In the U.S., where people spend about 90 percent of their time indoors, and as many as 50 percent of buildings have water damage, it is no surprise there is an increase in the detrimental health impacts of airborne mold exposure [i, ii].
Mold spores can enter your airways through your nose and mouth, and they may irritate your exposed eyes and skin as well. Once the spores have made their way into your body, your immune system will try to get rid of them by eliciting a series of physical responses from you, such as coughing or sneezing.
Modern building materials such as cellulose-based wallboard and ceiling tiles enable the growth of Stachybotrys chartarum, commonly known as “black mold,” in indoor environments.
Poor quality materials and insulation tactics that increase moisture, combined with more episodes of severe weather, allow black mold to spread in damp indoor environments [i, iii, iv, v].
In addition, prolonged periods of water damage allow mold to colonize building materials in a way that disperses airborne spores, preventing detection through conventional sampling methods. As a result, exposure to mold in water-damaged buildings has become a significant public health threat, significantly affecting industrialized nations [i, ii].
For over a century, the impact of airborne mold spores on the respiratory system has been well-established. At least 21 percent of U.S. asthma cases result from mold exposure [vi, iii].
However, the nonrespiratory systemic effects of mold exposure are only starting to be understood. Mycotoxins, the chemical compounds produced from mold, can be absorbed through the skin and airways, causing severe health conditions, such as neurological and autoimmune diseases, cancer, and even mortality [i, vi, vii].
Stachybotrys mold is one of the world’s ten most dangerous fungi, earning it the nickname “toxic black mold” due to the dangerous byproducts it releases [xi, iv]. These byproducts are known as mycotoxins, and the most deadly is trichothecene satratoxin [vi].
These mycotoxins are released at about 300 times the concentration of spores, meaning small exposures can result in catastrophic consequences [vi].
Research suggests that mycotoxins are even more toxic than pesticides [ii]. Although inhalation of mycotoxins can cause multisystemic effects in the body, the two nonrespiratory systems most impacted are the nervous and immune systems [ii, vi].
Research has found that 70 percent of patients exposed to black mold had multiple neurological deficits, and more than 80 percent had abnormal immune cell function [ii].
Laboratory studies show that mycotoxins cause the production of cytokines and chemokines, which are small proteins that help with communication between cells [iv]. Their release causes inflammation and disrupts the nervous system in the neuroimmune axis [vi].
The inflammation process is intended to repair injured tissues; however, constant activation of these pathways in the central nervous system (CNS) can shift the homeostasis of the cells, risking permanent neurological damage [i].
Exposure to black mold mycotoxins interferes with RNA transcription and translation [i]. As a result, adult neural cells cannot fully regenerate, causing extensive cellular damage and death, known as apoptosis [vi, v].
In addition, by depleting glutathione, an antioxidant that prevents cellular damage, mycotoxins can cause oxidative stress, which is an imbalance between free radicals and antioxidants [i].
Exposure can also endanger the blood-brain barrier, increasing susceptibility to other neurotoxins and binding to proteins involved in neuroplasticity, which is the process of the nervous system changing appropriately in response to stimuli [vi].
Neurological symptoms of airborne black mold exposure are wide-ranging and can include, but are not limited to: fatigue, sleep disturbances, memory problems, slurred speech, dizziness, weakness, headache, decreased balance, slow reflexes, and decreased visual field [i, ii].
Patient-reported symptoms include moderate to severe cognitive, physical, and emotional symptoms, with decreased cognitive functioning in multiple areas, especially memory and executive function [vi].
Testing has shown hypoactivation of the frontal cortex in patients with black mold exposure, which could be due to the involvement of the brain stem.
Neuropsychological testing bolsters this hypothesis, demonstrating impairments similar to those seen in mild-moderate traumatic brain injuries [vi]. The severity of these symptoms is proportional to the duration of exposure to mold [vi].
Disruptions to the Immune System
The immune system is essential for protecting against pathogens, including molds and mycotoxins. Innate and adaptive immunity is critical for eliminating infectious pathogens and toxins [viii].
Intact mucosal barriers of the body protect tissues by activating cellular responses to produce cytokines to recruit specific immune cells to fight off invading microbes [ix]. Mycotoxins can disrupt these barriers and suppress cellular immunity, leading to immune system dysfunction [x, ix].
After black mold exposure, the effects of mycotoxins are mediated through different cellular pathways. Macrophages, epithelial, and mast cells produce cytokines and chemokines, which act as mediators of inflammatory and immune system response [v, vi].
Mycotoxins can change how genes are expressed in these mediators, resulting in altered immune system responses to subsequent mold exposures [v]. These impacts are significant, with a sampling of those working in mold-infested buildings demonstrating a two-to-thousand-fold increase in the production of inflammatory and immune markers [ii].
Conditions associated with Mycotoxins
It is now widely accepted that black mold myotoxicity can lead to immunologic disorders, including autoimmune conditions, cancer, allergic and non-allergic chronic inflammatory disease, infectious disease progressions, and disruption of circadian rhythm [x].
Black mold and mycotoxin exposure are hazardous for individuals with pre-existing immune system dysregulation.
Mycotoxin damage to the central nervous system, frontal cortex, and brain tissues can increase amyloid plaques, similar to the neurological dysfunction and disease development of Alzheimer’s [i].
Studies are investigating the possibility of mycotoxin’s impact on the nervous system in amyotrophic lateral sclerosis (ALS), as well as a connection between mycotoxins and Parkinson’s disease [viii].
Research has also suggested that multiple sclerosis (M.S.) may primarily be a mold toxin caused by gliotoxin, a mycotoxin produced by the Aspergillus and Candida species [ii].
Additionally, there is a correlation between mycotoxins and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). One study indicated that 93 percent of ME/CFS patients had at least one mycotoxin in their urine [ii]. Evidence also suggests that individuals exposed to mold have higher indices of hypothyroidism [vii].
Clinically, combining information regarding nutritional deficiencies, environmental toxin exposure, and genetic testing can help identify patients most susceptible to mycotoxins [ii].
In addition, evaluating genetic single nucleotide polymorphisms (SNPs), proteomics, and other markers of cellular function in the immune and methylation system can direct potential treatment options [ii].
However, further research is needed to better understand the associations between black mold exposure and the effect of mycotoxins on a neurological and immunological function to develop the best possible treatments [vi].