| Allergen immunotherapy | The only treatment that modifies the disease rather than suppressing symptoms | 3–5 years of treatment; specialist-initiated10 |
| Surgery | Fixed structural obstruction — septal deviation, turbinate hypertrophy, polyps | Does not treat the underlying inflammation; medical therapy continues afterwards6 |
Nasal spray technique — where most treatment fails
An intranasal corticosteroid that is sprayed onto the septum or swallowed does nothing, and technique is wrong more often than it is right. The sequence that works:
Nosebleeds and crusting are almost always a technique problem — spray directed at the septum — rather than a reason to stop treatment.4
Allergen avoidance and environmental control
Avoidance is worth doing where it is achievable and not worth pretending where it is not. Single measures used alone rarely change symptoms; combinations aimed at a confirmed allergen are more useful.2
- House dust mite — mite-impermeable covers on mattress and pillows, weekly hot washing of bedding, reduce soft toys in the bed, hard floors in the bedroom where practical. Humidity control matters most in coastal Queensland.
- Grass pollen — check pollen forecasts in the warm season, keep car and bedroom windows shut on high-count and windy days, avoid mowing or wear a mask, shower and change clothes after outdoor work, dry washing indoors during peak counts.
- Pets — keep animals out of the bedroom; removing a family pet is a decision that needs an honest conversation about likely benefit.
- Mould — fix leaks and rising damp, ventilate wet rooms, clean visible mould, run a dehumidifier in humid months.
- Irritants — smoke, sprays, strong fragrances and dust; respiratory protection for occupational exposures.
Allergen immunotherapy
Immunotherapy — sublingual tablets or drops, or subcutaneous injections — delivers escalating doses of a confirmed allergen to induce tolerance. It is the only treatment that alters the natural history: benefit persists for years after a completed course, and in children it reduces the risk of developing asthma and of new sensitisations. It is considered when symptoms remain troublesome despite correct medical treatment, when a single or dominant allergen is confirmed, or when a person prefers not to take daily medication indefinitely. A course runs three to five years, and the first dose of any new subcutaneous course is given where anaphylaxis can be managed.10
Recognising deterioration
Reasons to seek review rather than escalate on your own: symptoms unchanged after four to six weeks of correctly used daily treatment; facial pain, fever or thick discoloured discharge lasting more than ten days; one-sided symptoms of any kind; new loss of smell; recurrent nosebleeds; or worsening asthma alongside the nasal symptoms.
Action plan
A written plan works the same way it does in asthma. It should name the daily treatment and when to start it (for seasonal disease, two to four weeks before the expected season), the add-on for breakthrough symptoms, the specific triggers to plan around, and the point at which to seek review. Anyone with coexisting asthma needs their asthma action plan alongside it, because rhinitis flares and asthma flares tend to arrive together.9
Medications
Medications for rhinitis
| Class | Examples | Onset | Main cautions |
|---|---|---|---|
| Intranasal corticosteroid | Mometasone, fluticasone, budesonide, ciclesonide | Hours; full effect 1–2 weeks | Local irritation and nosebleed from poor technique; minimal systemic effect at licensed doses |
| Intranasal antihistamine | Azelastine | 15–30 minutes | Bitter taste; short duration |
| Combination nasal spray | Azelastine with fluticasone | Within 30 minutes | Cost; still requires correct technique |
| Oral antihistamine (non-sedating) | Loratadine, cetirizine, fexofenadine, desloratadine | 1 hour | Cetirizine can be mildly sedating; little effect on blockage |
| Oral antihistamine (sedating) | Older agents | 1 hour | Not recommended — impaired sleep quality, next-day performance and driving |
| Topical decongestant | Oxymetazoline, xylometazoline | Minutes | Maximum 3–5 days — rebound congestion (rhinitis medicamentosa)11 |
| Saline | Isotonic or hypertonic rinse, spray, sachets | Immediate, symptomatic | Use cooled boiled, distilled or sterile water — never untreated tap water |
| Leukotriene receptor antagonist | Montelukast | Days | Neuropsychiatric adverse effects; reserve as adjunct |
Correct use of medications
The commonest failures are all fixable: using an intranasal corticosteroid "when the nose is bad" instead of every day, stopping at three days because nothing has happened yet, poor technique, and continuing a topical decongestant well past its safe window. An INCS is a preventer and behaves like one — daily, at the same time, whether or not the nose is blocked that morning.8
Order of medications
Saline first, then the medicated spray a few minutes later, on a cleared nose. Where an oral antihistamine is also used, timing between them does not matter. For seasonal disease, start before the season rather than in response to the first bad day — pre-emptive treatment is substantially more effective than catching up.1
Multi-system manifestations
Lower airway — the united airway
Rhinitis and asthma are two expressions of one inflamed airway. Around 80% of people with asthma have rhinitis, and roughly a quarter of people with allergic rhinitis have asthma. Untreated rhinitis is associated with worse asthma control, more exacerbations and more emergency presentations; treating the nose measurably improves the chest.5 Anyone with rhinitis who reports cough, wheeze, chest tightness or exercise limitation needs spirometry, not reassurance.9
Eyes
Allergic conjunctivitis accompanies allergic rhinitis in most cases — itch, redness, watering and gritty discomfort. Intranasal corticosteroids improve eye symptoms as well as nasal ones; where they persist, an ocular antihistamine or mast cell stabiliser is added.
