Risk from inhaled mycotoxins in indoor office and residential 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.

Diisocyanate emission from a paint product: a preliminary analysis.

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.