The NATO/CCMS Pilot Study on Indoor Air Quality.
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Biomedical subjects
Publications and source records attributed to M Maroni.
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Recent studies have suggested that somatostatin could reduce calcitonin plasma levels (CT) in normal subjects and in medullary thyroid carcinoma (MTC). The aim of this study was to examine the usefulness of the somatostatin analog, sandostatine (SMS 201.995) in MTC with elevated residual CT levels post-thyroidectomy with or without metastases. 18 patients (17-64 years, 12 men and 8 women) with CT greater than 850 pg/ml (N less than 150 pg/ml) and with metastases in 12 cases, were studied. MTC was sporadic in 11 cases, familial in 4 cases and of undefined form in 3. Initial posology was 300 micrograms/d of sandostatin (3 injections/day). It was then increased by 300 micrograms/d every 9 day till a maximum of 1500 micrograms/d. Treatment duration was 37 days in 11 cases and 60 days in 7 cases. Plasma CT and carcinoembryonic antigen levels (CEA) were measured before treatment and at the end of each dosage plateau. Morphologic evaluation of metastases was done at 0, 30, 60 days. 7/18 patients were reevaluated 2 to 8 months after with drawal of sandostatine. Treatment was well tolerated. Flushes improved in 4 out of 5 cases but diarrhea in only 2 out of 9 patients. Sandostatine was without any effect on plasma CEA. Heterogenous responses were observed for plasma CT levels (CT decreases greater than 20% in 8/18 patients when 900 to 1500 micrograms/day were administered). Patients were subdivised into 3 groups according to CEA levels and presence or absence of metastases. Group A (n = 9) had elevated CEA levels (greater than 10 mg/ml) and metastases.(ABSTRACT TRUNCATED AT 250 WORDS)
Biotechnology has been defined as the application of biological organisms, systems or processes to manufacturing and service industries. In considering health aspects of biotechnological development it must be underlined that the use of microorganisms in traditional industries, such as the production of food, bread, beer and dairy products, has not added significantly to the more usual industrial hazards. The risk factors encountered in the biotechnology industry can be defined as general, i.e., common to other industrial activities, and specific, i.e., depending on the presence of microorganisms and/or their metabolic products. The specific health risks vary according to the type of process, but can be grouped into three main categories: immunological diseases, toxic effects; pathological effects of microorganisms. Allergic immunological diseases such as bronchial asthma, contact dermatitis, oculo-rhinitis and extrinsic allergic alveolitis are by far the most frequent and well known diseases occurring among workers employed on biotechnological production. Toxic effects were observed among workers employed on the production of antibiotics and hormones or single cell proteins, where absorption of endotoxins has been described. Infectious diseases may arise from uncontrolled dissemination of pathogenic microorganisms through aerosols, dusts, aqueous and semisolid sludge effluents from biotechnological plants. The greatest risks occur in the production of antiviral vaccines, in research laboratories and in waste-water treatment plants. Risk of pathogenic effects has also been speculated from exposure to engineered microorganisms in laboratory and environmental or agricultural applications. Safety precautions consisting of protective measures, and effective barriers of containment (both physical and biological) have to be advised according to the hazardous characteristics of the organisms.(ABSTRACT TRUNCATED AT 250 WORDS)
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A cross-sectional study compared 55 transformer repairmen, 38 currently, and 17 previously exposed to polychlorinated biphenyls (PCBs) with 56 non-exposed subjects. PCBs exposures occurred from air and contaminated surfaces, predominantly from Aroclor 1260 with some exposure to Aroclor 1242. Each worker underwent: a questionnaire; standardized medical examination; delayed hypersensitivity testing; and determination of serum and adipose tissue lipid total PCB concentrations. Adipose and serum [PCBs] were significantly higher in the currently exposed, but previously exposed workers did not differ significantly from comparison subjects. No subjects had a classical syndrome of PCB poisoning. A number of neurobehavioral and irritant symptoms were significantly more prevalent in the exposed group, but were probably not related to PCBs. Comedones were more frequent in the exposed group, but no evidence of classical chloracne was noted. Cutaneous delayed hypersensitivity responses to mumps and to trichophyton antigens did not differ between the groups. The association of PCBs with job functions were explored.
Thirty-eight transformer repairmen currently exposed to polychlorinated biphenyls (PCBs), 17 former transformer repairmen, and 56 comparison workers not known to be exposed to PCBs were studied. Measurements were made of serum liver function tests, gamma-glutamyl transpeptidase (GGT), lipid profile, thyroid function tests, and other serum biochemistry; hemoglobin; white cell count; 24-hour excretion of delta-aminolevulinic acid, porphyrins, 17-hydroxycorticosteriods and 17-ketosteroids; sperm count; spirometry; and antipyrine half-life to evaluate microsomal mixed function oxidase induction. The total exposed group differed significantly from the comparison group in albumin, LDH, T4, T4-RT3 index, and actual/predicted FEV1. Significant differences among all three exposure groups were seen for albumin, T4, T4-RT3 index, and 17-hydroxycorticosteroid excretion. Differences in FEV1 were attributable to smoking. Significant correlations between serum PCBs and serum lipids were removed by adjustment for confounding variables. After adjustment for confounding variables, there was a statistically significant positive correlation between serum PCBs and GGT and a negative correlation between adipose PCBs and 17-hydroxycorticosteroid excretion. These may reflect subtle metabolic effects of PCBs.
