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BML-ENV-002environmental mouldUSA

Add-On: 15 Mold Panel: IgE

The 15 Mold Panel: IgE measures serum-specific IgE antibodies to fifteen common environmental moulds including Aspergillus, Alternaria, Penicillium, Stachybotrys, and others. It confirms Type I sensitisation in patients with suspected mould allergy presenting with chronic rhinitis, asthma, or allergic fungal disease and guides environmental control and immunotherapy.

15

Biomarkers

Blood (serum)

Sample

7–10 business days

Turnaround

No

Fasting

What is the 15 Mold IgE test?

The Add-On: 15 Mold Panel: IgE measures serum-specific IgE antibodies to fifteen common environmental moulds, each associated with indoor damp, outdoor spore exposure, or occupational settings. It is ordered to confirm Type I hypersensitivity in patients with suspected mould allergy who present with chronic rhinitis, asthma, or allergic fungal disease, and to guide environmental remediation, avoidance strategies, and allergen immunotherapy decisions. This panel is particularly relevant in patients whose symptoms correlate with damp indoor environments, water-damaged buildings, or seasonal outdoor mould exposure. Detection of specific IgE does not by itself constitute a diagnosis — clinical relevance is determined by correlating serological results with the patient's exposure history, symptom pattern, and response to avoidance. The panel is an add-on test, typically ordered alongside broader allergy evaluations or in conjunction with investigations for allergic bronchopulmonary aspergillosis or severe asthma with fungal sensitisation.

What does the 15 Mold IgE test measure?

1
Alt a IgE(Alternaria alternata-specific IgE)
Range: <0.35 kU/L typically considered negative; 0.35–0.69 equivocal; ≥0.70 positive.Optimal: Undetectable or <0.10 kU/L in non-atopic individuals.kU/L / IU/mL

Alternaria alternata is one of the most common outdoor moulds and a potent aeroallergen. Specific IgE antibodies reflect Type I hypersensitivity; exposure to spores triggers mast-cell degranulation in sensitised individuals, leading to rhinitis, asthma exacerbation, and less commonly atopic dermatitis or allergic fungal rhinosinusitis.

Alternaria sensitisation is a recognised risk factor for severe asthma and is more prevalent in patients with poorly controlled respiratory allergy. Detection guides environmental control, inhalant avoidance, and allergen immunotherapy decisions.

2
Asp f IgE(Aspergillus fumigatus-specific IgE)
Range: <0.35 kU/L negative; 0.35–0.69 equivocal; ≥0.70 positive.Optimal: Undetectable in non-sensitised individuals.kU/L / IU/mL

Aspergillus fumigatus is ubiquitous in soil, decaying organic matter, and indoor water-damaged environments. IgE to Asp f signals sensitisation; in the absence of invasive disease, elevations are seen in allergic bronchopulmonary aspergillosis (ABPA), severe asthma with fungal sensitisation, and allergic fungal rhinosinusitis.

Aspergillus-specific IgE is essential in the diagnosis of ABPA and guides management of severe asthma with fungal sensitisation. It is interpreted alongside total IgE, eosinophil count, precipitins, and imaging, not in isolation.

3
Pen ch IgE(Penicillium chrysogenum-specific IgE)
Range: <0.35 kU/L negative; ≥0.70 positive.Optimal: Undetectable in non-atopic individuals.kU/L / IU/mL

Penicillium species are common indoor moulds, particularly in damp buildings. P. chrysogenum (formerly P. notatum) is the species from which penicillin was originally isolated, though the allergen is distinct from the drug. Specific IgE reflects sensitisation to airborne spores and hyphal fragments.

Penicillium sensitisation is associated with chronic rhinitis and asthma exacerbated by indoor damp. Clinical significance is determined by the history of exposure and respiratory symptoms; cross-reactivity with other moulds is common.

4
Cla h IgE(Cladosporium herbarum-specific IgE)
Range: <0.35 kU/L negative; ≥0.70 positive.Optimal: Undetectable.kU/L / IU/mL

Cladosporium is one of the most abundant outdoor moulds worldwide and also found indoors in moisture-damaged materials. C. herbarum is the most allergenic species; specific IgE indicates Type I sensitisation to its spore and mycelial allergens.

