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A study was made via a clinical approach in the absence of environmental data with the aim of demonstrating a possible past exposure to asbestos in a working population that had never been examined before nor had ever undergone any specific health checks. It was deemed useful to compare this working population with a control population not exposed to asbestos. The population under study consisted of 126 employees of a single (thermonuclear) department of a metal engineering industry who reported having used asbestos as insulation material in all heat processes up to the beginning of the 1980's. Pleural plaques were observed in 13 workers that were also confirmed by high resolution TC (HRTC) except in one case. The control group consisted of subjects seen at the Clinica del Lavoro of Milan for non-asbestos related diseases in whom a fibrobronchoscopy with broncho-alveolar lavage (BAL) was performed for diagnostic purposes. In each group asbestos bodies were counted in the BAL liquid using a method with a detection limit of 0.1 bodies/ml. The asbestos bodies detected in the alveolar liquid of subjects in the control group were between a maximum of 0.25 and a minimum of 0 bodies/ml of liquid (mean = 0.03; SD = 0.64) whereas in the sample of subjects from the population under study who underwent BAL the results gave a concentration of asbestos bodies in the BAL liquid between a maximum of 9.0 and a minimum of 0.15 bodies/ml of liquid (mean = 2.38; SD = 2.72). In order to obtain a statistically significant difference between the control population, which was certainly not exposed, and the sample of subjects undergoing BAL from the population for which an occupational exposure was assumed, we applied the non-parametric Wilcoxon-Mann-Whitney test for independent samples in view of the asymmetric distribution of the values of asbestos body concentration in the alveolar liquid: the result was a statistically significant difference (p < 0.001) between the two populations. We also calculated the total asbestos bodies recovered in the BAL liquid of subjects from both populations. In the control group total asbestos bodies were between a maximum of 15 and a minimum of 0 (mean = 1.8; SD = 3.9) while in the group under study the concentration of total asbestos bodies recovered in BAL liquid was between a maximum of 990 and a minimum of 12.7 (mean = 206.5; SD = 270). The Wilcoxon-Mann-Whitney test was also applied to these data, the result of which was that the difference in exposure between the two populations was statistically significant (p < 0.001). Concluding, the study demonstrates the importance of asbestos body count in BAL liquid as an objective indicator of past occupational exposure to asbestos, thus providing documented proof that overcomes any doubts arising from case history and any lack of environmental data that could prove exposure.

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In order to define the need for removal versus conservative interventions regarding asbestos-cement roofs and the possible priorities, visual judgement of the state of deterioration or assessments based on the weight of the superficial friable material that can be removed with adhesives are not sufficient. Since in similar deterioration conditions the dispersion of fibres may vary considerably from case to case, only counting of the dispersed fibres will ensure a correct assessment of the pollution potential of an asbestos-cement weathered surface. The paper describes a simple method for measuring the atmospheric dispersion of fibres based on the well demonstrated fact that primary dispersion from the covering, as from many other sources of asbestos pollution, consists of course bundles that are subject to rapid sedimentation. By means of aluminium boxes containing object-holder slides installed under the edge of the covering for about one month, it is possible, using optical phase-contrast microscopy, to count the fibres that have sedimented and calculate the number of fibres/m2/day. If the method is used with the standardized criteria described, it gives reproducible results, involves low costs and has the advantage of balancing the possible variations in primary dispersion intensity due to changes in the local weather conditions over the relatively long sedimentation sampling period.

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The non-carcinogenic effects of vitreous fibres on the human respiratory apparatus have been the subjects of numerous studies on large exposed populations. No evidence seems to have been produced of the existence of a fibrogenic effect. However, no definite and agreed opinion has yet been expressed by the main Agencies and Institutions working in the field of prevention. As a contribution to the discussion, the paper presents the experience of the Clinica del Lavoro of Milano involving 1000 subjects who underwent broncho-alveolar lavage during assessment and checking for suspected occupational respiratory disease. A group of 23 cases was selected who were exposed to vitreous fibres without other significant exposures to factors considered hazardous for the respiratory apparatus, especially asbestos. We observed 7 cases of alveolitis; 6 cases with pleural thickening; 2 cases of interstitial disease. On the basis of the nature of exposure (duration, latency from beginning and from the end of hazardous occupation), of the data obtained from the examination of the bronchial lavage liquid (presence of vitreous fibres, siderocytes, cellularity), and of the clinical and laboratory data (X-ray, PFR), the view expressed is tendentially reassuring concerning the possible effects of vitreous fibres on the respiratory apparatus. Although the existence of an irritative type of lesion that manifests in the form of alveolitis and localised pleural thickening seems possible, albeit in a limited number of cases, it does however appear much more difficult to admit the existence of a fibrogenic effect.

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Olfactory testing has been of minor interest in Occupational Health due to the lack of testing methods able to detect malingering. On the other hand there is evidence that occupational exposure to several, mainly neurotoxic, substances may result in olfactory damage. We have combined three different testing methods in one package in order to assure a forensic-degree level of results. The package consists of: 1. primary neuron functionality testing with a single olfactory stimulant; 2. olfactory-trigeminal discrimination testing with regular sniff-test; 3. odor identification score by Doty's UPSIT test. Final judgement of a link between olfactory system impairment and occupational exposure to chemicals requires a good knowledge of the present and past occupational exposure and of the general conditions of the patient. It requires collaboration between the Occupational Health specialist and the expert in Olfactology and may be completed with endoscopy, radiography and other specific controls. We suggest that a more extensive use of appropriate olfactory testing should be established at least for special risk groups of workers. This will not only detect occupational health damage that would otherwise have remained unknown, but can also furnish new information on the neurotoxic effects of many inhalable chemicals.

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The paper describes a case of chronic interstitial lung disease due to exposure to hard metals, with progressive global respiratory insufficiency, treated with single lung transplant. Clinical conditions improved gradually after the operation and after more than two years the patient was in good health and had resumed an almost normal life and relationships.

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The aim of this study was to elucidate the site and detailed nature of peripheral nerve damage induced in the rat by chronic CS2 inhalation exposure in the light of the relationship between pathological and neurophysiological data. Adult male rats were exposed to 700 ppm of CS2 2 h/d, 5 d/week for 12 weeks and then followed-up for 18 weeks. The first alteration observed was a decrease in the nerve conduction velocity, discovered after only 3 weeks of exposure. Pathological lesions were first observed in the 10th week and consisted of a typical "giant axon" axonopathy. Obvious pathological lesions of the myelin sheaths were revealed much later, in the 3rd week after the end of exposure, when some nerve fibers were dying back. Recovery took place with the regeneration of new fibers which started in the 8th week after the end of exposure and was nearly complete in the 18th week. These findings demonstrate that CS2-induced polyneuropathy is an axonopathy very similar to that caused by other occupational neurotoxic agents like MnBK, n-hexane, and acrylamide. The timing of the pathological events within the nerve fibers suggests that the pathogenesis of the nerve lesions should probably be attributed to a primary energy failure of the axonal membrane induced by CS2.

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