[Sino-nasal inverted papillomas and occupational etiology]. / Papillomi invertiti naso-sinusali ed eziologia occupazionale.

The sino-nasal inverted papilloma is a rare benign tumour with certain aggressive features because of frequent relapses and the high probability of malignant degeneration. For these reasons, several studies have been made to evaluate the efficacy of the different courses of treatment, but only afew studies have been carried out to establish the etiology of this tumour, which is still uncertain. Although it is believed that viral infection, chronic inflammation and cigarette smoking can play an important etiological role, it has recently been suggested that occupational risk factors, such as those involved in malignant epithelial sino-nasal cancer (SNC), can also be involved in causing sino-nasal inverted papilloma. A group of 70 patients was examined who have been diagnosed with inverted papilloma from 1991 to 2003; the occupational history, collected via the standardized questionnaire, showed that risk factors like wood and leather dusts, chromium and nickel vapours or fumes and formaldehyde were associated with only 5% of all cases. This proportion is much lower than that established for SNC in several epidemiological studies. Although occupational environmental pollution can be a source of chronic sino-nasal mucosa irritation, on the basis of our results we believe that a causal relationship between exposure to occupational risk factors and inverted papilloma is not likely, differently from the suggestions made in other studies. Consequently, an epidemiological surveillance of inverted papilloma as a "sentinel" tumour, as has been proposed in Italy for SNC, is not considered necessary. Among the possible non-occupational risk factors we observed that 75% of the male patients were smokers and 40% of all patients suffered from chronic sinusitis and sino-nasal polyps. Lastly, among the 70 cases of inverted papilloma, we observed 5 with malignant degeneration.

[Protocol for health surveillance of workers exposed to repetitive arm movements]. / Protocollo di sorveglianza sanitaria di lavoratori esposti a movimenti ripetitivi dell'arto superiore.

BACKGROUND: Repetitive movements of the upper limbs at work can cause the onset of musculo-skeletal disorders and therefore an adequate planning of health surveillance is needed. A Work Group on this problem was constituted in Brescia, Italy, following the great interest raised by recent scientific meetings on this topic. OBJECTIVES: The aim of the Group was to prepare a proposal for a health surveillance protocol for the use of Occupational Health Physicians. RESULTS: Health surveillance for the prevention of upper limb disorders must be based on the degree of risk. The risk assessment procedure should be based on the methodology currently available for ergonomic analysis and should also consider the frequency of upper limb disorders in the exposed workers. In case of moderate risk, it is necessary to identify hyper-susceptible individuals, in order to reduce exposure to repetitive movements by means of an adequate task fitness evaluation and suitable health education programmes. In situations of medium-to-high risk, a specific programme of health surveillance must be planned in order to identify early disorders and prevent the onset of more severe damage using task fitness evaluation and rehabilitation therapies. The appropriate diagnostic procedure is indicated for this purpose and a classification is proposed to divide the upper limb disorders into two stages, according to the clinical picture: a first acute-subacute stage, which is potentially reversible, and a chronic-subchronic stage, which is non-reversible. Legal reports are required according to the stage of the disease identified and must be supported by an adequate risk assessment.

[The use of 1,1,1-trichloroethane (methylchloroform) in industrial operations: the neurotoxicity risk]. / Utilizzo di 1,1,1-tricloroetano (metilcloroformio) in lavorazioni industriali: il rischio neurotossicità.

1,1,1-Trichloroethane (1,1,1-TE) is a widely used organic solvent which is thought to be relatively safe. The present review is mainly focused on the neurotoxic effects of 1,1,1-TE. Concentrations above 350 ppm are considered capable of negatively conditioning the performance of the exposed person, in particular reaction time and manual abilities. Peripheral neuropathies have also been described. More recently the potential neurotoxicity of 1,1,1-TE has been underscored by animal studies investigating the effects of this substance in neurobehavioral tests and on neurochemical parameters. 1,1,1-TE alters the motor activity in small laboratory rodents. In fixed interval responding in mice, the effects of 1,1,1-TE are qualitatively similar to those of other volatile (ethanol) and non volatile (benzodiazepines and barbiturates) CNS depressants. In addition, in drug discrimination procedures 1,1,1-TE shares discriminative stimulus properties with barbiturates, toluene, halotane, and oxazepam indicating that this solvent has behavioral effects in common with central nervous system depressant drugs. From a neurochemical point of view long-term exposure to 1,1,1-TE induces astrogliosis in the cerebral cortex of gerbils as indicated by an increased concentration of glial fibrillary acidic protein. In addition low dose inhalation of 1,1,1-TE for 3 months decreases DNA concentrations in several brain regions of the gerbil. 1,1,1-TE affects also brain concentrations of cAMP and cGMP as well as calcium ion control, possibly through an action on voltage-dependent calcium channels. It has been also suggested that intermediate metabolites of 1,1,1-TE may give origin to condensation products with dopamine, ultimately impairing dopaminergic transmission. Some of the neurochemical effects of 1,1,1-TE are shared by other chlorinated organic solvents as well as by CNS depressants. The literature analyzed indicates that 1,1,1-TE may exert significant neurotoxic effects suggesting that more caution in its use is needed and that attention should be paid to the possibility of an additive effect of 1,1,1-TE and CNS depressants (ethanol, barbiturates, benzodiazepines and other volatile solvents) giving origin to severe neurotoxicity.

Plasma prolactin concentrations in lead exposed workers.

Plasma Prolactin (Prl) Zinc protoporphyrin (Zpp) and blood lead concentrations (PbB) were measured in 76 exposed male workers. All of them were employed in small (not more than 30 persons) pewter factories and were randomly selected from those regularly controlled by the National Health Service, Occupational Health Unit of Brescia (USSL 41). Although all plasma Prl values were within the normal range, the mean value of the subgroup having Zpp and PbB higher than 40 micrograms/dl was significantly higher (+47%) than that observed in the group of workers having Zpp and PbB less than 40 micrograms/dl. The data indicate the possibility of a lead-induced Prl secretion dysfunction, probably mediated by a decrease in dopaminergic inhibitory control.

[Toxicologic hazards at the endocrine level of heavy metals]. / Rischio tossicologico a livello endocrino dei metalli pesanti.

The effects of heavy metals (in particular Pb, Cd, Cr, Mn and Hg) on pituitary, thyroid, adrenal gland, pancreas and gonads are reviewed. The effect of these metals on the CNS centers regulating endocrine function is emphasized. On this time, the reviewed data stress the importance of studying the mechanisms of preclinical damage and the biological markers of it.

[The behavior of lecithin cholesterol acyltransferase (LCAT) in acute viral hepatitis and post-hepatitis cirrhosis]. / Comportamento della LCAT nelle epatiti acute virali e nelle cirrosi postepatitiche.

The behaviour of LCAT was examined in acute viral hepatitis and post-hepatic cirrhosis. In the former case, the enzyme was also investigated during remissions. The influence of cholestasis on LCAT activity was evaluated. Depression was noted in cirrhosis and the acute stage of hepatitis, whereas enhanced values were observed during remissions. Depression of the enzyme by cholestasis is explained in a variety of ways.