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.

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.

The basis for some common gypsum wallboard mold remediation practices was examined. The bottom inch of several gypsum wallboard panels was immersed in bottled drinking water; some panels were coated and others were untreated. The panels were examined and tested for a period of 8 weeks. This study investigated: (a) whether mold growth, detectable visually or with tape lift samples, occurs within 1 week on wet gypsum wallboard; (b) the types, timing, and extent of mold growth on wet gypsum wallboard; (c) whether mold growth is present on gypsum wallboard surfaces 6 inches from visible mold growth; (d) whether some commonly used surface treatments affect the timing of occurrence and rate of mold growth; and (e) if moldy but dried gypsum wallboard can be cleaned with simple methods and then sealed with common surface treatments so that residual mold particles are undetectable with typical surface sampling techniques. Mold growth was not detected visually or with tape lift samples after 1 week on any of the wallboard panels, regardless of treatment, well beyond the 24-48 hours often mentioned as the incubation period. Growth was detected at 2 weeks on untreated gypsum. Penicillium, Cladosporium, and Acremonium were early colonizers of untreated panels. Aspergillus, Epicoccum, Alternaria, and Ulocladium appeared later. Stachybotrys was not found. Mold growth was not detected more than 6 inches beyond the margin of visible mold growth, suggesting that recommendations to remove gypsum wallboard more than 1 foot beyond visible mold are excessive. The surface treatments resulted in delayed mold growth and reduced the area of mold growth compared with untreated gypsum wallboard. Results showed that simple cleaning of moldy gypsum wallboard was possible to the extent that mold particles beyond "normal trapping" were not found on tape lift samples. Thus, cleaning is an option in some situations where removal is not feasible or desirable. In cases where conditions are not similar to those of this study, or where large areas may be affected, a sample area could be cleaned and tested to verify that the cleaning technique is sufficient to reduce levels to background or normal trapping. These results are generally in agreement with laboratory studies of mold growth on, and cleaning of, gypsum wallboard.

Exposure of workers to diisocyanates in the polyurethane foam manufacturing industry is well documented. However, very little quantitative data have been published on exposure to diisocyanates from the use of paints and coatings. The purpose of this study was to evaluate emission of 2,4-toluene diisocyanate, 2,6-toluene diisocyanate (2,6-TDI), and isophorone diisocyanate from a commercially available two-stage concrete coating and sealant. A laboratory model of an outdoor deck coating process was developed and diisocyanate concentrations determined by derivatization with 1-(2-methoxyphenol)-piperazine and subsequent high performance liquid chromatographic analysis with UV detection. The detection limit for 2,4-toluene diisocyanate and 2,6-toluene diisocyanate urea derivatives was 0.6 microg TDI/gm wet product, and 0.54 microg IPDI/gm wet product for the isophorone diisocyanate urea derivative. No 2,4-toluene diisocyanate or isophorone diisocyanate was detected in the mixed product. A maximum mean 2,6-TDI emission rate of 0.32 microg of 2,6-TDI/gram of wet product applied/hour was observed for the 1-hour sampling time, 0.38 microg of 2,6-TDI/gram of wet product applied/hour was observed for the 5-hour sampling time, and 0.02 micrpg of 2,6-TDI/gram of wet product applied/hour was observed for the 15-hour sampling time. The decrease in rate of 2,6-TDI emission over the 15-hour period indicates that emission of 2,6-TDI is virtually complete after 5 hours. These emission rates should allow industrial hygienists to calculate exposures to isocyanates emitted from at least one curing sealant.

We conducted an evaluation of shredded paper insulation to identify potentially toxic components. The study was to provide a preliminary characterization of a few samples of insulation currently in use. The following samples were analyzed: previously produced insulation (PPI) containing fire retardants, shredded recycled paper (PPI feedstock), freshly produced insulation (FPI), and insulation which had been installed in a residence (II). Volatile constituents were analyzed by GC-MS from headspace air of samples held at room temperature or heated to 90 degrees C. Extractable constituents were sampled by extracting with methylene chloride, and analyzing by GC-MS. Formaldehyde analysis was done according to EPA Method TO11. Headspace air at room temperature contained no detectable quantities of volatile constituents for any sample measured. In headspace air at 90 degrees C, only PPI contained traces of aliphatic and aromatic hydrocarbons and higher aldehydes, and FPI traces of toluene. Extracts of PPI contained traces of octadecadienoic acid methyl ester and aliphatic and aromatic hydrocarbons and higher aldehydes. Extracts of PPI feedstock contained traces of a substituted cyclohexenecarboxylic acid. FPI contained extractable diethyl phthalate (30-50 micrograms/g). Extracts of II contained traces of methyl palmitate, an octadecenoic acid methyl ester, and a phthalate plasticizer. No formaldehyde was detected. PPI was composed of approximately 98 percent paper fiber and 2 percent pre-gelatinized starch. PPI samples agglomerated together with less than 0.01 percent separating from clumps as fine dust. Boron and sodium were expected and confirmed because they were added to PPI and FPI as fire retardants. Chromium, copper, iron, potassium, magnesium, manganese, phosphorus, and silicon were present at detectable concentrations. Study calculations indicate that an occupant would have to completely consume all the fine particles produced from 3.3 kg of insulation per day to have an intake of boron equivalent to the EPA RfD. No other constituent appeared to be present even close to toxicologically relevant amounts.