Does a positive result mean the patient has a mould problem in their home?

Not necessarily. A positive specific IgE confirms sensitisation, which could result from outdoor exposure (Alternaria, Cladosporium) or past indoor exposure. Correlation with environmental history, symptom timing, and sometimes environmental inspection is needed to attribute symptoms to current indoor mould.

Can this panel diagnose allergic bronchopulmonary aspergillosis?

It is one component. ABPA diagnosis requires elevated Aspergillus fumigatus-specific IgE plus markedly elevated total IgE, peripheral eosinophilia, Aspergillus-specific IgG precipitins, and compatible imaging. The panel alone does not establish the diagnosis.

Is fasting required for the mould IgE panel?

No. Specific IgE testing does not require fasting or special preparation.

What does it mean if multiple moulds are positive?

It may reflect genuine polysensitisation — the patient has mounted IgE responses to several moulds — or serological cross-reactivity among moulds sharing pan-allergens such as enolases. Exposure history and symptom patterns distinguish clinically relevant sensitisations from incidental cross-reactions.

Can this test diagnose toxic mould syndrome or mycotoxin illness?

No. Specific IgE measures type-I allergic sensitisation to mould proteins, not mycotoxin exposure. The concept of chronic mycotoxin illness from indoor mould exposure remains contested and is not established by IgE serology.

Should I stop antihistamines before the test?

No. Unlike skin-prick testing, blood IgE measurement is not affected by antihistamines, and they need not be discontinued.

How long does it take to receive results?

Turnaround is typically 7–10 business days from receipt at US BioTek, plus transport time from the draw site to the specialty laboratory.

BML-ENV-001environmental mouldUSA

15 Mold Panel: IgE

Q: What is the difference between mould allergy testing and environmental mould testing?

This serological panel measures the patient's immune response — specific IgE antibodies to mould allergens — confirming sensitisation. Environmental testing (air sampling, surface culture, PCR) identifies mould presence in a building but does not prove the patient is allergic. Clinical allergy requires both exposure and a positive immune response.

Q: Does a negative panel rule out mould allergy?

No. Sensitisation may develop after testing, titres may be suppressed by immunosuppressive medications, or symptoms may be caused by non-IgE mechanisms such as irritant effects or hypersensitivity pneumonitis. A negative panel supports alternative diagnoses but does not exclude mould exposure as a contributor.

The 15 Mold Panel: IgE quantifies serum-specific immunoglobulin E to 15 clinically relevant indoor and outdoor moulds, confirming type-I sensitisation in patients with suspected fungal allergy. It is ordered to attribute respiratory symptoms to mould exposure, guide environmental remediation, and support diagnosis of allergic bronchopulmonary aspergillosis when interpreted with total IgE and…

Biomarkers

Blood (serum)

Sample

7–10 business days

Turnaround

Fasting

What is the 15 Mold IgE Panel test?

The 15 Mold Panel: IgE quantifies serum-specific immunoglobulin E against a broad range of clinically relevant indoor and outdoor moulds, providing practitioners with a comprehensive snapshot of type-I fungal sensitisation. Mould allergy is underdiagnosed in patients with perennial or seasonally exacerbated rhinitis and asthma, and environmental history alone cannot reliably predict which moulds drive symptoms. This panel is ordered to confirm sensitisation when exposure to damp indoor environments or outdoor mould spores is suspected, to guide remediation priorities, and to support decisions about environmental control or allergen immunotherapy. Unlike culture or PCR-based environmental testing, which identifies mould presence in a building, this serological assay measures the patient's immune response. A positive specific IgE confirms sensitisation but does not alone diagnose clinical allergy — correlation with exposure timing and symptom patterns is essential. The panel includes the most frequently implicated allergens (Alternaria, Aspergillus, Penicillium, Cladosporium) alongside less common but contextually important species, making it suited to both routine allergy evaluation and investigation of building-related respiratory illness.

What does the 15 Mold IgE Panel test measure?

