Is it a Cold or the Mold?
In general, fungi grow as yeast or mold forms depending on external conditions that include temperature, water presence, and carbon dioxide concentrations. Some fungi produce mycotoxins (2,6) which can be deleterious to human beings and are more fully described in the text below. Although the terms fungi and molds are not identical in meaning, both words are used in discussions impacting human health. The term mold is used primarily in this review.
Molds are found in virtually every environment, indoors and outdoors. While most molds are innocuous, some molds are capable of causing allergic reactions and respiratory problems. (1,2,7) Patients exposed to molds may present with classic seasonal allergy symptoms throughout the year. The interesting characteristic of molds is their unique ability to adapt to different environments, acting as traditional allergens and/or potential pathogens. Molds grow and thrive in warm, damp and humid conditions. Living and/or working in water-damaged buildings are a common route of exposure. (1, 3, 4)
Exposure to molds has been linked to a variety of health problems, including Allergic Rhinitis and Asthma. (7,8,9,10) Extreme weather events such as thunderstorms can dramatically modify aerial antigen levels; this phenomenon is "thunderstorm asthma." During a thunderstorm, various mold spores and pollens are lifted into the air. Moisture from the storms then causes these pollens to rupture into tiny particles that are small enough to enter the lungs triggering acute asthma symptoms. In November 2016, an evening thunderstorm in the state of Victoria, Australia triggered asthma attacks. Thousands of people experiencing respiratory distress were rushed to hospitals, at least nine died. (11,12)
Recent analyses have found a number of fungi/molds especially Aspergillus, Candida, Fusarium, and others can be pathogenic and contribute to a variety of severe syndromes. (13,14,15) When mold species invade the human body, less common but severe mold induced respiratory syndromes can develop, as seen in individuals with Allergic Bronchopulmonary Aspergillosis (ABPA) and Hypersensitivity Pneumonitis (HP). ABPA is an allergic or hypersensitive reaction to Aspergillus fumigatus. Fungal spores are inhaled and then colonize in the lower airways and alveoli. HP is a disease that causes your lungs to become inflamed as an allergic reaction to inhaled molds, fungus, chemicals or dust. A few molds under the right conditions produce mycotoxins; secondary metabolites that may cause harmful effects in various organ systems.
Symptoms of mold exposure are often overlooked because patient symptoms are very similar to virus or bacterial infection symptoms, as well as the flu (see figure 1).
Identifying the immune response to molds through serum testing (16) may help distinguish the nature of an exposure. Measuring levels of Immunoglobulin E (IgE), Immunoglobulin G (igG) and Immunoglobulin A (IgA) to specific molds can identify if the patient is experiencing an acute or delayed hypersensitivity response.
Measuring IgE can assist in identifying if the symptoms are an acute allergic response to a mold. Positive IgG levels may suggest a recent, on-going or past exposure to a specific mold. Positive IgA levels suggest a strong mucosal response, usually associated with a recent respiratory or gastrointestinal exposure to specific molds.
It is important to recognize the sources of mold exposure are often hard to identify, unseen water leakage within walls or even houseplants can harbor large amounts of mold. Teachers working in a mold-damaged school for up to two years complained of symptoms of rhinitis. When tested for mold specific IgG, elevated levels were associated with the presence of rhinitis. (17) Elevated IgG and IgA responses have been reported in sawmill workers exposed chronically to mold in lumber. (18)
The ubiquitous nature of molds makes elimination of molds and mold spores improbable, however, many steps can be taken to significantly reduce the burdens of mold and fungi within indoor spaces. Reducing humidity to below 50% through the use of air conditioning or dehumidifiers will inhibit growth. Ensuring that windows, doors, and ducting are properly sealed and the proper use of high-efficiency particulate air (HEPA) filters for air conditioners, ducts, and furnaces will reduce spore and mold levels. The use of paints containing mold inhibitors should be used. Keeping dust levels down by frequent cleaning reduces fungal spores that have been brought in the home. Moving and/or removing houseplants can reduce mold burdens. Molds and fungi should be physically removed from homes as dead mold can still trigger immune responses. Mold inhibitors should be considered for refrigerator, or air conditioner drip pans and other places water collects. If leaks occur replace damaged wallboard, wallpaper, insulation, carpeting, and other materials where molds can colonize and thrive. (1)
In summary, exposure to fungi/ molds can result in a wide spectrum of clinical findings that include irritant effects, hypersensitivity conditions, or life-threatening disorders. In assessing individuals with possible mold/fungi-related ailments, potential environmental exposures within the home and work settings should be considered. Serologic testing to identify the 'culprit' allergen source(s) can be accomplished by performing immunologic IgE, IgG, and IgA assays. Since immune-suppressed persons can be at risk for fatal opportunistic fungal infections, this sub-group of individuals may require a more comprehensive clinical work-up to identify specific fungi by culture, molecular assays, or other test methods.