Cladosporium sensitisation is common in allergic rhinitis and asthma, particularly in children and adolescents with atopy. It is a frequent sensitiser in damp or water-damaged homes.

5
Fus p IgE(Fusarium proliferatum-specific IgE)
Range: <0.35 kU/L negative; ≥0.70 positive.Optimal: Undetectable.kU/L / IU/mL

Fusarium species are soil and plant pathogens found in water-damaged buildings and outdoor air. F. proliferatum is one of several Fusarium species implicated in respiratory allergy; specific IgE reflects sensitisation to inhaled spores.

Fusarium sensitisation is less common than Alternaria or Aspergillus but clinically relevant in occupational settings (agriculture, horticulture) and in patients with severe or refractory allergic rhinitis or asthma.

6
Sta c IgE(Stachybotrys chartarum-specific IgE)
Range: <0.35 kU/L negative; ≥0.70 positive.Optimal: Undetectable.kU/L / IU/mL

Stachybotrys chartarum, colloquially 'black mould,' grows on cellulose-rich materials in chronically damp indoor environments. It produces mycotoxins and allergens; specific IgE indicates Type I sensitisation. The clinical significance of Stachybotrys beyond IgE-mediated allergy remains debated.

Detection of Stachybotrys-specific IgE confirms sensitisation in patients with water-damaged building exposure and respiratory symptoms. Evidence for systemic toxicity from environmental exposure is limited, but sensitisation supports remediation and avoidance.

7
Cha g IgE(Chaetomium globosum-specific IgE)
Range: <0.35 kU/L negative; ≥0.70 positive.Optimal: Undetectable.kU/L / IU/mL

Chaetomium is a common indoor mould in water-damaged buildings, preferring cellulose substrates. C. globosum is the most prevalent species; specific IgE reflects sensitisation to its allergens.

Chaetomium sensitisation is a marker of indoor damp exposure and can contribute to allergic rhinitis and asthma. It is less commonly measured than Aspergillus or Penicillium but relevant in occupational or residential damp investigations.

8
Aur p IgE(Aureobasidium pullulans-specific IgE)
Range: <0.35 kU/L negative; ≥0.70 positive.Optimal: Undetectable.kU/L / IU/mL

Aureobasidium pullulans is a ubiquitous yeast-like fungus found on plant surfaces, in soil, and in indoor damp environments. Specific IgE indicates sensitisation; the fungus is a known cause of allergic respiratory symptoms in damp housing.

Sensitisation to Aureobasidium is common in patients with chronic rhinitis or asthma living in damp or mouldy environments. Cross-reactivity with other environmental moulds is frequent.

9
Epi p IgE(Epicoccum purpurascens-specific IgE)
Range: <0.35 kU/L negative; ≥0.70 positive.Optimal: Undetectable.kU/L / IU/mL

Epicoccum is a plant pathogen and saprophyte, common outdoors on dead plant material and indoors in damp conditions. E. purpurascens is the principal allergenic species; specific IgE denotes Type I sensitisation.

Epicoccum sensitisation is associated with seasonal allergic rhinitis and asthma, particularly in agricultural and horticultural workers and in patients exposed to outdoor and indoor mould.

10
Rhi s IgE(Rhizopus stolonifer-specific IgE)
Range: <0.35 kU/L negative; ≥0.70 positive.Optimal: Undetectable.kU/L / IU/mL

Rhizopus stolonifer, the common bread mould, is a fast-growing fungus found on decaying fruit, vegetables, and baked goods. Specific IgE indicates sensitisation to inhaled or contact allergens from this ubiquitous organism.

Rhizopus sensitisation is less common than Aspergillus or Penicillium but clinically relevant in occupational settings (food handling, composting) and in patients with refractory allergic rhinitis or asthma.

11
Muc r IgE(Mucor racemosus-specific IgE)
Range: <0.35 kU/L negative; ≥0.70 positive.Optimal: Undetectable.kU/L / IU/mL

Mucor species are ubiquitous environmental moulds found in soil, decaying vegetation, and spoiled food. M. racemosus is one allergenic species; specific IgE reflects Type I sensitisation.

