Histopathological findings in heart transplant patients under tacrolimus-mycophenolate mofetil versus cyclosporine microemulsion-azathioprine.
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Biomedical subjects
Publications and source records attributed to L Romeo.
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OBJECTIVES: To determine whether occupational exposure to hand-transmitted vibration is a risk factor for scleroderma (systemic sclerosis, SSc), two case-control studies were conducted in the provinces of Trento and Verona, northeastern Italy. METHODS: In the Trento study, 21 patients with a diagnosis of either systemic or localised scleroderma were recruited from those admitted to all hospitals of the province from 1 January 1976 to 31 December 1991. For each case, two age- and gender-matched controls were selected. In the Verona study, cases included 55 patients diagnosed with SSc and clinically followed at the rheumatology clinic of the local university hospital between 1 January 1997 and 30 June 1999. The controls included 171 subjects frequency-matched by gender and age group. In both studies, all subjects were interviewed by structured questionnaire containing items on personal characteristics, smoking and drinking habits, use of medicines, occupational history and complete medical history. Women were also investigated about silicone implants and cosmetic surgery. Jobs and job tasks involving the use of vibratory tools, with or without concomitant exposure to silica dust in mining and non-mining occupations, were carefully investigated. A minimum criterion of 6 months was required for exposure duration. RESULTS: In the Trento study, men with scleroderma were more likely than controls to have had exposure to hand-transmitted vibration (odds ratio (OR) 1.5, 95% confidence interval (95% CI) 0.1-74.1) or silica dust (OR 5.2, 95% Cl 0.5-74.1), but the association was not significant. The scleroderma patients were miners or stone workers who had operated jackhammers and rock drills. In the Verona study, a greater, although not statistically significant, odds of SSc was observed in men exposed to hand-transmitted vibration (OR 2.4, 95% CI 0.4-14.0) and in women exposed to silica (OR 2.4, 95% Cl 0.4-15.5). The SSc patients with vibration exposure were machinery operators or metal workers who had used grinders and impact wrenches. CONCLUSIONS: Our case-control studies did not show a significant association between scleroderma and hand-transmitted vibration, with or without concomitant exposure to silica dust. Owing to the rarity of the disease and the small number of cases in the present studies, a genetic susceptibility to connective tissue disorders in SSc patients with occupational exposure to hand-transmitted vibration and/or silica cannot be ruled out.
The occupational airborne exposure to benzene of 150 workers employed in petrol stations and a refinery plant was assessed using personal sampling pumps. All workers provided blood samples after the end of work and on the following morning before resuming work. Benzene concentrations in the blood of 243 non-occupationally-exposed subjects were also measured. The median occupational benzene exposure for all 150 workers studied was 80 micrograms/m3. Overall median blood benzene of all workers was 251 ng/l at the end of the shift, and 174 ng/l the following morning. The benzene concentrations measured in blood collected the following morning proved to be significantly lower than those measured at the end of the shift. Median blood benzene for the 243 'normal' subjects was 128 ng/l, which was significantly lower than that measured in the workers before a new work shift. The median blood benzene concentration was significantly higher in smokers than in non-smokers, both in the general population (210 ng/l vs. 110 ng/l) and in the exposed workers at the end of the shift (476 ng/l vs. 132 ng/l) and the following morning (360 ng/l vs. 99 ng/l). End-of-shift blood benzene correlated significantly with environmental exposure; this correlation was better in the 83 non-smokers than in the 67 smokers. In non-smokers with the median benzene occupational exposure of 50 micrograms/m3, no difference was found in blood benzene concentration in exposed and non-exposed subjects.
