Document 7RaGwGvO1YKxo6oBV1q3GyvZe

o Vol. 283 No. 13 EARTHENWARE CONTAINERS: SOURCE OF LEAD POISONINC-KLEIN ET AL. 669 EARTHENWARE CONTAINERS AS A SOURCE OF FATAL LEAD POISONING* Case Study and Public-Health Considerations Mic h a e l Kl e in , M.D., Ro s a l ie Na me r , El e a n o r Ha r p u r , M.D., a n d Ric h a r d Co r b in , M.D. Abstract Two young children suffered lead poi soning as a result of drinking juice stored in a modern handmade earthenware jug. One of the children died. Subsequent testing of 264 contempo rary earthenware glaze surfaces revealed that 50 per cent released sufficient lead to make them un safe for culinary use. Between 10 and 25 per cent of the pieces tested would have been capable of causing severe lead poisoning. Compounding of safe earthenware glazes is essential. LEAD poisoning in children is well known. It is J usually associated with pica under conditions of social deprivation found in large tenement dwell ings constructed before World War II, when leaded paints were routinely used. Lead poisoning in Can ada is rare and is almost unheard of in the children of middle-class suburbs. The cases that Follow are unusual, but they resulted in the identification of a serious public-health hazard. nous calcium disodium EDTA (16.5 mg per kilogram every 8 hours) was instituted in an alternating fashion according to the method of Chisolm.' The course continued unremitting ly downhill despite chelation therapy and the use of cerebral dehydrating agents. The patient died on the 3d hospital day while still on the respirator. Electroencephalograms for the 2 days before death were isoelectric. Autopsy revealed severe brain swelling, with hernigtion of the cerebellar tonsils and uncinate portions of the temporal lobes and ischemic necro-' sis of the pituitary gland.t Tissue levels of lead are shown in Table l. -' Ca s e Re p o r t s Cas e 1. JX-, a 2-year-old boy, was admitted to the Mont real Children's Hospital in a comatose state. Respiratory ar rest occurred in the Emergency Room, and assisted ventila tion was instituted. Three weeks previously, afebrile nausea and vomiting had begun. A physician diagnosed gastritis and advised rest and forced fluids. There was' no improvement, and 2 days before admission to a suburban hospital, the parents noted lethargy, anorexia and a marked increase in irritability. On admission anemia and basophilic stippling of erythrocytes were noted. The diagnosis of {end poisoning was considered, but no history of pica was obtained. Growth and development had been entirely normal, and there was no previous history of serious illness. On the next day, the patient had a grand-mal seizure followed by deep coma; He was transferred to the Montreal Children's Hospital. On examination, he was in deep coma and areflexic; die pupils were fixed apd dilated, and corneal reflexes were absent. The liver edge was palpable 6 cm below the right costal margin. Laboratory findings included a hemoglobin of 7 g per' 100 ml and a white-cell count of 8109, with a normal differential. A peripheral blood smear revealed anisocytosis, poikilocytosis and marked basophilic stippling. On urinalysis the sediment contained coarse granular casts, 35 to 40 red cells per high-power field and moderate glucose by glucoseoxidase paper; screening for coproporphyrins was positive, and paper chromatography demonstrated generalized ami noaciduria. Examination of the spinal fluid showed 1000 red cells and 10 lymphocytes per cubic millimeter and' a protein of 435 mg and glucose of 121 mg per 100 ml. Serum elec trolytes, Mood urea nitrogen and creatinine were normal. The serum glutamic oxalacetic transaminase was 92 U, and the serum glutamic pyruvic transaminase 117 U. The uri nary lead level was 5 mg per liter on admission and 138 mg per liter) on therapy (normal, 0.02 to 0.08 mg per liter). The diagnosis of lead poisoning was established wjthin an hour of admission, and therapy with intramuscular BAL (8 mg per kilogram of body weight every 8 hours) and iptrave- From the Department of Pediatrics. McGill University, and the Ceramics Department, Macdonald College of McGill University. Ste. Anne de Bellevue. Quebec, and the Montreal Children's Hospital (address reprint requests to Dr. Klein at the Department of Pediatrics, Strong Memorial Hospital, 260 Crittenden Bivd., Rochester, N.Y. 14620). tTwenty-hour sample collected in a lead-free plastic container. Table 1. Tissue Lead Levels. Tissue Liver Kidney Spleen Level, or Pa t k n t No r ma l Levee* mgllOO ml 1.33 0.05 - 0.94 1.82 0.02-0.08 1.13 0.01 -0.07 Brain: Basal ganglions Cortical gray matter Cortical white matter 0.196 0.218 0.037 0.01-0.10 Careful questioning of the parents disclosed that during the 4 weeks before admission, the patient had been drinking large quantities of apple juice that had been stored in a hand-crafted earthenware jug (Fig. 1). With the onset of the symptoms, the patient's juice consumption was further in creased, on medical advice. Subsequent