Mucor sensitisation is uncommon but may be relevant in occupational or residential exposures involving organic decay or compost. It is grouped with other zygomycetes for allergy evaluation.

12
Bot c IgE(Botrytis cinerea-specific IgE)
Range: <0.35 kU/L negative; ≥0.70 positive.Optimal: Undetectable.kU/L / IU/mL

Botrytis cinerea, the grey mould, is a plant pathogen found on grapes, berries, and other fruits. It is common in agricultural settings and wine production. Specific IgE indicates sensitisation to its airborne spores and allergens.

Botrytis sensitisation is relevant in occupational exposures (viticulture, horticulture) and in patients with allergic rhinitis or asthma triggered by fruit handling or damp agricultural environments.

13
Tri v IgE(Trichoderma viride-specific IgE)
Range: <0.35 kU/L negative; ≥0.70 positive.Optimal: Undetectable.kU/L / IU/mL

Trichoderma viride is a soil fungus and plant symbiont found in decaying wood and damp building materials. Specific IgE indicates Type I sensitisation to its allergens.

Trichoderma sensitisation is less frequently reported but may be relevant in indoor damp investigations and in agricultural or horticultural occupational exposures.

14
Cur l IgE(Curvularia lunata-specific IgE)
Range: <0.35 kU/L negative; ≥0.70 positive.Optimal: Undetectable.kU/L / IU/mL

Curvularia species are dematiaceous moulds found in soil, plants, and indoor damp environments. C. lunata is one allergenic species; specific IgE denotes sensitisation to its spores.

Curvularia sensitisation is associated with allergic rhinitis and asthma in patients with damp indoor exposure. It is less commonly tested than Alternaria or Cladosporium but relevant in comprehensive mould panels.

15
Hel h IgE(Helminthosporium halodes-specific IgE)
Range: <0.35 kU/L negative; ≥0.70 positive.Optimal: Undetectable.kU/L / IU/mL

Helminthosporium (also classified under Bipolaris) is a plant pathogen and allergen found outdoors and in damp indoor environments. H. halodes is one allergenic species; specific IgE reflects sensitisation.

Helminthosporium sensitisation is recognised in allergic rhinitis and asthma, particularly in agricultural workers and patients exposed to outdoor moulds. Cross-reactivity with other dematiaceous fungi is common.

Why is the 15 Mold IgE test ordered?

  • Patients with chronic rhinitis, asthma, or recurrent sinusitis whose symptoms worsen in damp indoor environments or after water-damage events
  • Evaluation of allergic bronchopulmonary aspergillosis (ABPA) or severe asthma with fungal sensitisation, where Aspergillus-specific IgE is a key diagnostic criterion
  • Investigation of occupational respiratory allergy in agricultural workers, horticulturists, composters, or workers in water-damaged buildings
  • Patients with poorly controlled allergic rhinitis or asthma despite standard therapy, where mould sensitisation is suspected but not yet confirmed
  • Allergic fungal rhinosinusitis work-up, to identify fungal sensitisation patterns that support the diagnosis and guide surgical and medical management
  • Paediatric or adult atopic patients with seasonal or perennial symptoms suggestive of outdoor mould exposure (Alternaria, Cladosporium)
  • Pre-immunotherapy evaluation where mould allergens are candidate antigens based on clinical history
  • Patients reporting symptoms triggered by specific indoor exposures (visible mould, musty odours, damp basements) or occupational environments

Sample collection and turnaround

Sample type

Blood (serum)

Fasting required

No

Collection method

Venipuncture at patient service centre

Turnaround

7–10 business days

Collection notes

Phlebotomy required; serum separated and shipped to US BioTek. No special preparation. Defer testing if the patient is on high-dose systemic corticosteroids or immunosuppressants, if clinically feasible, to avoid suppression of IgE response.

Specimen requirements

Minimum 1–2 mL serum, depending on the number of allergens tested. Separate from cells within two hours and refrigerate or freeze. Avoid haemolysed, lipaemic, or icteric specimens, which may interfere with immunoassay performance.

