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Mold health issues are potentially harmful effects of molds (US usage; British English "moulds").

Molds are ubiquitous in the biosphere, and mold spores are a common component of household and workplace dust. The vast majority of molds are not hazardous to humans, and reaction to molds can vary between individuals, with relatively minor allergic reactions being the most common.^[1] Nonetheless, the United States Centers for Disease Control and Prevention (CDC) reported in its June 2006 report, 'Mold Prevention Strategies and Possible Health Effects in the Aftermath of Hurricanes and Major Floods,' that "excessive exposure to mold-contaminated materials can cause adverse health effects in susceptible persons regardless of the type of mold or the extent of contamination."^[2] When mold spores are present in abnormally high quantities, they can present especially hazardous health risks to humans after prolonged exposure, including allergic reactions or poisoning by mycotoxins,^[3] or causing fungal infection (mycosis).^[4]

Health effects

Studies have shown that people who are atopic (sensitive), already suffer from allergies, asthma, or compromised immune systems^[5] and occupy damp or moldy buildings are at an increased risk of health problems such as inflammatory and toxic responses to mold spores, metabolites and other components.^[6] The most common health problem is an allergic reaction. Other problems are respiratory and/or immune system responses including respiratory symptoms, respiratory infections, exacerbation of asthma, and rarely hypersensitivity pneumonitis, allergic alveolitis, chronic rhinosinusitis and allergic fungal sinusitis. Severe reactions are rare but possible. A person's reaction to mold depends on their sensitivity and other health conditions, the amount of mold present, length of exposure, and the type of mold or mold products.

Some molds also produce mycotoxins, that can pose serious health risks to humans and animals. The term "toxic mold" refers to molds that produce mycotoxins, such as Stachybotrys chartarum, not to all molds.^[7] Exposure to high levels of mycotoxins can lead to neurological problems and in some cases death.^[8] Prolonged exposure, e.g., daily workplace exposure, can be particularly harmful.

The five most common genera of indoor molds are Cladosporium, Penicillium, Aspergillus, Alternaria, and Trichoderma.

Damp environments which allow mold to grow can also produce bacteria and help release volatile organic compounds.

Symptoms of mold exposure

Symptoms of mold exposure can include:^[9]

Nasal and sinus congestion, runny nose
Respiratory problems, such as wheezing and difficulty breathing, chest tightness
Cough
Throat irritation
Sneezing / Sneezing fits

Health effects linking to asthma

Infants may develop respiratory symptoms as a result of exposure to a specific type of fungal mold, called Penicillium. Signs that an infant may have mold-related respiratory problems include (but are not limited to) a persistent cough and/or wheeze. Increased exposure increases the probability of developing respiratory symptoms during their first year of life. Studies have shown that a correlation exists between the probability of developing asthma and increased exposure to Penicillium. The levels are deemed ‘no mold’ to ‘low level’, from ‘low’ to ‘intermediate’, and from ‘intermediate’ to ‘high’.^[10]

Mold exposures have a variety of health effects depending on the person. Some people are more sensitive to mold than others. Exposure to mold can cause a number of health issues such as; throat irritation, nasal stuffiness, eye irritation, cough and wheezing, as well as skin irritation in some cases. Exposure to mold may also cause heightened sensitivity depending on the time and nature of exposure. People at higher risk for mold allergies are people with chronic lung illnesses, and weak immune systems, which can often result in more severe reactions when exposed to mold.^[11]

There has been sufficient evidence that damp indoor environments are correlated with upper respiratory tract symptoms such as coughing, and wheezing in people with asthma.^[12]

Flood specific mold health effects

Among children and adolescents, the most common health effect post-flooding was lower respiratory tract symptoms, though there was a lack of association with measurements of total fungi.^[13] Another study found that these respiratory symptoms were positively associated with exposure to water damaged homes, exposure included being inside without participating in clean up.^[13] Despite lower respiratory effects among all children, there was a significant difference in health outcomes between children with pre-existing conditions and children without.^[13] Children with pre-existing conditions were at greater risk that can likely be attributed to the greater disruption of care in the face of flooding and natural disaster.^[13]^[14]

Although mold is the primary focus post flooding for residents, the effects of dampness alone must also be considered. According to the Institute of Medicine, there is a significant association between dampness in the home and wheeze, cough, and upper respiratory symptoms.^[15] A later analysis determined that 30% to 50% of asthma-related health outcomes are associated with not only mold, but also dampness in buildings.^[15] Another health effect associated with dampness and mold is Sick Building Syndrome (SBS), which is defined by manifestations of symptomatic illness as a result of poor indoor air quality and pollutant exposures.^[15] Signs of potentially illness-causing buildings include condensation on the windows, high humidity in the bathrooms, a moldy odor, or water leakage.^[16]

While there is a proven correlation between mold exposure and the development of upper and lower respiratory syndromes, there are still fewer incidences of negative health effect than one might expect.^[17] Barbeau and colleagues suggested that studies do not show a greater impact from mold exposure for a number of reasons: 1) the types of health effects are not severe and are therefore not caught; 2) people whose homes have flooded find alternative housing to prevent exposure; 3) self-selection, the healthier people participated in mold clean-up and were less likely to get sick; 4) exposures were time-limited as result of remediation efforts and; 5) the lack of access to health care post-flooding may result in fewer illnesses being discovered and reported for their association with mold.^[17] There are also certain notable scientific limitations in studying the exposure effects of molds on individuals because there are currently no known biomarkers that can prove that a person has been exposed to molds.^[18] Thus, it is currently impossible to prove correlation between mold exposure and symptoms.^[18]

Mold-associated conditions

Health problems associated with high levels of airborne mold spores include^[19]^{[unreliable medical source?]} allergic reactions, asthma episodes, irritations of the eye, nose and throat, sinus congestion, and other respiratory problems, although mold spores won't actually cause asthma, just irritate existing conditions. For example, residents of homes with mold are at an elevated risk for both respiratory infections and bronchitis.^[20] When mold spores are inhaled by an immunocompromised individual, some mold spores may begin to grow on living tissue,^[21] attaching to cells along the respiratory tract and causing further problems.^[22]^[23] Generally, when this occurs, the illness is an epiphenomenon and not the primary pathology. Also, mold may produce mycotoxins, either before or after exposure to humans, potentially causing toxicity.

Fungal infection

A serious health threat from mold exposure for immunocompromised individuals is systemic fungal infection (systemic mycosis). Immunocompromised individuals exposed to high levels of mold, or individuals with chronic exposure may become infected.^[24]^[25] Sinuses and digestive tract infections are most common; lung and skin infections are also possible. Mycotoxins may or may not be produced by the invading mold.

Dermatophytes are the parasitic fungi that cause skin infections such as athlete's foot and tinea cruris. Most dermataphyte fungi take the form of a mold, as opposed to a yeast, with appearance (when cultured) that is similar to other molds.

Opportunistic infection by molds^[26] such as Talaromyces marneffei and Aspergillus fumigatus is a common cause of illness and death among immunocompromised people, including people with AIDS or asthma.^[27]^[28]

Mold-induced hypersensitivity

The most common form of hypersensitivity is caused by the direct exposure to inhaled mold spores that can be dead or alive or hyphal fragments which can lead to allergic asthma or allergic rhinitis.^[29] The most common effects are rhinorrhea (runny nose), watery eyes, coughing and asthma attacks. Another form of hypersensitivity is hypersensitivity pneumonitis. Exposure can occur at home, at work or in other settings.^[29]^[30] It is predicted that about 5% of people have some airway symptoms due to allergic reactions to molds in their lifetimes.^[31]

Hypersensitivity may also be a reaction toward an established fungal infection in allergic bronchopulmonary aspergillosis.

Mycotoxin toxicity

Molds excrete toxic compounds called mycotoxins, secondary metabolites produced by fungi under certain environmental conditions. These environmental conditions affect the production of mycotoxins at the transcription level. Temperature, water activity and pH, strongly influence mycotoxin biosynthesis by increasing the level of transcription within the fungal spore. It has also been found that low levels of fungicides can boost mycotoxin synthesis.^[32]^[33] Certain mycotoxins can be harmful or lethal to humans and animals when exposure is high enough.^[34]^[35]

The common house mold, Trichoderma longibrachiatum, produces small toxic peptides containing amino acids not found in common proteins, like alpha-aminoisobutyric acid, called trilongins (up to 10% w/w). Their toxicity is due to absorption into cells and production of nano-channels that obstruct vital ion channels that ferry potassium and sodium ions across the cell membrane. This affects in the cells action potential profile, as seen in cardiomyocytes, pneumocytes and neurons leading to conduction defects. Trilongins are highly resistant to heat and antimicrobials making primary prevention the only management option.^[36]^[37]^[38]

Extreme exposure to very high levels of mycotoxins can lead to neurological problems and in some cases death; fortunately, such exposures rarely to never occur in normal exposure scenarios, even in residences with serious mold problems.^[39] Prolonged exposure, such as daily workplace exposure, can be particularly harmful.^[40]

It is thought that all molds may produce mycotoxins and thus all molds may be potentially toxic if large enough quantities are ingested, or the human becomes exposed to extreme quantities of mold. Mycotoxins are not produced all the time, but only under specific growing conditions. Mycotoxins are harmful or lethal to humans and animals only when exposure is high enough.^[41]^[42]

Mycotoxins can be found on the mold spore and mold fragments, and therefore they can also be found on the substrate upon which the mold grows. Routes of entry for these insults can include ingestion, dermal exposure, and inhalation.

Some mycotoxins cause immune system responses that vary considerably, depending on the individual. The duration of exposure, the frequency of exposure and the concentration of the insult (exposure) are elements in triggering immune system response.

Aflatoxin is an example of a mycotoxin. It is a cancer-causing poison produced by certain fungi in or on foods and feeds, especially in field corn and peanuts.^[43]

Toxic effects from mold were thought to be the result of exposure to the mycotoxins of some mold species, such as Stachybotrys chartarum. In 1927, Ismailson, a Soviet scientist, noted a form of mycotoxicosis in employees in a binder twine factory.^[44] In the 1940s, "Stachybotryotoxicosis" was identified in Ukraine as a new disease in humans in close contact with moldy hay, including inhalation of the associated dust, which caused, among other symptoms, a "haemorrhagic exúdate".^[45] Following cases of pulmonary hemorrhage in infants in Cleveland, Ohio in 1993–94, several related studies suggested a causal relationship between exposure to S. chartarum and the disease.^[46]^[47]^[48]^[49]^[50]^[51] An anonymous panel from within the CDC revisited the cases and argued that the link was not proven.^[52]^[53]^[54] Subsequent studies with mice and rats exposed to S. chartarum and associated mycotoxins showed that pulmonary hemorrhage could occur, suggesting the link is plausible.^[55]^[56]^[57] The American Academy of Pediatrics also found the link plausible^[58], and subsequent analysis and case studies with humans have further noted the association^[59]^[60]^[61].

Innate Immune Activation

The health hazards produced by mold have been associated with Sick Building Syndrome (SBS), but previously, controversy existed around whether studies had sufficiently demonstrated that normal indoor exposures to these common organisms posed a significant threat.^[62] In 1986, a study noted an airborne outbreak of toxicosis from trichothecenes associated with "Stachybotrys atra" in a Chicago house affecting a family including their maid; symptoms included diarrhea, headaches, fatigue, dermatitis, malaise, and severe leg pains, which resolved following remediation of the mold contamination.^[63] This study drew attention to how mycotoxins in indoor environments might impact health. In the early 2000s, several small studies concluded that individuals with significant dampness and mold exposure displayed cognitive and neurological deficits on par with mild-to-moderate traumatic brain injury along with immunological changes.^[64]^[65]^[66] These studies were criticised for their methodologies, such as by not showing a possible mechanism of action for the harm, and not controlling for the possibility of malingering by mold-exposed individuals involved in litigation, although the associated critiques were also problematic.^[67]^[68]^[69] Researchers also contested whether the amount of spores that could be breathed in by humans would be sufficient to cause a toxic effect and that no association between spore counts and adverse health effects existed.^[70]^[71]^[72] However, when also considering spore fragments (that have more surface area to carry mycotoxins) as well as whole spores, the amount of exposure was estimated to be 1,000x to 1,000,000x higher than previously thought.^[73]^[74] Moreover, inhalational exposure "provides a pathway to the central nervous system along the olfactory and trigeminal nerve axons in the nasal sensory epithelium that bypasses the blood–brain barrier."^[75]