Alt a IgE(Alternaria alternata IgE)

Range: <0.35 kU/L negative; 0.35–0.69 equivocal; ≥0.70 positive.Optimal: Undetectable (<0.35 kU/L) indicates no type-I sensitisation. Titres above 0.70 kU/L confirm sensitisation; higher levels correlate loosely with symptom severity but do not define clinical allergy in the absence of relevant exposure and symptoms.kU/L / IU/mL

Alternaria alternata is an outdoor dematiaceous mould ubiquitous in soil and on decaying vegetation; its spores peak in warm dry weather. Specific IgE recognises protein epitopes on spore surfaces and mycelium; major allergen Alt a 1 is a beta-barrel protein unique to Alternaria. Cross-reactivity with other moulds is uncommon. Elevated specific IgE reflects type-I sensitisation, not active infection.

Alternaria is a leading cause of allergic rhinitis and a well-recognised trigger of severe exacerbations in atopic asthma. Detection of IgE aids attribution when exposure history and symptom timing implicate outdoor mould, and guides targeted environmental control.

Asp f IgE(Aspergillus fumigatus IgE)

Range: <0.35 kU/L negative; 0.35–0.69 equivocal; ≥0.70 positive.Optimal: Undetectable (<0.35 kU/L). Titres ≥0.70 kU/L confirm sensitisation; ABPA typically produces markedly elevated total IgE and Aspergillus-specific IgE, whereas simple sensitisation may show low-positive titres.kU/L / IU/mL

Aspergillus fumigatus is the most clinically important thermotolerant Aspergillus species, found in compost, soil, and water-damaged buildings. Its small conidia are easily inhaled. Specific IgE targets multiple protein allergens; major allergens include Asp f 1, Asp f 2, and Asp f 3. Cross-reactivity among Aspergillus species occurs but is incomplete.

Aspergillus fumigatus IgE is central to the diagnosis of allergic bronchopulmonary aspergillosis in patients with asthma or cystic fibrosis, and marks type-I sensitisation in allergic rhinitis and allergic fungal sinusitis. It does not diagnose invasive aspergillosis, which is a tissue-invasive mycosis in immunocompromised hosts.

Pen ch IgE(Penicillium chrysogenum IgE)

Range: <0.35 kU/L negative; 0.35–0.69 equivocal; ≥0.70 positive.Optimal: Undetectable. Positive titres (≥0.70 kU/L) reflect sensitisation; clinical relevance depends on exposure history and symptom correlation.kU/L / IU/mL

Penicillium chrysogenum (formerly P. notatum) thrives in damp indoor environments, on wallpaper, carpet, and in humidifiers. Specific IgE binds to allergenic proteins in spores and hyphal fragments. Cross-reactivity with Aspergillus and other moulds is partial and allergen-dependent.

Penicillium is a frequent indoor allergen implicated in perennial allergic rhinitis and asthma exacerbations. Detection of specific IgE supports the diagnosis of mould allergy when indoor exposure and temporal symptom patterns align.

Cla h IgE(Cladosporium herbarum IgE)

Range: <0.35 kU/L negative; 0.35–0.69 equivocal; ≥0.70 positive.Optimal: Undetectable. Sensitisation is confirmed at ≥0.70 kU/L; clinical allergy requires corroborating exposure and symptoms.kU/L / IU/mL

Cladosporium herbarum is the most common airborne outdoor mould in temperate climates; spore counts peak in summer and autumn. Allergens include Cla h 8 (mannitol dehydrogenase) and enolase. Cross-reactivity with Alternaria is limited.

Cladosporium sensitisation is linked to seasonal allergic rhinitis and asthma. IgE detection helps distinguish mould-triggered symptoms from pollen allergy when outdoor exposure predominates.

Aur p IgE(Aureobasidium pullulans IgE)

Range: <0.35 kU/L negative; 0.35–0.69 equivocal; ≥0.70 positive.Optimal: Undetectable. Positive IgE (≥0.70 kU/L) indicates sensitisation; clinical significance depends on exposure context.kU/L / IU/mL

Aureobasidium pullulans is a dematiaceous yeast-like fungus colonising damp wood, painted surfaces, and bathroom grout. Specific IgE targets glycoproteins released by budding cells and hyphae.