Ears and hearing
Mucosal swelling around the eustachian tube opening causes ear fullness, popping, muffled hearing and, in children, otitis media with effusion — a recognised contributor to hearing loss and speech delay in the preschool years.2
Sleep and daytime function
Nasal obstruction fragments sleep, and severity of rhinitis correlates with impaired sleep quality independent of other factors. The consequences — daytime sleepiness, irritability, reduced concentration, measurable falls in school and work performance — are usually attributed to anything but the nose.12 Rhinitis also worsens snoring and increases upper airway resistance, and untreated nasal obstruction reduces tolerance of continuous positive airway pressure therapy in obstructive sleep apnoea.
Sinuses and sense of smell
Persistent mucosal inflammation obstructs sinus drainage and predisposes to acute and chronic rhinosinusitis; chronic rhinosinusitis with nasal polyps sits at the severe end of the same inflammatory spectrum.6 Reduced smell affects appetite, food enjoyment and safety — detecting smoke, gas and spoiled food.
Facial growth and dental development in children
Long-standing mouth breathing in a growing child is associated with an altered facial growth pattern, a high narrow palate and malocclusion. It is a reason to treat childhood nasal obstruction properly rather than wait for it to be outgrown.
Living with rhinitis
Through the Central Queensland year
The local pattern differs from the southern Australian one. Grass pollen dominates and the warm-season exposure is long; humidity keeps dust mite and mould loads high year round; and dust, smoke and cane burning add irritant load. Practically, this means most people here need year-round baseline treatment with seasonal escalation, rather than a short spring course.
Sleep
Treat the nose before buying equipment. Beyond that: a slightly elevated head of bed, dust-mite covers, no pets in the bedroom, windows closed on high-pollen nights, and saline plus INCS in the evening rather than only in the morning.
Exercise and sport
Nasal obstruction forces mouth breathing during exercise, which delivers cold, dry, unfiltered air to the lower airway and worsens exercise-induced symptoms. Treating rhinitis is part of treating exercise-induced breathlessness, and nasal breathing at low and moderate intensity is worth training deliberately.
Work and study
Where symptoms track with work, occupational rhinitis should be documented and exposures controlled — it commonly precedes occupational asthma, and early action changes the outcome. Non-sedating antihistamines matter for anyone driving or operating machinery.
Travel
Take enough spray for the trip and keep it in hand luggage, expect a different pollen calendar at the destination, and start treatment before travelling into a known trigger season.
Pregnancy
Rhinitis of pregnancy is common and hormonally driven. Saline is first-line and safe. Several intranasal corticosteroids have a long safety record in pregnancy, and treatment decisions should be made with the treating doctor or midwife rather than by stopping everything — untreated nasal obstruction disturbs sleep and worsens coexisting asthma, which carries its own risk.4
Prognosis
Rhinitis is a long-term condition that is highly controllable. Most people achieve good control with saline, a correctly used intranasal corticosteroid and an antihistamine when needed. Childhood allergic rhinitis often improves in adult life but seldom disappears; non-allergic rhinitis tends to persist. Immunotherapy is the only treatment that changes the underlying trajectory. The main avoidable harms are years of poor control from incorrect spray technique, dependence on topical decongestants, and unrecognised asthma sitting behind the nasal symptoms.1
Role of the physiotherapist
Medical therapy controls the inflammation; the physiotherapist deals with what the obstructed nose has done to the breathing pattern. That means breathing pattern assessment and retraining — restoring nasal, diaphragmatic breathing after months or years of mouth breathing, which does not simply revert when the nose clears. It means teaching saline rinsing and nasal spray technique properly, with the device in the patient's hand, since technique is the single most common reason treatment fails.7 It means checking inhaler technique and looking actively for the asthma that so often accompanies rhinitis, and separating exercise-induced nasal obstruction from bronchoconstriction, laryngeal obstruction and deconditioning in someone who is breathless on exertion. Where rhinitis coexists with snoring or sleep apnoea, addressing nasal patency and breathing pattern improves both symptoms and tolerance of therapy.5
Part 1 · References
- Bousquet J, Schünemann HJ, Togias A, et al. Next-generation Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines for allergic rhinitis based on Grading of Recommendations Assessment, Development and Evaluation (GRADE) and real-world evidence. J Allergy Clin Immunol 2020;145(1):70–80.
