Change in pulmonary diffusing capacity for carbon monoxide (DL) with ambient temperature was investigated to compare the relation between DL and pulmonary capillary blood volume (Vc) with that occurring during exercise in the previous study and to examine the possibility of evaluating the potential capacity for increase in Vc. Five subjects were exposed to ambient temperatures of 12, 20, 28 and 36°C for about 100 min. The average DL increased by about 30% from 27.2 at 36°C to 34.9 ml/min/Torr at 12°C. DL was primarily determined by acute change in Vc which might be well related to determinants of change in stroke volume rather than cardiac output. It was implied that the mechanism of change in DL at rest might be different that during exercise. The best parameter matching for change in DL was mean skin temperature, which was considered to make possible the detection of changes in Vc. Comparison with the previous study revealed that the magnitude and pattern of change in DL with Vc was uniform whether Vc was altered either by change in ambient temperature or by performing exercise. This means that it is not always necessary to have a patient perform exercise in order to examine the potential increase in Vc. On the other hand, change in DL in this study seemed to depend mainly on the characteristics of the pulmonary arterial system while change in DL during exercise seemed to depend on the total number of the pulmonary capillaries in the previous study. Therefore, it was implied that selection of stimulation, which could either be change in thermal condition at rest or an exercise regime, could assist in the differentiation of various characteristics of pulmonary diseases.
Automobile gasoline samples, 214 in total, were collected in 14 major cities in various parts of Japan in the autumn of 1983, and analyzed for aromatic and other contents on a Silicone OV 101 capillary GC column. n-Hexane, benzene, toluene and xylenes (3 isomers plus ethylbenzene) contents were 5.7, 1.4, 8.1 and 10.4% (v/v) as grand means, respectively. There was no remarkable vairation in contents between the samples from different cities nor the samples of different brands. Comparison with the results of a 1976 study disclosed no apparent changes in aromatic contents in the past 7 years.
Pathological changes in lung tissues of Sprague Dawley rats after single intratracheal administration of 1 mg, 5 mg or 10 mg of zinc stearate were examined to ascertain whether lung fibrosis such as that described in Uotila's case report is caused by exposure to this dust. The results obtained were as follows: 1. The lungs of rats administered 1-10 mg of zinc stearate did not show any evident formation of dust foci or proliferation of collagen fibers after nine months, whereas such changes were evident in the rats administered 10 mg of quartz. 2. The hydroxyproline content of the lung, as an indicator of collagen fiber formation, was significantly less in the zinc stearate groups than in the rats ad-ministered 10 mg of quartz. 3. The Zn content of the lung tissues increased soon after the administration of the dust and then decreased rapidly. The incresed dust content of whole lungs of rats administered 10 mg of zinc stearate was 641 pg after week and 53 pg after nine months. From the above results, it was considered that zinc stearate by itself might not always act as a severe chemical irritant or a main facter in fatal pneumoconiosis.
In rats intraperitoneal injection of lead (8 mg/kg as Pb-acetate) over a period of 15 days induced histoenzymic and histological alterations in the testes. Histopathological examination revealed at places degeneration of seminiferous tubules. There were patchy areas showing marked loss in the activity of succinic dehydrogenase and adenosine triphosphatase whereas alkaline phosphatase activity showed only slight inhibition in treated rats. These alterations suggest that in the initial stage of exposure to lead, the disruption of cellular energetics and cation transport in the testicular tissue may be responsible for altering the germinal function of the testis.