What can affect 15 Mold IgE results?

reducesRecent corticosteroid or immunosuppressive therapy

Systemic corticosteroids and immunosuppressants can suppress IgE production and reduce measured specific IgE titres; defer testing until after a washout period if clinically feasible.

variableAge and atopic status

Specific IgE titres tend to be higher in atopic children and decline with age. Non-atopic individuals rarely show detectable specific IgE, so low titres in a non-atopic adult may have limited clinical significance.

variableCross-reactivity between mould allergens

Moulds share homologous proteins, so sensitisation to one species may yield positive IgE to others without true independent sensitisation. Interpretation should consider the dominant moulds in the patient's environment.

elevatesTiming relative to acute exposure or exacerbation

Recent intense exposure or an acute allergic exacerbation can transiently elevate specific IgE; serial testing may be needed to establish baseline sensitisation.

variableTotal IgE concentration

Very high total IgE (as in ABPA or hyper-IgE syndromes) can lead to non-specific binding and false-positive specific IgE results; interpret specific IgE in the context of total IgE and clinical picture.

variableSample handling and interference

Haemolysis, lipaemia, or high bilirubin can interfere with immunoassays. Samples should be centrifuged promptly and grossly abnormal specimens rejected.

What do 15 Mold IgE results mean?

Elevated

Detectable or elevated specific IgE (≥0.35 kU/L, and particularly ≥0.70 kU/L) confirms sensitisation to the corresponding mould. Clinical relevance depends on correlation with exposure history and symptoms. Aspergillus fumigatus-specific IgE ≥0.35 kU/L is a diagnostic criterion for ABPA when accompanied by elevated total IgE, eosinophilia, and compatible imaging. Alternaria and Cladosporium sensitisation are common outdoor mould allergies; indoor moulds (Penicillium, Stachybotrys, Chaetomium) suggest damp building exposure. Multiple positive results may reflect cross-reactivity or polysensitisation and warrant environmental assessment.

Normal

Undetectable specific IgE (<0.35 kU/L) is the expected finding in non-sensitised individuals. A negative panel in a patient with suggestive symptoms prompts consideration of non-allergic rhinitis, irritant exposure, or sensitisation to allergens not included in the panel.

Reduced

Specific IgE below 0.10 kU/L is typically undetectable and argues against Type I sensitisation to that mould. Absence of IgE does not exclude non-IgE-mediated hypersensitivity (Type III or IV) or irritant responses, which are not captured by this assay.

Note: Specific IgE confirms sensitisation but not necessarily clinical allergy; asymptomatic sensitisation is common in atopic individuals. Correlation with exposure history, symptom pattern, and response to avoidance is essential. Cross-reactivity between moulds means that not every positive result represents an independent sensitisation. For ABPA diagnosis, Aspergillus-specific IgE must be interpreted with total IgE, eosinophil count, precipitins, lung function, and imaging. Reference ranges and positivity thresholds are assay-specific; US BioTek intervals may differ from other platforms.

Frequently asked questions

Total IgE measures the overall concentration of IgE in serum and is elevated in atopy, parasitic infection, and conditions such as ABPA. Specific IgE identifies antibodies directed against individual allergens (in this case, moulds) and confirms which allergens the patient is sensitised to.

How to access the 15 Mold IgE test

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About this page

Published: October 7, 2026

Last reviewed: October 7, 2026

References:
  1. Agarwal R, et al. International Society for Human and Animal Mycology (ISHAM) working group report on allergic bronchopulmonary aspergillosis complicating asthma. Clin Exp Allergy. (2013)
  2. Denning DW, et al. The link between fungi and severe asthma: a summary of the evidence. Eur Respir J. (2006)
  3. Bush RK, Portnoy JM. The role and abatement of fungal allergens in allergic diseases. J Allergy Clin Immunol Pract. (2001)
  4. Crameri R, et al. Fungi: the neglected allergenic sources. Allergy. (2014)
  5. Simon-Nobbe B, et al. The spectrum of fungal allergy. Int Arch Allergy Immunol. (2008)

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.