- Wise SK, Damask C, Roland LT, et al. International consensus statement on allergy and rhinology: allergic rhinitis — 2023. Int Forum Allergy Rhinol 2023;13(4):293–859.
- Australian Bureau of Statistics. National Health Survey: chronic conditions. Canberra: ABS, 2023.
- Australasian Society of Clinical Immunology and Allergy. Allergic rhinitis (hay fever) — clinical update. Sydney: ASCIA, 2024.
- Global Initiative for Asthma. Global strategy for asthma management and prevention: 2026 update. GINA, 2026.
- Fokkens WJ, Lund VJ, Hopkins C, et al. European Position Paper on Rhinosinusitis and Nasal Polyps 2020. Rhinology 2020;58(Suppl S29):1–464.
- Head K, Snidvongs K, Glew S, et al. Saline irrigation for allergic rhinitis. Cochrane Database Syst Rev 2018;6:CD012597.
- Wallace DV, Dykewicz MS, Oppenheimer J, Portnoy JM, Lang DM. Pharmacologic treatment of seasonal allergic rhinitis: synopsis of guidance from the 2017 Joint Task Force on Practice Parameters. Ann Intern Med 2017;167(12):876–881.
- National Asthma Council Australia. Australian Asthma Handbook, version 3.0. Melbourne: National Asthma Council Australia, 2025.
- Roberts G, Pfaar O, Akdis CA, et al. EAACI guidelines on allergen immunotherapy: allergic rhinoconjunctivitis. Allergy 2018;73(4):765–798.
- Ramey JT, Bailen E, Lockey RF. Rhinitis medicamentosa. J Investig Allergol Clin Immunol 2006;16(3):148–155.
- Colás C, Galera H, Añibarro B, et al. Disease severity impairs sleep quality in allergic rhinitis (the SOMNIAAR study). Clin Exp Allergy 2012;42(7):1080–1087.
References are numbered in citation order (Vancouver/BMJ style) and were current at the time of writing. Guidelines are living documents — verify against the latest version before clinical use.
Clinical evidence
Part 1 covers the same condition without the technical detail. What follows is the evidence base behind it, written for clinicians — the literature, the reasoning and the gaps.
For clinicians: this summary supports clinical reasoning and is not a protocol. Check current guidelines and local policy before applying it, and read it alongside the key references and guidelines directory.
Framing. Rhinitis is the most prevalent chronic respiratory condition in Australia and the one most consistently under-treated. Two facts drive most of the clinically useful reasoning. First, the upper and lower airway behave as a single organ: rhinitis is present in around 80% of people with asthma, and untreated rhinitis is associated with worse asthma control and more exacerbations.1 Second, the treatment that works best is the one patients are least likely to be using correctly — an intranasal corticosteroid (INCS), taken daily, delivered with technique that actually reaches the mucosa. The therapeutic problem in rhinitis is rarely drug choice; it is diagnosis, adherence and delivery, all three of which sit squarely within physiotherapy scope alongside medical management.
Classification and what it changes
- The Allergic Rhinitis and its Impact on Asthma (ARIA) framework classifies by duration (intermittent or persistent) and by functional impact (mild or moderate–severe), not by allergen or season.2 The practical consequence: sleep disruption or interference with work, school or sport defines moderate–severe disease and mandates an INCS as first-line, irrespective of how modest daytime symptoms sound.
