Mold Spore Analysis and Toxicity

¶ … Mold Spore Trapping

Current Scientific Knowledge

People are exposed to aeroallergens in a variety of settings, both at home and at work. Fungi are ubiquitous airborne allergens and are important causes of human diseases, especially in the upper and lower respiratory tracts. These diseases occur in persons of various ages.

Airborne spores and other fungi particles are ubiquitous in nonpolar landscapes, especially amongst field crops, and often form the bulk of suspended biogenic debris. The term mold often is used synonymously with the term fungi. A more precise definition would specify that molds lack macroscopic reproductive structures but may produce visible colonies. Respiratory illness in subjects exposed to rust and dark-spored imperfecti fungi was described more than 60 years ago, and physicians worldwide now recognize a sensitization to diverse fungi.

Since fungus particles commonly are derived from wholly microscopic sources, exposure hazards are assessed largely through direct sampling of a suspect atmosphere. Because of their small size, fungal emanations present special collection requirements to ensure particle viability for culture-based studies.

Fungi have two basic structures. Yeast grows as single cells by central division of eccentric budding to form daughter units. Most other familiar fungi are composed of branching threads, 3-10 mcm in width, termed hyphae. A mycelium is an aggregate of hyphae. Hyphae are modified to bear the simple reproductive parts of many microfungi and form the structural tissue of fleshy fungi (eg, mushrooms, puff balls).

In general, familiar allergenic molds reproduce asexually. However, two large and distinctive classes, Ascomycetes and Basidiomycetes, also produce innumerable sexual spores for atmospheric dispersion. In its life cycle, a single fungus organism produces both sexual and asexual spores from morphologically different structures, respectively termed perfect and imperfect stages.

Statistics of Occurrence

There are 35 million persons with sinus problems and 15 million persons with asthma reported in the United States alone. Clinically, physicians know that a sinus infection can contribute significantly to the frequency and severity of asthma attacks.

Toxicity of Mold and Physiology of Affectation

The physiology of mucus in individuals with asthma is similar to that of nasal mucus. Mucociliary clearance (MCC) involves cilia and the layers of mucus on the ciliated epithelium and refers to the movement of particles along a desired path for maximum health. In the upper respiratory tract, cilia propel the mucus and its trapped bacteria and particles to the nasopharynx, where it drops to the hypopharynx and is swallowed. The stomach acid then disposes of the unwanted invaders.

In the lower respiratory tract, the cilia that line the trachea and bronchial tree similarly move the mucus blanket up the trachea and into the hypopharynx for swallowing.

The science of rheology investigates the makeup of this liquid and studies its viscosity and elasticity. Two layers of mucus are present over the ciliated cell; an outer, thick, viscoelastic, semisolid mucus layer, which the cilia do not strike directly, is found over a layer of watery serous fluid. Due to the lowered viscosity of the layer of watery serous fluid, the cilia are able to beat normally and to move the watery lower layer, thereby, affecting movement of the upper thick layer. Changes in these properties affect movement of the mucus blanket and play a major role in pulmonary and sinus disease. If the movement of the blanket is slowed, bacteria are able to multiply as the mucus thickens and stagnates.

Mold Infectious Processes

Fungal exposure can also come from a volatile compound (VOC) that a fungi or mold creates through primary or secondary metabolism that then becomes airborne. Note that primary metabolic processes are those necessary to sustain the life of an organism. These volatile compounds may be constantly created as the fungus consumes its food source during the primary metabolic process. VOCs can irritate the mucous membranes of the eyes and respiratory system.

Fungi that consume certain organic sources can release highly toxic gases. For example, a fungus that grows on wallpaper often releases toxic gas arsine directly from the wallpaper that contains arsenic pigments. Thus, fungi and molds can release dangerous materials when they break down the host material. This can cause mucous membrane irritation in sensitized individuals.