A 2003 paper by the American College of Occupational and Environmental Medicine (ACOEM), which claimed the link between mold and building-related symptoms was "weak and unproven", was published without disclosing conflicts of interest by the authors and to substantial critique of the science.^[76]^[77]^[78] Dr. Harriet Ammann, who authored the chapter on mold toxicity in a relevant book by the Institute of Medicine, notably criticised the methodology used in the ACOEM paper: "They took hypothetical exposure and hypothetical toxicity and jumped to the conclusion there is nothing there."^[79] Her associated review in 2004 did find insufficient evidence of causation at that time but still acknowledged evidence of "potential relationships between mycotoxin exposure and pulmonary hemorrhage, immunosuppression, neurotoxicity, respiratory and dermal responses."^[80]^[81] Similarly, Frederick J. Passman points out another critique: "The Hardin group’s calculations are rendered moot by recent reports of airborne mycotoxins associated with particles substantially smaller than spores".^[82]^[83]^[84] A 2006 position paper by the American Academy of Allergy, Asthma & Immunology (AAAAI) maintained a similarly sceptical position as the ACOEM paper in denying that mold in indoor environments could cause severe effects, but was co-authored by one of the same authors as the 2003 paper and was similarly problematic.^[85]^[86]^[87]^[88]^[89] Julie Rehmeyer, a prominent science writer, recounted this controversy in her book, Through the Shadowlands, noting that it took 12 years for scientists to prevail in making both ACOEM and AAAAI sunset these flawed and misrepresentative position papers, with the ACOEM paper now marked as "CONTENT NOT FOR REUSE".^[90]^[91]^[92] Despite this, both papers are still being referenced as of 2020 in support of the notion that adverse health effects from mold and dampness are limited mostly to respiratory and dermatological effects.^[93]^[94]

Regardless, studies are suggesting that the so-called "toxic effects" are actually the result of chronic activation of the immune system, leading to chronic inflammation.^[95]^[96]^[97]^[98] In 2008, the United States Government Accountability Office published a report on indoor mold, reviewing the literature to date and acknowledging the possibility of immune and toxic effects, while calling for further research.^[99] By 2009, the WHO noted a strong association between dampness and inflammatory responses, while also recognising that "synergistic interactions among microbial agents" might make it "difficult to detect and implicate specific exposures in the causation of damp building-associated adverse health effects."^[100] Gram-negative bacteria, which create endotoxins known to produce inflammatory responses, might also be partly responsible, as might actinomycetes and their associated exotoxins.^[101]^[102] A ten-year longitudinal study also found that dampness and mold seemed to be an underlying cause of sick-building syndrome.^[103] A 2018 review of 16 associated studies found that people exposed to molds and mycotoxins had "symptoms affecting multiple organs, including the lungs, musculoskeletal system, as well as the central and peripheral nervous systems" and also noted that such exposure has now been implicated in the pathogenesis of autism-spectrum disorder.^[104] An in vitro study of human neurological system cells showed damage caused by inflammatory and immune processes (along with disruption of the blood-brain barrier) in response to mycotoxins at exposure levels that would be expected in water-damaged buildings.^[105] Ex vivo studies of human peripheral blood mononuclear cells showed inflammatory and innate immune responses upon exposure to specific molds and mycotoxins, such as S. chartarum (and an associated mycotoxin, Satratoxin G) and various strains of Aspergillus.^[106]^[107] Studies exposing mice to controlled doses of S. chartarum spores similarly show activation of the innate immune system, along with neural, cognitive, and emotional dysfunction, even when the spores are denatured of their mycotoxins.^[108]^[109] As well, several studies have now shown cognitive deficits, immune activation, and behavioral dysregulation in humans.^[110]^[111]^[112] Furthermore, children living in water-damaged homes show systemic inflammation, immune activation, and probably poorer cognitive function, too.^[113]^[114]^[115] Tellingly, the affected biomarkers, hormones, and pathways in individuals affected by inhaled mycotoxins are consistent with studies of ingested mycotoxins, such as trichothecene exposure.^[116]^[117] Two studies using volumetric MRIs have suggested that affected individuals display structural changes in the brain, associated with the forebrain parenchymal, cortical gray matter, pallidum volumes, and the caudate nucleus.^[118]^[119] Correlating to this, Dale Bredesen, a neurodegenerative researcher, has noted a subtype of Alzheimer's Disease associated with this chronic inflammatory response, calling it an "unrecognized—and treatable—epidemic".^[120]^[121] Arnold R. Eiser, Professor Emeritus of Medicine at Drexel University College of Medicine, has suggested that environmental factors such as dampness and mold may be a contributing factor for why Finland has the highest death rate from dementia in the world.^[122]

The WHO estimates the prevalence of significant dampness and mold in buildings to be at least 20%, while other estimates of US homes suggest a prevalence as high as 47%.^[123]^[124] Preliminary research suggests that around 25% of the population have HLA DR/DQ genes associated with a poor antigen response to biotoxins, which can result in a chronic inflammatory response, but it is unknown how many actually experience such symptoms due to frequent misdiagnosis.^[125] Sleeping disorders are also associated with exposure to dampness and mold, consistent with the decrease in α-melanocyte stimulating hormone (α-MSH) associated with this syndrome.^[126]^[127] Patients may also present with psychological symptoms given the neuroinflammatory markers involved.^[128]^[129]^[130] However, correction of the underlying neuroinflammation can correct psychological symptoms, whereas the referral of patients suffering an autoimmune disorder strictly into psychological therapies is unlikely to result in improvement.^[131]^[132]

Recognition of research in this area has been poor, in part due to the aforementioned scientific controversy, along with highly variable and sometimes non-specific nomenclatures such as: Mold Illness, Mycotoxicosis, Mixed Mold Mycotoxicosis (MMT), Indoor Mold Sensitivity, Sick Building Syndrome (SBS), Damp Building-Related Illnesses (DBRI), Biotoxin-Related Illnesses, Toxic Mold Syndrome, Toxiciant-Induced Loss of Tolerance (TILT), Chronic Inflammatory Response Syndome (CIRS), and Dampness and Mold Hypersensitivity Syndrome (DMHS).^[133] Related syndromes likely include Byssinosis^[134]^[135], Pfiesteria-associated human illness^[136]^[137], and Chronic Ciguatera^[138]^[139], given the related biotoxin exposure, genetic susceptibility as per HLA DR/DQ genes, and similar immunological and inflammatory responses.

Exposure sources and prevention

The main sources of mold exposure are from the indoor air in buildings with substantial mold growth, and from ingestion of food with mold growths.

Air

Prevention of mold exposure and its ensuing health issues begins with prevention of mold growth in the first place by avoiding a mold-supporting environment such as humid air. Extensive flooding and water damage can support extensive mold growth. Following hurricanes, homes with greater flood damage, especially those with more than 3 feet (0.91 m) of indoor flooding, demonstrated higher levels of mold growth compared with homes with little or no flooding.^[140]^[141] The aftermath of a hurricane is the worst-case scenario, but the concept of water damage supporting widespread mold growth is more generally applicable.

It is useful to perform an assessment of the location and extent of the mold hazard in a structure. Various practices of remediation can be followed to mitigate mold issues in buildings, the most important of which is to reduce moisture levels.^[142] Removal of affected materials after the source of moisture has been reduced and/or eliminated may be necessary.^[143] Thus, the concept of mold growth, assessment, and remediation is essential in prevention of mold health issues.

A common issue with mold hazards in the household is the placement of furniture, and the lack of ventilation which this causes to certain parts of the wall. The simplest method of avoiding mold in a home so affected is to move the furniture in question.

Adverse respiratory health effects are associated with occupancy in buildings with moisture and mold damage.^[144]

Molds may excrete liquids or low-volatility gases, but the concentrations are so low that frequently they cannot be detected even with sensitive analytical sampling techniques. Sometimes, these by-products are detectable by odor, in which case they are referred to as "ergonomic odors", meaning the odors are detectable, but do not indicate toxicologically significant exposures.

Food

Molds that are often found on meat and poultry include members of the genera Alternaria, Aspergillus, Botrytis, Cladosporium, Fusarium, Geotrichum, Mortierella, Mucor, Neurospora, Paecilomyces, Penicillium, and Rhizopus.^[145] Grain crops in particular incur considerable losses both in field and storage due to pathogens, post-harvest spoilage, and insect damage. A number of common microfungi are important agents of post-harvest spoilage, notably members of the genera Aspergillus, Fusarium, and Penicillium.^[145] A number of these produce mycotoxins (soluble, non-volatile toxins produced by a range of microfungi that demonstrate specific and potent toxic properties on human and animal cells^[146]) that can render foods unfit for consumption. When ingested, inhaled, or absorbed through skin, mycotoxins may cause or contribute to a range of effects from reduced appetite and general malaise to acute illness or death in rare cases.^[147]^[148]^[149] Mycotoxins may also contribute to cancer. Dietary exposure to the mycotoxin aflatoxin B1, commonly produced by growth of the fungus Aspergillus flavus on improperly stored ground nuts in many areas of the developing world, is known to independently (and synergistically with Hepatitis B virus) induce liver cancer.^[150] Mycotoxin-contaminated grain and other food products have a significant impact on human and animal health globally. According to the World Health Organization, roughly 25% of the world's food may be contaminated by mycotoxins.^[147]

Prevention of mold exposure from food is generally to consume food that has no mold growths on it.^[43] Also, mold growth in the first place can be prevented by the same concept of mold growth, assessment, and remediation that prevents air exposure. In addition, it is especially useful to clean the inside of the refrigerator, and to ensure dishcloths, towels, sponges, and mops are clean.^[43]

Ruminants are considered to have increased resistance to some mycotoxins, presumably due to the superior mycotoxin-degrading capabilities of their gut microbiota.^[147] The passage of mycotoxins through the food chain may also have important consequences on human health.^[151] For example, in China in December 2011, high levels of carcinogen aflatoxin M1 in Mengniu brand milk were found to be associated with the consumption of mold-contaminated feed by dairy cattle.^[152]

Bed

Over 47 species have been identified in pillows.^[153]

Flooding

Flooding in houses causes a unique opportunity for mold growth which may be attributed to adverse health effects in people exposed to the mold, especially children and adolescents. In a study on the health effects of mold exposure after hurricanes Katrina and Rita, the predominant types of mold were Aspergillus, Penicillum, and Cladosporium with indoor spore counts ranging from 6,142 – 735,123 spores m⁻³.^[17] Molds isolated following flooding were different from mold previously reported for non-water damaged homes in the area.^[17] Further research found that homes with greater than three feet of indoor flooding demonstrated significantly higher levels of mold than those with little or no flooding.^[17]

Mitigation

Recommended strategies to prevent mold include: avoiding mold-contamination; utilization of environmental controls; the use of personal protective equipment (PPE), including skin and eye protection and respiratory protection; and environmental controls such as ventilation and suppression of dust.^[154] When mold cannot be prevented, the CDC recommends clean-up protocol including first taking emergency action to stop water intrusion.^[154] Second, they recommend determining the extent of water damage and mold contamination. And third, they recommend planning remediation activities such as establishing containment and protection for workers and occupants; eliminating water or moisture sources if possible; decontaminating or removing damaged materials and drying any wet materials; evaluating whether the space has been successfully remediated; and reassembling the space to control sources of moisture.^[154]

History

In the 1930s, mold was identified as the cause behind the mysterious deaths of farm animals in Russia and other countries. Stachybotrys chartarum was found growing on wet grain used for animal feed. Illness and death also occurred in humans when starving peasants ate large quantities of rotten food grains and cereals that were heavily overgrown with the Stachybotrys mold.^[155]

In the 1970s, building construction techniques changed in response to changing economic realities including the energy crisis. As a result, homes and buildings became more airtight. Also, cheaper materials such as drywall came into common use. The newer building materials reduced the drying potential of the structures making moisture problems more prevalent. This combination of increased moisture and suitable substrates contributed to increased mold growth inside buildings.^[156]

In April 2015, a tree fell on the home of Lucy Wicks, a Federal Liberal MP of Australia, causing water damage. Afterwards, she fell ill with neurological symptoms, environmental sensitivity, and fatigue, and was eventually diagnosed with Chronic Inflammatory Response Syndrome (CIRS) (see Innate Immune Activation).^[157]^[158] This led to a Federal Inquiry into Biotoxin-related Illnesses in 2018.^[159]^[160] The Australian Government's Department of Health are yet to respond to or implement any of the recommendations made in the subsequent report.^[161]^[162] However, the National Construction Code was updated in 2019 to implement higher standards regarding condensation management in building design.^[163]^[164]^[165]

Today, the US Food and Drug Administration and the agriculture industry closely monitor mold and mycotoxin levels in grains and foodstuffs in order to keep the contamination of animal feed and human food supplies below specific levels. In 2005 Diamond Pet Foods, a US pet food manufacturer, experienced a significant rise in the number of corn shipments containing elevated levels of aflatoxin. This mold toxin eventually made it into the pet food supply, and dozens of dogs and cats died before the company was forced to recall affected products.^[166]^[167]

Litigation

In 2002, the U.S. International Trade Commission reported that according to one estimate, US insurers paid over $3 billion in mold-related lawsuits, more than double the previous year's total.^[168] According to the Insurance Information Institute, in 2003 there were over 10,000 mold-related lawsuits pending in US state courts.^[169] Most were filed in states with high humidity, but suits were on the rise in other states as well.^[169] By 2004, many mold litigation settlements were for amounts well past $100,000.^[170] In 2005, the U.S. International Trade Commission reported that toxic mold showed signs of being the "new asbestos" in terms of claims paid.^[168] In 2012, a key appellate court in Manhattan found a consensus in the scientific literature for a causal relationship between the presence of mold and resultant illness.^[171]

