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A series of controlled experiments has been undertaken to study the dependence of neutron counting efficiency on the type of liquid phosphor and on the geometry and light collection efficiency of the liquid container. Five hydrogenous scintillating liquids have been compared in various container geometries. From differential lead absorption measurements using a calibrated polonium‐beryllium neutron source, neutron counting efficiencies from 5.4±2 percent to 17.9±6 percent have been obtained.

Increased lead absorption was found in 1972 in 56% of 256 children aged 1 to 18 years who lived within 1.6 km of a lead-emitting ore smeltery in El Paso, Tex. Engineering improvements have subsequently reduced emissions from the smeltery, and levels of lead in air, dust, and soil have declined. To evaluate the impact of these environmental improvements on lead absorption, we conducted a follow-up study in 1977 of blood lead levels in 140 children aged 1 through 18 years who lived within 1.6 km of the smeltery. Mean blood lead levels were found to have decreased from 41.4 to 17.7 μg/dL in children living within 0.8 km of the plant and from 31.2 to 20.2 μg/dL in children living at 0.8 to 1.6 km. These data argue for the feasibility of reducing children's lead absorption near primary lead smelteries. ( JAMA 242:739-741, 1979)

A COMPARISON OF THE MEASUREMENT OF FREE ERYTHROCYTE PORPHYRIN (FEP) AND RED CELL AMINOLEVULINIC ACID DEHYDRASE ACTIVITY (ALAD) AS MEANS OF DETERMINING EXCESSIVE LEAD ABSORPTION

To the Editor.— The recent discovery of unexpected increased lead absorption in children of female battery workers strikingly reflects the impact on clinical practice of the increased participation by women in the work force. This experience illustrates other epidemiologic principles that we believe need wider appreciation. We have detailed these points to pediatricians 1 and wish now to reiterate them for a more general medical audience. Report of a Case.— A 24-year-old woman had intermittent headache, dizziness, and amnesia. Results of neurological evaluation were normal, but anemia with basophilic stippling was found. Her work involved burning lead battery terminals, but the importance of this information was not appreciated until her 20-month-old son showed a high blood lead level on routine screening. Subsequently, increased lead absorption was disclosed in the woman, and chelation therapy produced clinical and biochemical improvement. Three of her children, and children in the families of five other

Current questions about lead exposure focus on the consequences of levels too low to have erupted into blatantly discernible defects. The present paper addresses two sets of interrelated problems derived from this issue. One is how to define the behavioral consequences of asymptomatic lead absorption, and the second focuses on behavioral assessment procedures. Current primary prevention programs emphasize environmental monitoring, and early detection programs emphasize lead body burden measurements. The evaluation of behavioral problems in school children as a function of body burden is rarely performed. Epidemiologic data indicate sufficient natural variability to determine the degree of association between indices of total body burden and behavior. Assessment procedures are described and research suggestions offered that sample concretely defined target behaviors in social environments.

Five siblings aged 5-11 years, children of a smelter worker, living within 500 meters of a primary lead smelter, were found to have persistently raised blood lead levels (above 30μg/dl) on two occasions with at least a two-month interval between measurements). Three of the children had levels greater than 50μg/dl. All had lines of increased density at the lower femoral metaphyses, three had lead lines on their gums and two had hypochromic microcytic anaemia. The eldest also showed reduced nerve conduction velocity. It is likely that these children had lifelong exposure to lead. Renal function studies including serum creatinine level (Cr), urinary aminoacids and urine phosphorus to urine creatinine concentration ratio (UP/UCr) were within normal limits for the their age. Haematological and neurological effects of increased lead absorption have been studied extensively, but there is less information on the renal effects.

Drs. Kaemmer and Johnson have rightfully pointed out that the patient in question had a single lead level of 64µg/100 ml and X-rays of the wrists and knees demonstrating lead lines as the only evidence of systemic lead absorption. The authors recognized that treatment with BAL and calcium EDTA was started too hastily but felt that a discussion of treatment was not germane to the reporting of the unusual source of the lead poisoning in this article.

It has been suggested that the solvent methylN-butyl ketone (MBK) may cause peripheral neuropathy in humans. An Investigation was undertaken after two cases of peripheral neuropathy among spray painters at one work site were reported to the National Institute for Occupational Safety and Health. Twenty-six painters were interviewed and examined. Two were found to have definite peripheral neuropathy and one had a probable case. Although one of these men had been exposed to lead in the past, there are strong reasons to believe that MBK was responsible for his neuropathy. There was nothing to suggest excessive lead absorption in the other two men. (JAMA235:1455-1457, 1976)

