Pleural fibrosis due to asbestos exposure was fully appreciated considerably later than pulmonary interstitial fibrosis due to similar exposure. This is well exemplified by the fact that pleura face on was included in the International Labour Office's International Classification of Radiographs of Pneumoconioses only in the last revision of the Classification. The functional relevance of pleural fibrosis, in particular circumscribed pleural fibrosis, has remained controversial. Since pleural fibrosis can occur at various sites (diaphragmatic plaques, chest wall in profile and face on, mediastinal) and can be of different thickness and extent, a comprehensive integrative assessment of pleural fibrosis was undertaken in order to permit a quantitative study of relationships between pleural fibrosis and pulmonary function. This approach was used for chest X-ray films of 1,584 asbestos insulation workers examined (1981-1983); 1,185 (75%) had pleural fibrosis. The distribution pattern of the integrative pleural index was found to be different in the subgroup with circumscribed (n = 975) from that with diffuse (n = 197) pleural fibrosis, with a higher profusion of high INDEX values in the latter. Stepwise regression analysis indicated that there was a significant inverse relationship between forced vital capacity (FVC) and the integrative index of pleural fibrosis in the subgroup with circumscribed pleural fibrosis. In the subgroup with diffuse pleural fibrosis, the obliteration of costophrenic angle(s), even with pleural fibrosis of limited extent, resulted in marked decrement in FVC% predicted; higher values of INDEX did not result in additional significant reductions of FVC. In those with both parenchymal and pleural abnormalities (n = 862) the pleural index was found to make a significant contribution, independent of that of parenchymal abnormalities, to decrements of FVC. Since pleural fibrosis has gradually become the predominant radiologically detectable abnormality in asbestos exposed workers, establishing its quantifiable functional relevance is useful.
This study was undertaken to determine the relation between radiographic and histological manifestations of pulmonary asbestosis (interstitial fibrosis) in insulation workers who had died of lung cancer. Of 450 confirmed deaths from lung cancer a chest radiograph suitable for determining evidence of pneumoconiosis was obtained in 219. Of these cases, 138 also had a tissue specimen submitted that was suitable for histological study to determine the extent of histological fibrosis. There was a significant albeit limited correlation between the radiographic and histological findings (r = 0 27, p < 0-0013). All 138 cases had histological evidence of parenchymal fibrosis; in 25 (18%), however, there was no radiographic evidence of parenchymal fibrosis. In 10 cases (7%) both parenchymal and pleural disease were undetectable on the radiograph. Thus a negative chest radiograph does not exclude the presence of interstitial fibrosis (asbestosis) in a substantial proportion of insulation workers previously exposed to asbestos who develop lung cancer.
In an effort to assess exposure among workers engaged in capacitors manufacture, PCB concentration was determined in plasma (290) and adipose tissue (61). In general, males had higher concentrations of PCBs than females. The correlation of plasma concentration (1-546 ppb) of the more highly chlorinated PCBs, which had been used in past, with total duration of employment suggested accumulation over time. The gc-ec pattern of these PCB peaks was, in most cases, characteristic of exposure to a PCB mixture with 54% chlorine. The less highly chlorinated PCBs, di-, tri-, and tetrachlorobiphenyls, were the source of current exposure, and were observed in concentrations of 6-2530 ppb in plasma. Higher exposure occurred among persons with direct contact with PCBs in jobs such as capacitor filling. Adipose tissue concentrations, for both the more highly chlorinated PCBs (1-165 ppm) and lower chlorinated PCBs (0.6-414 ppm), were proportional to those in plasma.
This paper presents a study of renal function in I02 patients with lead poisoning admitted to the Occupational Diseases Clinic in Bucharest during the past IO years; nearly half the patients had no history of lead colic. Every possible cause of renal damage, other than lead, was excluded by a careful differential diagnosis.Renal function was investigated by repeated determinations of blood urea, creatinine and uric acid, urea clearance, and endogenous creatinine clearance tests.Significant decreases of the clearance values (less than 50 ml./min. urea clearance and less than 8o ml./min. creatinine clearance), persistent high blood urea (more than 50 mg./Ioo ml.), and high blood creatinine (more than I-2 mg./ioo ml.) were found in a significant number of cases. These signs of impaired renal function were more frequent in the group of patients with chronic lead poisoning who had had several episodes of colic and an occupational exposure of more than IO years. A high blood pressure was also found more frequently in this group of patients.Undercompensated and decompensated renal failure was found in I7 patients, most of whom had been exposed to lead for more than IO years and had a history of several attacks of colic. Arterial hypertension accompanied the chronic renal failure in 13 patients, the renal impairment generally preceding the rise in blood pressure by several years.The duration of occupational lead exposure, the high absorption in the past, and the long period of observation of these patients, most of whom were repeatedly hospitalized, may explain the relatively high incidence (17 cases) of nephropathy with chronic renal failure in the present group. Impairment of urea clearance seems to be the earliest sign, at a time when the creatinine clearance is still normal. As the duration of exposure lengthens and the patient is subjected to active episodes of poisoning the creatinine clearance also deteriorates. Persistent urea retention and high creatininaemia may follow in time, accompanied rather frequently by arterial hypertension. A study of some of the cases followed for several years demonstrated this progressive evolution of lead nephropathy.A functional and transitory impairment of renal function is very probably caused by an impairment of intrarenal circulation, resulting from marked vasoconstriction of the renal vessels, forming part of the generalized vasoconstriction of lead poisoning. Prolonged exposure and frequently recurring episodes of acute poisoning may lead to progressive impairment of renal function and to the development of organic lesions.Special attention should be paid to renal function tests in all cases with prolonged exposure to lead in order to prevent the development of severe lead nephropathy.The question whether lead poisoning can cause certain pathological states earlier than has been a chronic nephropathy is of interest at the present possible hitherto. time not only in occupational medicine but also inIn the past, many authors have held that chronic paediatrics, general medicin...
Reports of acute arsenic poisoning arising from environmental exposure are rare. Two cases of acute arsenic intoxication resulting from ingestion of contaminated well water are described. These patients experienced a variety of problems: acute gastrointestinal symptoms, central and peripheral neurotoxicity, bone marrow suppression, hepatic toxicity, and mild mucous membrane and cutaneous changes. Although located adjacent to an abandoned mine, the well water had been tested for microorganisms only and was found to be "safe." Regulations for testing of water from private wells for fitness to drink are frequently nonexistent, or only mandate biologic tests for microorganisms. Well water, particularly in areas near mining activity, should be tested for metals.
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