In 1999, an Austin, Texas, woman was awarded $32 million when she sued her insurer over mold damage in her 22-room mansion.^[170]

In 2001, a jury awarded a couple and their eight-year-old son $2.7 million, plus attorney’s fees and costs, in a toxic mold-related personal injury lawsuit against the owners and managers of their apartment in Sacramento, California.^[172]

In 2003, The Tonight Show co-host Ed McMahon received $7.2 million from insurers and others to settle his lawsuit alleging that toxic mold in his Beverly Hills home made him and his wife ill and killed their dog.^[173] That same year environmental activist Erin Brockovich received settlements of $430,000 from two parties and an undisclosed amount from a third party to settle her lawsuit alleging toxic mold in her Agoura Hills, California, home.^[174]

In 2006, a Manhattan Beach, California family received a $22.6 million settlement in a toxic mold case.^[175] The family had asserted that moldy lumber had caused severe medical problems in their child.^[175] That same year, Hilton Hotels received $25 million in settlement of its lawsuit over mold growth in the Hilton Hawaiian Village's Kalia Tower.^[176]

In 2010, a jury awarded $1.2 million in damages in a lawsuit against a landlord for neglecting to repair a mold-infested house in Laguna Beach, California.^[177] The lawsuit asserted that a child in the home suffered from severe respiratory problems for several years as a result of the mold.^[177]

In 2011, in North Pocono, Pennsylvania, a jury awarded two homeowners $4.3 million in a toxic mold verdict.^[178]

Policy

While there is a national policy regarding mold, each state is responsible for independently creating and administering their own policy. For example, following Hurricane Harvey, the governor of Texas sought to expand the emergency response to allow mold remediation companies to come from out of state.^[179]

References

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^ Gent JF, Ren P, Belanger K, Triche E, Bracken MB, Holford TR, Leaderer BP (December 2002). "Levels of household mold associated with respiratory symptoms in the first year of life in a cohort at risk for asthma". Environmental Health Perspectives. 110 (12): A781-6. doi:10.1289/ehp.021100781. PMC 1241132. PMID 12460818.
^ "Best Air Purifiers for Mold and Mildew Removal Reviews UPDATED OCT 2019!". www.freshairguide.com. Retrieved 2019-11-19.
^ Cohen, Aaron. "WHO Guidelines for Indoor Air Quality: Dampness and Mould" (PDF). World Health Organization. Retrieved November 18, 2011. {{cite web}}: Unknown parameter |name-list-format= ignored (|name-list-style= suggested) (help)
^ ^a ^b ^c ^d Rabito FA, Iqbal S, Kiernan MP, Holt E, Chew GL (March 2008). "Children's respiratory health and mold levels in New Orleans after Katrina: a preliminary look". The Journal of Allergy and Clinical Immunology. 121 (3): 622–5. doi:10.1016/j.jaci.2007.11.022. PMID 18179814.
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External links

CDC.gov Mold
US EPA: Mold Information — U.S. Environmental Protection Agency
US EPA: EPA Publication #402-K-02-003 "A Brief Guide to Mold, Moisture, and Your Home"
NIBS: Whole Building Design Guide: Air Decontamination
NPIC: Mold Pest Control Information — National Pesticide Information Center
Mycotoxins in grains and the food supply:
- indianacrop.org
- cropwatch.unl.edu
- agbiopubs.sdstate.edu (PDF)

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[135] Middleton, D; Logan, J S; Magennis, B P; Nelson, S D (1979-05-01). "HLA antigen frequencies in flax byssinosis patients". Occupational and Environmental Medicine. 36 (2): 123–126. doi:10.1136/oem.36.2.123. ISSN 1351-0711.

[136] Grattan, Lynn M; Oldach, David; Perl, Trish M; Lowitt, Mark H; Matuszak, Diane L; Dickson, Curtis; Parrott, Colleen; Shoemaker, Ritchie C; Kauffman, C Lisa; Wasserman, Martin P; Hebel, J Richard (1998-08-15). "Learning and memory difficulties after environmental exposure to waterways containing toxin-producing Pfiesteria or Pfiesteria-like dinoflagellates". The Lancet. 352 (9127): 532–539. doi:10.1016/S0140-6736(98)02132-1. ISSN 0140-6736.

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[139] Shoemaker, Ritchie C.; House, Dennis; Ryan, James C. (2010). "Defining the neurotoxin derived illness chronic ciguatera using markers of chronic systemic inflammatory disturbances: A case/control study". Neurotoxicology and Teratology. 32 (6): 633–639. doi:10.1016/j.ntt.2010.05.007. ISSN 0892-0362.

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[141] Shoemaker RC, House DE (2006). "Sick building syndrome (SBS) and exposure to water-damaged buildings: time series study, clinical trial and mechanisms". Neurotoxicology and Teratology. 28 (5): 573–88. doi:10.1016/j.ntt.2006.07.003. PMID 17010568.

[control-142] Kumar, Manisha; Verma, Rajesh K (September 2010). "Fungi diversity, their effects on building materials, occupants and control– a brief review". Journal of Scientific and Industrial Research. 69 (9): 657–661. ISSN 0975-1084. {{cite journal}}: Unknown parameter |name-list-format= ignored (|name-list-style= suggested) (help)

[143] Wilson SC, Holder WH, Easterwood KV, et al. (2004). Identification, remediation, and monitoring processes used in a mold-contaminated high school. Advances in Applied Microbiology. Vol. 55. pp. 409–23. doi:10.1016/S0065-2164(04)55016-5. ISBN 9780120026579. PMID 15350804. {{cite book}}: |journal= ignored (help)

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[foodborne_fungi-145] Samson RA, Hoekstra ES, Frisvad JC (2000). Introduction to food- and airborne fungi (6., rev. ed.). Utrecht, The Netherlands: Centraalbureau voor Schimmelcultures. ISBN 978-9070351427.

[146] Kankolongo M, Hell K, Nawa I (June 2009). "Assessment for fungal, mycotoxin and insect spoilage in maize stored for human consumption in Zambia". J. Sci. Food Agric. 89 (8): 1366–75. doi:10.1002/jsfa.3596.

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[148] Reddy K, Salleh B, Saad B, Abbas H, Abel C, Shier W (2010). "An overview of mycotoxin contamination in foods and its implications for human health". Toxin Reviews. 29 (1): 3–26. doi:10.3109/15569541003598553.

[149] He J, Zhou T (June 2010). "Patented techniques for detoxification of mycotoxins in feeds and food matrices". Recent Patents on Food, Nutrition & Agriculture. 2 (2): 96–104. doi:10.2174/1876142911002020096. PMID 20653554.

