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Whereas most idiosyncratic environmental sensitivity complaints do not fit known diagnoses, the multiple chemical sensitivities syndrome (MCS) is an extreme presentation that has defined diagnostic criteria. MCS symptomatics claim that they acquired a sensitized state as the result of a chemical exposure, usually to a solvent or pesticide, but not to a fragrance. Before this exposure, they did not experience symptoms. Following sensitization, symptoms increasing in number and severity with time are attributed by the MCS symptomatic to various exposures that are innocuous to most individuals. Although phenomenological studies have provided no evidence that particular odors elicit MCS symptoms, low levels of fragrances and perfumes are frequently associated with the reporting of MCS symptoms. This evaluation examines proposed mechanisms by which odorants and fragrances might cause either sensitization or elicitation of MCS symptoms, including altered odor sensitivity, primary irritancy or irritancy-induced upper airway reactivity, neurogenic switching of trigeminal irritancy signals, time-dependent sensitization and limbic kindling, CNS toxicity, and various psychiatric conditions. In no case was there persuasive evidence that any olfactory mechanism involving fragrance underlies either induction of a sensitized state or the triggering of MCS symptoms. Fragrances and other odorants could, however, be associated with symptoms as claimed by MCS symptomatics, because they are recognizable stimuli, but fragrance has not been demonstrated to be causal in the usual sense.

The Environmental Health and Safety Council of the American Health Foundation has examined current estimates of cancer risks associated with the presence of asbestos-containing materials (ACM) in public buildings. The Council finds that even complete removal of asbestos from all of these buildings will provide no measurable benefit to public health. The removal of nonfriable ACM only can be postulated to protect the public against a small hypothetical risk that cannot be measured epidemiologically. Moreover, examination of the assumptions used in the risk assessment calculations leads to the conclusion that these small calculated risks are likely to represent overestimates. In recent surveys, the measured asbestos levels in indoor air cast some doubt on whether occupant exposure to asbestos levels are contributed to significantly by ACM even when some of the material is friable or in bad condition. Furthermore, the models used for cancer risk estimates assume no threshold level for cancer and conclude that any exposure is carcinogenic. This may be unjustified in light of information on the mechanisms for some asbestos-caused disease. Based on the best available data, it is very unlikely that cancer will result from indoor asbestos exposure, especially where ACM is well maintained.Copyright 1994, 1999 Academic Press, Inc.

Contemporary Issues in Fiber Toxicology. Warheit, D. B., Driscoll, K. E., Oberdoerster, G., Walker, C., Kuschner, M., and Hesterberg, T. W. (1995). Fundam. Appl. Toxicol. 25, 171 - 183. Copyright 1995, 1999 Academic Press

Squamous cell carcinomas of bronchial origin have been produced in lungs of rats exposed to the beta radiation of 106Ru and 32P sources. Utilizing intrabronchial pellets implanted by surgical techniques, the spacial relationships of the emitting pellet to the bronchial origin of tumor has been defined, permitting dose in rads to the target tissue to be directly calculated. Previously reported experiments with electroplated 106Ru sources have shown a rad dose-related incidence of tumor yield. These doses based on time of death with cancer rather than time of initiation of malignant change included some “wasted” radiation. Serial sacrifice experiments with rats exposed to 5 microc 106Ru sources have demonstrated earlier finding of cancer providing for minimum estimates of the period of “wasted” radiation. Spontaneous deaths in the serial sacrifice pool have confirmed the cancer incidences of previous experiments at the 5 microc level. A hollow plastic pellet has been devised for the examination of dose rate effect on tumor induction with the use of isotopes of varying half life. An initial experiment with Phosphorus-32 delivering doses of 103, 104, 105 rads has resulted in a yield of tumors at these levels comparable to the yield from the same dose in rads delivered by 106Ru pellets. Thus, within these limits, there has been no dose-rate dependence for tumor yield.

The radon hazard is presumed to be lung cancer induced by alpha irradiation of basal cells in the bronchial epithelium. The effective dose is calculated by a relatively complete analysis which includes (1) the distribution of atmospheric activity by size and daughter, (2) the prediction of alpha decay in the bronchial regions from a model of mucus flow superimposed on calculated regional deposition, (3) measurements of epithelial thickness to determine accessibility of basal cells, and (4) classification of dose by inhaled daughter, size, alpha particle, region, and tissue depth. The cancer-related dose, taken as the largest dose to exceptionally shallow basal cells, associated with one working level of radon daughters is estimated to be 20 rads/yr for nose breathing at 15 l./min, and it may be higher. Comparison with animal experiments suggests that the working level may not be safe and that 30 pc/l. of daughters (0.1 WL) may not be too conservative for the MPC.