Mould exposure is a recognised cause of respiratory illness, with the World Health Organization confirming sufficient evidence linking indoor dampness and mould to asthma exacerbation, respiratory infections, and allergic rhinitis. In our 24 years of forensic mould assessments, we have observed a consistent pattern: buildings with elevated indoor mould concentrations above 500 CFU/m³ frequently have occupants reporting respiratory symptoms. Here is what the science actually shows about how mould affects your lungs and overall health.

How Mould Affects the Respiratory System

Mould affects human health through three primary mechanisms: allergenicity, irritancy, and in some species, toxicity. Understanding these pathways is critical because each produces different symptoms, affects different populations, and requires different interventions.

Allergenic responses are the most common health effect. Mould spores contain proteins that can trigger IgE-mediated immune responses in sensitised individuals. When inhaled, these allergens cause the immune system to overreact, producing symptoms identical to hay fever: nasal congestion, sneezing, watery eyes, and post-nasal drip. Approximately 10-20% of the Australian population is sensitised to one or more mould allergens. The most allergenic genera include Alternaria, Cladosporium, Aspergillus, and Penicillium — all extremely common in Australian indoor environments.

Irritant responses can affect anyone regardless of allergy status. Mould produces beta-glucans (cell wall components), microbial volatile organic compounds (MVOCs — responsible for the characteristic “musty” smell), and fine particulate fragments. These substances irritate mucous membranes and airways on direct contact. Unlike allergic responses, irritant effects are dose-dependent and can affect previously healthy individuals exposed to high concentrations.

The Asthma and Mould Connection

The relationship between mould exposure and asthma is among the strongest and most well-documented in environmental health literature. A landmark meta-analysis published in the journal Indoor Air found that living in a damp or mouldy home increased the risk of current asthma by 30-50% and the risk of asthma development by 30-70%, depending on the study population.

In Australia, where approximately 2.7 million people have asthma (11% of the population), this connection is particularly significant. Australian homes in coastal subtropical and tropical regions — from Sydney northward through Brisbane, the Gold Coast, Cairns, and Darwin — face high ambient humidity levels that can exceed 80% RH for extended periods, creating ideal conditions for indoor mould colonisation. The Australian Institute of Health and Welfare has identified housing conditions, including dampness and mould, as modifiable risk factors for respiratory disease burden.

For existing asthmatics, mould exposure can trigger acute exacerbations including wheezing, chest tightness, and severe bronchospasm. Studies have linked Alternaria alternata exposure specifically to life-threatening asthma attacks in sensitised individuals. The mechanism involves direct airway inflammation from inhaled spores, fragments, and secondary metabolites that provoke both immediate and delayed-type hypersensitivity reactions in the bronchial epithelium.

Specific Respiratory Conditions Linked to Mould

Beyond the general categories of allergic and irritant responses, several specific clinical conditions are recognised in the medical literature as being caused or exacerbated by indoor mould exposure.

Hypersensitivity Pneumonitis

Hypersensitivity pneumonitis (HP), also known as extrinsic allergic alveolitis, is an inflammatory lung disease caused by repeated inhalation of organic antigens — including mould spores, fragments, and hyphal elements. Unlike allergic rhinitis, which affects the upper airways, HP involves inflammation of the alveoli (air sacs) deep in the lung tissue. Acute HP presents with cough, breathlessness, fever, and malaise typically 4-8 hours after exposure. Chronic HP from sustained low-level exposure can progress to pulmonary fibrosis — irreversible scarring of lung tissue that permanently reduces respiratory capacity.

HP is not limited to exposure to “toxic” mould species. Any mould in sufficient airborne concentration can trigger HP in susceptible individuals. I have assessed properties where occupants developed HP from exposure to common Penicillium and Aspergillus species — genera that would not typically be labelled “toxic” but were present at high airborne concentrations due to hidden water damage behind wall linings. This is one reason why the fixation on “toxic black mould” is counterproductive — it distracts from the reality that any mould at high concentration can cause serious illness.