Research is demonstrating that fungal-volatile compounds may impact the "common chemical sense" which senses pungency and responds to it. This sense is primarily associated with the trigeminal nerve. The sensory and motor nerves respond to pungency by trying to hold the breath, discomfort, or through sensations such as itching, burning, and skin crawling. Changes in sensation, swelling of mucous membranes, constriction of the respiratory smooth muscle, or dilation of surface blood vessels may be part of fight or flight reactions in response to trigeminal nerve stimulation.

Reactions often include a reduced attention level, general disorientation, lowered reflex time, dizziness, headache, burning sensation in the mucosa, and so on.

Volatile compounds found in or around homes can be responsible for mucous membrane irritants. It is now believed that fungi can add to the already existing compounds when breaking down certain organic substances. A mold-contaminated building may have a significant contribution from fungal contaminants that are added to common VOCs (e.g., building materials, paints, plastics, and cleaning chemicals).

VOCs in general can result in symptoms that include lowered attention span, headaches, lack of concentration, and dizziness.

Reaction to Mold Odors

Some individuals have very strong reactions to the smells given off by molds. Among humans, there is a high degree of variation in ability to detect these odors. Certain individuals can detect low levels of VOCs, while others can only detect relatively high levels. Those individuals who are particularly susceptible to mold odors may react with headache, nasal stuffiness, nausea, or even vomiting.

Asthmatics often exhibit extreme symptoms when exposed to certain mold-induced odors.

Toxicities

Molds also produce secondary metabolites such as antibiotics and poisonous substances produced by a fungus known as mycotoxins. Sometimes it is possible to isolate antibiotics from the molds themselves in order to utilize some of their properties in fighting infections.

Secondary metabolisms are not necessary for maintaining the existence of a mold - either by creating energy or synthesizing structural components, informational molecules, or enzymes. They do, however, function to provide molds with advantages over other mold and bacteria and are toxic to certain plant and human cells.

Toxic conditions exist when a human is exposured to these mycotoxins - either through ingesting mycotoxin-containing mold spores or with skin contact to toxic mold itself.

Mycotoxins are nearly all cytotoxic (substances produced by microorganisms that are toxic to individual cells), which disrupt various cellular structures such as membranes, and interrupt important processes, including protein, RNA, and DNA synthesis.

Mycotoxins vary in the danger they pose for humans. Mycotoxins pose a threat to larger organisms, not because they are specifically targeting them, but rather because these large organisms inadvertently come across the byproduct of the competing molds all battling for the same ecological niche.

Numerous mold types produce mycotoxins, including some found indoors in contaminated homes and office buildings. Another factor that determines the mycotoxins that are produced by specific molds usually depends on the materials or organisms that they grow on.

It used to be thought that dangerous molds were primarily contaminants in foods. This notion is quickly changing. Recently, researchers have become more concerned with multiple mycotoxins that develop from many types of mold spores growing in moist indoor environments.

Health effects from exposures to such mold mixtures can differ from those related to single mycotoxins in controlled laboratory exposures. Although it is difficult to predict how exposure to multiple toxigenic molds can affect an individual - a synergetic effect can occur - the following table provides possible poor health effects from mycotoxin exposure to multiple molds indoors.

Problems with:

Results in:

Vascular System

Increased vascular fragility, the possibility of hemorrhaging into body tissues.

Possible molds include: aflatoxin, satratoxin, and roridins

Digestive System

Diarrhea, vomiting, intestinal hemorrhaging, liver necrosis, liver fibrosis

Aflatotoxin produces damage to mucous membranes

Respiratory System

Respiratory distress, hemorrhaging from the lungs and surrounding lung tissues

Cutaneous System

Rash, burning sensations, sloughing of skin

Urinary System

Painful and burning urination, increase in infections of the urethra, bladder, and kidneys

Reproductive System

Infertility and changes in the reproductive cycles, menses, and sperm motility

Immune System

Many mycotoxins can produce changes or weakenings of the immune system and can shorten the life span of those with compromised immunity systems (i.e, HIV / AIDS).

Table 1.1. Mycotoxins and their effects on human physiology

Unfortunately, not all types or species of molds have been tested for the presence of mycotoxins. The production of toxins varies according to the type of mold, the substrate on which it grows, and seasons of the year.