- Allergic and non-allergic rhinitis overlap frequently, and mixed rhinitis is common. Non-allergic disease is largely neurogenic; it responds to INCS and to intranasal antihistamine but not to allergen avoidance or immunotherapy, so the distinction changes management even though it does not change the symptom list.3
- Symptom-based diagnosis alone over-attributes to allergy. Skin prick testing or allergen-specific immunoglobulin E identifies which allergen where a specific intervention is contemplated; it does not establish disease, and testing without a matching exposure history generates sensitisation findings that mislead more than they help.3
Pharmacological evidence
- INCS outperform oral antihistamines across all nasal symptoms including obstruction, and improve ocular symptoms as well — a finding that repeatedly surprises clinicians who add an antihistamine when an INCS is already prescribed.4
- Adding an oral antihistamine to an INCS adds little. The 2017 Joint Task Force synopsis recommends against routine combination of an INCS with an oral antihistamine in adults with seasonal allergic rhinitis, and recommends INCS monotherapy for moderate–severe disease.4 Where an INCS is insufficient, the evidence-supported step is a combination intranasal antihistamine plus corticosteroid, which outperforms either component alone and acts within 30 minutes.3
- Time course is the commonest reason for apparent failure. INCS act on the late-phase eosinophilic response; meaningful benefit takes days and maximal effect one to two weeks. A patient who stopped at day three has not had a trial of the drug.2
- Saline irrigation improves symptoms with very low risk. The Cochrane review found benefit in allergic rhinitis with no adverse effects of consequence, on low-quality evidence — a profile that justifies routine use as an adjunct rather than a claim of efficacy comparable to topical steroid.5
- Leukotriene receptor antagonists are inferior to INCS and carry a neuropsychiatric safety warning; their role is a narrow adjunct, largely where asthma coexists.6
- Topical decongestants beyond three to five days produce rebound congestion (rhinitis medicamentosa), which is a genuinely iatrogenic obstruction and worth asking about explicitly in anyone whose nose has been blocked for months.7
Delivery and adherence — where the effect size is actually lost
- Trial efficacy assumes correct technique and daily use. Real-world use is intermittent and technique is frequently wrong: head extended, nozzle aimed at the septum, forceful sniff, dose swallowed. Each of these reduces mucosal deposition, and together they can account for the entire difference between trial and clinic outcomes.3
- Epistaxis and crusting are usually a technique finding — septal deposition — rather than an indication to stop. Treating them as a drug adverse effect ends effective treatment for a mechanical reason.3
- Pre-seasonal initiation, two to four weeks before expected exposure, is more effective than reactive treatment, and the priming phenomenon explains why: once mucosal reactivity is established, smaller allergen doses sustain symptoms.2
- Objective monitoring is available and rarely used. Peak nasal inspiratory flow is cheap and repeatable, and a validated symptom score tracked over weeks is far more informative than the patient's recall of a bad week.3
Allergen avoidance
- Single-measure avoidance performs poorly in trials. The Cochrane review of house dust mite avoidance for perennial allergic rhinitis found insufficient evidence to support mite-impermeable bedding as a standalone intervention.8
- The defensible position is combined, allergen-specific measures where sensitisation is confirmed and exposure is genuinely modifiable — and honesty where it is not. Recommending an unaffordable or impractical measure with a weak evidence base costs credibility that is then unavailable for the interventions that do work.
Allergen immunotherapy — the only disease-modifying option
- Subcutaneous and sublingual immunotherapy both reduce symptoms and medication use in allergic rhinoconjunctivitis, with benefit persisting after a completed three-to-five-year course.9
- The Grass Sublingual Immunotherapy Tablet Asthma Prevention (GAP) trial did not meet its primary endpoint of reduced asthma incidence, but showed reduced asthma symptoms and medication use during and after treatment — a nuance frequently over-claimed in both directions.10
- Candidate selection matters more than modality: a confirmed single or dominant allergen, symptoms persisting despite correct pharmacotherapy, and a patient prepared to commit to years of treatment.9
The united airway
- Roughly a quarter of people with allergic rhinitis have asthma, and rhinitis precedes asthma often enough to function as a marker of risk.1 Spirometry with reversibility testing in any patient with rhinitis plus cough, wheeze or exertional limitation is a higher-yield investigation than allergy testing.