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@@ Line 73: / Line 73: @@
 === Innate Immune Activation ===
-The health hazards produced by mold have been associated with [[sick building syndrome|Sick Building Syndrome]], but previously, controversy existed around whether studies had sufficiently demonstrated that normal indoor exposures to these common organisms posed a significant threat.<ref>{{cite journal | vauthors = Weinhold B | title = A spreading concern: inhalational health effects of mold | journal = Environmental Health Perspectives | volume = 115 | issue = 6 | pages = A300-5 | date = June 2007 | pmid = 17589582 | pmc = 1892134 | doi = 10.1289/ehp.115-a300 }}</ref> In 1986, a study noted an airborne outbreak of toxicosis from [[Trichothecene|trichothecenes]] associated with [[Stachybotrys chartarum|"Stachybotrys atra"]] in a Chicago house affecting a family including their maid; symptoms included diarrhea, headaches, fatigue, dermatitis, malaise, and severe leg pains, which resolved following remediation of the mold contamination.<ref>{{Cite journal|last=Croft|first=William A.|last2=Jarvis|first2=Bruce B.|last3=Yatawara|first3=C. S.|date=1986|title=Airborne outbreak of trichothecene toxicosis|url=http://www.sciencedirect.com/science/article/pii/000469818690096X|journal=Atmospheric Environment (1967)|language=en|volume=20|issue=3|pages=549–552|doi=10.1016/0004-6981(86)90096-X|issn=0004-6981|via=}}</ref> This study drew attention to how mycotoxins in indoor environments might impact health. In the early 2000s, several small studies concluded that individuals with significant dampness and mold exposure displayed cognitive and neurological deficits on par with mild-to-moderate traumatic brain injury along with immunological changes.<ref>{{cite journal|vauthors=Baldo JV, Ahmad L, Ruff R|date=2002|title=Neuropsychological performance of patients following mold exposure|journal=Applied Neuropsychology|volume=9|issue=4|pages=193–202|doi=10.1207/s15324826an0904_1|pmid=12584073|s2cid=22966117}}</ref><ref>{{cite journal|vauthors=Crago BR, Gray MR, Nelson LA, Davis M, Arnold L, Thrasher JD|date=August 2003|title=Psychological, neuropsychological, and electrocortical effects of mixed mold exposure|journal=Archives of Environmental Health|volume=58|issue=8|pages=452–63|doi=10.3200/aeoh.58.8.452-463|pmid=15259424|s2cid=13957522}}</ref><ref>{{cite journal|vauthors=Gray MR, Thrasher JD, Crago R, Madison RA, Arnold L, Campbell AW, Vojdani A|date=July 2003|title=Mixed mold mycotoxicosis: immunological changes in humans following exposure in water-damaged buildings|journal=Archives of Environmental Health|volume=58|issue=7|pages=410–20|doi=10.1080/00039896.2003.11879142|pmid=15143854|s2cid=9653550}}</ref> These studies were criticised for their methodologies, such as by not showing a possible mechanism of action for the harm, and not controlling for the possibility of malingering by mold-exposed individuals involved in litigation, although the associated critiques were also problematic.<ref>{{cite journal|vauthors=Fox DD, Greiffenstein MF, Lees-Haley PR|date=2005|title=Commentary on cognitive impairment with toxigenic fungal exposure|journal=Applied Neuropsychology|volume=12|issue=3|pages=129–33|doi=10.1207/s15324826an1203_1|pmid=16131338|s2cid=28445744}}</ref><ref>{{cite journal|vauthors=McCaffrey RJ, Yantz CL|date=2005|title="Cognitive impairment associated with toxigenic fungal exposure": a critique and critical analysis|journal=Applied Neuropsychology|volume=12|issue=3|pages=134–7|doi=10.1207/s15324826an1203_2|pmid=16131339|s2cid=38601840}}</ref><ref>{{cite journal|vauthors=Gordon WA, Cantor JB, Spielman L, Ashman TA, Johanning E|date=2006|title=Cognitive impairment associated with toxigenic fungal exposure: a response to two critiques|journal=Applied Neuropsychology|volume=13|issue=4|pages=251–7|doi=10.1207/s15324826an1304_6|pmid=17362145|s2cid=20541284}}</ref> Researchers also contested whether the amount of spores that could be breathed in by humans would be sufficient to cause a toxic effect and that no association between spore counts and adverse health effects existed.<ref>{{Cite journal| vauthors = Nevalainen A, Pasanen AL, Niininen M, Reponen T, Kalliokoski P, Jantunen MJ |date=1991-01-01|title=The indoor air quality in Finnish homes with mold problems |journal=Environment International|series=Healthy Buildings|language=en|volume=17|issue=4|pages=299–302|doi=10.1016/0160-4120(91)90015-I|issn=0160-4120}}</ref><ref>{{cite journal | vauthors = Garrett MH, Rayment PR, Hooper MA, Abramson MJ, Hooper BM | title = Indoor airborne fungal spores, house dampness and associations with environmental factors and respiratory health in children | journal = Clinical and Experimental Allergy | volume = 28 | issue = 4 | pages = 459–67 | date = April 1998 | pmid = 9641573 | doi = 10.1046/j.1365-2222.1998.00255.x }}</ref><ref>{{cite journal | vauthors = Strachan DP, Flannigan B, McCabe EM, McGarry F | title = Quantification of airborne moulds in the homes of children with and without wheeze | journal = Thorax | volume = 45 | issue = 5 | pages = 382–7 | date = May 1990 | pmid = 2382244 | doi = 10.1136/thx.45.5.382 | pmc = 462482 }}</ref> However, when also considering spore fragments (that have more surface area to carry mycotoxins) as well as whole spores, the amount of exposure was estimated to be 1,000x to 1,000,000x higher than previously thought.<ref>{{cite journal | vauthors = Reponen T, Seo SC, Grimsley F, Lee T, Crawford C, Grinshpun SA | title = Fungal Fragments in Moldy Houses: A Field Study in Homes in New Orleans and Southern Ohio | journal = Atmospheric Environment | volume = 41 | issue = 37 | pages = 8140–8149 | date = December 2007 | pmid = 19050738 | doi = 10.1016/j.atmosenv.2007.06.027 | pmc = 2153459 | bibcode = 2007AtmEn..41.8140R }}</ref><ref>{{cite journal | vauthors = Nevalainen A, Täubel M, Hyvärinen A | title = Indoor fungi: companions and contaminants | journal = Indoor Air | volume = 25 | issue = 2 | pages = 125–56 | date = April 2015 | pmid = 25601374 | doi = 10.1111/ina.12182 }}</ref>
+The health hazards produced by mold have been associated with [[sick building syndrome|Sick Building Syndrome]] (SBS), but previously, controversy existed around whether studies had sufficiently demonstrated that normal indoor exposures to these common organisms posed a significant threat.<ref>{{cite journal | vauthors = Weinhold B | title = A spreading concern: inhalational health effects of mold | journal = Environmental Health Perspectives | volume = 115 | issue = 6 | pages = A300-5 | date = June 2007 | pmid = 17589582 | pmc = 1892134 | doi = 10.1289/ehp.115-a300 }}</ref> In 1986, a study noted an airborne outbreak of toxicosis from [[Trichothecene|trichothecenes]] associated with [[Stachybotrys chartarum|"Stachybotrys atra"]] in a Chicago house affecting a family including their maid; symptoms included diarrhea, headaches, fatigue, dermatitis, malaise, and severe leg pains, which resolved following remediation of the mold contamination.<ref>{{Cite journal|last=Croft|first=William A.|last2=Jarvis|first2=Bruce B.|last3=Yatawara|first3=C. S.|date=1986|title=Airborne outbreak of trichothecene toxicosis|url=http://www.sciencedirect.com/science/article/pii/000469818690096X|journal=Atmospheric Environment (1967)|language=en|volume=20|issue=3|pages=549–552|doi=10.1016/0004-6981(86)90096-X|issn=0004-6981|via=}}</ref> This study drew attention to how mycotoxins in indoor environments might impact health. In the early 2000s, several small studies concluded that individuals with significant dampness and mold exposure displayed cognitive and neurological deficits on par with mild-to-moderate traumatic brain injury along with immunological changes.<ref>{{cite journal|vauthors=Baldo JV, Ahmad L, Ruff R|date=2002|title=Neuropsychological performance of patients following mold exposure|journal=Applied Neuropsychology|volume=9|issue=4|pages=193–202|doi=10.1207/s15324826an0904_1|pmid=12584073|s2cid=22966117}}</ref><ref>{{cite journal|vauthors=Crago BR, Gray MR, Nelson LA, Davis M, Arnold L, Thrasher JD|date=August 2003|title=Psychological, neuropsychological, and electrocortical effects of mixed mold exposure|journal=Archives of Environmental Health|volume=58|issue=8|pages=452–63|doi=10.3200/aeoh.58.8.452-463|pmid=15259424|s2cid=13957522}}</ref><ref>{{cite journal|vauthors=Gray MR, Thrasher JD, Crago R, Madison RA, Arnold L, Campbell AW, Vojdani A|date=July 2003|title=Mixed mold mycotoxicosis: immunological changes in humans following exposure in water-damaged buildings|journal=Archives of Environmental Health|volume=58|issue=7|pages=410–20|doi=10.1080/00039896.2003.11879142|pmid=15143854|s2cid=9653550}}</ref> These studies were criticised for their methodologies, such as by not showing a possible mechanism of action for the harm, and not controlling for the possibility of malingering by mold-exposed individuals involved in litigation, although the associated critiques were also problematic.<ref>{{cite journal|vauthors=Fox DD, Greiffenstein MF, Lees-Haley PR|date=2005|title=Commentary on cognitive impairment with toxigenic fungal exposure|journal=Applied Neuropsychology|volume=12|issue=3|pages=129–33|doi=10.1207/s15324826an1203_1|pmid=16131338|s2cid=28445744}}</ref><ref>{{cite journal|vauthors=McCaffrey RJ, Yantz CL|date=2005|title="Cognitive impairment associated with toxigenic fungal exposure": a critique and critical analysis|journal=Applied Neuropsychology|volume=12|issue=3|pages=134–7|doi=10.1207/s15324826an1203_2|pmid=16131339|s2cid=38601840}}</ref><ref>{{cite journal|vauthors=Gordon WA, Cantor JB, Spielman L, Ashman TA, Johanning E|date=2006|title=Cognitive impairment associated with toxigenic fungal exposure: a response to two critiques|journal=Applied Neuropsychology|volume=13|issue=4|pages=251–7|doi=10.1207/s15324826an1304_6|pmid=17362145|s2cid=20541284}}</ref> Researchers also contested whether the amount of spores that could be breathed in by humans would be sufficient to cause a toxic effect and that no association between spore counts and adverse health effects existed.<ref>{{Cite journal| vauthors = Nevalainen A, Pasanen AL, Niininen M, Reponen T, Kalliokoski P, Jantunen MJ |date=1991-01-01|title=The indoor air quality in Finnish homes with mold problems |journal=Environment International|series=Healthy Buildings|language=en|volume=17|issue=4|pages=299–302|doi=10.1016/0160-4120(91)90015-I|issn=0160-4120}}</ref><ref>{{cite journal | vauthors = Garrett MH, Rayment PR, Hooper MA, Abramson MJ, Hooper BM | title = Indoor airborne fungal spores, house dampness and associations with environmental factors and respiratory health in children | journal = Clinical and Experimental Allergy | volume = 28 | issue = 4 | pages = 459–67 | date = April 1998 | pmid = 9641573 | doi = 10.1046/j.1365-2222.1998.00255.x }}</ref><ref>{{cite journal | vauthors = Strachan DP, Flannigan B, McCabe EM, McGarry F | title = Quantification of airborne moulds in the homes of children with and without wheeze | journal = Thorax | volume = 45 | issue = 5 | pages = 382–7 | date = May 1990 | pmid = 2382244 | doi = 10.1136/thx.45.5.382 | pmc = 462482 }}</ref> However, when also considering spore fragments (that have more surface area to carry mycotoxins) as well as whole spores, the amount of exposure was estimated to be 1,000x to 1,000,000x higher than previously thought.<ref>{{cite journal | vauthors = Reponen T, Seo SC, Grimsley F, Lee T, Crawford C, Grinshpun SA | title = Fungal Fragments in Moldy Houses: A Field Study in Homes in New Orleans and Southern Ohio | journal = Atmospheric Environment | volume = 41 | issue = 37 | pages = 8140–8149 | date = December 2007 | pmid = 19050738 | doi = 10.1016/j.atmosenv.2007.06.027 | pmc = 2153459 | bibcode = 2007AtmEn..41.8140R }}</ref><ref>{{cite journal | vauthors = Nevalainen A, Täubel M, Hyvärinen A | title = Indoor fungi: companions and contaminants | journal = Indoor Air | volume = 25 | issue = 2 | pages = 125–56 | date = April 2015 | pmid = 25601374 | doi = 10.1111/ina.12182 }}</ref> Moreover, inhalational exposure "provides a pathway to the central nervous system along the olfactory and trigeminal nerve axons in the nasal sensory epithelium that bypasses the blood–brain barrier."<ref>{{Citation|last=Ammann|first=Harriet M.|title=Inhalation Exposure and Toxic Effects of Mycotoxins|date=2016|url=https://doi.org/10.1007/978-3-319-29137-6_20|work=Biology of Microfungi|pages=495–523|editor-last=Li|editor-first=De-Wei|series=Fungal Biology|place=Cham|publisher=Springer International Publishing|language=en|doi=10.1007/978-3-319-29137-6_20|isbn=978-3-319-29137-6|access-date=2020-08-31}}</ref>