Allergic Bronchopulmonary Aspergillosis (ABPA)

ABPA is a complex immunological reaction to Aspergillus fumigatus colonisation of the airways, occurring almost exclusively in people with pre-existing asthma or cystic fibrosis. The immune system mounts an exaggerated response to Aspergillus antigens, causing airway inflammation, mucus plugging, bronchiectasis (permanent airway dilation), and progressive lung damage. Symptoms include worsening asthma control, cough productive of brown or greenish-brown mucus plugs, recurrent fevers, and pulmonary infiltrates visible on chest X-ray or CT.

ABPA requires specialist diagnosis and management by a respiratory physician, typically involving oral corticosteroids and antifungal therapy (itraconazole). From an environmental perspective, identifying and eliminating the indoor source of Aspergillus fumigatus is critical to reducing ongoing exposure and preventing relapse. Our assessments specifically identify Aspergillus species because of this clinical significance.

Allergic Fungal Rhinosinusitis

Allergic fungal rhinosinusitis (AFRS) is a chronic sinus condition characterised by thick, dark (“peanut butter-like”) mucin containing eosinophils and fungal hyphae. It is most commonly associated with Aspergillus, Alternaria, and Curvularia species. AFRS can cause sinus obstruction, nasal polyposis, and in severe cases, bony erosion of the sinuses. Like ABPA, it represents an exaggerated immune response to fungal antigens rather than direct infection. Treatment typically involves surgery, corticosteroids, and environmental control measures to reduce ongoing mould exposure.

Vulnerable Populations at Higher Risk

While mould can affect anyone, certain populations face disproportionately greater health risks. Identifying whether vulnerable individuals occupy a building is a critical factor in assessing urgency during our mould inspections.

• Infants and young children — developing respiratory and immune systems are more susceptible; Australian research shows children under 5 in mouldy homes have significantly higher rates of lower respiratory tract infections
• Elderly individuals — reduced immune function and often pre-existing respiratory conditions compound mould exposure effects
• Immunocompromised individuals — organ transplant recipients, chemotherapy patients, and those with advanced HIV face risk of invasive fungal infections (aspergillosis, mucormycosis) that can be life-threatening
• People with chronic respiratory disease — COPD, cystic fibrosis, and bronchiectasis patients may experience accelerated lung function decline with sustained mould exposure
• Atopic individuals — people with a genetic predisposition to allergic conditions (eczema, hay fever, allergic asthma) are significantly more likely to become sensitised to mould allergens and develop symptoms at lower exposure concentrations
• Individuals with confirmed mould allergy — diagnosed by skin prick testing or specific IgE blood tests, these individuals react to concentrations that would not affect non-sensitised people

The Australian Institute of Occupational Hygienists (AIOH) recommends that any indoor mould contamination in buildings occupied by immunocompromised individuals be treated with heightened urgency and more stringent remediation standards than would apply to a general-population setting.

Mycotoxins and MVOCs: Beyond Allergies

Beyond allergic and irritant effects, certain mould species produce mycotoxins — toxic secondary metabolites that can cause systemic health effects. The mycotoxins most relevant to indoor environments include:

• Trichothecenes (from Stachybotrys chartarum, Fusarium) — cytotoxic, immunosuppressive, can cause dermatitis on skin contact
• Ochratoxin A (from Aspergillus ochraceus, Penicillium verrucosum) — nephrotoxic, classified as a possible human carcinogen (IARC Group 2B)
• Sterigmatocystin (from Aspergillus versicolor) — genotoxic, commonly found in water-damaged buildings
• Gliotoxin (from Aspergillus fumigatus) — immunosuppressive, relevant to invasive aspergillosis

Microbial volatile organic compounds (MVOCs) are produced by actively growing mould and are responsible for the characteristic musty or earthy odour in damp buildings. Common MVOCs include 1-octen-3-ol (“mushroom alcohol”), geosmin, and 2-methylisoborneol. While individual MVOC concentrations in buildings are typically below occupational exposure limits, the mixture effects of multiple MVOCs at low concentrations are not well characterised. In our experience, a persistent musty odour is one of the most reliable indicators of hidden mould growth, even when no mould is visually apparent.

Duration and Intensity: Why Exposure Context Matters

The health impact of mould exposure is not simply about presence or absence — it depends critically on concentration, duration, and individual susceptibility. A brief encounter with elevated outdoor mould spores during a walk is fundamentally different from sleeping 8 hours per night in a bedroom with active Aspergillus growth behind the wall lining.