Sensitisation is less common than to Alternaria or Aspergillus but relevant in damp indoor environments. Detection aids attribution of respiratory symptoms when building moisture problems are documented.

Fus p IgE(Fusarium proliferatum IgE)

Range: <0.35 kU/L negative; 0.35–0.69 equivocal; ≥0.70 positive.Optimal: Undetectable. Positive IgE reflects sensitisation; clinical relevance requires symptom-exposure correlation.kU/L / IU/mL

Fusarium species are soil-borne moulds and plant pathogens; indoor growth occurs in water-damaged buildings. Fusarium proliferatum shares allergens with other Fusarium species, including enolases and ribosomal proteins.

Fusarium sensitisation is less frequently documented than Alternaria or Aspergillus but can contribute to perennial allergic rhinitis and occupational allergy in agricultural and greenhouse workers.

Sta c IgE(Stachybotrys chartarum IgE)

Range: <0.35 kU/L negative; 0.35–0.69 equivocal; ≥0.70 positive.Optimal: Undetectable. Positive IgE indicates sensitisation; interpreting Stachybotrys results requires clear distinction between allergy (IgE-mediated) and non-specific building-related illness.kU/L / IU/mL

Stachybotrys chartarum ('black mould') colonises cellulose-rich materials in chronically damp indoor environments. It produces macrocyclic trichothecene mycotoxins, but specific IgE measures type-I sensitisation to allergenic proteins, not toxin exposure.

Media attention has amplified concern, but IgE-mediated sensitisation to Stachybotrys is relatively uncommon. Detection in this panel helps address patient and practitioner questions when water damage is documented, but IgE positivity does not confirm mycotoxin illness.

Muc r IgE(Mucor racemosus IgE)

Range: <0.35 kU/L negative; 0.35–0.69 equivocal; ≥0.70 positive.Optimal: Undetectable. Positive IgE indicates type-I sensitisation in the appropriate exposure context.kU/L / IU/mL

Mucor species are zygomycetes widespread in soil and decaying organic matter; indoor growth follows water intrusion. Mucor allergens are less well characterised than those of Aspergillus or Alternaria.

Sensitisation is uncommon. IgE positivity may point to indoor dampness but does not diagnose invasive mucormycosis, an opportunistic infection in immunosuppressed patients.

Rhi n IgE(Rhizopus nigricans IgE)

Range: <0.35 kU/L negative; 0.35–0.69 equivocal; ≥0.70 positive.Optimal: Undetectable. Positive IgE reflects sensitisation; significance requires symptom correlation.kU/L / IU/mL

Rhizopus nigricans is a fast-growing zygomycete found on bread, fruit, and in soil. It is ubiquitous but rarely a dominant allergen.

Sensitisation is infrequent. Detection may be incidental; clinical relevance is established by temporal correlation with exposure.

Bot c IgE(Botrytis cinerea IgE)

Range: <0.35 kU/L negative; 0.35–0.69 equivocal; ≥0.70 positive.Optimal: Undetectable. Positive IgE indicates sensitisation; occupational exposure should be explored.kU/L / IU/mL

Botrytis cinerea is a plant pathogen causing grey mould on grapes and soft fruits. Outdoor spore exposure occurs during harvest; indoor growth is less common.

Sensitisation is relevant in viticulture and agricultural settings. Detection aids occupational allergy evaluation.

Cur l IgE(Curvularia lunata IgE)

Range: <0.35 kU/L negative; 0.35–0.69 equivocal; ≥0.70 positive.Optimal: Undetectable. Positive IgE confirms sensitisation; clinical significance depends on exposure.kU/L / IU/mL

Curvularia species are dematiaceous moulds found on grasses and in soil; indoor contamination follows water damage. Allergens overlap partially with other dematiaceous moulds.

Sensitisation is less common than to Alternaria or Cladosporium but contributes to allergic rhinitis when outdoor or indoor exposure is documented.

Epi p IgE(Epicoccum purpurascens IgE)

Range: <0.35 kU/L negative; 0.35–0.69 equivocal; ≥0.70 positive.Optimal: Undetectable. Positive IgE reflects sensitisation in appropriate exposure settings.kU/L / IU/mL

Epicoccum is a saprophytic mould on plants and in soil; spore release is seasonal. Allergen characterisation is limited.