-A 2003 paper by the [[American College of Occupational and Environmental Medicine]] (ACOEM), which claimed the link between mold and building-related symptoms was "weak and unproven", was published without disclosing conflicts of interest by the authors and to substantial critique of the science.<ref>{{Cite journal|last=Hardin|first=Bryan D.|last2=Kelman|first2=Bruce J.|last3=Saxon|first3=Andrew|date=2003|title=Adverse human health effects associated with molds in the indoor environment|url=https://pubmed.ncbi.nlm.nih.gov/12762072/|journal=Journal of Occupational and Environmental Medicine|volume=45|issue=5|pages=470–478|doi=10.1097/00043764-200305000-00006|issn=1076-2752|pmid=12762072|via=}}</ref><ref>{{Cite journal|last=Craner|first=James|date=2008-10-01|title=A Critique of the ACOEM Statement on Mold: Undisclosed Conflicts of Interest in the Creation of an “Evidence-Based” Statement|url=https://doi.org/10.1179/oeh.2008.14.4.283|journal=International Journal of Occupational and Environmental Health|volume=14|issue=4|pages=283–298|doi=10.1179/oeh.2008.14.4.283|issn=1077-3525|pmid=19043916}}</ref><ref>{{Cite journal|last=Ladou|first=Joseph|last2=Teitelbaum|first2=Daniel T.|last3=Egilman|first3=David S.|last4=Frank|first4=Arthur L.|last5=Kramer|first5=Sharon N.|last6=Huff|first6=James|date=2007-10-01|title=American College of Occupational and Environmental Medicine (ACOEM): A Professional Association in Service to Industry|url=https://doi.org/10.1179/oeh.2007.13.4.404|journal=International Journal of Occupational and Environmental Health|volume=13|issue=4|pages=404–426|doi=10.1179/oeh.2007.13.4.404|issn=1077-3525|pmid=18085054}}</ref> Dr. Harriet Ammann, who authored the chapter on mold toxicity in a relevant book by the Institute of Medicine, notably criticised the methodology used in the ACOEM paper: "They took hypothetical exposure and hypothetical toxicity and jumped to the conclusion there is nothing there."<ref>{{Cite news|last=Armstrong|first=David|date=2007-01-10|title=Amid Suits Over Mold, Experts Wear Two Hats|language=en-US|work=Wall Street Journal|url=https://www.wsj.com/articles/SB116831654647871083|access-date=2020-08-26|issn=0099-9660}}</ref><ref>{{Cite book|last=Institute of Medicine (États-Unis). Committee on Damp Indoor Spaces and Health.|url=http://worldcat.org/oclc/1015583620|title=Damp indoor spaces and health.|date=2004|publisher=National academies Press|isbn=0-309-09193-4|oclc=1015583620}}</ref> Similarly, Frederick J. Passman points out another critique: "The Hardin group’s calculations are rendered moot by recent reports of airborne mycotoxins associated with particles substantially smaller than spores".<ref>{{Cite journal|last=Ph.D|first=Frederick J. Passman|date=2008-01-28|title=Metalworking Fluid Microbes—What We Need to Know to Successfully Understand Cause-and-Effect Relationships|url=https://doi.org/10.1080/10402000701691720|journal=Tribology Transactions|volume=51|issue=1|pages=107–117|doi=10.1080/10402000701691720|issn=1040-2004}}</ref><ref>{{Cite journal|last=Górny|first=Rafał L.|last2=Reponen|first2=Tiina|last3=Willeke|first3=Klaus|last4=Schmechel|first4=Detlef|last5=Robine|first5=Enric|last6=Boissier|first6=Marjorie|last7=Grinshpun|first7=Sergey A.|date=2002|title=Fungal Fragments as Indoor Air Biocontaminants|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC126767/|journal=Applied and Environmental Microbiology|volume=68|issue=7|pages=3522–3531|doi=10.1128/AEM.68.7.3522-3531.2002|issn=0099-2240|pmid=12089037|via=}}</ref><ref>{{Cite journal|last=Brasel|first=T. L.|last2=Martin|first2=J. M.|last3=Carriker|first3=C. G.|last4=Wilson|first4=S. C.|last5=Straus|first5=D. C.|date=2005|title=Detection of Airborne Stachybotrys chartarum Macrocyclic Trichothecene Mycotoxins in the Indoor Environment|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1287651/|journal=Applied and Environmental Microbiology|volume=71|issue=11|pages=7376–7388|doi=10.1128/AEM.71.11.7376-7388.2005|issn=0099-2240|pmc=1287651|pmid=16269780|via=}}</ref> A 2006 position paper by the [[American Academy of Allergy, Asthma, and Immunology|American Academy of Allergy, Asthma & Immunology]] (AAAAI) maintained a similarly sceptical position as the ACOEM paper in denying that mold in indoor environments could cause severe effects, but was co-authored by one of the same authors as the 2003 paper and was similarly problematic.<ref>{{Cite journal|last=Bush|first=Robert K.|last2=Portnoy|first2=Jay M.|last3=Saxon|first3=Andrew|last4=Terr|first4=Abba I.|last5=Wood|first5=Robert A.|date=2006-02-01|title=The medical effects of mold exposure|url=http://www.sciencedirect.com/science/article/pii/S0091674905025911|journal=Journal of Allergy and Clinical Immunology|language=en|volume=117|issue=2|pages=326–333|doi=10.1016/j.jaci.2005.12.001|issn=0091-6749}}</ref><ref>{{Cite journal|last=Shoemaker|first=Ritchie C.|last2=Ammann|first2=Harriett|last3=Lipsey|first3=Richard|last4=Montz|first4=Edward|date=2006-09-01|title=Rigor, transparency, and disclosure needed in mold position paper|url=https://www.jacionline.org/article/S0091-6749(06)01520-X/abstract|journal=Journal of Allergy and Clinical Immunology|language=English|volume=118|issue=3|pages=764–766|doi=10.1016/j.jaci.2006.07.018|issn=0091-6749|pmid=16950306}}</ref><ref>{{Cite journal|last=Lieberman|first=Allan|last2=Rea|first2=William|last3=Curtis|first3=Luke|date=2006|title=Adverse health effects of indoor mold exposure|url=https://pubmed.ncbi.nlm.nih.gov/16950304/|journal=The Journal of Allergy and Clinical Immunology|volume=118|issue=3|pages=763; author reply 767–768|doi=10.1016/j.jaci.2006.06.037|issn=0091-6749|pmid=16950304|via=}}</ref><ref>{{Cite journal|last=Kilburn|first=Kaye H.|last2=Gray|first2=Michael|last3=Kramer|first3=Sharon|date=2006|title=Nondisclosure of conflicts of interest is perilous to the advancement of science|url=https://pubmed.ncbi.nlm.nih.gov/16950307/|journal=The Journal of Allergy and Clinical Immunology|volume=118|issue=3|pages=766–767; author reply 767–768; discussion 768|doi=10.1016/j.jaci.2006.07.009|issn=0091-6749|pmid=16950307|via=}}</ref><ref>{{Cite journal|last=Strickland|first=Maurice H. V.|date=2006|title=How solid is the Academy position paper on mold exposure?|url=https://pubmed.ncbi.nlm.nih.gov/16950305/|journal=The Journal of Allergy and Clinical Immunology|volume=118|issue=3|pages=763–764; author reply 767–768|doi=10.1016/j.jaci.2006.07.008|issn=0091-6749|pmid=16950305|via=}}</ref> Julie Rehmeyer, a prominent science writer, recounted this controversy in her book, ''Through the Shadowlands'', noting that it took 12 years for scientists to prevail in making both ACOEM and AAAAI sunset these flawed and misrepresentative position papers, with the ACOEM paper now marked as "CONTENT NOT FOR REUSE".<ref>{{Cite book|last=Rehmeyer, Julie.|url=http://worldcat.org/oclc/995760832|title=Through the Shadowlands : a Science Writer's Odyssey into an Illness Science Doesn't Understand.|date=2017|publisher=Rodale Inc|isbn=978-1-62336-766-4|oclc=995760832}}</ref><ref>{{Cite web|title=ACOEM Takes Down Position Paper commonly Used to Defend against Mold Claims {{!}} Dr. Ritchie Shoemaker|url=https://www.survivingmold.com/legal-resources/works-citing-dr.-shoemaker/acoem-takes-down-position-paper-commonly-used-to-defend-against-mold-claims|access-date=2020-08-27|website=www.survivingmold.com}}</ref><ref>{{Cite web|last=Miller|first=Ben|date=2015-03-09|title=ACOEM Takes Down Position Paper commonly Used to Defend against Mold Claims|url=http://www.workcompcentral.com/|url-status=live|archive-url=|archive-date=|access-date=2020-08-27|website=WorkCompCentral|language=English}}</ref> Despite this, both papers are still being referenced as of 2020 in support of the notion that adverse health effects from mold and dampness are limited mostly to respiratory and dermatological effects.<ref>{{Cite web|last=|first=|date=|title=Papers citing Hardin et al (2003)|url=https://scholar.google.com/scholar?cites=7121341673404550863&as_sdt=2005&sciodt=0,5&hl=en|url-status=live|archive-url=|archive-date=|access-date=2020-08-26|website=Google Scholar}}</ref><ref>{{Cite web|last=|first=|date=|title=Papers citing Bush et al (2006)|url=https://scholar.google.com/scholar?cites=15302957015752618732&as_sdt=2005&sciodt=0,5&hl=en|url-status=live|archive-url=|archive-date=|access-date=2020-08-26|website=Google Scholar}}</ref>
+A 2003 paper by the [[American College of Occupational and Environmental Medicine]] (ACOEM), which claimed the link between mold and building-related symptoms was "weak and unproven", was published without disclosing conflicts of interest by the authors and to substantial critique of the science.<ref>{{Cite journal|last=Hardin|first=Bryan D.|last2=Kelman|first2=Bruce J.|last3=Saxon|first3=Andrew|date=2003|title=Adverse human health effects associated with molds in the indoor environment|url=https://pubmed.ncbi.nlm.nih.gov/12762072/|journal=Journal of Occupational and Environmental Medicine|volume=45|issue=5|pages=470–478|doi=10.1097/00043764-200305000-00006|issn=1076-2752|pmid=12762072|via=}}</ref><ref>{{Cite journal|last=Craner|first=James|date=2008-10-01|title=A Critique of the ACOEM Statement on Mold: Undisclosed Conflicts of Interest in the Creation of an “Evidence-Based” Statement|url=https://doi.org/10.1179/oeh.2008.14.4.283|journal=International Journal of Occupational and Environmental Health|volume=14|issue=4|pages=283–298|doi=10.1179/oeh.2008.14.4.283|issn=1077-3525|pmid=19043916}}</ref><ref>{{Cite journal|last=Ladou|first=Joseph|last2=Teitelbaum|first2=Daniel T.|last3=Egilman|first3=David S.|last4=Frank|first4=Arthur L.|last5=Kramer|first5=Sharon N.|last6=Huff|first6=James|date=2007-10-01|title=American College of Occupational and Environmental Medicine (ACOEM): A Professional Association in Service to Industry|url=https://doi.org/10.1179/oeh.2007.13.4.404|journal=International Journal of Occupational and Environmental Health|volume=13|issue=4|pages=404–426|doi=10.1179/oeh.2007.13.4.404|issn=1077-3525|pmid=18085054}}</ref> Dr. Harriet Ammann, who authored the chapter on mold toxicity in a relevant book by the Institute of Medicine, notably criticised the methodology used in the ACOEM paper: "They took hypothetical exposure and hypothetical toxicity and jumped to the conclusion there is nothing there."<ref>{{Cite news|last=Armstrong|first=David|date=2007-01-10|title=Amid Suits Over Mold, Experts Wear Two Hats|language=en-US|work=Wall Street Journal|url=https://www.wsj.com/articles/SB116831654647871083|url-status=live|access-date=2020-08-26|archive-url=http://www.armstrongjournalism.com/wp-content/uploads/2014/12/Amid-Suits-Over-Mold-Experts-Wear-Two-Hats.pdf|archive-date=2014-12-28|issn=0099-9660}}</ref> Her associated review in 2004 did find insufficient evidence of causation at that time but still acknowledged evidence of "potential relationships between mycotoxin exposure and pulmonary hemorrhage, immunosuppression, neurotoxicity, respiratory and dermal responses."<ref>{{Cite book|last=Institute of Medicine (États-Unis). Committee on Damp Indoor Spaces and Health.|url=http://worldcat.org/oclc/1015583620|title=Damp indoor spaces and health.|date=2004|publisher=National academies Press|isbn=0-309-09193-4|oclc=1015583620}}</ref><ref>{{Cite web|last=May 10|first=Eric S. Strober {{!}}|last2=AM|first2=2010 at 12:00|title=The Past, Present and Future of Mold Litigation|url=https://www.law.com/newyorklawjournal/almID/1202457764938/|access-date=2020-08-31|website=New York Law Journal|language=en}}</ref> Similarly, Frederick J. Passman points out another critique: "The Hardin group’s calculations are rendered moot by recent reports of airborne mycotoxins associated with particles substantially smaller than spores".<ref>{{Cite journal|last=Ph.D|first=Frederick J. Passman|date=2008-01-28|title=Metalworking Fluid Microbes—What We Need to Know to Successfully Understand Cause-and-Effect Relationships|url=https://doi.org/10.1080/10402000701691720|journal=Tribology Transactions|volume=51|issue=1|pages=107–117|doi=10.1080/10402000701691720|issn=1040-2004}}</ref><ref>{{Cite journal|last=Górny|first=Rafał L.|last2=Reponen|first2=Tiina|last3=Willeke|first3=Klaus|last4=Schmechel|first4=Detlef|last5=Robine|first5=Enric|last6=Boissier|first6=Marjorie|last7=Grinshpun|first7=Sergey A.|date=2002|title=Fungal Fragments as Indoor Air Biocontaminants|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC126767/|journal=Applied and Environmental Microbiology|volume=68|issue=7|pages=3522–3531|doi=10.1128/AEM.68.7.3522-3531.2002|issn=0099-2240|pmid=12089037|via=}}</ref><ref>{{Cite journal|last=Brasel|first=T. L.|last2=Martin|first2=J. M.|last3=Carriker|first3=C. G.|last4=Wilson|first4=S. C.|last5=Straus|first5=D. C.