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Environmental Medicine: Integrating a Missing Element into Medical Education Reprinted from the Journal of the American Medical Association May 11, 1984, Volume 251 Copyright 1984, American Medical Association Brief Reports Seasonal Arsenic Exposure From Burning Chromium-Copper-Arsenate-Treated Wood Henry A.Peters, MD; William A.Croft, DVM, PhD; Edwin A.Woolson, PhD; Barbara A.Darcey; Margaret A.Olson • All eight members of a rural Wisconsin family experienced recurring neurological and medical illness over three years, especially during the winter months. Arsenic, in concentrations of 12 to 87 ppm, was noted in the hair of the mother and father, and analysis of hair and fingernails of all family members demonstrated pathological levels of arsenic. For four years the five-room home had been heated with a small wood stove in which outdoor or marine plywood and wood remnants had been preferentially burned. Stove ashes that contained more than 1,000 ppm of arsenic contaminated the living area, and the ratio of copper, chromium, and arsenic pentoxide in this ash matched the ratio used in the chromium-copper-arsenate-treated wood. (JAMA 1984;251:2393–2396) WOOD IS the major construction material used in the United States, but is susceptible to rapid attack by insects, fungi, and other microorganisms. Treatment of wood with pentachlorophenol, inorganic arsenicals, or creosote preservatives extends its utility and useful life. The burning of chromium-copper-arsenate (CCA) preservative-impregnated wood was associated with a family’s many health problems. High arsenic content was noted on hair and nail analysis. History A rural family living in northern Wisconsin included the parents, two boys, and four girls ranging from 1 to 30 years old. From the Department of Neurology, Center for Health Sciences (Dr Peters and Mss Darcey and Olson). and the Department of Environmental Toxicology (Dr Croft). University of Wisconsin, Madison; and the Agricultural Environmental Quality Institute, US Department of Agriculture. Beltsville, Md (Dr Woolson). Reprint requests to Department of Neurology. University Hospital and Clinics. Center for Health Sciences, University of Wisconsin, 600 Highland Ave, Madison, WI 53792 (Dr Peters). For three years the parents and children experienced various health problems including sensory hyperesthesias, muscle cramps, recurrent pruritic conjunctivitis, earaches and otitis media, sinusitis, bronchitis, and pneumonitis. A 4-week-old premature neonate was diagnosed as having viral pneumonia and because of recurring respiratory exacerbations was treated with a permanent tracheotomy. The children displayed recurrent “measleslike” rashes consisting of pinpoint hyperemic pruritic dermatitis. The children, who went barefoot, experienced reddened thickened skin on the soles of the feet, and in babies, who crawled on the floor, a rash on the legs, diaper and stomach area, hands, arms, and face developed, which later became desquamated. The youngest member of the family experienced a thrombosed penile artery. All family members complained of malaise, easy fatigue, and a “loose feeling” (lack of sensation) in the arms, hands, feet, and legs. Muscle cramps occurred during the evening hours, often causing the children to awaken the parents from sleep. By the spring of 1982, headaches were frequent, and the parents complained of “blacking out” for periods of up to two hours followed by feelings of disorientation. The two youngest children had multiple seizures described as grand mal from birth to 1 year. All members experienced frequent nosebleeds and easy bruising. One child was diagnosed by a local physician as having idiopathic thrombocytopenic purpura. The mother’s fifth pregnancy resulted in a premature birth diagnosed as placenta previa or abruptio placenta. Most striking was recurring seasonal alopecia, ranging from thinning of hair in the parents to complete baldness in the youngest children. The alopecia was most prominent during the months of March and April, and there was considerable hair regrowth by November and December, after which the cycle would repeat itself (Table 1). All symptoms alleviated during summer months and each year seemed progressively worse in terms of the symptomatology. During the last year the father was unemployed, although he had previously worked in construction and bridge repair. The mother worked as a waitress. Concerned that the house was the source of the family’s health problems, an environmental health group had analyzed blood and urine specimens of family members for carbon monoxide, nitrates, nitrites, thallium, arsenic, calcium, copper, iron, lead, mercury, and zinc, but all results were reported normal. Air analysis of the home by the State Board of Health for carbon monoxide and formaldehyde was within acceptable limits. Concern that the fish in the area might contain heavy metals caused by acid rain, the family had stopped eating fish. Well-water analysis by the State Department of Hygiene was normal for heavy metals, organic compounds, nitrates, nitrites, and radioactivity. Physical Examination of the Family The father was admitted to University Hospital, Madison, in June 1982. Reprinted with permission from JAMA 251(18):2393–6, Copyright 1984, American Medical Association.