Urinary creatinine is used as an adjustment factor of the concentration of metabolites excreted in urinary random samples. The usefulness of this practice is longtime disputed. The aim of this study, made in 94 workers, is to estimate if the creatinine-adjustment of V and Ni urinary concentrations brings a true advantage in his capacity to predict the amount of metal excreted in 24 hours. The results shown this practice is pointless and that also in case of urinary samples at anomalous dilution. A greater accuracy in expression of analytical results of V and Ni excretion may be obtained collecting the urinary samples with a known amount, that is to say more representative of the daily diuresis.
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The target enzyme in organophosphorous-induced delayed neuropathy (OPIDN) has been designated neuropathy target esterase or neurotoxic esterase (NTE). NTE activity can be measured in blood lymphocytes and platelets, which could be of use as biomonitors in man at risk for the development of OPIDN. Separation of lymphocytes and platelets from whole blood, recovery, purity, storage and expression of data were examined. A substantial amount of the NTE activity of a human lymphocyte preparation made using Ficoll/Pacque was due to contamination by platelets; further purification was achieved by sucrose-gradient centrifugation. In an easily prepared sample of human platelets less than 10% of NTE was associated with contaminating white cells. We were unable to preserve NTE activity of platelets or lymphocytes at -80 degrees C either 'dry' or with added buffer and glycerol. In 68 male subjects, NTE activity in platelets averaged 8.36 +/- 1.54 nmol min-1 mg protein-1 and NTE activity in lymphocytes, obtained from blood after removal of platelets, 13.34 +/- 2.42 nmol min-1 mg protein-1. A good correlation was found between platelet and lymphocyte NTE activity. NTE activity in platelets may be a preferable method for measuring exposure to axonopathic organophosphorous compounds because of the ease and purity of separation. No correlation with other neuropathic risk factors such as age, smoking and alcohol intake was noted.
A multinational epidemiological study on the neurotoxic effects of long-term, low-level exposure to organophosphorus pesticides (OPs) is being supported in ten European countries by the United Nations Development Programme (UNDP) jointly with the World Health Organization (WHO) Regional Office for Europe. The protocol developed for the study is directed at the assessment of OP exposure and absorption, abnormal neurological findings, and behavioral changes in both agricultural and industrial workers. The biological monitoring tests adopted in the study have been standardized and submitted to quality assurance programmes.
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Twenty-two female subjects working in a factory in which 1,1,1-trichloroethane was the only solvent used were investigated by means of clinical, neurophysiological and psychometric methods so that the neurotoxicity of the solvent could be evaluated. On the basis of the ambient air concentrations of 1,1,1-trichloroethane ranging from 110 to 990 ppm, the workers were divided into three risk groups and compared with a reference group. No significant difference was observed between the exposed and unexposed females with respect to clinical features, maximal motor conduction velocity, conduction velocity of slow fibers, and psychometric data. The most frequent complaints of the workers were of the "neurotic" type with a slightly higher, but not significant, difference in the exposed group. The results obtained favor the absence of a manifest neurotoxic effect of 1,1,1-trichloroethane under the specific work conditions of the investigation; generally unfavorable work conditions seem to have played a prominent role in the genesis of the neurotic complaints. The importance of a global methodological approach in the study of work-related risks, particularly in neurological and psychological surveys, is stressed.
Acephate is a water-soluble organophosphate insecticide whose action on insects has been related to its conversion to methamidophos, a very potent anticholinesterase agent which has caused delayed neuropathy in man. Inhalation and skin exposure to acephate was evaluated in four workers engaged in 8-day campaigns with the formulation of the 97%-pure technical product. Before, during, and after exposure, the workers were monitored for the urine content of acephate and methamidophos, and for erythrocyte (AChE) and plasma (PChE) cholinesterase levels. Median air concentrations (8-hr TWA) ranged from 0.278 to 2.170 mg/m3; median total-body skin deposition ranged from 26.1 to 41.9 mg/day. Based on these values, daily workers' absorption of acephate was estimated to be in the order of 10-20 mg. Urinary excretion of unchanged acephate followed a pattern consistent with exposure, showing peak values of excretion during the workshift or in the eight hr after the end of the workshift. The urine levels of unchanged acephate were found to vary from 1 to 10 mg/L. Methamidophos was not detected in any urine sample (detection limit: 30 micrograms/L). High correlation (r = 0.78) was found between skin exposure level and urine acephate elimination. No changes in AChE or PChE were observed for the workers whose urinary concentrations of acephate were 1 or 2 mg/L. One subject who had urinary acephate excretion between 3 and 8 mg/L, showed slightly decreased values of PChE during exposure and of AChE after exposure.
This article reviews the biological indicators available for monitoring human neurotoxicity by exogenous chemicals with reference to the phases in which the neurotoxic process takes place, namely delivery, receptor-linkage, and toxicodynamic phase. Among the delivery phase tests, indicators are available for metals (lead, mercury) and some organic substances (CS2, n-hexane, DDT, etc.), but a correlation between neurotoxic effects and these indices is rather loose or not yet proved. The receptor-phase tests comprise well known enzymes, such as cholinesterase, less known but promising indicators, such as neuropathy target esterase (NTE), and new tools under study, such as acrylamide-hemoglobin adducts or 2,5-hexanedione-protein adducts. The toxicodynamic phase tests, which mainly consist of measuring substances released from the nervous system, have provided so far rather poor results, but more specific techniques of measurement (monoclonal antibodies) could offer new possibilities in the future.
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