- Treating rhinitis is associated with better asthma control and fewer exacerbations, and Australian guidance directs co-management of the upper airway as part of asthma care rather than as an optional extra.6
- Nasal obstruction drives mouth breathing, which delivers cold, dry, unfiltered air to the lower airway and worsens exercise-induced bronchoconstriction — a mechanical contribution that is treatable and routinely overlooked in the assessment of exertional breathlessness.1
Clinical reasoning
- Ask about sleep before asking about sneezing. Severity of rhinitis correlates with impaired sleep quality, and the resulting daytime dysfunction is what actually disables patients — while being the least likely symptom to be volunteered or attributed to the nose.11
- "Failed INCS" is usually a delivery or adherence finding. Before escalating, watch the patient use the device, ask how many days a week it is genuinely used, and confirm the trial ran for at least two weeks.4
- Rhinitis in poorly controlled asthma is a treatable cause, not a coincidence. Escalating inhaled therapy while leaving the nose untreated is a common and avoidable pattern.6
- Unilateral anything is not rhinitis. One-sided obstruction, discharge, bleeding, facial pain or complete anosmia require examination and specialist assessment, not another spray.3
- Screen for medication-induced and rebound rhinitis. Angiotensin-converting enzyme inhibitors, beta-blockers, non-steroidal anti-inflammatory drugs and prolonged topical decongestant use are all reversible contributors.7
- Occupational rhinitis is an early warning for occupational asthma. Symptoms that track with the working week warrant documentation and exposure control while the disease is still confined to the nose.3
Physiotherapy implications
- Technique training for nasal spray and saline delivery addresses the dominant cause of treatment failure and uses the same teach-back approach as inhaler technique. The rationale is mechanistic rather than a demonstrated treatment effect: delivery error is the accepted explanation for the efficacy–effectiveness gap, but technique training has not been tested as an intervention in adequately powered trials.5
- Chronic nasal obstruction establishes a mouth-breathing pattern that does not spontaneously revert when the nose clears; breathing pattern retraining is therefore part of managing the sequelae rather than the inflammation.
- In exertional breathlessness, nasal obstruction should be assessed alongside exercise-induced bronchoconstriction, inducible laryngeal obstruction and deconditioning — the four are commonly conflated and the nasal component is the cheapest to test and treat.
- Where continuous positive airway pressure therapy is poorly tolerated, untreated nasal obstruction is a frequent and modifiable contributor.3
Evidence gaps
- No adequately powered trials of technique training as an intervention, despite delivery error being the accepted explanation for the efficacy–effectiveness gap.
- Non-allergic and mixed rhinitis are under-represented in trials; most evidence is generated in seasonal allergic rhinitis and extrapolated.
- Avoidance measures lack trials of combined, allergen-specific packages in real households — the way they are actually prescribed.8
- Whether treating rhinitis reduces asthma exacerbations as a primary endpoint remains inadequately tested, despite consistent associative data.1
- Australian pollen and mould exposure data are sparse outside the major southern cities, so seasonal advice in subtropical and inland regions rests on limited local evidence.
References for the clinical evidence summary
- Global Initiative for Asthma. Global strategy for asthma management and prevention: 2026 update. GINA, 2026.
- Bousquet J, Schünemann HJ, Togias A, et al. Next-generation Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines for allergic rhinitis based on GRADE and real-world evidence. J Allergy Clin Immunol 2020;145(1):70–80.
- Wise SK, Damask C, Roland LT, et al. International consensus statement on allergy and rhinology: allergic rhinitis — 2023. Int Forum Allergy Rhinol 2023;13(4):293–859.
- Wallace DV, Dykewicz MS, Oppenheimer J, Portnoy JM, Lang DM. Pharmacologic treatment of seasonal allergic rhinitis: synopsis of guidance from the 2017 Joint Task Force on Practice Parameters. Ann Intern Med 2017;167(12):876–881.
- Head K, Snidvongs K, Glew S, et al. Saline irrigation for allergic rhinitis. Cochrane Database Syst Rev 2018;6:CD012597.
- National Asthma Council Australia. Australian Asthma Handbook, version 3.0. Melbourne: National Asthma Council Australia, 2025.
- Ramey JT, Bailen E, Lockey RF. Rhinitis medicamentosa. J Investig Allergol Clin Immunol 2006;16(3):148–155.
- Sheikh A, Hurwitz B, Nurmatov U, van Schayck CP. House dust mite avoidance measures for perennial allergic rhinitis. Cochrane Database Syst Rev 2010;7:CD001563.
- Roberts G, Pfaar O, Akdis CA, et al. EAACI guidelines on allergen immunotherapy: allergic rhinoconjunctivitis. Allergy 2018;73(4):765–798.
- Valovirta E, Petersen TH, Piotrowska T, et al. Results from the 5-year SQ grass sublingual immunotherapy tablet asthma prevention (GAP) trial in children with grass pollen allergy. J Allergy Clin Immunol 2018;141(2):529–538.
- Colás C, Galera H, Añibarro B, et al. Disease severity impairs sleep quality in allergic rhinitis (the SOMNIAAR study). Clin Exp Allergy 2012;42(7):1080–1087.
Corrections: If something on this page is wrong, out of date or unclear, we want to know. Email reception@inspireclinic.au with the page name and what you believe is incorrect. Substantive corrections are made promptly, and the guide’s version and last-updated date are changed to reflect it.