Sensitisation is uncommon. Inclusion in broad panels aids comprehensive environmental allergy evaluation.

Pho b IgE(Phoma betae IgE)

Range: <0.35 kU/L negative; 0.35–0.69 equivocal; ≥0.70 positive.Optimal: Undetectable. Positive IgE indicates sensitisation; interpretation is context-dependent.kU/L / IU/mL

Phoma species are plant pathogens and soil inhabitants; indoor presence is uncommon. Allergens are poorly characterised.

Sensitisation is rare. IgE detection may be incidental; clinical relevance requires documented exposure and symptom correlation.

Cha g IgE(Chaetomium globosum IgE)

Range: <0.35 kU/L negative; 0.35–0.69 equivocal; ≥0.70 positive.Optimal: Undetectable. Positive IgE confirms sensitisation; clinical significance depends on exposure history.kU/L / IU/mL

Chaetomium globosum colonises cellulose substrates in chronically damp buildings, similar to Stachybotrys. Specific IgE targets protein allergens.

Sensitisation is uncommon but relevant in water-damaged indoor environments. Detection aids comprehensive mould allergy evaluation.

Tri v IgE(Trichoderma viride IgE)

Range: <0.35 kU/L negative; 0.35–0.69 equivocal; ≥0.70 positive.Optimal: Undetectable. Positive IgE reflects sensitisation; interpretation requires exposure correlation.kU/L / IU/mL

Trichoderma viride is a soil fungus and biocontrol agent; indoor growth follows water damage. Allergens are not well characterised.

Sensitisation is rare. Inclusion in comprehensive mould panels supports thorough environmental allergy work-up.

Why is the 15 Mold IgE Panel test ordered?

Evaluation of perennial or seasonally worsening allergic rhinitis or asthma when environmental history suggests mould exposure
Work-up of suspected allergic bronchopulmonary aspergillosis in patients with asthma or cystic fibrosis, interpreted alongside total IgE, eosinophil count, and imaging
Investigation of respiratory symptoms attributed to water-damaged buildings, particularly when remediation or relocation decisions depend on confirming sensitisation
Occupational allergy assessment in agricultural, greenhouse, or indoor cultivation workers with work-related respiratory symptoms
Patients with poorly controlled asthma despite optimal pharmacotherapy, where unrecognised mould sensitisation may be a contributing trigger
Pre-immunotherapy screening when sublingual or subcutaneous allergen therapy for mould is being considered
Evaluation of suspected allergic fungal sinusitis, interpreted with imaging and clinical presentation
Patients requesting objective testing after media or public health messaging about 'toxic mould' exposure

Sample collection and turnaround

Sample type

Blood (serum)

Fasting required

Collection method

Venipuncture at patient service centre

Turnaround

7–10 business days

Collection notes

Standard phlebotomy; serum separation required. No special preparation. If the patient is on omalizumab or high-dose corticosteroids, note this on the requisition as it may influence interpretation.

Specimen requirements

Minimum 1.0 mL serum; gel separator acceptable. Separate from cells within two hours and freeze if shipment to US BioTek will exceed 48 hours. Avoid repeated freeze-thaw cycles.

What can affect 15 Mold IgE Panel results?

reducesRecent high-dose systemic corticosteroids or immunosuppressive therapy

Immunosuppression can blunt IgE production and lower specific IgE titres, potentially producing false-negative results during or shortly after treatment.

reducesOmalizumab (anti-IgE monoclonal antibody)

Omalizumab binds free and B-cell-surface IgE, reducing measurable specific IgE; testing should ideally precede initiation or be interpreted with caution during therapy.

reducesAge — very young children

Sensitisation develops over time; infants and toddlers may not yet have mounted detectable IgE responses even with significant exposure.

variableTotal IgE deficiency or hyper-IgE syndromes

Patients with very low total IgE may have proportionally low specific IgE, while those with markedly elevated polyclonal IgE may show multiple low-positive results reflecting background rather than true sensitisation.

variableCross-reactivity among mould allergens and with other environmental allergens

Pan-allergens such as enolases and ribosomal proteins can produce positive results across multiple moulds; correlation with exposure and clinical history distinguishes true polysensitisation from serological cross-reactivity.

variableSpecimen handling and storage

IgE is relatively stable, but prolonged storage at room temperature or multiple freeze-thaw cycles can degrade antibodies; specimens should be processed or frozen promptly.