Epidemiological studies conducted in the 1980s revealed that people working in the rubber manufacturing industry had an increased risk of cancer. Even now, workers employed in rubber processing are still at risk despite the measures adopted to improve their working conditions. The aim of the study was to evaluate the presence of a genotoxic risk in a rubber industry and to verify whether or not it was possible to locate the most dangerous position among the different rubber-working processes. The mutagenic activity of airborne particulate was evaluated in samples collected in the mixing department of a rubber manufacturing plant. Ambient air samples were taken over 3-h period in two stable positions near the mixing (Banbury mixer) and calendering areas. Personal air samples were taken over 2-h period during a normal workday from five workers employed in different rubber processing operations (mixing, weighing, calendering, compounding and extruding). The mutagenic activity of the air samples was determined by plate incorporation assay using Salmonella typhimurium strains (TA 98, TA 98NR, TA 100, YG 1021) with and without metabolic activation. Polycyclic aromatic hydrocarbon (PAH) concentrations were determined by high-performance liquid chromatography (HPLC); the presence of other presumable contaminants were carried out by gas chromatography-mass spectrometry (GC-MS). The results showed substantial direct and indirect frameshift mutagenicity in both ambient and personal samples. No mutagenic activity was present in S. typhimurium TA 100, except in the personal sample from a worker employed on the Banbury mixer. HPLC analysis revealed very low concentrations of PAHs. GC-MS analysis showed the presence of compounds such as azulene derivative, 1,2-dihydro-2,2,4-trimethylquinoline, N-methyl N-phenylbenzenamine, diphenylamine, bis(2-ethylhexyl)phthalate and bis(methyl-propyl)phthalate. We conclude that the high levels of mutagenic activity in ambiental and personal samples indicate the presence of substances with high genotoxic potency; no substantial differences were seen among the several rubber processing operations. PAHs were not involved in indoor pollution. GC-MS analysis revealed the presence of compounds which may be produced by high temperatures to which the raw materials are subjected during rubber manufacturing processes. These substances are potential carcinogen though their mutagen properties have not been clearly determined.
OBJECTIVE: To study the blood benzene levels resulting from environmental and occupational benzene exposure. METHODS: Benzene in venous blood was measured in 243 nonoccupationally exposed subjects ("normal" people) and in 167 workers occupationally exposed to benzene. All exposed workers gave blood samples at the end of the work shift and on the following morning before resuming work. Blood benzene was assayed by gas chromatography (GC)-mass spectrometry. Occupational benzene exposure was monitored by environmental personal samplers and measured by GC analysis. RESULTS: The mean occupational benzene exposure for all 167 workers studied was 186 ng/l (58 ppb; range 5 1535 ng/l, 2-500 ppb). Overall, the mean blood benzene level of all workers was 420 ng/1 at the end of the shift and 287 ng/l on the morning thereafter. The blood benzene levels measured the morning after turned out to be significantly lower (t=3.6; P < 0.0001) than those measured at the end of the shift. The mean blood benzene level of the 243 "normal" subjects was 165 ng/l, which was significantly lower than that measured in the workers on the morning thereafter (t=5.8: P < 0.0000001). The mean blood benzene concentration was significantly higher in smokers than in nonsmokers in both the general population (264 versus 123 ng/l) and in the exposed workers. In the group of nonsmoking workers, whose workplace exposure to benzene was lower than 100 ng/l, blood benzene levels were similar (210-202 ng/l) to those measured in the nonsmoking general population (165 ng/l). End-of-shift blood benzene correlated significantly with environmental exposure (y=0.91x + 251; r=0.581; n=162; P < 0.00001). Finally, there was also a significant correlation between blood benzene measured at the end of the shift and that determined on the morning thereafter (y=0.45x + 109; r=0.572; n=156; P < 0.00001). CONCLUSION: Nonsmoking workers occupationally exposed to benzene at environmental levels lower than 100 ng/l (mean 35 ng/l) and the nonsmoking general population exposed to ubiquitous benzene pollution have similar blood benzene concentrations. This suggests that it is impossible to distinguish between occupational and environmental exposure when the benzene level in the workplace is less than 100 ng/l.
The report concerns a 30-year-old factory worker, employed in a small galvanizing plant for over ten years in the burnishing, copper- and nickel-plating of small metal articles for the shoe industry. Acute arsine poisoning was attributed to the use of a dilute solution of CuSO4 (3%), HCl (32%), and As2O3 (2%) for burnishing metal (Fe-Zn) shoelace eyelet holes, in the absence of local exhaust ventilation and with no respiratory protection. Arsine caused severe intravascular hemolysis with a rapid drop in hematocrit and hemoglobin levels. Other body organs were involved as a result of the hypoxic effect of anemia and hemolysis, or as a direct toxic effect of the arsine itself. Our experience confirms that exchange transfusion is capable of rapidly arresting the adverse effects of arsine. The importance of preventive measures and worker information to avoid acute arsine poisoning is emphasized.
Among the elements of toxicological relevance, inorganic arsenic (As) probably exhibits the most complex metabolism, and we deemed it interesting to identify and quantify the different As species excreted after an occupational acute intoxication with arsine. For this purpose total As and five As species were determined using an hybrid analytical method coupling liquid chromatography with inductively coupled plasma mass spectrometry. The highest urinary elimination of total As was observed in the first 5 d after admission. The As species mostly excreted were monomethylarsonate (MMA), dimethylarsinate (DMA), As3+, arsenobetaine (AsB), and to a lesser extent As5+. The amount of AsB excreted in urine by the subject does not appear to be completely justified by AsB intake through food. Arsenic is excreted mainly via the urine with a clearance of 7.8 ml/h/kg and follows a triphasic model with periods of 28 h, 59 h, and 9 d, respectively. The evidence that DMA excretion culminates after a few days, when the excretion of the inorganic form is substantially reduced (while that of MMA is still elevated), seems to confirm the existence of two successive methylating enzyme activities. Furthermore, the elimination rate of As from blood follows a three-phase model and the half-lives of different species vary from about 27 to 86 h with the following gradient As5+ < MMA < As3+ < DMA < AsB.