National Allergy Bureau

This agency considers mold counts in the air 0-900 as low, 2500 as moderate, 25,000 as high, and above 25,000 as very high. At "high" levels most individuals with any sensitivity will experience symptoms. Acceptable levels for individual species vary since species toxicity varies widely as does spore size, weight, and other features, which affect risk to building occupants.

Allergies are probably the most common reaction to contact with molds. Atopic individuals (i.e., those experiencing allergic reactions that are hereditary) who are exposed to mold, mold spores, or mold byproducts may manifest allergic reactions once they become sensitized to the particular strain of toxic mold.

The reactions can run the spectrum, from very mild and temporary reactions to acute, chronic, and end-system illness.

According to The Institute of Medicine:

in 5 Americans suffer from allergic rhinitis - the most common chronic disease in human beings in 9 Americans suffer from allergen-related sinusitis in 10 Americans have allergen-related asthma in 11 Americans suffer from allergic dermatitis

Approximately 1 in 100 Americans suffer from serious chronic allergic diseases

Current-Day Understanding

The biological system's response and effects of widespread chemical contamination of earth's air, food, and water has been widely documented and published in scientific and medical literature.

Currently, human's sensitivity to chemicals can be defined as an "adverse reaction to ambient levels of toxic chemicals, which are generally accepted as being "subtoxic," in environmental air (home and public buildings), food, and water."

The manifestation of adverse reactions depends on the tissues or organs involved; the chemical and pharmacologic nature of the substances involved; the individual susceptibility of the exposed person (nutritional state, genetic make-up, and toxic load at the time of exposure); the length of time, amount, and variety of other body stressors (total load); and the response of synergism among these at the time of reaction.

It is often difficult, and at times impossible, to distinguish between allergic and toxic responses, and chemical sensitivities may encompass both. Chemical allergies may involve an antigen-antibody reaction and are a small but significant part of the overall spectrum of chemical sensitivity. Another type has been found in survivors of acute poisoning who develop chemical sensitivity.

In two large incidences - the gassing of troops during World War I and the cyanide accident in Bhopal, India - exposed persons have developed chemical sensitivities. In contrast, the etiology of those who have become chemically sensitive following long-term subacute toxic exposures is often difficult to determine.

A significant number of persons are involved in the reaction of toxic airborne pathogens; perhaps as much as 20% of the population. The pathogen-sensitive person may develop reactions quite suddenly or gradually over a period of years. The concentration of the causative pathogens needed to trigger a response diminishes and reaction to a minimal amount of toxic mold may be possible.

This progression is probably related to an overload of the enzyme detoxification systems. Chemical sensitivity is usually manifested in one main organ with secondary effects in others, and symptoms are usually multiple. The end-organ responses are often in the smooth muscles of neuro-cardiovascular, gastrointestinal, urogenital, and respiratory systems, as well as the skin, but any organ may be involved.

Pathophysiology

The total body load is the total of all incitants to which the body has to respond to maintain homeostasis.

Pollutants may be biological (pollens, dusts, molds, viruses, bacterias), chemical (organic or inorganic), or physical (heat, cold, electromagnetic radiation, light, radon, and positive and negative ions).

To prevent disease, the body must manage this burden through use or elimination. If the load is excessive, symptoms may occur as a response to disturbance of the body's immune and enzyme detoxification systems.

Acute toxilogic tolerance demonstrated as masking or adaptation is a change in the steady rate induced by the internal or external environment, with the accommodation of body function adjusting to a new set point.

Adaptation and masking are acute survival mechanisms in which the person apparently adjusts to a constant acute toxic exposure to survive initially but then later pays the price with a long-term decrease in efficient functioning and, perhaps, longevity. Because of this phenomenon, the total body load may increase without the person be aware of such changes in their systemic responses.

Even though no correlated symptoms are apparent, repeated exposures continue to damage the immune and enzyme detoxification systems, and the eventual result is end-organ failure.