testing revealed that apple juice stored in the jug for 3 hours contained 157 mg per liter (ppm) of lead. Juice stored for 3 days contained 1300 mg per liter (ppm) of lead. Cas e 2. C.L., the four-year-old brother of J.L., was admit ted to the Montreal Children's Hospital on the same day. He ha4 been drinking apple juice from the same container. He also had a 3-week history of intermittent afebrile nausea and vomiting, but at the time of admission he was asymptomatic. On examination he appeared well. The only positive finding was a liver edge palpable 4 cm below the right costal mar gin. The hemoglobin was 8.5 g per 100 ml, the hematocrit 26.5 per cent, and the white-cell count 8600, with a nor mal differential. Anisocytosis, poikilocytosis and basophilic stip pling were seen on the peripheral blood smear. Urinalysis revealed only occasional fine granular casts in the sediment. Urine screening for coproporphyrins was positive, and gener alized aminoaciduria was present. The serum glutamic oxala cetic and pyruvic transaminases were both 110 U. Blood urea nitrogen, creatinine and serum electrolytes were nor mal. The urinary lead level was 62.6 mg per liter. Examina tion of spinal fluid gave normal Tesults. Electroencepha lography showed only slight abnormality. t Pathology courtesy of Dr. F. W. Wlgglesworth. 5Lead determinations in urine and apple juice were performed by atomic absorption. N3695J 670 THE NEW ENGLAND JOURNAL OF MEDICINE Sept. 24. 1970 Figure 1. Hand-Crafted Pitcher Used for the Storage of Apple Juice. Therapy with BAL and calcium disodium EDTA was insti tuted according to the same schedule used in Case 1. The padent was asymptomatic throughout and was discharged on the 5th hospital day. The whole-blood lead level (normal less than 40 ng per 100 ml) at the end of the 5-day course of BAL and calcium disodium EDTA was 8 ftg per 100 ml.* Three days after this therapy was completed the blood lead level had rebounded to 75 fig per 100 ml. At this point d-penicillamine therapy was started (100 mg per kilogram for 5 days and 40 mg per kilogram for 60 days). Blood lead levels were 47 and 27 fig per 100 ml X and 2 months after the institution of this therapy, respectively. The patient has remained well without treatment for 5 months. Ep id e mio l o g y The solubility of lead glazes on earthenware de signed for household use has long been a matter of great importance, and in some countries is regulated by legislation* At present in Canada, no govern mental standards exist setting the levels of safety for ceramics intended for culinary use. The United States Potter's Association and the United States Food and Drug Administration have recently defined 7 ppm as the maximum lead release of glazes recommended for use on ceramic items intended for food and drink.1 The high extractable lead con tent of the jug implicated in the two cases resulted in the following study by one of us (R.N.). Blood lead determinations were carried out by the Baltimore Health Department laboratory with the use of a dithizone method. Samples One hundred and seventeen samples of earthen ware pottery of unknown glaze composition, both domestic and imported, handcrafted and commer cial, were obtained from handicraft shops and de partment stores. One hundred and forty-seven samples were pre pared in the ceramics laboratory, with the use of 49 different glaze compositions in use by various schools, clubs, studios and potters. These were fired at 1750, 1850 and 2050F on containers of identical size and clay composition. These are the three tem peratures at which most hand-craftsmen fire their earthenwares. Pr o c e d u r e The testing procedure was standardized with that outlined by the Department of Consumer and Corporate Affairs, Standards Branch, Ottawa, Ontario, and was as follows: pottery samples were washed with dilute alkaline-detergent solution, rinsed with distilled water; samples were filled to the top with 4 per cent acetic acid solution, and the volume recorded; samples were covered with plastic film and allowed to stand at room temperature for 18 hours; and lead was determined by atomic absorption tech nic^ reported as metallic lead in micrograms per milliliter (ppm). The report of lead extractions from 264 earthenware glaze surfaces is shown in Table 2. Dis c u s s io n The feet that lead-glazed pottery could result in poisoning was known in antiquity and has been periodically rediscovered as certain cultural changes allowed lead glazes to be produced improperly or used under inappropriate conditions. The Greeks used earthenware vessels for cooking, but under carefully controlled conditions.