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Blood styrene was measured by a gas chromatography-mass spectrometry method in 81 "normal people" and in 76 workers exposed to styrene. In the normal subjects, styrene was also tested in alveolar and environmental air. Styrene was found in nearly all (95%) blood samples. Average styrene levels in the normal subjects were 221 ng/l in blood (Cb), 3 ng/l in alveolar air (Ca) and 6 ng/l in environmental air (Ci). Styrene levels did not differ significantly between smokers and nonsmokers, 95% of values being below 512 ng/l in Cb, 7 ng/l in Ca and 15 ng/l in Ci. In workers with an average exposure to styrene of 204 micrograms/l, at the end of the workshift, mean blood styrene concentration was 1211 micrograms/l. In blood samples collected at the end of the Thursday shift, styrene levels were significantly higher (1590 micrograms/l) than those found at the end of the Monday shift (1068 micrograms/l). A similar difference was found in samples taken the morning after exposure (60 and 119 micrograms/l, respectively). Significant correlations between blood and environmental styrene were found both at the end of the shift and the morning after exposure (r = 0.61 and 0.41, respectively). In workers occupationally exposed to styrene, 16 h after the end of the workshift, blood styrene (94 micrograms/l) was significantly higher than that found in the normal subjects (0.22 microgram/l). The half-life of blood styrene was 3.9 h.
The concentrations of Fe, Mn, Pb and Cr have been determined in broncho-alveolar lavage (BAL) fluid of 25 subjects without occupational or abnormal environmental exposure to metals, using the AAS method. The numerous factors which can interfere with the results in pre-analytical and in analytical phases are stressed. Metals concentrations in BAL are expressed in micrograms/l. They were not correlated with the volume of fluid recovered, the total cells, alveolar macrophages and erythrocytes. The results were not modified by stratification considering age and sex. Iron concentrations were higher than others, probably due to higher environmental exposure and partly to its essential role in humans. The diagnostic significance of element determination in BAL fluid and the relationship with exposure and lung load is discussed.
Blood benzene was determined by gas chromatography-mass spectrometry in 431 "normal" subjects, subdivided into 155 rural subjects and 276 urban subjects. Blood benzene (mean value 262 ng/l) was significantly lower in rural (200 ng/l) than in urban (296 ng/l) workers, as well as differing significantly between 293 non-smokers and 138 smokers (205 ng/l and 381 ng/l, respectively). Among non-smokers, values were significantly higher (307 ng/l) in 76 chemical workers. In the total study population, in 95% of cases blood benzene was less than 718 ng/l, the 95th percentile being 514 ng/l in non-smokers vs 901 ng/l in smokers and 576 ng/l in rural vs 822 ng/l in urban subjects. Within each population subgroup, the difference between non-smokers and smokers was statistically significant, except among office workers (non-smokers 234 ng/l, smokers 304 ng/l). Blood benzene (y) was directly proportional to the number of cigarettes smoked (x) (y = 201 + 12x; r = 0.44; n = 431), and inversely proportional to the interval between the last cigarette and the time at which the blood samples was taken (z) (log y = 6.167-0.0015z; r = -0.461; n = 135). The blood half-life of benzene was about 8h. The multiple correlation between blood benzene (Cb), number of cigarettes per day (x) and time since the last cigarette (z) is: Cb = 417 + 7.2x - 0.41z (n = 135; R = 0.20; P less than 0.00001).