Chronic low-level exposure in residential settings is the most concerning scenario because it is sustained, often unrecognised, and difficult to quantify retrospectively. Our assessment methodology addresses this by measuring both current airborne concentrations and indicators of historical contamination through surface sampling. Indoor air spore counts above 500 CFU/m³, or concentrations exceeding the concurrent outdoor baseline by more than a factor of two, indicate an active indoor source. Counts exceeding 1,000 CFU/m³ are considered elevated by most occupational hygiene guidelines and warrant prompt investigation.

Importantly, even dead mould can affect health. Mycotoxins remain active on dried spores and fragments, and dead mould retains its allergenic proteins. This is why simply “killing” mould with bleach or biocide without physical removal does not eliminate health risks — the allergenic and potentially toxic material remains in place. Effective remediation requires physical removal of contaminated materials, not just surface treatment.

Documenting Health Effects for Insurance and Legal Purposes

In my experience preparing reports for insurance claims, tenancy disputes, and litigation, establishing a causal link between mould exposure and health effects requires three categories of evidence, and the strength of the case depends on having all three.

Medical evidence is the foundation. Affected individuals should see their GP and request referral to a respiratory physician or clinical immunologist/allergist. Specific diagnostic investigations include skin prick testing for mould allergens (Alternaria, Aspergillus, Cladosporium, Penicillium panels), serum-specific IgE testing, spirometry (lung function testing), and where indicated, high-resolution CT of the chest. Written medical opinions that explicitly reference mould exposure as a contributing factor to the patient’s condition carry significant weight.

Environmental evidence comes from an independent professional assessment. Quantified air and surface sampling data from a NATA-accredited laboratory, combined with moisture mapping and building condition documentation, establishes what the occupant was actually exposed to. Our reports quantify airborne spore concentrations, identify species present, compare indoor concentrations to outdoor baselines, and assess whether the indoor environment meets WHO guidelines. This objective data transforms a subjective health complaint into a documented exposure scenario.

Temporal correlation is the connecting thread. A symptom diary recording when symptoms occur, their severity, and critically, when they improve — particularly when the occupant is away from the property for several days — establishes the pattern that links the specific building to the health effects. Courts and tribunals find this temporal evidence particularly persuasive. If symptoms consistently worsen at home and improve during holidays or while staying elsewhere, the inference of building-related causation is strong.

When to Seek Professional Assessment and Medical Advice

If building occupants are experiencing persistent respiratory symptoms — particularly symptoms that improve when away from the property for extended periods (such as during holidays) — a professional mould assessment is warranted. This pattern of symptom improvement with absence from the building is a strong clinical indicator of building-related illness.

Specific triggers for seeking professional assessment include: unexplained worsening of existing asthma requiring increased reliever medication; persistent cough, wheeze, or breathlessness without obvious infectious cause; recurrent respiratory infections in building occupants; visible mould growth exceeding approximately 1 m² in total area; persistent musty or earthy odours without visible mould (indicating hidden growth); and any situation where vulnerable individuals occupy the property.

At Test Australia, our assessments include systematic moisture mapping using calibrated pin-type and pinless moisture meters, thermal imaging cameras, air sampling using calibrated impaction samplers, surface sampling via tape-lift and swab methods, and detailed environmental condition documentation including relative humidity, temperature, and ventilation assessment. All samples are analysed by an independent NATA-accredited laboratory, and our reports are prepared to forensic standards suitable for insurance claims, tenancy disputes, or legal proceedings. We do not provide remediation services or refer to remediation contractors, maintaining the arms-length independence essential for credible assessment.

Concurrently with environmental assessment, affected individuals should consult their GP or request referral to a respiratory physician or clinical immunologist. Specific testing for mould allergy (skin prick tests, specific IgE panels for Alternaria, Aspergillus, Cladosporium, and Penicillium) can confirm sensitisation and guide both medical treatment and environmental remediation priorities. Where hypersensitivity pneumonitis or ABPA is suspected, specialist investigation including CT imaging and precipitin antibody testing may be warranted. For further information or to arrange an assessment, contact Test Australia.