Mold Causes Asthma!

Mold Causes Asthma!
Last year, we posted an article with the question, “Does Mold Cause Asthma?
The question was partially answered by a research team in Finland who conducted a study in 2001. They surveyed 10,000 students on the dampness of their homes and questioned how often they developed colds and other respiratory infections. The research concluded that damp homes may cause asthma and was partly conclusive.
Up until now, mold was considered an asthma trigger that could exacerbate the condition and even the Centers for Disease Control and Prevention (CDC) believes there is some link between the onset of asthma and damp buildings.
Basically, all previous studies have found QUALITATIVE or ANECDOTAL associations between mold and asthma, but no clear, definitive cause and effect, i.e. MOLD CAUSES ASTHMA!
Last month, a research team from the University of Cincinnati in the United States published a study in the Journal of Allergy and Clinical Immunology that showed a definite QUANTITATIVE link between mold and asthma.
Tiina Reponen, co-author of the study, said while it is known that mold is a risk factor for asthma, this is the first study that quantitatively measured mold and after adjusting for commonly known risk factors, found an association with asthma. Previously, other studies had shown qualitative or anecdotal associations, she said.
The study evaluated about 300 children between the ages of one and seven. The researchers found that there are three species of mold which are particluarly harmful to children: Aspergillus ochraceus, Aspergillus unguis and Penicillium variabile. These molds, common to water-damaged homes, cause children to develop asthma. Based on this study, an allergist at the Medical College of Wisconsin, Monica Vasudev, believes that expectant mothers and infants should try to avoid living in water-damaged homes.
“It’s proof of common sense that you want to take care of mold in the home. It’s just proving that if you don’t do that, your kids are more likely to develop asthma.” (Gary Steven, an allergist at the Allergy, Asthma & Sinus Center in Milwaukee)
Well stated Mr. Steven!

12 thoughts on “Mold Causes Asthma!

  1. Bharat B Dikshit, Cell.: 91 9376229651 India.

    Dear Sanjayji,
    Very Informative Article. Interested in” Effect of Negative ion air purifiers on
    Molds” other Indoor pollutants.
    Thanks with regards.
    Bharat Dikshit(Scientist/President,APRS,Baroda,India)


    This article, has generated quite a few comments on some of the LinkedIn Groups we shared this article with. Below are some of the comments we received. Thanks so much for feedback and comments.


    This is definitely an interesting study, but the small sample size and questionable outcomes means that there need to be many more like it to really have any valid quantitative link.

    Of 289 children followed, 69 had “chronic lung disease”, including asthma. The study of potential causation of asthma in up to 69 children does not make a valid numerical conclusion unless it is proven to be repeatable in a larger set.

    It also appears that the study utilized a PCR screen of 36 mold species, and identified 3 that were statistically associated with asthma. They did not, however, assess any of the other millions of mold species to identify the statistical association of those species. If the average holds up, and approximately 10% of mold species can be “statistically” and “quantitatively” associated with asthma, then their findings are really not much help to investigators.

    I do not see any information to identify how closely the allergen skin test screens corresponded to the mold species that were tested by PCR. There is significant doubt about the allergen screens, since only 12% (8 children) exhibited allergic response to mold. That leaves a very significant question of the asthma/respiratory illness mechanism in the other 61 children…what causes their symptoms?

    This study is a very, very small incremental step, but I am not going to jump on the bandwagon of “guilt by association” based on statistical evidence garnered from 8 children with mold allergies and asthma, and 61 children with otherwise unexplained asthma, just because PCR samples are statistically analyzed and pointed to as conclusive.

    (Bobby R)


    I strongly suggest that we’re careful – and accurate – about the claims we might make.

    1. This paper does NOT conclude that mold CAUSES asthma. (See Conclusion at the end of the abstract below.)
    2. It’s unfortunate that the ERMI, with all its limitations and inconsistencies, forms the basis of the authors’ conclusions.
    3. The cite to this paper, which is not listed here nor in the Milwaukee Journal-Sentinel article, is:

    Reponen, T., et al (2012) “Infant origins of childhood asthma associated with specific molds”, Journal of Allergy and Clinical Immunology, In-Press Corrected Proof, 12 July 2012 (10.1016/j.jaci.2012.05.030)


    The specific cause or causes of asthma development must be identified to prevent this disease.

    Our hypothesis was that specific mold exposures are associated with childhood asthma development.

    Infants were identified from birth certificates. Dust samples were collected from 289 homes when the infants were 8 months of age. Samples were analyzed for concentrations of 36 molds that comprise the Environmental Relative Moldiness Index (ERMI) and endotoxin, house dust mite, cat, dog, and cockroach allergens. Children were evaluated at age 7 years for asthma based on reported symptoms and objective measures of lung function. Host, environmental exposure, and home characteristics evaluated included a history of parental asthma, race, sex, upper and lower respiratory tract symptoms, season of birth, family income, cigarette smoke exposure, air conditioning, use of a dehumidifier, presence of carpeting, age of home, and visible mold at age 1 year and child’s positive skin prick test response to aeroallergens and molds at age 7 years.

    Asthma was diagnosed in 24% of the children at age 7 years. A statistically significant increase in asthma risk at age 7 years was associated with high ERMI values in the child’s home in infancy (adjusted relative risk for a 10-unit increase in ERMI value, 1.8; 95% CI, 1.5-2.2). The summation of levels of 3 mold species, Aspergillus ochraceus, Aspergillus unguis, and Penicillium variabile, was significantly associated with asthma (adjusted relative risk, 2.2; 95% CI, 1.8-2.7).