|date=2005|title=Detection of Airborne Stachybotrys chartarum Macrocyclic Trichothecene Mycotoxins in the Indoor Environment|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1287651/|journal=Applied and Environmental Microbiology|volume=71|issue=11|pages=7376–7388|doi=10.1128/AEM.71.11.7376-7388.2005|issn=0099-2240|pmc=1287651|pmid=16269780|via=}}</ref> A 2006 position paper by the [[American Academy of Allergy, Asthma, and Immunology|American Academy of Allergy, Asthma & Immunology]] (AAAAI) maintained a similarly sceptical position as the ACOEM paper in denying that mold in indoor environments could cause severe effects, but was co-authored by one of the same authors as the 2003 paper and was similarly problematic.<ref>{{Cite journal|last=Bush|first=Robert K.|last2=Portnoy|first2=Jay M.|last3=Saxon|first3=Andrew|last4=Terr|first4=Abba I.|last5=Wood|first5=Robert A.|date=2006-02-01|title=The medical effects of mold exposure|url=http://www.sciencedirect.com/science/article/pii/S0091674905025911|journal=Journal of Allergy and Clinical Immunology|language=en|volume=117|issue=2|pages=326–333|doi=10.1016/j.jaci.2005.12.001|issn=0091-6749}}</ref><ref>{{Cite journal|last=Shoemaker|first=Ritchie C.|last2=Ammann|first2=Harriett|last3=Lipsey|first3=Richard|last4=Montz|first4=Edward|date=2006-09-01|title=Rigor, transparency, and disclosure needed in mold position paper|url=https://www.jacionline.org/article/S0091-6749(06)01520-X/abstract|journal=Journal of Allergy and Clinical Immunology|language=English|volume=118|issue=3|pages=764–766|doi=10.1016/j.jaci.2006.07.018|issn=0091-6749|pmid=16950306}}</ref><ref>{{Cite journal|last=Lieberman|first=Allan|last2=Rea|first2=William|last3=Curtis|first3=Luke|date=2006|title=Adverse health effects of indoor mold exposure|url=https://pubmed.ncbi.nlm.nih.gov/16950304/|journal=The Journal of Allergy and Clinical Immunology|volume=118|issue=3|pages=763; author reply 767–768|doi=10.1016/j.jaci.2006.06.037|issn=0091-6749|pmid=16950304|via=}}</ref><ref>{{Cite journal|last=Kilburn|first=Kaye H.|last2=Gray|first2=Michael|last3=Kramer|first3=Sharon|date=2006|title=Nondisclosure of conflicts of interest is perilous to the advancement of science|url=https://pubmed.ncbi.nlm.nih.gov/16950307/|journal=The Journal of Allergy and Clinical Immunology|volume=118|issue=3|pages=766–767; author reply 767–768; discussion 768|doi=10.1016/j.jaci.2006.07.009|issn=0091-6749|pmid=16950307|via=}}</ref><ref>{{Cite journal|last=Strickland|first=Maurice H. V.|date=2006|title=How solid is the Academy position paper on mold exposure?|url=https://pubmed.ncbi.nlm.nih.gov/16950305/|journal=The Journal of Allergy and Clinical Immunology|volume=118|issue=3|pages=763–764; author reply 767–768|doi=10.1016/j.jaci.2006.07.008|issn=0091-6749|pmid=16950305|via=}}</ref> Julie Rehmeyer, a prominent science writer, recounted this controversy in her book, ''Through the Shadowlands'', noting that it took 12 years for scientists to prevail in making both ACOEM and AAAAI sunset these flawed and misrepresentative position papers, with the ACOEM paper now marked as "CONTENT NOT FOR REUSE".<ref>{{Cite book|last=Rehmeyer, Julie.|url=http://worldcat.org/oclc/995760832|title=Through the Shadowlands : a Science Writer's Odyssey into an Illness Science Doesn't Understand.|date=2017|publisher=Rodale Inc|isbn=978-1-62336-766-4|oclc=995760832}}</ref><ref>{{Cite web|title=ACOEM Takes Down Position Paper commonly Used to Defend against Mold Claims {{!}} Dr. Ritchie Shoemaker|url=https://www.survivingmold.com/legal-resources/works-citing-dr.-shoemaker/acoem-takes-down-position-paper-commonly-used-to-defend-against-mold-claims|access-date=2020-08-27|website=www.survivingmold.com}}</ref><ref>{{Cite web|last=Miller|first=Ben|date=2015-03-09|title=ACOEM Takes Down Position Paper commonly Used to Defend against Mold Claims|url=http://www.workcompcentral.com/|url-status=live|archive-url=|archive-date=|access-date=2020-08-27|website=WorkCompCentral|language=English}}</ref> Despite this, both papers are still being referenced as of 2020 in support of the notion that adverse health effects from mold and dampness are limited mostly to respiratory and dermatological effects.<ref>{{Cite web|last=|first=|date=|title=Papers citing Hardin et al (2003)|url=https://scholar.google.com/scholar?cites=7121341673404550863&as_sdt=2005&sciodt=0,5&hl=en|url-status=live|archive-url=|archive-date=|access-date=2020-08-26|website=Google Scholar}}</ref><ref>{{Cite web|last=|first=|date=|title=Papers citing Bush et al (2006)|url=https://scholar.google.com/scholar?cites=15302957015752618732&as_sdt=2005&sciodt=0,5&hl=en|url-status=live|archive-url=|archive-date=|access-date=2020-08-26|website=Google Scholar}}</ref>
-Regardless, studies are suggesting that the so-called "toxic effects" are actually the result of chronic activation of the immune system, leading to chronic inflammation.<ref>{{cite journal | vauthors = Kuhn DM, Ghannoum MA | title = Indoor mold, toxigenic fungi, and Stachybotrys chartarum: infectious disease perspective | journal = Clinical Microbiology Reviews | volume = 16 | issue = 1 | pages = 144–72 | date = January 2003 | pmid = 12525430 | pmc = 145304 | doi = 10.1128/CMR.16.1.144-172.2003 }}</ref><ref>{{cite web|last1=Shoemaker|first1=Ritchie C.|last2=Mark|first2=Laura|last3=McMahon|first3=Scott | name-list-format = vanc |date=2010|year=2010|title=Research Committee Report on Diagnosis and Treatment of Chronic Inflammatory Response Syndrome Caused by Exposure to the Interior Environment of Water-Damaged Buildings|url=https://www.survivingmold.com/docs/POA_MOLD_7_27_10_final.pdf|url-status=live|archive-url=|archive-date=|access-date=2020-08-14|website=Surviving Mold|publisher=Policyholders of America}}</ref><ref>{{cite journal | vauthors = Morris G, Berk M, Walder K, Maes M | s2cid = 14712633 | title = The Putative Role of Viruses, Bacteria, and Chronic Fungal Biotoxin Exposure in the Genesis of Intractable Fatigue Accompanied by Cognitive and Physical Disability | journal = Molecular Neurobiology | volume = 53 | issue = 4 | pages = 2550–71 | date = May 2016 | pmid = 26081141 | doi = 10.1007/s12035-015-9262-7 }}</ref><ref>{{cite journal | vauthors = Valtonen V | title = Clinical Diagnosis of the Dampness and Mold Hypersensitivity Syndrome: Review of the Literature and Suggested Diagnostic Criteria | language = English | journal = Frontiers in Immunology | volume = 8 | pages = 951 | date = 2017 | pmid = 28848553 | doi = 10.3389/fimmu.2017.00951 | pmc = 5554125 }}</ref> In 2008, the United States Government Accountability Office published a report on indoor mold, reviewing the literature to date and acknowledging the possibility of immune and toxic effects, while calling for further research.<ref>{{Cite journal|last=U.S. Government Accountability Office|first=|date=2008|title=Indoor Mold: Better Coordination of Research on Health Effects and More Consistent Guidance Would Improve Federal Efforts|url=https://www.gao.gov/products/GAO-08-980|journal=|volume=|issue=GAO-08-980|pages=|via=}}</ref> By 2009, the [[World Health Organization|WHO]] noted a strong association between dampness and inflammatory responses, while also recognising that "synergistic interactions among microbial agents" might make it "difficult to detect and implicate specific exposures in the causation of damp building-associated adverse health effects."<ref>{{Cite web | date=2009|title=WHO guidelines for indoor air quality: dampness and mould|url=https://www.euro.who.int/en/health-topics/environment-and-health/air-quality/publications/2009/who-guidelines-for-indoor-air-quality-dampness-and-mould|url-status=live |access-date=2020-08-03|website=www.euro.who.int|page=91|language=en}}</ref> Gram-negative bacteria, which create endotoxins known to produce inflammatory responses, might also be partly responsible, as might [[Actinomycetales|actinomycetes]] and their associated exotoxins.<ref>{{cite journal|vauthors=Hope J|date=2013-04-18|title=A review of the mechanism of injury and treatment approaches for illness resulting from exposure to water-damaged buildings, mold, and mycotoxins|journal=TheScientificWorldJournal|volume=2013|pages=767482|doi=10.1155/2013/767482|pmc=3654247|pmid=23710148}}</ref><ref>{{Cite journal|last=Thrasher|first=Jack D.|last2=Crawley|first2=Sandra|date=2009|title=The biocontaminants and complexity of damp indoor spaces: more than what meets the eyes|url=https://pubmed.ncbi.nlm.nih.gov/19793773/|journal=Toxicology and Industrial Health|volume=25|issue=9-10|pages=583–615|doi=10.1177/0748233709348386|issn=1477-0393|pmid=19793773|via=}}</ref> A 2018 review of 16 associated studies found that people exposed to molds and mycotoxins had "symptoms affecting multiple organs, including the lungs, musculoskeletal system, as well as the central and peripheral nervous systems" and also noted that such exposure has now been implicated in the pathogenesis of [[Autism spectrum|autism-spectrum disorder]].<ref>{{Cite journal|last=Ratnaseelan|first=Aarane M.|last2=Tsilioni|first2=Irene|last3=Theoharides|first3=Theoharis C.|date=2018-06-01|title=Effects of Mycotoxins on Neuropsychiatric Symptoms and Immune Processes|url=http://www.sciencedirect.com/science/article/pii/S0149291818302297|journal=Clinical Therapeutics|language=en|volume=40|issue=6|pages=903–917|doi=10.1016/j.clinthera.2018.05.004|issn=0149-2918}}</ref> An [[In vitro|''in vitro'']] study of human neurological system cells showed damage caused by inflammatory and immune processes (along with disruption of the [[Blood–brain barrier|blood-brain barrier]]) in response to mycotoxins at exposure levels that would be expected in water-damaged buildings.<ref>{{cite journal | vauthors = Karunasena E, Larrañaga MD, Simoni JS, Douglas DR, Straus DC | s2cid = 319228 | title = Building-associated neurological damage modeled in human cells: a mechanism of neurotoxic effects by exposure to mycotoxins in the indoor environment | journal = Mycopathologia | volume = 170 | issue = 6 | pages = 377–90 | date = December 2010 | pmid = 20549560 | doi = 10.1007/s11046-010-9330-5 }}</ref> ''[[Ex vivo]]'' studies of human [[Peripheral blood mononuclear cell|peripheral blood mononuclear cells]] showed inflammatory and innate immune responses upon exposure to specific molds and mycotoxins, such as ''[[Stachybotrys chartarum|S. chartarum]]'' (and an associated mycotoxin, Satratoxin G) and various strains of [[Aspergillus]].<ref>{{cite journal | vauthors = Rosenblum Lichtenstein JH, Hsu YH, Gavin IM, Donaghey TC, Molina RM, Thompson KJ, Chi CL, Gillis BS, Brain JD | display-authors = 6 | title = Environmental mold and mycotoxin exposures elicit specific cytokine and chemokine responses | journal = PLOS ONE | volume = 10 | issue = 5 | pages = e0126926 | date = 2015-05-26 | pmid = 26010737 | pmc = 4444319 | doi = 10.1371/journal.pone.0126926 | bibcode = 2015PLoSO..1026926R }}</ref><ref>{{cite journal | vauthors = Punsmann S, Liebers V, Lotz A, Brüning T, Raulf M | title = Ex vivo cytokine release and pattern recognition receptor expression of subjects exposed to dampness: pilot study to assess the outcome of mould exposure to the innate immune system | journal = PLOS ONE | volume = 8 | issue = 12 | pages = e82734 | date = 2013-12-10 | pmid = 24340055 | pmc = 3858334 | doi = 10.1371/journal.pone.0082734 | bibcode = 2013PLoSO...882734P }}</ref> As well, several studies have now shown cognitive deficits, immune activation, and behavioral dysregulation in humans.<ref>{{cite journal | vauthors = Shoemaker RC, House DE | title = Sick building syndrome (SBS) and exposure to water-damaged buildings: time series study, clinical trial and mechanisms | journal = Neurotoxicology and Teratology | volume = 28 | issue = 5 | pages = 573–88 | date = 2006-09-01 | pmid = 17010568 | doi = 10.1016/j.ntt.2006.07.003 }}</ref><ref>{{cite journal | vauthors = Kilburn KH | s2cid = 1692592 | title = Neurobehavioral and pulmonary impairment in 105 adults with indoor exposure to molds compared to 100 exposed to chemicals | journal = Toxicology and Industrial Health | volume = 25 | issue = 9–10 | pages = 681–92 | date = 2009-10-01 | pmid = 19793776 | doi = 10.1177/0748233709348390 }}</ref><ref>{{cite journal | vauthors = Morris G, Berk M, Walder K, Maes M | s2cid = 14712633 | title = The Putative Role of Viruses, Bacteria, and Chronic Fungal Biotoxin Exposure in the Genesis of Intractable Fatigue Accompanied by Cognitive and Physical Disability | language = English | journal = Molecular Neurobiology | volume = 53 | issue = 4 | pages = 2550–71 | date = May 2016 | pmid = 26081141 | doi = 10.1007/s12035-015-9262-7 }}</ref> Studies exposing mice to controlled doses of ''[[Stachybotrys chartarum|S. chartarum]]'' spores similarly show activation of the innate immune system, along with neural, cognitive, and emotional dysfunction, even when the spores are denatured of their mycotoxins.