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...

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Sixteen working welders with more than seven years' exposure and a chest radiograph suggestive of siderosis and I3 healthy unexposed men were studied. Each subject had a comprehensive medical and work history, physical examination, standard chest film, and pulmonary function investigation (lung volumes, ventilatory capacities, pulmonary compliance in static and dynamic conditions, specific compliance, and elastic work of breathing).Seven of the welders had some exertional dyspnoea and three complained of cough. Although spirographic values were generally within the normal range, the arc welders had a statistically significant reduction in static and functional compliance. Seven had a functional compliance under the lower limit of the control group. Differences in elastic work of breathing and specific compliance were not significant.The possible causes of pulmonary function impairment in welders are discussed.Since I936, when Doig and McLaughlin reported their first cases, several studies have been devoted to the clinical, epidemiological, roentgenological, and functional aspects of welders' siderosis.Most authors are agreed in considering this condition as harmless, with no impairment of the general health or respiratory function (Collen, I947; Doig and Duguid, ig5i; Doig and Challen, I964; Enzer and Sander, I938; Sander, I944). However, some recent papers have questioned this view (Charr, I955, I956; Friede and Rachow, I96I; Kierst, Uselis, Graczyk, and Krynicki, I964; Sevcik, Chalupa, Klhufkova, and Hrazdira, I960).The purpose of the present work is to examine some aspects of pulmonary ventilation in welders at work and to assess the possible impairment of pulmonary elasticity. Material and MethodsFifty-two subjects were picked at random from the 70 welders of a metallurgical plant. Sixteen were then selected as having over seven years' exposure as arc welders and chest radiographs suggestive of siderosis. The International Labour Office (1959) criteria for evaluation of chest films were used. All subjects had a complete medical and work history, clinical examination, and standard chest postero-anterior film. Individuals with chronic cardiopulmonary disease or acute respiratory illness during the last six months period were excluded.These i6 welders were compared with a control group of 13 normal individuals with no dust exposure. The ages and heights of subjects are presented in Table I. No significant differences in height, age, or smoking habits were found between the groups. The average duration of exposure was I7-I years (range 7 to 30 years).Lung function tests comprised determinations of lung volumes, forced expiratory volumes, helium-mixing time, and pulmonary mechanics. All determinations were carried out on fasting subjects in a sitting position.