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Environmental Medicine: Integrating a Missing Element into Medical Education Table 1.—Summary of Family Health Condition During the Last Three Years Family Members No. 1 2 3 4 5 6 7 8 Age, yr 1 2.5 5.5 7 8 9.5 30 30 Sex M F F F F M F M Eye irritations + + + + + + + + Penicillamine and digestion + + + + + + + + Headaches + + + + + + + + Penicillamine and seizures + + − − − − + + Nosebleeds + + + + + + + + Alopecia + + + + + + + + Diarrhea + + + + + + + + Diagnoses + + + + + + + + Other diagnoses Thrombosed penile artery + … … … … … … … Severe viral pneumonia … + … … … … … … ITP asthma* … … … … + … … … Scarlet fever … … … … … + … … Placenta previa, placenta abruptio … … … … … … + … Sinusitis and severe hepatitis … … … … … … … + *ITP indicates idiopathic thrombocytopenic purpura. Table 2.—Analysis of Hair and Fingernails Taken From Family Members at Initial Visit at Clinic for Arsenic Determination* Family Members Age, yr Hair Arsenic, ppm Fingernail Arsenic, ppm 1 30 87.0† 0.73–2.5 2,988 2 30 Bruehinge‡ 17.4 1,452 Prodmal cut (12 cm) 12.15 … Middle cut (12 cm) 1.59 … Distal cut (12 cm) 0.49 … 3 9.5 0.3 … 4 8 0.5–4.7 105 5 7 0.39–1.2 1,731 6 5.5 0.17–2.2 1,000 7 2.5 … 434 8 1 … 5,066 *Normal values for hair, less than 0.65 ppm; fingernails. 0.9 to 1.8 ppm. †Unwashed hair. ‡Removed from hairbrush. Somewhat anxious, he admitted to drinking more beer than he should. Physical and neurological examination findings were normal except for congenital clubbing of the fingers and toes. Nerve conduction studies and electromyography (EMG) were normal. Urine zinc excretion of 2.4 mg/L was slightly elevated, with normal levels of copper, lead, and arsenic excretion. Urine thallium levels, done elsewhere, had been reported as normal and were not repeated. Because the alopecia could not be attributed to thallium intoxication, hair samples were analyzed for arsenic, which can also produce hair loss.1 The hair was found to contain 87 ppm (normal, 0.65 ppm).2 Arsenic levels were determined by atomic-absorption spectroscopy after acid digestion.3 Urine, fingernail, and multiple hair samples were collected from the mother and children and analyzed for arsenic. Although no arsenic was detected in the urine, extremely high concentrations were found in the fingernails. Some of the hair arsenic levels were also elevated. Ranges are reported in Table 2. The administration of penicillamine (250 mg three times daily for one week) to the father and one child failed to produce notable urinary arsenic excretion. Clinically, we were unable to detect Mees’ lines4 (characteristic of acute extreme arsenic exposure) in the fingernails or toenails of the parents or children. Minimal hyperkeratosis was noted on the palm’s surface of the three youngest children. Despite subjective complaints of numbness and tingling, no sensory shading or other sensory abnormality was evident on neurological examination. Family pictures confirmed the history of severe alopecia in the children. The hair loss, although less severe, was still present during the summer. Home Visit Foul play was initially suspected, but because both parents were clinically involved, the likelihood of intentional poisoning was lessened. The family lived in a three-bedroom ranch-style house that had been enlarged room by room from a small cabin as the family grew. Multiple food samples, paint, broiler grease, dust from wall heaters, and ash from a wood-burning kitchen stove (the principal source of heat) were collected and analyzed for arsenic. In addition, air samples were taken to be analyzed for arsenic. The food samples contained insignificant quantities of arsenic. The air sample contained 0.300 µg of arsenic per cubic meter of air and 0.040 µg of arsenic per cubic meter of air for the background sample. The ashes from the stove and chimney area contained arsenic in excess of 1,000 ppm. Specimens of dust and ash collected from around the stove area contained arsenic at 100 to 600 ppm. The high arsenic content in the ash from the stove covering parts of the floor suggested this as a probable source of poisoning. After the analyses were complete, the father reported that for four years he had been burning large amounts of plywood remnants in the kitchen stove. These wood scraps were made available to him from a construction site where he had worked. Much of the plywood had been CCA treated with a solution of 47% chromium oxide, 19% copper oxide, and 34% arsenic pentoxide. The CCA solution was factory applied at a rate of 4.0 to 6.4 kg/cu m of wood.5 The proportions of these metals in the ash were the same as in the treatment solution (2.2:1:1.8).5 The small wood stove located in the kitchen-dining area was loaded from the top. Adding plywood and wood scraps would allow the escape of ashes and
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Environmental Medicine: Integrating a Missing Element into Medical Education volatilized fumes from the stove. The father would at times remove the stovepipe from the chimney during the winter and carry it through the dining room and hallway outdoors where the flue ash was removed. Usually the stove continued to burn while this maneuver took place. Soot and ashes were prominent in the kitchen, especially on the floor. Because this was the warmest room in the house, the smallest children played in it and the mother also spent most of her time there. Since June of 1982 when the diagnosis of arsenic poisoning was made, the family has stopped burning the CCA-treated wood, and cleanup operations were made of the home along with attempts to resettle the family in a noncontaminated environment. Because of lack of funds, the family has been unable to relocate, and current efforts are directed at additional cleaning of the house itself, in which the walls and even the soil around the cabin showed arsenic content. The fourth youngster who had a tracheostomy and slept under oxygen at night has had the tracheostomy closed. The dermatologic, respiratory, neurological, and