Search

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.

Clinical practice always necessitates proper diagnosis and correct treatment. For most clinical fields, determining the cause of the illness is irrelevant to the intervention. An oncologist, for example, has no need to explore the “cause” of the patient’s lymphoma. Allergists, by contrast, have tools and the need to examine the relevant allergen which is the putative “cause” of the patient’s allergic symptomatology. In the context of a legal claim, the “cause” of the symptoms or disorder is central, because it determines financial responsibility. However, in the case of an allergic disorder and identified allergen, a claim requires more. Whose allergen? Where did it come from? These are crucial questions that must be answered. This paper explores the approaches to causal assessment which are important for the clinical allergist as he/she navigates the interface between clinical practice and legal proceedings. Its purpose is to help the allergist understand that interface, and to be prepared to enter an unfamiliar legal arena.

There is no uniformity in the suggested guidelines for acceptable levels of fungi in indoor ambient air. Thus, health professionals have no way to determine what levels of fungi may pose a threat to human health. The authors reviewed the published literature to identify data reported for noncomplaint structures, that is, structures in which occupants did not have health concerns associated with the quality of the indoor air. For both commercial and residential structures, fungal concentrations detected were often higher than currently suggested guidance values. The average indoor air concentration in 149 noncomplaint commercial buildings was 233 colony forming units (CFU) per cubic meter, whereas outdoor ambient air levels averaged 983 CFU/m(3). Total indoor spore counts ranged from 610 to 1040 spores/m(3) in three commercial buildings. Outdoor total spore counts associated with these buildings ranged from 400 to 80,000 spores/m(3). The average indoor concentration reported for 820 noncomplaint residential structures was 1252 CFU/m(3) with an average outdoor level of 1524 CFU/m(3). Total spore counts detected indoors at 85 residential structures ranged from 68 to 2307 spores/m(3). Outdoor spore levels associated with these structures ranged from 400 to 80,000 spores/m(3). A large proportion of both commercial and residential noncomplaint structures have indoor ambient air fungal concentrations above 500 CFU/m(3), a level often advocated as requiring remediation in structures when occupants complain of nonspecific adverse health symptoms.

The fundamental issue in the multiple chemical sensitivity (MCS) debate is whether this phenomenon is primarily a psychogenic or toxicodynamic disorder, that is, whether symptoms are due to an emotional response to perceived chemical toxicity or to a pathological interaction between chemical agents and organ systems. The distinction between psychogenic or toxicodynamic is essential to the medical management of an MCS patient. A behavioral origin leads to a behavioral therapy, whereas a toxicodynamic etiology may necessitate avoidance and exposure control methodologies. Regulatory, legislative, judicial, and occupational control responses are also dependent upon the critical distinction between psychogenic and organic etiologies. If people are being poisoned by low levels of chemicals, one set of responses follows. If, on the other hand, MCS sufferers are symptomatic for emotional reasons, the response is different. Everything that is known about MCS to date strongly suggests behavioral and psychogenic explanations for symptoms. The premature use of the term multiple chemical sensitivities has hampered effective exploration of and response to this phenomenon, because it suggests, to the lay person, a physiological explanation. It is time that this disorder be properly characterized so that sufferers receive the care they need and so that new "victims" are not recruited.

Today’s newest growth industry-environmental health litigation-is straining our court system’s search for the truth. The newness of the subject matter has spawned an abundance of inexpert experts coming before courts which are unprepared to discern valuable from misleading testimony. As a result, scientifically worthless testimony, misleading rather than helpful to the triers of fact, abounds. Here we will consider the proper role of modern science in the assessment of environmentally caused illnesses. We will see how offhanded, nonscientific testimony is often admitted in violation of Federal Rules of Evidence against such admissions. Finally, I shall present recommendations to permit the courts to assess the methodology employed, and hence, the admissibility, of evidence presented by medical expert witnesses in these proceedings.

A patient with the preoperative diagnosis of indeterminate pulmonary nodule which proved at operation to be a single left pulmonary vein has been presented. No resection was performed and delayed postoperative pulmonary angiography confirmed the operative diagnosis. We discuss differential diagnosis and a retrospective analysis of how unnecessary thoracotomy might have been avoided.

This report describes the twenty-first case of intrahepatic cystic dilatation of the biliary tree and the first with an associated choledochal cyst. The age, incidence, and clinical manifestations of this disease are extremely varied and the prognosis, although unpredictable, has generally been unfavorable. Although this disease appears to be quite uncommon, it is likely that it will be seen more frequently as awareness of its existence is more widely disseminated. One should consider this diagnosis in cases of repeated jaundice or cholangitis when extrahepatic obstruction cannot be identified.

Complications following ilesostomy are not uncommon. Fluid and electrolyte imbalance, skin excoriation and breakdown, stenosis of the stoma and mechanical small bowel obstruction are the usual problems which may occur. Recently, a new complication following total colectomy and ileostomy has been recognized. Uric acid urolithiasis, usually associated with gout, leukemia or polycythemia, has been found in a significant number of patients after total colectomy. 1 Prospective studies report this complication in 9% to 13% of all patients with established ileostomies. 2,3 Loss of fluid and electrolytes from the gastrointestinal tract may contribute to this unusually high incidence of uric acid lithiasis, but confirming clinical data is lacking. The purpose of this study is to determine alterations in uric acid excretion in patients with established ileostomies and uric acid calculi. Based on these findings, methods of prevention and management of this complication will be discussed. Patients Three patients with established ileostomies