Industrial hygienists (IHs) are called upon to investigate exposures to mold in indoor environments, both residential and commercial. Because exposure standards for molds or mycotoxins do not exist, it is important for the industrial hygienist to have a broad knowledge of the potential for exposure and health effects associated with mold in the indoor environment. This review focuses on the toxic effects of molds associated with the production of mycotoxins, and the putative association between health effects due to mycotoxin exposure in the indoor environment. This article contains background information on molds and mycotoxins, and a brief summary and review of animal exposure studies, case reports, and epidemiological studies from the primary literature concerning inhalation of mycotoxins or potentially toxin-producing molds. The relevance of the findings in the reviewed articles to exposures to mold in indoor, non-agricultural environments is discussed. Although evidence was found of a relationship between high levels of inhalation exposure or direct contact to mycotoxin-containing molds or mycotoxins, and demonstrable effects in animals and health effects in humans, the current literature does not provide compelling evidence that exposure at levels expected in most mold-contaminated indoor environments is likely to result in measurable health effects. Even though there is general agreement that active mold growth in indoor environments is unsanitary and must be corrected, the point at which mold contamination becomes a threat to health is unknown. Research and systematic field investigation are needed to provide an understanding of the health implications of mycotoxin exposures in indoor environments.

This report is based on proceedings from the Exposure Assessment Tools for Hypersensitivity Pneumonitis (HP) Workshop, sponsored by the American Thoracic Society, that took place on May 18, 2019, in Dallas, Texas. The workshop was initiated by members from the Environmental, Occupational, and Population Health and Clinical Problems Assemblies of the American Thoracic Society. Participants included international experts from pulmonary medicine, occupational medicine, radiology, pathology, and exposure science. The meeting objectives were to 1 ) define currently available tools for exposure assessment in evaluation of HP, 2 ) describe the evidence base supporting the role for these exposure assessment tools in HP evaluation, 3 ) identify limitations and barriers to each tool’s implementation in clinical practice, 4 ) determine which exposure assessment tools demonstrate the best performance characteristics and applicability, and 5 ) identify research needs for improving exposure assessment tools for HP. Specific discussion topics included history-taking and exposure questionnaires, antigen avoidance, environmental assessment, specific inhalational challenge, serum-specific IgG testing, skin testing, lymphocyte proliferation testing, and a multidisciplinary team approach. Priorities for research in this area were identified.

Intravenous administration of lipid is a relatively new treatment in the management of toxicity from lipophilic compounds. It is used in human medicine in the treatment of toxicity from lipophilic local anaesthetics and cardiotoxic drugs and can result in dramatic improvement in clinical status. We present six cases of poisoning in dogs successfully treated with lipid infusion after ingestion of ivermectin (3), moxidectin (2) and baclofen (1). The dogs ranged in age from eight weeks to 14 years, and weighed 4-30 kg. Intravenous lipid therapy was started between six and eight hours and 22 hours after ingestion, and all the dogs responded well. In four dogs, there was clinical improvement within one hour; one had improved within two hours and the other within 4.5 hours of lipid administration. The only adverse effect of lipid infusion reported was mild swelling and pain after extravasation in one case which resolved with conservative management. All the dogs were discharged within 24-52 hours after exposure (7-46 hours after the start of lipid administration), and none developed any apparent sequelae.

Intravenous administration of lipid is a relatively new treatment in the management of toxicity from lipophilic compounds. It is used in human medicine in the treatment of toxicity from lipophilic local anaesthetics and cardiotoxic drugs and can result in dramatic improvement in clinical status. We present six cases of poisoning in dogs successfully treated with lipid infusion after ingestion of ivermectin (3), moxidectin (2) and baclofen (1). The dogs ranged in age from eight weeks to 14 years, and weighed 4–30 kg. Intravenous lipid therapy was started between six and eight hours and 22 hours after ingestion, and all the dogs responded well. In four dogs, there was clinical improvement within one hour; one had improved within two hours and the other within 4.5 hours of lipid administration. The only adverse effect of lipid infusion reported was mild swelling and pain after extravasation in one case which resolved with conservative management. All the dogs were discharged within 24–52 hours after exposure (7–46 hours after the start of lipid administration), and none developed any apparent sequelae.

Mycotoxins are known to produce veterinary and human diseases when consumed with contaminated foods. Mycotoxins have also been proposed to cause adverse human health effects after inhalation exposure to mold in indoor residential, school, and office environments. Epidemiologic evidence has been inadequate to establish a causal relationship between indoor mold and nonallergic, toxigenic health effects. In this article, the authors model a maximum possible dose of mycotoxins that could be inhaled in 24 h of continuous exposure to a high concentration of mold spores containing the maximum reported concentration of aflatoxins B1 and B2, satratoxins G and H, fumitremorgens B and C, verruculogen, and trichoverrols A and B. These calculated doses are compared to effects data for the same mycotoxins. None of the maximum doses modeled were sufficiently high to cause any adverse effect. The model illustrates the inefficiency of delivery of mycotoxins via inhalation of mold spores, and suggests that the lack of association between mold exposure and mycotoxicoses in indoor environments is due to a requirement for extremely high airborne spore levels and extended periods of exposure to elicit a response. This model is further evidence that human mycotoxicoses are implausible following inhalation exposure to mycotoxins in mold-contaminated home, school, or office environments.