<ref>{{cite journal | vauthors = Harding CF, Pytte CL, Page KG, Ryberg KJ, Normand E, Remigio GJ, DeStefano RA, Morris DB, Voronina J, Lopez A, Stalbow LA, Williams EP, Abreu N | display-authors = 6 | title = Mold inhalation causes innate immune activation, neural, cognitive and emotional dysfunction | journal = Brain, Behavior, and Immunity | volume = 87 | pages = 218–228 | date = July 2020 | pmid = 31751617 | doi = 10.1016/j.bbi.2019.11.006 | pmc = 7231651 }}</ref><ref>{{cite journal| vauthors = Harding CF, Liao D, Persaud R, Lin K, Page K, Pytte C |s2cid=53155076|date=2015-10-01|title=Environmental mold exposure, brain inflammation, and spatial memory deficits |journal=Brain, Behavior, and Immunity|series=PsychoNeuroImmunology Research Society's 22nd Annual Scientific Meeting |volume=49|pages=e42|doi=10.1016/j.bbi.2015.06.160 }}</ref> Furthermore, children living in water-damaged homes show systemic inflammation, immune activation, and probably poorer cognitive function, too.<ref>{{cite journal | vauthors = Mustonen K, Karvonen AM, Kirjavainen P, Roponen M, Schaub B, Hyvärinen A, Frey U, Renz H, Pfefferle PI, Genuneit J, Vaarala O, Pekkanen J | display-authors = 6 | title = Moisture damage in home associates with systemic inflammation in children | journal = Indoor Air | volume = 26 | issue = 3 | pages = 439–47 | date = June 2016 | pmid = 25924948 | doi = 10.1111/ina.12216 }}</ref><ref>{{cite journal | vauthors = Jedrychowski W, Maugeri U, Perera F, Stigter L, Jankowski J, Butscher M, Mroz E, Flak E, Skarupa A, Sowa A | display-authors = 6 | title = Cognitive function of 6-year old children exposed to mold-contaminated homes in early postnatal period. Prospective birth cohort study in Poland | journal = Physiology & Behavior | volume = 104 | issue = 5 | pages = 989–95 | date = October 2011 | pmid = 21763705 | doi = 10.1016/j.physbeh.2011.06.019 | pmc = 3758954 }}</ref><ref>{{Cite journal|last=Casas|first=Lidia|last2=Torrent|first2=Maties|last3=Zock|first3=Jan-Paul|last4=Doekes|first4=Gert|last5=Forns|first5=Joan|last6=Guxens|first6=Mònica|last7=Täubel|first7=Martin|last8=Heinrich|first8=Joachim|last9=Sunyer|first9=Jordi|date=2013-11-01|title=Early life exposures to home dampness, pet ownership and farm animal contact and neuropsychological development in 4 year old children: A prospective birth cohort study|url=http://www.sciencedirect.com/science/article/pii/S1438463912001496|journal=International Journal of Hygiene and Environmental Health|language=en|volume=216|issue=6|pages=690–697|doi=10.1016/j.ijheh.2012.12.013|issn=1438-4639}}</ref> Tellingly, the affected biomarkers, hormones, and pathways in individuals affected by inhaled mycotoxins are consistent with studies of ingested mycotoxins, such as [[trichothecene]] exposure.<ref>{{Cite journal|last=Lebrun|first=Bruno|last2=Tardivel|first2=Catherine|last3=Félix|first3=Bernadette|last4=Abysique|first4=Anne|last5=Troadec|first5=Jean-Denis|last6=Gaigé|first6=Stéphanie|last7=Dallaporta|first7=Michel|date=2015-07-01|title=Dysregulation of energy balance by trichothecene mycotoxins: Mechanisms and prospects|url=http://www.sciencedirect.com/science/article/pii/S0161813X15000649|journal=NeuroToxicology|language=en|volume=49|pages=15–27|doi=10.1016/j.neuro.2015.04.009|issn=0161-813X}}</ref><ref>{{Cite journal|last=Terciolo|first=Chloé|last2=Maresca|first2=Marc|last3=Pinton|first3=Philippe|last4=Oswald|first4=Isabelle P.|date=2018-11-01|title=Review article: Role of satiety hormones in anorexia induction by Trichothecene mycotoxins|url=http://www.sciencedirect.com/science/article/pii/S0278691518306781|journal=Food and Chemical Toxicology|language=en|volume=121|pages=701–714|doi=10.1016/j.fct.2018.09.034|issn=0278-6915}}</ref> Two studies using volumetric MRIs have suggested that affected individuals display structural changes in the brain, associated with the forebrain [[Parenchyma|parenchymal]], cortical [[Grey matter|gray matter]], [[pallidum]] volumes, and the [[caudate nucleus]].<ref>{{cite journal | vauthors = Shoemaker RC, House D, Ryan JC | title = Structural brain abnormalities in patients with inflammatory illness acquired following exposure to water-damaged buildings: a volumetric MRI study using NeuroQuant® | journal = Neurotoxicology and Teratology | volume = 45 | pages = 18–26 | date = 2014 | pmid = 24946038 | doi = 10.1016/j.ntt.2014.06.004 }}</ref><ref>{{Cite journal| vauthors = McMahon SW, Shoemaker RC, Ryan JC |date=2016|title=Reduction in Forebrain Parenchymal and Cortical Grey Matter Swelling across Treatment Groups in Patients with Inflammatory Illness Acquired Following Exposure to Water-Damaged Buildings|url=https://www.survivingmold.com/docs/NQ_II_4_12_2016.PDF|journal=Journal of Neuroscience & Clinical Research|language=en|volume=1|issue=1|pages=1–4|via=}}</ref> Correlating to this, Dale Bredesen, a neurodegenerative researcher, has noted a subtype of [[Alzheimer's disease|Alzheimer's Disease]] associated with this chronic inflammatory response, calling it an "unrecognized—and treatable—epidemic".<ref>{{cite journal | vauthors = Bredesen DE | title = Inhalational Alzheimer's disease: an unrecognized - and treatable - epidemic | journal = Aging | volume = 8 | issue = 2 | pages = 304–13 | date = February 2016 | pmid = 26870879 | pmc = 4789584 | doi = 10.18632/aging.100896 }}</ref><ref>{{Cite journal|last=Bredesen|first=Dale E.|date=2015|title=Metabolic profiling distinguishes three subtypes of Alzheimer's disease|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4586104/|journal=Aging (Albany NY)|volume=7|issue=8|pages=595–600|issn=1945-4589|pmc=4586104|pmid=26343025|via=}}</ref> Arnold R. Eiser, Professor Emeritus of Medicine at [[Drexel University College of Medicine]], has suggested that environmental factors such as dampness and mold may be a contributing factor for why [[Finland]] has the highest death rate from [[dementia]] in the world.<ref>{{Cite journal|last=Eiser|first=Arnold R.|date=2017-09-15|title=Why does Finland have the highest dementia mortality rate? Environmental factors may be generalizable|url=http://www.sciencedirect.com/science/article/pii/S0006899317302901|journal=Brain Research|language=en|volume=1671|pages=14–17|doi=10.1016/j.brainres.2017.06.032|issn=0006-8993}}</ref>
+Regardless, studies are suggesting that the so-called "toxic effects" are actually the result of chronic activation of the immune system, leading to chronic inflammation.<ref>{{cite journal | vauthors = Kuhn DM, Ghannoum MA | title = Indoor mold, toxigenic fungi, and Stachybotrys chartarum: infectious disease perspective | journal = Clinical Microbiology Reviews | volume = 16 | issue = 1 | pages = 144–72 | date = January 2003 | pmid = 12525430 | pmc = 145304 | doi = 10.1128/CMR.16.1.144-172.2003 }}</ref><ref>{{cite web|last1=Shoemaker|first1=Ritchie C.|last2=Mark|first2=Laura|last3=McMahon|first3=Scott | name-list-format = vanc |date=2010|year=2010|title=Research Committee Report on Diagnosis and Treatment of Chronic Inflammatory Response Syndrome Caused by Exposure to the Interior Environment of Water-Damaged Buildings|url=https://www.survivingmold.com/docs/POA_MOLD_7_27_10_final.pdf|url-status=live|archive-url=|archive-date=|access-date=2020-08-14|website=Surviving Mold|publisher=Policyholders of America}}</ref><ref>{{cite journal | vauthors = Morris G, Berk M, Walder K, Maes M | s2cid = 14712633 | title = The Putative Role of Viruses, Bacteria, and Chronic Fungal Biotoxin Exposure in the Genesis of Intractable Fatigue Accompanied by Cognitive and Physical Disability | journal = Molecular Neurobiology | volume = 53 | issue = 4 | pages = 2550–71 | date = May 2016 | pmid = 26081141 | doi = 10.1007/s12035-015-9262-7 }}</ref><ref>{{cite journal | vauthors = Valtonen V | title = Clinical Diagnosis of the Dampness and Mold Hypersensitivity Syndrome: Review of the Literature and Suggested Diagnostic Criteria | language = English | journal = Frontiers in Immunology | volume = 8 | pages = 951 | date = 2017 | pmid = 28848553 | doi = 10.3389/fimmu.2017.00951 | pmc = 5554125 }}</ref> In 2008, the United States Government Accountability Office published a report on indoor mold, reviewing the literature to date and acknowledging the possibility of immune and toxic effects, while calling for further research.<ref>{{Cite journal|last=U.S. Government Accountability Office|first=|date=2008|title=Indoor Mold: Better Coordination of Research on Health Effects and More Consistent Guidance Would Improve Federal Efforts|url=https://www.gao.gov/products/GAO-08-980|journal=|volume=|issue=GAO-08-980|pages=|via=}}</ref> By 2009, the [[World Health Organization|WHO]] noted a strong association between dampness and inflammatory responses, while also recognising that "synergistic interactions among microbial agents" might make it "difficult to detect and implicate specific exposures in the causation of damp building-associated adverse health effects."<ref>{{Cite web | date=2009|title=WHO guidelines for indoor air quality: dampness and mould|url=https://www.euro.who.int/en/health-topics/environment-and-health/air-quality/publications/2009/who-guidelines-for-indoor-air-quality-dampness-and-mould|url-status=live |access-date=2020-08-03|website=www.euro.who.int|page=91|language=en}}</ref> Gram-negative bacteria, which create endotoxins known to produce inflammatory responses, might also be partly responsible, as might [[Actinomycetales|actinomycetes]] and their associated exotoxins.<ref>{{cite journal|vauthors=Hope J|date=2013-04-18|title=A review of the mechanism of injury and treatment approaches for illness resulting from exposure to water-damaged buildings, mold, and mycotoxins|journal=TheScientificWorldJournal|volume=2013|pages=767482|doi=10.1155/2013/767482|pmc=3654247|pmid=23710148}}</ref><ref>{{Cite journal|last=Thrasher|first=Jack D.|last2=Crawley|first2=Sandra|date=2009|title=The biocontaminants and complexity of damp indoor spaces: more than what meets the eyes|url=https://pubmed.ncbi.nlm.nih.gov/19793773/|journal=Toxicology and Industrial Health|volume=25|issue=9-10|pages=583–615|doi=10.1177/0748233709348386|issn=1477-0393|pmid=19793773|via=}}</ref> A ten-year longitudinal study also found that dampness and mold seemed to be an underlying cause of sick-building syndrome.<ref>{{Cite journal|last=Zhang|first=Xin|last2=Sahlberg|first2=Bo|last3=Wieslander|first3=Gunilla|last4=Janson|first4=Christer|last5=Gislason|first5=Thorarinn|last6=Norback|first6=Dan|date=2012-07-15|title=Dampness and moulds in workplace buildings: Associations with incidence and remission of sick building syndrome (SBS) and biomarkers of inflammation in a 10year follow-up study|url=http://www.sciencedirect.com/science/article/pii/S0048969712005724|journal=Science of The Total Environment|language=en|volume=430|pages=75–81|doi=10.1016/j.scitotenv.2012.04.040|issn=0048-9697}}</ref> A 2018 review of 16 associated studies found that people exposed to molds and mycotoxins had "symptoms affecting multiple organs, including the lungs, musculoskeletal system, as well as the central and peripheral nervous systems" and also noted that such exposure has now been implicated in the pathogenesis of [[Autism spectrum|autism-spectrum disorder]].<ref>{{Cite journal|last=Ratnaseelan|first=Aarane M.|last2=Tsilioni|first2=Irene|last3=Theoharides|first3=Theoharis C.|date=2018-06-01|title=Effects of Mycotoxins on Neuropsychiatric Symptoms and Immune Processes|url=http://www.sciencedirect.com/science/article/pii/S0149291818302297|journal=Clinical Therapeutics|language=en|volume=40|issue=6|pages=903–917|doi=10.1016/j.clinthera.2018.05.004|issn=0149-2918}}</ref> An [[In vitro|''in vitro'']] study of human neurological system cells showed damage caused by inflammatory and immune processes (along with disruption of the [[Blood–brain barrier|blood-brain barrier]]) in response to mycotoxins at exposure levels that would be expected in water-damaged buildings.<ref>{{cite journal | vauthors = Karunasena E, Larrañaga MD, Simoni JS, Douglas DR, Straus DC | s2cid = 319228 | title = Building-associated neurological damage modeled in human cells: a mechanism of neurotoxic effects by exposure to mycotoxins in the indoor environment | journal = Mycopathologia | volume = 170 | issue = 6 | pages = 377–90 | date = December 2010 | pmid = 20549560 | doi = 10.1007/s11046-010-9330-5 }}</ref> ''[[Ex vivo]]'' studies of human [[Peripheral blood mononuclear cell|peripheral blood mononuclear cells]] showed inflammatory and innate immune responses upon exposure to specific molds and mycotoxins, such as ''[[Stachybotrys chartarum|S. chartarum]]'' (and an associated mycotoxin, Satratoxin G) and various strains of [[Aspergillus]].