What do 15 Mold IgE Panel results mean?

Elevated

A specific IgE titre ≥0.70 kU/L for any mould confirms type-I sensitisation to that allergen. The pattern of positives helps attribute symptoms: outdoor moulds (Alternaria, Cladosporium) suggest seasonal exacerbations, while indoor species (Aspergillus, Penicillium, Stachybotrys, Chaetomium) point to damp building exposure. Very high Aspergillus fumigatus IgE (often >0.35–1.0 kU/L), especially with markedly elevated total IgE and peripheral eosinophilia, raises suspicion for allergic bronchopulmonary aspergillosis. Multiple positive results may reflect genuine polysensitisation or cross-reactivity among moulds sharing pan-allergens; exposure history and symptom timing guide clinical relevance. Sensitisation without temporal symptom-exposure correlation does not constitute clinical allergy and does not mandate intervention beyond environmental control.

Normal

Undetectable specific IgE across the panel is the expected baseline in non-sensitised individuals. This result supports alternative diagnoses (non-allergic rhinitis, irritant-induced bronchospasm, hypersensitivity pneumonitis, or non-mould allergens) and suggests that remediation for mould allergy is not indicated, though other building-related exposures may still be relevant.

Reduced

Specific IgE below the detection threshold (<0.35 kU/L) indicates no measurable type-I sensitisation to that mould at the time of testing. A negative panel does not exclude mould allergy entirely — sensitisation may develop later, titres may be suppressed by recent immunosuppression, or symptoms may be driven by non-IgE mechanisms such as irritant effects or hypersensitivity pneumonitis.

Note: Specific IgE measures sensitisation, not clinical allergy. Positive results must be interpreted alongside exposure history, symptom timing, and physical examination. The panel does not diagnose invasive fungal infection, hypersensitivity pneumonitis (which is a type-III/IV process), or non-specific building-related illness. Stachybotrys IgE does not confirm mycotoxin-mediated disease. Reference ranges and assay performance are method-dependent; US BioTek uses a fluorescent enzyme immunoassay, and results should not be directly compared to ImmunoCAP or other platforms without understanding assay-specific characteristics. When ABPA is suspected, order total IgE, eosinophil count, Aspergillus-specific IgG (precipitins), and imaging in addition to specific IgE.

Frequently asked questions

This serological panel measures the patient's immune response — specific IgE antibodies to mould allergens — confirming sensitisation. Environmental testing (air sampling, surface culture, PCR) identifies mould presence in a building but does not prove the patient is allergic. Clinical allergy requires both exposure and a positive immune response.

How to access the 15 Mold IgE Panel test

The 15 Mold IgE Panel reference page is free and open to all practitioners. Create a free practitioner account to see pricing, save tests to your list, and generate requisition forms. Verification takes 1–2 business days.

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About this page

Published: October 7, 2026

Last reviewed: October 7, 2026

References:

Chowdhary A, et al. Mould allergy and fungal sensitisation in patients with respiratory allergy in India. Mycoses. (2014)
Agarwal R, et al. Allergic bronchopulmonary aspergillosis: review of literature and proposal of new diagnostic and classification criteria. Clin Exp Allergy. (2013)
Bush RK, Portnoy JM. The role and abatement of fungal allergens in allergic diseases. J Allergy Clin Immunol Pract. (2016)
Simon-Nobbe B, et al. The spectrum of fungal allergy. Int Arch Allergy Immunol. (2008)
Horner WE, et al. Fungal allergens. Clin Microbiol Rev. (2004)

This content is for licensed healthcare practitioners only and does not constitute medical advice. Clinical decisions should be based on the full clinical picture and not on any single test result.