The past 15 years has witnessed a great expansion in the understanding of lead exposure in humans. This progress has taken place on a number of fronts, only some of which are strictly scientific, fulfilling the statement made by Rene Dubos a number of years ago that the subject of lead exposure offers a piece of action to practically every field of human endeavor. An example of this is the recent action taken by the Environmental Protection Agency to reduce further the permissible lead content in gasoline, surely as important a step as any current scientific discovery in the field. Amelioration of lead exposure will never occur without the broad cooperation of not only bench scientists, behavioralists, and clinical people, but also public health, legal, legislative, and governmental persons sharing common concerns. The subject matter of this volume represents just this kind of cooperative effort, as one can easily see

Screening programs for Pb poisoning emphasize measurements of blood Pb and erythrocyte protoporphyrin (EP). A far more sensitive index of the size of chelatable and potentially toxic Pb stores, the EPT, has yet to be evaluated in children with mild-moderate increased lead absorption. EPT's were performed in 20 such children: 4 CDC Class II (Pb 30-49μg/dl, EP 50-109μg/dl) and 16 in Class III, who were further subdivided: IIIa (Pb 30-49μg/dl, EP > 110μg/d1) and IIIb (Pb 50-69μg/dl, EP>50μg/dl). CaNa2EDTA (500 mg/m2/dose) was given q 12 H × 2, and the 24-hour urinary Pb (uPb) excretion was measured. A positive EPT was defined as urinary excretion of Pb ≥ 500μg/24H. Conclusions: 1) Measurements of blood Pb and/or EP are imprecise indicators of chelatable Pb, as determined by the EPT, in children with mild-moderate increased Pb absorption; 2) 70% of all children in this study required 5 days of treatment for increased Pb absorption; 3) Based on conventional screening tests, these children may have gone untreated; 4) We suggest that all children with blood Pb>30 and EP>50 should have careful assessment of the size of chelatable Pb stores by a precise method, namely, the CaNa2EDTA provocative test.

The experimental observations described in the following paragraphs were prompted by the reports of Holmes and his associates1on the beneficial effects of the administration of ascorbic acid to persons suffering from chronic lead poisoning. These investigators noted a decided reduction in the symptoms of exposed workmen and an apparent decrease in the lead content of the blood and the urine following the daily ingestion of ascorbic acid. This was associated with an increase in the number of erythrocytes, a decrease in the number of stippled erythrocytes and an increase in the hemoglobin content of the blood. They inferred that ascorbic acid combined with lead to form a relatively insoluble or unionized compound that might be eliminated through the bile into the feces. The importance of these conclusions, from a practical point of view, stimulated our efforts to verify them. If they proved to be true in our hands

The increasing recognition of lead poisoning as an industrial hazard has stimulated the search for a rapid, reliable stain for the stipple cells found after lead absorption. Further experimentation with the Henderson stain 1 has demonstrated that Wright's blood stain may be substituted for the staining mixture recommended by Henderson. With this change it is possible not only to note and to count the stipple cells but also to make the usual differential count of the white blood cells at a single examination. The three reagents required are kept for convenience in covered Coplin jars. The technic is as follows: Fix dried smear in acetone-free methyl alcohol for from three to five minutes and transfer directly to Wright's stain (staining time predetermined for each lot of stain used) ; wash in tap water and transfer to dilute ammonia water (2.5 cc. of stronger ammonia water in

Whether bullets remaining in tissues can give rise to lead poisoning has long been a subject of discussion. The great body of opinion, first expressed by Pare, holds that bullets in tissues will not cause intoxication, but there have also been proponents of the opposite point of view, and cases of plumbism from retained bullets have been reported from time to time, the earliest record being that of Bronvin 1 in 1867. Among the more than fifty publications on this subject there are reports of forty cases in which the clinical diagnosis of plumbism resulting from retained bullets has been made. 2 The entire assumption of the occurrence of plumbism from retained bullets being dependent on the occurrence of clinically identifiable lead poisoning, it would seem desirable at the outset to state the criteria on which my associates and I base such a diagnosis. They are the existence of (1)

In spite of intense medical and sociologic effort, the incidence of lead poisoning remains high among children in many areas of the United States and the case fatality rate of lead encephalopathy continues to be approximately 25%. Of the survivors of pediatric plumbism, many have been reported to have significant residuals. Because the symptoms and signs of childhood lead intoxication may be vague or may mimic other common disorders, the diagnosis can be fraught with difficulty. During the past ten years in Cincinnati, a period in which 273 cases of excessive lead absorption have been documented among children, it has been observed repeatedly that a child initially may be labeled as having lead poisoning on the basis of a history of pica together with other signs and symptoms of possible lead intoxication, only to have analytic studies of the lead content of the objects chewed and of the child's blood

THE tendency of the young of a given species to be more prone to lead poisoning than the adult has been observed by several authors1, and we have investigated whether one of the reasons for this could be an increased absorption of lead from the intestine during an early stage of life.