About the Authors:
Dr. Gordon Siek has over 35 years of experience in Clinical Laboratories and diagnostic assay development. He received his PhD in Pharmacology from Boston University. Prior to becoming Laboratory Director at Alletess Medical Laboratory, Dr Siek was involved in several start-ups and was instrumental in getting CLIA and CAP certification for two laboratories, as well as the development of seven FDA cleared diagnostic kits.
After receiving her degree from University of Massachusetts Amherst, Veronica Kent, President of Alletess Medical Laboratory has worked in all areas of the company. She has over 30 years of experience working in high complexity laboratories and is excited to lead Alletess to its next level of success as the company's leader.
Joanne Sherman, MLS [ASCP.sup.cm] is our Laboratory Supervisor. She has over 43 years of experience working in various clinical laboratories, her expertise in compliance and laboratory protocols is essential to the day to day operations at Alletess Medical Laboratory.
(1.) EPA, A brief guide to mold, moisture, and your home http://www.epa.gov/mold/pdfs/moldguide.pdf (accessioned 7/25/2018.
(2.) Gorman C. Fungus, Mold & Mycotoxins 6th edition 2011 Caleta Press, Piano TX 75085.
(3.) Quansah, R., Jaakola, M.S., Hugg, TT, Heikkinen, S.A.M., Jaakkola J.J.K. Residential Dampness and Molds and the Risk of Developing Asthma: A systemic Review and Meta-Analysis. PLoS One 2012; 7:e47526: 1-9.
(4.) Kanchongkittiphon W1, Mendell MJ, Gaffin JM, Wang G, Phipatanakul W. Indoor Environmental Exposures and Exacerbation of Asthma: An Update to the 2000 Review by the Institute of Medicine Environmental Health Perspectives 2015, 123:6-20.
(5.) Oren I. and Paul M. Up to date epidemiology, diagnosis and management of invasive fungal infections. Clin. Microbiol. And Infect. 2014; 20 (Suppl 6) 1-4.
(6.) Bennett JW and Klich M. Mycotoxins Clin. Microbiol. Rev. 2003;16:497-516.
(7.) Glass D, Amedee RG. Allergic Fungal Rhinosinusitis: A Review. The Ochsner Journal 2011, 11:271-275.
(8.) Mendell, MJ, Mirer AG, Cheung K., Tong M, Douwes J. Respiratory and Allergic Health Effects of Dampness, Mold, and Dampness-related Agents: A review of the Epidemiologic Evidence. Environ. Health. Perspect. 2011; 119:748-756.
(9.) Jaakkola, JJK, Hwang B-F, and Jaakola N. Home Dampness and Molds, Parental Atopy, and Asthma in Childhood: A Six Year Population-Based Cohort Study. Environ. Health. Perspect. 2005; 113:357-361.
(10.) O'Driscoll BR, Hopkinson LC, Denning DW. Mold sensitization is common amongst patients with severe asthma requiring multiple hospital admissions. BMC Pulm Med. 2005; 18: 4.
(11.) Cecchi L, DAmato G, Ayres JG, Galan C, Forastiere F, Forsberg B, Gerritsen J, Nunes C, Behrendt H, Akdis C, Dahl R, Annesi-Maesano I. Projections of the effects of climate change on allergic asthma: the contribution of aerobiology. Allergy 2010; 65:1073-1098.
(12.) Reid CE, Gamble JL. Aeroallergens, Allergic Disease, and Climate Change: Impacts and Adaptation. EcoHealth 2009; 6, 458-470.
(13.) Lacasse Y and Cormier Y Hypersensitivity Pneumonitis. Orphanet Journal of Rare Diseases 2006; 1: 25.
(14.) Lacasse Y, Girard M, Cormier Y. Recent Advances in Hypersensitivity Pneumonitis. Chest 2012; 142(1):208-217.
(15.) Natarajan S, and Subramanian P. Allergic bronchopulmonary aspergillosis: A clinical review of 24 patients: Are we right in frequent serologic monitoring? Annals of Thoracic Medicine 2014; 9:214-220.
(16.) Crameri, R and Blaser K. Eur Respir J Allergy and immunity to fungal infections and colonization. 2002; 19: 151-157.
(17.) Patovirta R-L, Reiman M, Husman T, Haverinen U, Toivola M and Nevalainen A. Mould Specific TgG Antibodies Connected with Sinusitis in Teachers of Mould Damaged School: A Two Year Follow-up Study. Intern. J Occup Med and Environ Health 2003; 16:221-230.
(18.) Rydjord B, Eduard W, Stensby B, Sandven P, Michaelsen TE, and Wiker HG. Antibody Response to Long-term, High-dose Mould-exposed Sawmill Workers. Scand. J of Immunol. 2007;66:711-718.
by: Gordon Siek, PhD, Veronica Kent, BS, Joanne Sherman, MLS [ASCP.sup.cm]
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|Author:||Siek, Gordon; Kent, Veronica; Sherman, Joanne|
|Date:||Sep 1, 2018|
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