Avoidance of the offending substance for four days may unmask associated symptoms. Initial withdrawal symptoms may even occur. However, subsequent re-exposure will produce an immediate and clearly definable reaction because cause and effect are easily distinguished.

When exposed to a toxic substance, the body initially develops a bipolar response, with a stimulatory phase followed by a depressive phase. The detoxification systems begin to work.

If the incitant is virulent, biochemically active, or of substantial volume or duration (as in the case of toxic mold infusion), the detoxification systems may be depressed by the very act of overstimulation. At the same time, a person may perceive a stimulatory reaction in the brain and initially feel that the inciting substance is not harmful but actually pleasurable. Therefore, the person may continue to subject him or herself to more exposures; with time (i.e., minutes to years), however, the body's defenses can break down and depression-exhaustion symptoms develop. This stimulation and the resultant response has been observed with many pollutant exposures, including ozone and airborne pathogens.

Biochemical individuality accounts for individual susceptibility. Each person has differing quantities of carbohydrates, fats, proteins, enzymes, vitamins, minerals, and immune parameters with which to respond to environmental factors. This individuality allows us to clear noxious substances or to contribute to our own body burden. Biochemical individuality depends on at least three factors: genetics, the state of the fetus's nutritional health and toxic body burden during pregnancy, and the person's toxic body burden in later life in relation to nutritional state at the time of exposure.

For example, some persons are born with significantly less of a specific enzyme. Although that person may be able to respond to an environmental stimulant, this response is often considerably less than that of the person who was born with 100% of the expected detoxifying enzyme and immune parameters.

Mechanisms of Sensitivity

Figure 1.1 Krebs respiratory cycle (normal)

Figure 1.2. Krebs respiratory cycle (abnormal)

Our understanding of the mechanisms involved in chemical sensitivity is becoming clearer. Pollutant injury of the lungs or liver leads to free radical generation and subsequent disturbances at the cellular, subcellular, and molecular levels. This reaction can be either immunologic or nonimmunologic through the enzyme detoxification systems. Then, vascular-autonomic nervous system dysfunction occurs with a myriad of end-organ responses.

Type I hypersensitivity is usually found in classic examples of angioedema, urticaria, and anaphylaxis caused by sensitivity to mold and other incitants.

10% of systemically compromised patients appear to fall into this category.

Nonimmune Enzyme Detoxification

Nonimmune triggering of the vessel wall may occur. Complement may be triggered directly through the alternate pathway by molds, foods, or toxic chemicals. Mediators such as kinins and prostaglandins may also be directly triggered. These reactions then cause vascular spasm with resultant hypoxic release of lysozyme, which further accelerates the cycle with more spasm and hypoxia. Eventually, if left untreated and exposed to the triggering pathogen, end-organ failure will occur.

Triggering of the enzyme detoxification systems also may occur in any organ but more frequently in the liver and respiratory mucosa.

Diagnosis

Controversy still exists regarding the exact criteria for diagnosis and the exact regimen for treatment. Although not perfected, recent evidence supports the theory that AFS (allergic fungal sinusitis) represents an immunologic, rather than infectious, disease process. An improved understanding of this underlying disease process has lead to an evolution in the treatment of AFS and other mold-related problems.

Medical therapy has begun to shift from an emphasis on systemic antifungal therapy to various forms of topical treatment and immunomodulation. Likewise, surgical treatment of AFS, still a crucial component of the overall treatment plan of the patient, has shifted from radical to a more conservative but complete, usually endoscopic, approach.

Although important, surgery alone does not lead to a long-term disease-free state. A comprehensive management plan incorporating medical, surgical, and immunological care remains the most likely means of providing long-term disease control for AFS. The exact combination continues to be strongly debated.

Treatment

Injection therapy for inhalants such as toxic molds may help alleviate a chemically-induced hypersensitivity. These can be done daily, but usually are given every four to seven days. Vitamin and mineral supplementation is often necessary to replace any deficiencies occurring from direct toxic damage, an increased metabolism required for detoxification, or competition with direct absorption.