<ref>{{cite journal | vauthors = Rosenblum Lichtenstein JH, Hsu YH, Gavin IM, Donaghey TC, Molina RM, Thompson KJ, Chi CL, Gillis BS, Brain JD | display-authors = 6 | title = Environmental mold and mycotoxin exposures elicit specific cytokine and chemokine responses | journal = PLOS ONE | volume = 10 | issue = 5 | pages = e0126926 | date = 2015-05-26 | pmid = 26010737 | pmc = 4444319 | doi = 10.1371/journal.pone.0126926 | bibcode = 2015PLoSO..1026926R }}</ref><ref>{{cite journal | vauthors = Punsmann S, Liebers V, Lotz A, Brüning T, Raulf M | title = Ex vivo cytokine release and pattern recognition receptor expression of subjects exposed to dampness: pilot study to assess the outcome of mould exposure to the innate immune system | journal = PLOS ONE | volume = 8 | issue = 12 | pages = e82734 | date = 2013-12-10 | pmid = 24340055 | pmc = 3858334 | doi = 10.1371/journal.pone.0082734 | bibcode = 2013PLoSO...882734P }}</ref> Studies exposing mice to controlled doses of ''[[Stachybotrys chartarum|S. chartarum]]'' spores similarly show activation of the innate immune system, along with neural, cognitive, and emotional dysfunction, even when the spores are denatured of their mycotoxins.<ref>{{cite journal | vauthors = Harding CF, Pytte CL, Page KG, Ryberg KJ, Normand E, Remigio GJ, DeStefano RA, Morris DB, Voronina J, Lopez A, Stalbow LA, Williams EP, Abreu N | display-authors = 6 | title = Mold inhalation causes innate immune activation, neural, cognitive and emotional dysfunction | journal = Brain, Behavior, and Immunity | volume = 87 | pages = 218–228 | date = July 2020 | pmid = 31751617 | doi = 10.1016/j.bbi.2019.11.006 | pmc = 7231651 }}</ref><ref>{{cite journal| vauthors = Harding CF, Liao D, Persaud R, Lin K, Page K, Pytte C |s2cid=53155076|date=2015-10-01|title=Environmental mold exposure, brain inflammation, and spatial memory deficits |journal=Brain, Behavior, and Immunity|series=PsychoNeuroImmunology Research Society's 22nd Annual Scientific Meeting |volume=49|pages=e42|doi=10.1016/j.bbi.2015.06.160 }}</ref> As well, several studies have now shown cognitive deficits, immune activation, and behavioral dysregulation in humans.<ref>{{cite journal|vauthors=Shoemaker RC, House DE|date=2006-09-01|title=Sick building syndrome (SBS) and exposure to water-damaged buildings: time series study, clinical trial and mechanisms|journal=Neurotoxicology and Teratology|volume=28|issue=5|pages=573–88|doi=10.1016/j.ntt.2006.07.003|pmid=17010568}}</ref><ref>{{cite journal|vauthors=Kilburn KH|date=2009-10-01|title=Neurobehavioral and pulmonary impairment in 105 adults with indoor exposure to molds compared to 100 exposed to chemicals|journal=Toxicology and Industrial Health|volume=25|issue=9–10|pages=681–92|doi=10.1177/0748233709348390|pmid=19793776|s2cid=1692592}}</ref><ref>{{cite journal|vauthors=Morris G, Berk M, Walder K, Maes M|date=May 2016|title=The Putative Role of Viruses, Bacteria, and Chronic Fungal Biotoxin Exposure in the Genesis of Intractable Fatigue Accompanied by Cognitive and Physical Disability|journal=Molecular Neurobiology|language=English|volume=53|issue=4|pages=2550–71|doi=10.1007/s12035-015-9262-7|pmid=26081141|s2cid=14712633}}</ref> Furthermore, children living in water-damaged homes show systemic inflammation, immune activation, and probably poorer cognitive function, too.<ref>{{cite journal | vauthors = Mustonen K, Karvonen AM, Kirjavainen P, Roponen M, Schaub B, Hyvärinen A, Frey U, Renz H, Pfefferle PI, Genuneit J, Vaarala O, Pekkanen J | display-authors = 6 | title = Moisture damage in home associates with systemic inflammation in children | journal = Indoor Air | volume = 26 | issue = 3 | pages = 439–47 | date = June 2016 | pmid = 25924948 | doi = 10.1111/ina.12216 }}</ref><ref>{{cite journal | vauthors = Jedrychowski W, Maugeri U, Perera F, Stigter L, Jankowski J, Butscher M, Mroz E, Flak E, Skarupa A, Sowa A | display-authors = 6 | title = Cognitive function of 6-year old children exposed to mold-contaminated homes in early postnatal period. Prospective birth cohort study in Poland | journal = Physiology & Behavior | volume = 104 | issue = 5 | pages = 989–95 | date = October 2011 | pmid = 21763705 | doi = 10.1016/j.physbeh.2011.06.019 | pmc = 3758954 }}</ref><ref>{{Cite journal|last=Casas|first=Lidia|last2=Torrent|first2=Maties|last3=Zock|first3=Jan-Paul|last4=Doekes|first4=Gert|last5=Forns|first5=Joan|last6=Guxens|first6=Mònica|last7=Täubel|first7=Martin|last8=Heinrich|first8=Joachim|last9=Sunyer|first9=Jordi|date=2013-11-01|title=Early life exposures to home dampness, pet ownership and farm animal contact and neuropsychological development in 4 year old children: A prospective birth cohort study|url=http://www.sciencedirect.com/science/article/pii/S1438463912001496|journal=International Journal of Hygiene and Environmental Health|language=en|volume=216|issue=6|pages=690–697|doi=10.1016/j.ijheh.2012.12.013|issn=1438-4639}}</ref> Tellingly, the affected biomarkers, hormones, and pathways in individuals affected by inhaled mycotoxins are consistent with studies of ingested mycotoxins, such as [[trichothecene]] exposure.<ref>{{Cite journal|last=Lebrun|first=Bruno|last2=Tardivel|first2=Catherine|last3=Félix|first3=Bernadette|last4=Abysique|first4=Anne|last5=Troadec|first5=Jean-Denis|last6=Gaigé|first6=Stéphanie|last7=Dallaporta|first7=Michel|date=2015-07-01|title=Dysregulation of energy balance by trichothecene mycotoxins: Mechanisms and prospects|url=http://www.sciencedirect.com/science/article/pii/S0161813X15000649|journal=NeuroToxicology|language=en|volume=49|pages=15–27|doi=10.1016/j.neuro.2015.04.009|issn=0161-813X}}</ref><ref>{{Cite journal|last=Terciolo|first=Chloé|last2=Maresca|first2=Marc|last3=Pinton|first3=Philippe|last4=Oswald|first4=Isabelle P.|date=2018-11-01|title=Review article: Role of satiety hormones in anorexia induction by Trichothecene mycotoxins|url=http://www.sciencedirect.com/science/article/pii/S0278691518306781|journal=Food and Chemical Toxicology|language=en|volume=121|pages=701–714|doi=10.1016/j.fct.2018.09.034|issn=0278-6915}}</ref> Two studies using volumetric MRIs have suggested that affected individuals display structural changes in the brain, associated with the forebrain [[Parenchyma|parenchymal]], cortical [[Grey matter|gray matter]], [[pallidum]] volumes, and the [[caudate nucleus]].<ref>{{cite journal | vauthors = Shoemaker RC, House D, Ryan JC | title = Structural brain abnormalities in patients with inflammatory illness acquired following exposure to water-damaged buildings: a volumetric MRI study using NeuroQuant® | journal = Neurotoxicology and Teratology | volume = 45 | pages = 18–26 | date = 2014 | pmid = 24946038 | doi = 10.1016/j.ntt.2014.06.004 }}</ref><ref>{{Cite journal| vauthors = McMahon SW, Shoemaker RC, Ryan JC |date=2016|title=Reduction in Forebrain Parenchymal and Cortical Grey Matter Swelling across Treatment Groups in Patients with Inflammatory Illness Acquired Following Exposure to Water-Damaged Buildings|url=https://www.survivingmold.com/docs/NQ_II_4_12_2016.PDF|journal=Journal of Neuroscience & Clinical Research|language=en|volume=1|issue=1|pages=1–4|via=}}</ref> Correlating to this, Dale Bredesen, a neurodegenerative researcher, has noted a subtype of [[Alzheimer's disease|Alzheimer's Disease]] associated with this chronic inflammatory response, calling it an "unrecognized—and treatable—epidemic".<ref>{{cite journal | vauthors = Bredesen DE | title = Inhalational Alzheimer's disease: an unrecognized - and treatable - epidemic | journal = Aging | volume = 8 | issue = 2 | pages = 304–13 | date = February 2016 | pmid = 26870879 | pmc = 4789584 | doi = 10.18632/aging.100896 }}</ref><ref>{{Cite journal|last=Bredesen|first=Dale E.|date=2015|title=Metabolic profiling distinguishes three subtypes of Alzheimer's disease|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4586104/|journal=Aging (Albany NY)|volume=7|issue=8|pages=595–600|issn=1945-4589|pmc=4586104|pmid=26343025|via=}}</ref> Arnold R. Eiser, Professor Emeritus of Medicine at [[Drexel University College of Medicine]], has suggested that environmental factors such as dampness and mold may be a contributing factor for why [[Finland]] has the highest death rate from [[dementia]] in the world.<ref>{{Cite journal|last=Eiser|first=Arnold R.|date=2017-09-15|title=Why does Finland have the highest dementia mortality rate? Environmental factors may be generalizable|url=http://www.sciencedirect.com/science/article/pii/S0006899317302901|journal=Brain Research|language=en|volume=1671|pages=14–17|doi=10.1016/j.brainres.2017.06.032|issn=0006-8993}}</ref>
 The [[World Health Organization|WHO]] estimates the prevalence of significant dampness and mold in buildings to be at least 20%, while other estimates of US homes suggest a prevalence as high as 47%.<ref>{{Cite book| last1 = Heseltine | first1 = Elisabeth | last2 = Rosen | first2 = Jerome | name-list-format = vanc |title=WHO guidelines for indoor air quality : dampness and mould|date=2009|publisher=WHO Regional Office for Europe|isbn=978-92-890-4168-3|oclc=429024432}}</ref><ref>{{cite journal | vauthors = Mudarri D, Fisk WJ | title = Public health and economic impact of dampness and mold | journal = Indoor Air | volume = 17 | issue = 3 | pages = 226–35 | date = June 2007 | pmid = 17542835 | doi = 10.1111/j.1600-0668.2007.00474.x | url = https://digital.library.unt.edu/ark:/67531/metadc896583/ }}</ref> Preliminary research suggests that around 25% of the population have [[Human leukocyte antigen|HLA DR/DQ genes]] associated with a poor antigen response to biotoxins, which can result in a chronic inflammatory response, but it is unknown how many actually experience such symptoms due to frequent misdiagnosis.<ref>{{Cite book|last=Shoemaker | first = Ritchie C. | name-list-format = vanc |title=Surviving mold : life in the era of dangerous buildings| year = 2010 |isbn=978-0-9665535-5-0|oclc=852680195}}</ref> Sleeping disorders are also associated with exposure to dampness and mold, consistent with the decrease in α-melanocyte stimulating hormone (α-MSH) associated with this syndrome.<ref>{{Cite journal|date=2020-06-01|title=Dampness and mold at home and at work and onset of insomnia symptoms, snoring and excessive daytime sleepiness|url=https://www.sciencedirect.com/science/article/pii/S0160412020301008|journal=Environment International|language=en|volume=139|pages=105691|doi=10.1016/j.envint.2020.105691|issn=0160-4120}}</ref><ref>{{Cite journal|last=Shoemaker|first=Ritchie C.|last2=House|first2=Dennis|last3=Ryan|first3=James C.|date=2013|title=Vasoactive intestinal polypeptide (VIP) corrects chronic inflammatory response syndrome (CIRS) acquired following exposure to water-damaged buildings|url=https://www.survivingmold.com/docs/VIP_published_3_2013.pdf|journal=Health|volume=05|issue=03|pages=396–401|doi=10.4236/health.2013.53053|issn=1949-4998|via=}}</ref> Patients may also present with psychological symptoms given the neuroinflammatory markers involved.<ref>{{cite journal | vauthors = Osimo EF, Pillinger T, Rodriguez IM, Khandaker GM, Pariante CM, Howes OD | title = Inflammatory markers in depression: A meta-analysis of mean differences and variability in 5,166 patients and 5,083 controls | journal = Brain, Behavior, and Immunity | volume = 87 | pages = 901–909 | date = July 2020 | pmid = 32113908 | doi = 10.1016/j.bbi.2020.02.010  | pmc = 7327519 }}</ref><ref>{{cite journal | vauthors = Shenassa ED, Daskalakis C, Liebhaber A, Braubach M, Brown M | title = Dampness and mold in the home and depression: an examination of mold-related illness and perceived control of one's home as possible depression pathways | journal = American Journal of Public Health | volume = 97 | issue = 10 | pages = 1893–9 | date = October 2007 | pmid = 17761567 | pmc = 1994167 | doi = 10.2105/AJPH.2006.093773 }}</ref><ref>{{cite journal | vauthors = Bhattacharya A, Derecki NC, Lovenberg TW, Drevets WC | s2cid = 14265548 | title = Role of neuro-immunological factors in the pathophysiology of mood disorders | journal = Psychopharmacology | volume = 233 | issue = 9 | pages = 1623–36 | date = May 2016 | pmid = 26803500 | doi = 10.1007/s00213-016-4214-0 }}</ref> However, correction of the underlying neuroinflammation can correct psychological symptoms, whereas the referral of patients suffering an autoimmune disorder strictly into psychological therapies is unlikely to result in improvement.<ref>{{cite journal | vauthors = Selinheimo S, Vuokko A, Hublin C, Järnefelt H, Karvala K, Sainio M, Suojalehto H, Paunio T | display-authors = 6 | title = Psychosocial treatments for employees with non-specific and persistent physical symptoms associated with indoor air: A randomised controlled trial with a one-year follow-up | journal = Journal of Psychosomatic Research | volume = 131 | pages = 109962 | date = February 2020 | pmid = 32078837 | doi = 10.1016/j.jpsychores.2020.109962 }}</ref><ref>{{cite journal | vauthors = Benros ME, Waltoft BL, Nordentoft M, Ostergaard SD, Eaton WW, Krogh J, Mortensen PB | title = Autoimmune diseases and severe infections as risk factors for mood disorders: a nationwide study | journal = JAMA Psychiatry | volume = 70 | issue = 8 | pages = 812–20 | date = August 2013 | pmid = 23760347 | doi = 10.1001/jamapsychiatry.2013.1111 | doi-access = free }}</ref>