* In the second and first century B.C. Greek cookery was introduced into the aristocratic class of Roman civilization, but the taboos of the Greeks were lost and acidic solutions were stored in earthenware. Wine was stored in this way, and relaxations on the drinking of wine by aristocratic women may have resulted in chronic lead poisoning and sterility. It is believed that this in turn substantially reduced the size of the next generation and may very well have contributed to the rapid extinction of the aristocratic class. From this reasoning, lead poisoning has been alleged to have contributed to the fell of the Roman Empire* In 1723 the Massachusetts Bay Colony forbade rum distillation from leaded stills, a practice that was known to result in a condition of abdominal tPerkin-Elmer Model 303 Atomic Absorption Spectrophotometer with the following operating conditions: wavelength 283. range u.v.. slit 4 (I mm. 7A); source, lead hollow cathode 8-10 ma; fud flow (acetylene) 9.0, and airflow 9.0. * ^ i I j 1 ! ' J j | J ` i , DUP050315178 Vol. 283 No. 13 EARTHENWARE CONTAINERS: SOURCE OF LEAD POISONING-KLEIN ET AL. 671 Table 2. Report of Lead Extractions from 264 Earthenware Glaze Surfaces. - Sa mp l e Gr o u p * No. OF Le a d Ex t r a c t io n Gl a z e Su r f a c e s - <0.5 0l 5-7 7-20 20-100 >100 100- 500- - PPM PPM PPM PPM PPM 500 1000 PPM PPM " A Imported pottery 29 9 5 6 6 3__ Domestic commercial ware 48 17 7 4 IS 5 Domestic handcraft 40 10 4 4 6 16 -- _ 1 Totals tl7 36 16 14 27 24 - - 1B 147 36 36 32 14 - 10 19 r discomfort called "dry gripes."8 In 1754, the year for their manufacture. The term "earthenware" is after his treatise on scurvy was published, John correctly used to name pottery that has been fired Lind warned that lemon or wine juices should not between 1085 and 2174F, either glazed or un- t be stored in earthenware jugsJ In 1767 Sir glazed. Ceorge Baker read his "Essay on the Cause of the `Endemic Colic of Devonshire" at the College of Ceramic Glazes Physicians and Surgeons of London, in which he blamed the use of lead-lined troughs in the produc tion of apple cider, a discovery for which in 1772 he was denounced from the pulpit as a faithless son of Devon.7 In 1958, some Japanese tableware was found to be unsafe.8 Two years later, in Britain, lead poison ing resulted from the drinking of homemade wine stored in earthenware.- In 1961 Yugoslavian authors described 40 patients poisoned in six years by ear thenware pots used for pickling and wine making.10 In 1967 a case similar to ours was reported in a physician who had ingested 3.2 mg of lead per night for two years by drinking a cola from an ear thenware mug made by his son in a university A glaze is a thin layer of glass fused onto the sur face of clay wares. The basic glass former in ceram ic glazes is silica, an element that combines freely with other oxides to form a variety of complex sili cates. Silica has a very high fusion point and is therefore used in combination with oxides with low melting points. This mixture when fired forms a glass or glaze suitable for earthenware clays. Lead is a common constituent of earthenware glazes. In the past lead has often been used as the sole glass former or glaze on low-fired wares. De spite the toxicity of lead compounds, they are inval uable to the potter, for they impart characteristics to a glaze unequaled by other oxides. ceramics class." Two years later Mexican pottery was implicated in serious poisoning in the five Earthenware -- Glazes of Low Solubility members of a physician's family, and the suggestion In compounding lead-bearing glazes of low solu was made that such pottery might be a source of bility the following principles apply: serious disease and disability in Mexican peas ants. Lead compounds such as lead oxide, lead car Within the past 15 years there has been an im bonate and lead monosilicate are highly soluble, pressive revival of interest In handcrafts in North even when fused. The lead bisilicate and lead America. In the field of ceramics, this has resulted trisilicate have comparatively low solubility. In all in an increasing number of amateur and profession cases the ratio of silica to lead should not be less al craftsmen and small pottery industries. The pur than 2:1 (2 parts silicon dioxide to 1 lead monox suit of pottery for recreation or as an artistic expres ide) in molecular equivalents. sion demands little knowledge of chemistry. Most of Alumina (aluminum oxide) is effective in de the textbooks and periodicals available for the ama creasing the solubility of lead silicate mixtures, teur are nontechnical. Glaze "recipes" are obtained and is always used. from the literature, and commercial glazes -- unla Alkalies, particularly boric oxide, increase the beled for chemical composition -- are readily avail solubility of lead silicate mixtures. This effect able. A basic understanding of the chemical and must be counteracted by large additional in physical interactions of the compounds composing a creases of alumina and silica. The alkaline earths glaze is essential. (calcium oxide and barium oxide) are also instru Earthenware mental in decreasing lead solubility. Lead-bearing glazes, properly compounded to Most of the world's pottery has been earthenware yield low lead release, may be profoundly because of the abundance of these clay