Can You Test for Mold in a Patient?
No validated laboratory test exists to assess human exposure to toxigenic mold, and routine testing for mold exposure is not recommended. 1
What Testing Should Be Avoided
The following tests have no clinical utility and should not be ordered:
- Mycotoxin testing in blood or urine – These assays are not standardized for clinical use, lack validation, and have no established correlation with health effects 1
- Serum IgG antibody testing to mold – This does not reliably indicate exposure or disease 1
- Environmental mold sampling as part of medical evaluation – This is not recommended by the American Academy of Pediatrics 1
When Laboratory Testing May Be Appropriate
Testing is only indicated when you suspect specific mold-related diseases, not for general "mold exposure":
For Immunocompromised Patients with Suspected Invasive Fungal Disease
Immediate removal from mold exposure takes absolute priority. 1 Then proceed with:
- Serum galactomannan antigen testing for Aspergillus 1
- Microbiological cultures from respiratory specimens (sputum, BAL) 2
- CT imaging (superior to plain radiography for invasive disease) 1
- Immunological evaluation of immune function 1
- Beta-D-glucan testing (though less specific, can be positive with multiple fungal infections) 2
For Immunocompetent Patients with Suspected Allergic Disease
- Skin prick testing with standardized mold extracts (Alternaria, Aspergillus, Cladosporium, Penicillium) to identify IgE-mediated sensitization in patients with atopic history and respiratory symptoms 1, 3
- Mold-specific serum IgE as an alternative to skin testing 1
For Suspected Hypersensitivity Pneumonitis
- High-resolution CT (HRCT) looking for centrilobular ground-glass nodules, mosaic attenuation, air-trapping, and three-density sign 1
- Serum antigen-specific IgG or IgA antibodies can support a putative mold exposure when exposure history is unclear, but should never be used alone to confirm or exclude the diagnosis 1
Critical caveat: Serum precipitins have poor diagnostic performance with sensitivity of only 39-76% and specificity of 61-82%. In one cohort, 60% of patients with positive mold precipitins reported no identifiable exposure, while 32% with negative precipitins had demonstrable exposure. 1
For Suspected Coccidioidomycosis (Endemic Areas Only)
Use multiple tests including:
- Direct visualization and culture of sputum, BAL, or biopsy material 2
- Urine and serum antigen testing (particularly in immunocompromised patients) 2
- Serology (serum antibody testing) 2
The Correct Clinical Approach
Instead of laboratory testing for "mold exposure," focus on:
Detailed exposure history – Ask specifically about visible mold growth, water damage, musty odors in home/workplace, timing of symptoms relative to exposure 1
Assess immune status – Immunosuppression, chemotherapy, transplant status, HIV/AIDS, chronic granulomatous disease 1
Identify specific mold-related syndromes:
Environmental remediation is the definitive treatment – Medical interventions cannot be effective until source elimination is complete 5
Common Pitfalls
- Do not order "mold panels" or "mycotoxin screens" – These are not evidence-based and may reinforce false beliefs about mold toxicity 1
- Do not rely solely on serum precipitins for hypersensitivity pneumonitis diagnosis given their poor sensitivity and specificity 1
- Do not test asymptomatic patients or those without specific risk factors for mold-related disease 1
- Remember that outdoor molds are more important allergens than indoor molds for most allergic individuals 6