My purpose in this paper is to review briefly, from the point of view of the industrial physician, the various signs and symptoms commonly associated with plumbism and to discuss more fully some of those observations which may usually be considered of the greatest value in its early diagnosis. It is obvious to those acquainted with this problem in industry that efforts to reduce the incidence of industrial plumbism will be greatly handicapped if emphasis is not placed on such observations as may be considered presumptive evidence of lead absorption or lead intoxication. From an early date medical literature has been replete with reports dealing with the toxic effects of lead. With few exceptions the signs and symptoms considered in the present discussion have been fully described by early medical workers. Later scientists are to be given credit for experimental studies made to determine the action of lead on the

A recent series of articles in another journal has detailed the methods and the major results of our studies of lead absorption and lead poisoning during the past ten years. 1 So far as they are concerned with normal lead absorption and excretion, the results may be summarized briefly as follows: 1. Two groups of native Mexican Indians, whose mode of life and environment were devoid of opportunities for contact with the lead-containing products of highly organized and industrialized populations, were found to have lead in their blood and to excrete lead in their feces and urine, as a consequence of the occurrence of lead in the soil and hence in vegetation and animal products employed as food. 2. Various groups of healthy children and adults in the United States, with no occupational exposure, were shown to have lead in their tissues and in their excreta, chiefly because of regular

Since 1935 the Bureau of Laboratories of the Baltimore City Health Department has provided a routine laboratory service for the quantitative estimation of lead in blood and other body fluids as an index of abnormal lead absorption in cases of suspected lead poisoning. 1 The cooperation of those physicians and hospitals who made use of this service was solicited in order to make available the clinical histories of the persons whose bloods were examined for lead. In this way considerable information was obtained about the local occurrence of both industrial and nonindustrial lead poisoning. A summary of the incidence of lead poisoning in the city of Baltimore during the period 1931-1940 is shown in table 1. These data were obtained from the followingsources: (1) reports of occupational lead poisoning, (2) reports of deaths from lead poisoning and (3) cases ascertained in a follow-up of the blood lead laboratory

Because of the inability of engineering to eliminate lead exposure at its source, the scientifically proved method of control by Aub and his associates has been applied to lead absorption and its acute toxic episodes in the supervision and treatment of approximately 500 cases of lead exposure, 200 of absorption, and 100 of intoxication. The present demonstration of these principles has been effected by a diagnostic division of cases into absorption (1) plus severe intoxication requiring hospitalization, (2) plus mild intoxication, not disabling, (3) plus only laboratory signs of intoxication, and (4) without even laboratory signs of latent intoxication. Except for the first actually disabled group, the other three potentially disabled groups have been treated with the worker at work. Such treatment must (1) start before disability, (2) utilize calcium advisedly but not as a routine, and (3) consider under perfect laboratory and clinical control that artificial deleading is superior

THE ACUTE symptoms of lead poisoning were recognized by Nikander as early as the second century, BC, and they were correctly attributed to "cerussa" (white lead). 1 However, the "Devonshire colic" of 1724 was initially thought to be an epidemic pestilence. Tronchin correctly identified lead in the drinking water of Amsterdam as the cause of the epidemic colic of that city in 1757, and Baker showed ten years later that the cider made in Devon contained large amounts of lead, which produced the colic. 1 During the 200 years since, the literature has been replete with studies of lead poisoning, and although the industrial sources have been largely eliminated, the home brewing of wine 2,3 or whiskey 4,5 has continued to be a considerable source of chronic lead absorption in some areas. There has been universal agreement about the acute symptoms of plumbism, but the nature of the delayed effects remains controversial. In 1863

The following investigation was undertaken at the request of Dr. Alice Hamilton, special investigator of lead-poisoning for the federal Bureau of Labor, because of the availability in our laboratory of normal human gastric juice. The relative importance of the skin, the lungs, and the digestive tract as avenues of the lead absorption in workers in the lead industries seems to be determined only to this extent that the skin is the least important. While lead may be absorbed through the intact skin under special conditions of prolonged application of lead compounds to the skin, it may be questioned whether under ordinary working conditions absorption through the skin contributes to industrial plumbism. There remains, then, to consider the lungs and the digestive tract. Meillere 1 seems to show that while poisoning may occur by absorption of lead from the lungs, this is not a channel of absorption of practical importance in

Anomalies in the lead absorption curve of the vertical component of cosmic radiation have been reported by several authors using counter telescopes (Aiya 1944; George and Appapillai 1945; Swann and Morris 1947; Kellermann and Westerman 1949; Fenyves and Haiman 1950; Mazzolli de Mathov. 1951; Abd EI-Wahab Khalil 1952). However, in a recent detailed series of experiments, results of which were published as the experiment to be described here was nearing completion, Heyland and Duncanson (1953) found no evidence of any anomaly in the absorption curve.