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The objective of the present study was to determine whether workers in stainless steel production with low exposure to various forms of chromium show an increase in micronucleated nasal cells or an excess of nasal symptoms or disease. Altogether, 48 workers employed in a stainless steel production chain were studied, 29 of them in the steel melting shop with exposure to hexavalent chromium (Cr(6+)), 14 in the sintering and crushing departments of the ferrochromium plant with exposure to trivalent chromium (Cr(3+)) and five in the mine with exposure to chromite ore (Cr(3+)). Thirty-nine workers from the cold rolling mill, with very low exposure to chromium, served as referents. All the subjects were never smokers with a minimum of 14 years employment in the same department. There were no significant differences between the exposure groups and the referents regarding the mean frequency of centromere-negative or centromere-positive micronuclei (studied by pancentromeric fluorescence in situ hybridization), nasal diseases and symptoms or mucociliary clearance of the nasal cavity. No statistically significant differences in the incidence of cell atypia or inflammatory cells were detected between the exposed workers and the reference group, except for an increase in lymphocytes among the chromite ore workers. Anterior rhinoscopy indicated slight inflammatory changes in nasal mucosa and secretion more often in the Cr(6+) and Cr(3+) groups than in the referents, the Cr(6+)-exposed workers showing more livid or oedemic epithelium. In conclusion, the stainless steel production workers, with low exposure to dusts or fumes containing hexavalent or trivalent chromium, did not show clinical changes in the nasal mucosa or an increase in nasal cell micronuclei or symptoms of nasal diseases, except for slight changes in the nasal epithelium and secretion.

In 1985, Brown Coal Liquefaction (Victoria) Pty Ltd (BCLV) commenced operation of a pilot plant that investigated the feasibility of producing oil from brown coal. The plant operated for five years. This study aimed to use exposure and health information routinely collected by the company to characterize various health parameters of the workforce and to investigate whether any adverse health measures were exposure-related. About 1680 persons were employed at some time or other by BCLV, and the primary study population consisted of 408 workers who had a medical examination at the end of employment and who consented to being in an epidemiological study. Reported photosensitivity was associated with higher cumulative skin exposure (RR = 1.85; 95% CI = 1.22-2.78), with an exposure-response relationship of increasing risk with increasing skin exposure being suggested. There was no consistent evidence that chemical exposure at BCLV had any negative effect on the haematological, biochemical, endocrine or lung function of workers at the plant. However, the maximum follow-up period of less than eight years limits the ability of the study to detect any emerging chronic effects.

A previously described HPLC method for determining hyaluronate in effusions was used to analyze a consecutive series of effusions from 1039 patients with pleural fluids and from 571 patients with peritoneal fluids. A mesothelioma was verified histologically in 50 of the cases. The results were used to estimate the clinical utility of the analysis. With a cutoff of 75 mg/L for hyaluronate-derived uronic acid, assay specificity for a malignant mesothelioma was 100% and the sensitivity 56%. Only 20% of the effusions from the mesothelioma patients showed no evidence of increased production of hyaluronate. Cytological smears from the associated cell pellets were evaluated as malignant or suspicious for malignancy in only 28% or in a further 46% of the mesothelioma cases, respectively, leaving 30% of the pellets as cytologically false-negative. We also analyzed effusions from selected cases submitted from other hospitals, 154 of which had been diagnosed histologically as mesotheliomas. Concentrations of hyaluronate were increased in these cases too, but a considerable proportion of the samples showed evidence of losses of hyaluronate; consequently, the sensitivity of the assay in these samples was lower.

This paper describes the role of detectable blood alcohol in fatal work injuries. An attempt was made to identify all work-related fatalities that occurred throughout Australia in the period 1982-1984. A research team examined coroners' records and classified 1737 fatal injury cases as being work-related according to study definitions. The following were also extracted from data in coroners' records: (i) whether or not the description of the fatal event indicated that inebriation was likely to have been a factor; (ii) whether or not there was documentation of blood alcohol concentration (BAC), and if so, what it was. The likelihood of inebriation was assessed without knowledge of the victim's BAC. In 1030 (59 per cent) of the 1737 fatal work injury cases, a BAC determination was documented. Zero levels were detected in 867 fatalities (84 per cent), and 163 cases (16 per cent) had non-zero BAC. In the latter group the median BAC was 104 mg%. Sixty-five per cent of measurable BAC cases had BAC greater than 50 mg%. Fatality risk in the non-zero BAC group relative to that of the zero BAC group was elevated for the following factors: marital status--single (risk ratio (RR) = 1.7, 95 per cent confidence interval (CI) 1.1-2.8) or separated/divorced (RR = 2.4, CI 1.5-3.8); occupation as manager, executive or administrator (RR = 2.5, CI 1.5-5.8); and commuting (RR = 1.6, CI 1.2-2.0).(ABSTRACT TRUNCATED AT 250 WORDS)