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n-Hexane levels were determined by gas chromatography and mass spectrometry in environmental air and in the alveolar air, blood and urine of a group of subjects aged on average of 38 years who had not been occupationally exposed to this hydrocarbon. n-Hexane was found in all environmental air samples examined (n = 49), with the mean concentration being 104 ng/l (limit values, 1-279 ng/l). It was also found in all 49 samples of alveolar air, with the mean concentration being 50 ng/l (variation limit, 1-304 ng/l). In 64 samples of urine, n-hexane was found in only 50 samples, with the mean concentration being 1,417 ng/l (limit values, 34-8,820 ng/l). In 77 of the 90 blood samples taken, a mean concentration of 608 ng/l was detected (variation limit, 15-7,684 ng/l). Particularly the haematic and urinary concentration showed significant differences among the nine groups of individuals classified according to their work activity. The lowest levels were found in the blood and urine of farmers: 270 and 298 ng/l, respectively. The highest values were found for chemical workers (1,377 and 411 ng/l), respectively printers (585 and 2,691 ng/l respectively), and traffic wardens (740 and 8,820 ng/l, respectively). In all, 95% of the determinations of n-hexane yielded values of less than 255 ng/l in environmental samples, less than 105 ng/l in alveolar air, less than 1,475 ng/l in blood and less than 5,875 ng/l in urine. A comparison of these data revealed a significant correlation between environmental levels and alveolar (r/s = 0.769; P less than 0.00001), haematic (r/s = 0.624; P less than 0.0002), and urinary (r/s = 0.597; P less than 0.0005) values for n-hexane.
Benzene was measured in blood and alveolar air of 168 men, aged 20-58 years, subdivided into four groups: blood donors, hospital staff, chemical workers occupationally exposed to benzene, and chemical workers not occupationally exposed to benzene. The group of exposed workers was employed in work places with a mean environmental exposure to benzene of 1.62 mg/M3 (8 hr TWA). Non-exposed workers were employed elsewhere in the same plant, with an environmental exposure to benzene lower than 0.1 mg/M3. Blood and alveolar air samples were collected in the morning, before the start of the work shift for the chemical workers. The group of exposed workers was found to be significantly different from the other three groups, both for blood and alveolar benzene concentrations. The mean blood benzene concentration was 789 ng/l in the exposed workers, 307 ng/l in the non-exposed workers, 332 ng/l in the hospital staff, and 196 ng/l in the blood donors. Apart from the exposed workers, blood benzene concentration was significantly higher in smokers than in non-smokers. The mean alveolar benzene concentration was 92 ng/l in the exposed workers, 42 ng/l in the non-exposed workers, 22 ng/l in the hospital staff, and 11 ng/l in the blood donors. Alveolar benzene concentration was significantly higher in smokers than in non-smokers in the groups of the hospital staff and non-exposed workers, but not in the blood donors and exposed workers. In the three groups without occupational exposure considered altogether, the alveolar benzene concentration correlated significantly with environmental benzene concentration measured at the moment of the individual examinations, both in the smokers (r = .636; p less than .001) and non-smokers (r = .628; p less than .001). In the same three groups and in the exposed workers, alveolar benzene concentration showed a significant correlation with the blood benzene concentration.
Benzene, toluene, cumene and styrene were measured in the breath and blood of two groups of individuals. The first group included individuals belonging to a hospital staff, the second group included chemical workers who were not exposed to the abovementioned chemicals. The chemical workers were examined in plant infirmaries on the morning before the start of the workshift, and the hospital staff in the hospital infirmaries. One environmental air sample was taken in the infirmaries for each individual at the moment of the biological samplings. The environmental concentrations of benzene and styrene were significantly higher in the infirmaries of the chemical plant than in the infirmaries of the hospital. On the other hand, the environmental concentrations of toluene and cumene were not significantly different in the plant infirmaries and in the hospital infirmaries. In the hospital staff the alveolar concentrations of benzene, toluene and styrene were significantly lower than those in the chemical workers. In the hospital staff the blood concentrations of benzene, toluene and styrene were not significantly different from those in the chemical workers. Only the blood cumene concentration was significantly higher in the chemical workers. In hospital staff, smokers showed alveolar and blood concentrations of benzene and toluene that were significantly higher than those measured in the non smoker hospital staff. With reference to chemical workers, only alveolar benzene concentration was significantly higher in smokers than in non smokers.(ABSTRACT TRUNCATED AT 250 WORDS)
Statural growth and its relation to growth potential, renal function, blood urea nitrogen (BUN), mineral metabolism hormones and dietary intake were studied in 17 prepubertal children (aged 1.6-9.3 years) on conservative treatment for chronic renal failure due to tubulo-interstitial nephropathy. Statural growth (height SDS) was related to the degree of renal failure, was more retarded than ossification, and was independent of the chronological age of the patients. We observed that the lower the glomerular filtration rate (GFR), the lower was the growth potential (increased bone age/statural age ratio). Growth velocity may be normal regardless of statural and bone maturation delay and the degree of renal insufficiency. Impaired growth rate correlated with parathyroid hormone levels, caloric intake and increased blood urea nitrogen during the year of observation. These data show that comprehensive monitoring and suitable treatment must be performed in order to prevent growth retardation at any GFR level.