The ability of the filamentous molds to grow on foods, animal feeds, or the raw material used in their manufacture makes them a problem in that they spoil these commodities and make them potentially dangerous to health. Mold spores are ubiquitously distributed in nature and under suitable environmental conditions in the field or in storage, they will germinate and fungal growth will flourish. Molds on their own may be innocuous. During their growth process, however, toxic secondary metabolites, known collectively as mycotoxins, may be synthesized. Mycotoxins are a broad group of natural products, which have the potential to disrupt n o r d metabolism in man and animals. In their 1975 review of mycotoxins, Hardwig and Munro suggested that the economic importance of mycotoxins and mycotoxicoses in Canada and their implication regarding human and animal health were largely unknown. This uncertainty was due, in part, to limited data on the natural occurrence of these toxins and an inadequate knowledge of their effects on human and animal health. This uncertainty remains today. Should distressed grains, grains contaminated with fungi and mycotoxins, be used in feeds or foods to recover or reduce losses? Problems associated with mold contamination concern many sectors of the agriculture industry. The grain producer suffers economic loss owing to the downgrading when mold is visible on his crop. The feed manufacturer is reluctant to accept contaminated grains for use in diet formulation. A recent case involving alleged mycotoxicosis in swine (Schiefer and O'Ferrd 1981), in which the court held a feed manufacturer responsible for the disease, will cause manufacturers to exercise even greater caution in formulating diets. Farmers are faced with the prospect of their animals growing poorly, becoming ill, or both. The situation becomes most acute for the livestock producer who has home-grown moldy feed. In 1980, unusually wet weather conditions promoted Fusarium mold growth in Ontario white winter wheat and Quebec spring wheat. This was a serious infestation as at least 60% of the 700 800 ton harvest was affected. When the trichothecene, deoxynivalenol, was identified as the predominant mycotoxin, regulatory agencies adopted a cautious management posture. The grain was downgraded to feed grade and a practical solution for its use was adopted. That is, the contaminated wheat was blended with noncontaminated wheat to reduce the dietary exposure to the mycotoxin and decrease the health risk to an acceptable level. This may be an adequate solution when the level of contamination is low and the amount of grain affected is relatively small. However, if the entire Prairie wheat crop were affected, the problem of obtaining sufficient quantities of suitable blending material might prove impractical. Under field conditions, mycotoxieosis in animals is commonly caused by the exposure to a group of mycotoxins, with one or two prominent constituents serving as the major causative agent(s). While the acute effects of purified mycotoxins are well described and we are beginning to understand their metabolism, the potential for synergistic relationships between the various mycotoxins has not been adequately researched. The number of demonstrated cases of mycotoxicoses in Canada is relatively small; however, there are many suspected cases of mycotoxicoses. While the acute effect of mycotoxins is known, the significance of long-term exposure to these food contaminants is not well understood. Pier and Mchughlin (1985) noted that several mycotoxins diminish the effectiveness of native and acquired resistance to infectious disease at dietary levels below those required to produce the clinical symptoms of mycotoxicosis. They suggest that mycotoxins cause animals to be unthrifty or to succumb to infectious pathogens, and since the underlying mycotoxin etiology is not recognized, the symptoms are attributed solely to the infecting agent. In western Canada, the presence of ochratoxin A in the blood of slaughter pigs (Marquardt et d. 1988), T-2 toxin on grain from the Peace River district of northern Alberta and British Columbia (Puls and Greenway 19761, and de-oxynivalenol in Manitoba wheat (Clear and Abrmson 1986) are causes for concern. Ochratoxin A is a potent nephrotoxin and has been associated with endemic neuropathy in human populations. In Denmark, swine carcasses containing oxhratoxin A residues are condemned by law. It has been suggested that the trichothecene mycotoxins, including T-2 toxin and deoxynivalenol, are involved in the causation of esophageal cancer (Schoenea$ 1983), as well as impairing the effectiveness of innate defence mechanisms and immunogenesis (RobbanaB a m t et al. 19881, Therefore, while the absolute levels of these mycotoxins in the food chain may be low, the effect of chronic exposure to such compounds may not be insignificant. The efforts of Dr. Bruce B. Virgo, Special Editor for the Mycotoxin Symposium, and Mrs. Lynda Hendrickson, Editorial Assistant, Canadian Journal of Physiology and Pharmacology, are very gratefully recognized, The financial support of Canada Packers Inc. and Prairie Pools Inc. are gratefully acknowledged.