    In this birth cohort study exposure during infancy to 3 mold species common to water-damaged buildings was associated with childhood asthma at age 7 years.

    (Wane B.)


    Not quite true. The study showed that when looking at a variety of possible (predicted) allergens in a setting where children are known to be genetically vulnerable the only three allergens that were found to positively correlate with their development of asthma at age 7 were 3 species of fungi detected in samples taken from carpets.

    Most of the asthmatic children showed no allergic reaction to moulds when tested.

    All they really showed was that if those moulds were present in the homes then they were twice as likely to develop asthma. Those moulds might be there and the asthma might occur for the same reason (e.g. damp), so the two are linked, but this is not conclusive evidence that those moulds caused that asthma.

    Damp causes asthma – that is pretty clear using data that is proving to be consistent over several large studies, but why it does we still do not know with confidence.

    This study is another piece of the jigsaw, not the last piece.

    (Graham A.)


    “The researchers found that there are three species of mold which are particluarly harmful to children: Aspergillus ochraceus, Aspergillus unguis and Penicillium variabile. These molds, common to water-damaged homes, cause children to develop asthma.”

    Do peanuts cause children to develop asthma? Do cats? This study seems badly flawed to me. It uses ERMI, the algorithm for which places Alternaria alternata in the denominator. If Alternaria is such a well-known asthmagen, why does it reflect a “safer” environment in the ERMI calculation. This is bad science all around. I see Vesper is a co-author. He promotes ERMI, whether it is a useful tool or not.

    Anyone care to defend this study as being good science?

    (Steven T.)


    The actions are the same as they have been for the last few decades: fix water leaks and clean up mold. I agree with the general comment by Gary Steven, although I would not use the words “proof” or “common sense”. The only thing “common” about common sense is that everyone has their own idea of what it means. I would prefer to say that there is increasing evidence, a common body of knowledge, and standards of practice. The WHO publication on dampness and mold provides ample evidence of increased risk of respiratory illness, and in my opinion this study adds very little, if anything, to that document.

    (Bobby R.)


    I am always skeptical of articles that use the term “cause”. Cause and effect in complex matters like asthma is a very difficult chasm to cross. You have to eliminate all other potential variables and present the subjects with nothing other than that independent variable and look for the change. I can get on board with the idea that it is a contributing factor and may even be a major contributing factor but air pollution, indoor voc’s, genetic predisposition, childhood trauma, illness (that may not even be documented) etc. can all contribute to the overall system reaction creating asthma symptoms.

    (Bill R.)


    Sanjay, in my youth, as a graduate Medical Physics student, my thesis involved a study into the effect of negative air ions on Asthma. The study was conducted on two groups of asthmatics and held under double blind, corssover conditions. That is, neither the asthmatics, nor the medical doctors, supervising the trials knew whether the ionisers being used were real or dummy. The trial was an ABACA and ACABA format, where A represents a lead-in and/or wash-out period, and B represents exposure to an real ioniser and C represents exposure to a dummy ioniser. To be statistically significant, the Placebo effect needs to be taken into consideration. I suggest that in order to determine absolutely whether any type of mold causes asthma, such a double blind crossover trial needs to be done. Naturally, exposing anyone (particularly children) to potential harm has been and always will be avoided at all costs. It makes no sense to intentionally expose anyone to a potential asthma causing agent. That is why it is going to take decades of data collection, patient history review etc before any certainty can be achieved. Even then, much patient history records very subjective information. At least in my investigation, I was able to use the PEFR (Peak Expiratory Flow Rate) as a relatively objective measure of the “patient”‘s condition.

    (David S.)


    The Vesper paper form EPA put out in early 2011 was a 7 years study which, beyond a doubt proved the link between Asthma and mold (old news guys). FYI, less than 2% of all people exposed to mold actually have an invasive fungal infection (IFI). The rest are sick from the secondary metabolites produced from the fungal spore i.e. mycotoxins and beta glucans. In a water damaged structure there are always more than one pathogen, environmental and medical sciences has failed to understand this. The presence of Mycobacteria, Endotoxins, environmental bacteria and other pathogens go unnoticed by our industry day in and day out. People who suffer from these exposures always have a co-exposure (more than one pathogen) involved.

    (Michael P.)


    Michael, I really have to question the basis for these comments. Where does the 2% number come in? What does it actually refer to? If anywhere close to 2% of people exposed to mold got invasive infections, the world would have been rid of humans long ago, since we are exposed to fungal spores “day in and day out”. Even so, I fail to see what infection has to do with this topic, which is about asthma. You seem to focus on poorly understood links of metabolites, and miss the better defined link to allergens.

    The EPA study which you reference, published in 2011 (a year ago) is hardly “old news”. Even so, it still does not attain what this study attempts to do, which is to define a quantitative link. The EPA study was, like other before it, qualitative and putative. Yes, it “proved” a link, but it does not define what that link is, or what causes it, or what the quantitative threshold is for causation.

    I dispute that “environmental and medical sciences” fail to understand multiple pathogens, or leave them unnoticed. What we in our industry fail to do is quantitatively sample for them and prove a scientific link between their presence and the illness of the individual. Of course we fail to do this because there is not an economical way of sampling, or a means of interpretation of these samples because there is no economical way to tie the exposure to the clinical history of the exposed. The closest we have come is testing for allergic reaction to a few dozen species, and testing for the presence of the allergens of those few dozen species. Therefore, I would suggest that, rather than “ignoring” or “not noticing” the presence of other potential pathogens, which may or may not have a causative role, we are working with and developing the best science we have available.

    (Bobby R.)

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