deposits and affected by the addition of various oxides. Intro the relative ease ofreaching the temperatures needed duced for color and textures, these oxides may DUP050315179 672 THE NEW ENGLAND JOURNAL OF MEDICINE Sept. 24, 1970 sufficiently alter the final fired glaze composition to render it soluble. Glaze compositions are designed for specific temperatures and days. Because of the toxic nature of lead, all pottery designed for table use must have a glaze that does not dissolve at all. Absorption and inhalation of lead compounds used in the workshop present an additional hazard. Lead can be converted into compounds that are nontoxic to the workers han dling them by a process called fritting. Lead Frits A frit is a glassy material made by fusion of vari ous glaze components. A frit is designed for use as a constituent of glaze, although entire glazes may be fritted. There is a common misconception that commercial frits are "safe," and they are often used as the complete glaze. Frit compositions vary exten sively, and many lead-bearing frits are highly solu ble. The use of frits of low solubility, alone or in combination with other compounds or frits, does not guarantee a fired glaze of low solubility. Unfortu nately, commercial frits are not labeled for chemical composition, nor are they classified for solubility. For example, the glaze on the earthenware jug referred to in the case histories was a lead-bearing frit. This frit is highly soluble and difficult to use safely even as a minor glaze constituent* The craftsman had repeatedly used this frit as the glaze, believing all frits were "safe" and purchasing it by catalogue number from a well known North Ameri can chemical company. Co n c l u s io n s There is a considerable health hazard due to lead release from earthenware glaze on handcrafted, commercial domestic wares and some imported pottery. Fifty per cent of all glaze surfaces tested were unsafe for table use (more than 7 ppm). Twenty-five per cent of all domestic handcraft, and 10 per cent of imported and commercial earthenware released over 100 ppm of lead. Lead release in the range of 100 ppm would be expected to result in severe acute poison ing in small children under the conditions re *0.7 PbO 0.3 CaO 0.4 B,Oj 0.41 S;CL 1 molecularequivalents. > ported in the two cases presented above. Con tinuous use of containers releasing lead in the range of 7 to 20 ppm could give rise to chronic lead poisoning. In that event, the symptoms would be more insidious, and diagnosis diffi cult because of their similarity to common func tional complaints. Though the reported frequency of lead poison ing from pottery has been low, the true figure may be considerably higher. Fortunately, rela tively few earthenware containers are used for storage of acidic solutions, and many are used only for decorative purposes. Public demand for hand-made pottery is leading to increased production and availability. Unless this is matched by an increased awareness of the prob lem by potters and governments, one can ex pect to see an increase in lead poisoning from this source. We are indebted to Dr. B. Warkentin, of the Department of Soil Science, Macdonald College, Dr. M. P. Cescas, of Laval University, Quebec, Dr. Robert Lennox, of the Depart ment of Maternal and Child Health, and many other mem bers of the Department of National Health and Wellare, Ottawa, Ontario, Canada, to many members of the Depart ment of Consumer and Corporate Affairs, Ottawa, Ontario, Canada and Canadian Industries Limited, the T. Eaton Co., Limited, of Canada, and Centrale d'artisanat du Quebec and, finally, to Dr. Julian Chisolm for advice on treat ment. Re f e r e n c e s 1. Chisolm JJ Jr: The use of chelating agents in the treatment of acute and chronic lead intoxication in childhood. J Pediat 73:1-38. 1968 2. Kehoe RA: Cited by Cantamw A, Tnimper M: Lead Poisoning. Baltimore, Wifiiams and Wilkins Company, 1944, p 14 3. Pottery (Health) Special Regulations October 7. 1947, Minister of Labor and National Service under Section 60 of the Factory Act 1937, Great Britain and the Pottery (Health and Welfare) Special Regulations I9S0. January 16, 1950, SL 1950, No 65, Great Britain 4. Ceramic Industry 94:6, Match, 1970 (newsletter) 5. Gllfillan SC: Lead poisoning and the fall of Rome. J Occup Med 7:53-60, 1965 6. McCord CP: Lead and lead poisoning in early America: the pew ter era. Indust Med Sutg 22: 573-577, 1953 7. Meicklejohn A: The mill reek and the Devonshire colic. Brit J Indusu- Med 11:40-44, 19S4 8. Leonard A, Lynch G: Dishware as a possible source of lead poi soning. Calif Med 89:414-416. 1958 9. Whitehead TP, Prior AP: Lead poisoning from home-made wine. Lancet 2:1343-1344. 1960 10. BerUic T, Stahuljak D: Lead poisoning from lead-glazed pottery. Lancet 1:669. (96t 11. Hareis RW, Elsea WR: Ceramic glaze as a source of lead poison ing. JAMA 202:544-546, 1967 12. Block JL: The accident that saved five lives. Good Housekeepiog 169:60-70, November, 1969 DUP050315180