Adjuvant activities of isogenic Salmonella enterica, serovar Typhimurium, O-6,7 and O-4,5,12 lipopolysaccharide (LPS), lipid A and Bordetella pertussis LPS were compared by immunizing groups of mice subcutaneously with diphtheria and tetanus toxoid vaccine alone or mixed with one of the LPS derivatives. Five weeks later the mice were bled and the tetanus and diphtheria antibodies in the sera were measured. All the LPS derivatives efficiently increased the antibody responses when compared to the vaccine alone, but the mannose-rich O-6,7 LPS and lipid A were significantly more potent than O-4,5,12 LPS and B. pertussis LPS. We conclude that the quality of the O antigen influences the adjuvant activity of LPS.

Sera from 30 infants with suspected chlamydial pneumonitis were studied by enzyme immunoassay (EIA) with three antigens: reticulate bodies (RB), purified major outer membrane protein ( MOMP ) of Chlamydia trachomatis strain L2, and purified lipopolysaccharide from Re mutants of Salmonella (Re LPS), which shows complete cross-reaction with chlamydial glycolipid. The immunofluorescence test (I/RB IFAT), which detected IgM antibodies (titer of greater than or equal to 1:64) in 16 patients whose clinical picture was consistent with chlamydial pneumonitis, was the standard method. EIA measured IgM antibodies to the purified antigens but not to RB; 15 sera were positive with the MOMP antigen and two with the Re LPS antigen. High-titered IgG antibodies were detected by I/RB IFAT in 15 and by MOMP EIA in 13 of the 30 sera. By the RB EIA, 17 sera were positive. The MOMP EIA was thus as sensitive and specific as the I/RB IFAT. Because the EIA can be automated, it would make possible the screening of all children younger than six months of age with respiratory-tract symptoms and IgM antibodies to Chlamydia.

Thyrotropin releasing hormone (TRH), 10 pmol kg-1 injected in the region of locus coeruleus, caused a rapid (within 1 min) rise of mean arterial pressure in the urethane-anaesthetized rat. No clear-cut effects in heart rate or ventilation were observed. When TRH was injected into the lateral ventricle, a dose more than 10-fold higher was required to achieve a comparable rise in arterial pressure. It is concluded that TRH may have a physiological role in central cardiovascular regulation.

A cohort of 343 men from a viscose rayon factory in Finland with at least five years of exposure in carbon disulphide (CS2) was followed from 1967 to 1975 with respect to coronary heart disease (CHD) mortality. The exposed cohort had over twofold excess death rate from CHD relative to a matched reference group. Statistical separation of causes other than CHD revealed a difference of two years in the life expectancies of the two populations for the age interval of 25 to 54 years. The coronary mortality had, however, decreased since protective measures were instituted at the plant after the fifth year of follow-up, leaving only one-fifth of the original group exposed and reducing the level of CS2 exposure for them to less than 10 ppm. This trend, although tentative due to the limited experience after the intervention, seems to suggest that the risk of coronary death for the formerly excessively exposed workers can be influenced and lessened to a normal level.

Risk function analysis was performed in order to clarify the relationship between coronary heart disease death rate and occupational carbon disulfide exposure along with two other important risk factors, elevated diastolic blood pressure and older age, in a data set obtained from a 10-year prospective follow-up of coronary mortality in two cohorts of over 340 male industrial workers in Finland. The sole effect of carbon disulfide on the coronary mortality was statistically significant (relative risk = 2.3), and it was largely independent of the level of the other two risk factors. Log-linear models were fitted to predict coronary heart disease deaths. The analysis identified the dual role of raised blood pressure in the potential mechanism of coronary death. Relative risks ranging up to 48 were obtained for the joint non-synergistic effect of these three factors in the exposed group compared to a subgroup of nonexposed, 40-year-old normotensive men. The effect of carbon disulfide exposure on the risk of coronary death, while clearly distinguishable from the effect of hypertension and aging, stayed subordinate to them, but nevertheless remained an important risk element in the work environment.