Retention and clearance of chromium in the lung, heart, liver, kidney, spleen, plasma and blood cells were investigated in rats after a single exposure to either hexavalent chromium (Cr (VI)) or trivalent chromium (Cr (III)) aerosols with different chromium levels (7.415.9 mg Cr/m3) and different particle size distributions. The investigation was carried out from 0.5 h up to 7 days after exposure. Exposure to Cr (VI) aerosol showed more toxic effects than exposure to Cr (III). Initial cocentrations of lung chromium were in proportion to the exposure levels for each inhalation series of Cr (VI) or Cr (III) compounds. Chromium clearance from the lungs in the Cr (VI) groups was dependent on the size distribution of the aerosol particles. In the groups exposed to smaller Cr (VI) aerosol particles the lung chromium clearance showed two phases. The biological half-time of the first phase was 31.5 h and that of the following second phase was 732 h. Chromium clearance from lungs exposed to larger particles of Cr (VI) or to Cr (III) aerosols showed a single phase, the biological half-time of which ranged from 151 to 175 h. Chromium transport from the lungs into the blood, kidneys and liver was more rapid in the Cr (VI) groups than in the Cr (III) groups. In the former groups, the kidneys and liver also showed two-phase chromium clearance. These results suggest that considerable amount of chromium deposited in lung alveoli as the hexavalent form are rapidly transfered into the blood and taken up by erythrocytes or visceral organs, especially the liver and kidneys, before being reduced to the trivalent state.
Benzanthrone, a popular anthraquinone dye-intermediate is known to cause skin and other toxicological manifestations in industrial workers exposed to it. The uptake of benzanthrone through the systemic circulation, in the form of serum protein binding, was characterised by gel filtration and fluorescence quench-ing studies. Fractionation of benzanthrone-protein complex on Sephadex G-200 column revealed that albumin was responsible for the binding with benzanthrone. Addition of benzanthrone quenched the fluorescence intensity of bovine serum al-bumin or human serum albumin with a concomitant enhancement in the fluorescence intensity of benzanthrone. The quenching of albumin fluorescence and the increase in fluorescence of benzanthrone levelled off when the molar ratio of benzanthrone to albumin reached a value of one. This was in accordance with the Scatchard plot analysis. The binding was maximum in the pH range of 7.0-8.0. Stern-Volmer plot showed a linear relationship and downward curving with human serum albumin and bovine serum albumin having an association constant of 6.17 × 105M-1 and 6.54 × 105M-1, respectively. Tryptophan was found to interact with benzanthrone and it also elicited a concentration dependent quenching of its fluorescence with a simultaneous increase in the fluorescence of benzanthrone. The likely involvement in the type II residual tryptophan in the neighbourhood of apolar hydrophobic amino acids of protein chain was anticipated. Binding potential of this dye intermediate with carrier albumin may explain the mode of transport and the ultimate toxicity in the target tissues.
Male and female albino rats given different oral doses (0.75, 2.5, 5.0 and 0.25, 0.75, 1.5 mg/kg/D) of endosulfan respectively for a period of 30 days elicited signs of toxicity such as hyperexcitability, tremor, dyspnea and salivation for a brief period. At the tested dose levels, endosulfan produced no significant change in the organ body weight ratio, biochemical, histological, haematological and fertility indices. Residue analysis using GLC techniques of different organs revealed a higher level of α isomer in the fatty tissue of male and female rats, than in other organs. There was no significant accumulation of the α and β iso-mers of endosulfan in the vital organs inspite of repeated exposure which seems to be the reason for the absence of a severe toxicological response in the rats. The lower doses of endosulfan, however, showed none of the toxicological effects in male (0.75 and 2.5 mg/kg/D) and female (0.25 and 0.75 mg/kg/D) rats.
The frequency of sister chromatid exchanges (SCE), structural chromo-somal aberrations and the number of chromosomes in the peripheral blood lympho-cytes from stainless steel welders were studied. The surveys were carried out three times during a period of three years. There were no significant differences in the mean value and variance of SCE frequency among these three surveys both inthe welders and in the controls. In the results from these three surveys, there were statistical differences in the variance of SCE frequency between the welderand control groups. Futhermore, there was significant difference in the mean values of SCE frequency between smokers and non-smokers among the welders. The incidences of structural chromosomal aberrations in the welders were slightly but sinificantly higher than those in the controls with respect to aberrant metaphases, chromatid and chromo-some gaps, chromatid breaks, dicentric chromosomes and chromatid exchanges. As for the number of chromosomes, two welders with 47 chromosomes in about 70% of total metaphases were found, and their chromosome findings were confirmed to be 46, XY/47, XXY.