other problems have lessened considerably. Close monitoring of this family’s health problems will continue. Comment An eight-member family from northern Wisconsin experienced health problems involving the eyes, respiratory system, CNS, gastrointestinal (GI) tract, blood, reproductive system, skin, and hair. The exposure to arsenic, copper, and chromium occurred through ingestion, inhalation, and direct contact. This resulted in chronic exposure (1) to the skin and eyes where it caused a pruritic dermatitis; (2) to the respiratory system where it caused severe irritation and some pneumonic problems (almost fatal to the fourth child); (3) to the GI tract where it caused severe diarrhea; (4) to the CNS where it caused loss of sensation, seizures, blackouts, and headaches; and the most puzzling lesions of all, (5) the seasonal hair loss among all the family members. The youngest members of the family experienced the greatest health problems probably because they were crawling on the floor where the ash had accumulated. The reddened soles of the feet and thickened skin of the palms can be explained by exposure to arsenic6 in the ash. It is interesting to note that the two youngest children experienced seizures primarily between the ages of 4 months to 1 year, when they were constantly crawling in the kitchen-dining area. Note that the fingernails contained up to 5,066 ppm of arsenic (Table 2). Unfortunately, detailed EEG studies were not possible. The exact amount of arsenic, chromium, and copper to which each family member was exposed could not be determined. Only in acute poisoning can arsenic be detected in both blood and urine. Because no arsenic was detected in the urine of family members even after the administration of penicillamine to two members during the summer, we conclude that their exposure was not recent and hope that the body burden is not excessive. Arsenic reacts with protein sulfhydryl groups and any excess leaves the body. Hair and fingernails are the accepted choice for the determination of chronic arsenic exposure.1,7–12 Levels detected in the hair of the family members indicated the exposure to, but not the exact dose of, arsenic. Mees’ lines were not clinically evident when the father was first studied in June 1982. This was because the exposure was chronic and uniform, and not acute and intermittent, or less likely, because Mees’ lines had grown out and were clipped off before we saw the family. Also, the penta form of arsenic is less likely to produce Mees’ lines and also does not produce the melanotic darkening of the skin or the hyperkeratosis that is commonly produced by the more toxic or lethal trioxide form of arsenic. The signs and symptoms of chronic low-level exposure to inorganic arsenic in humans have been described,1,8,13 and arsenic oxide or pentavalent arsenic induces symptoms and signs similar to those experienced by this family.1,7,13–15 In the commercial process of making outdoor wood and marine plywood, arsenic pentoxide (combined with chromium and copper solution) was used to treat the wood scraps burned by this family. The temperature of wood burning (far less than in smelting) did not change the form of arsenic V oxide, because arsenic was present in the ash as arsenate. Ginsburg14 in 1965 reported that arsenic V was absorbed by the proximal renal tubules and excreted in the trioxide form in dogs.14 However, arsenic trioxide, a potentially more toxic form of arsenic, was not detected in our environmental or biologic samples.15 Since in winter the father took the chimney off the still smouldering stove for brief periods several times a month to clean the stack of creosote, carbon monoxide inhalation may also have added to the toxic hazard. We did not see the family during winter, so unfortunately no carbon monoxide air levels could be measured, and the father only removed the chimney when windows and doors to the kitchen were wide open. The combined effect of arsenic V, chromium, and copper exposure in the human is unknown and needs further study. We were unable to show changes in EMG and nerve conduction studies (on the father). It is possible that the more lethal trioxide form of arsenic would have produced more severe damage to the peripheral nerves. The children, because of the normalcy of their neurological examination results and other practical constraints, were not available for EMG and nerve conduction studies. The father experienced severe sinusitis of the maxillary sinus and had recent surgery to reopen fused bones in this area. Nasal septum ulcerations have been reported in cases of long industrial elemental arsenic exposures.17 The youngest members of this family demonstrated thickened, reddened, peeling soles. Similar lesions have been described in Taiwanese people living where soil and water were high in arsenic and toxic fluorescent alkaloids.6 A high incidence of skin cancer was also reported.6 Although arsenic has been associated with carcinogenesis in humans,16 no suggestive changes have been detected in this family. In the past, inorganic arsenicals were used in agriculture as insecticides, soil sterilants, and herbicides.17 Monitoring by the Food and Drug Administration has indicated that the level of arsenic in US food supplies is low.18 Most arsenic is found in the meat-fish-poultry diet, with seafood containing the highest levels.
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Environmental Medicine: Integrating a Missing Element into Medical Education Sources of environmental arsenic include smelters, electric power plants using arsenic-rich coal, and soil and water found in certain parts of the world.18 Human poisoning from the burning of CCA-impregnated wood has not been previously reported and represents the probable source of arsenic exposure in this family. Fowler18 warned in 1977 that the burning of CCA-treated wood should be studied as a potential health hazard. Our studies of the kitchen-living area were done in the summer and disclosed notable contamination with CCA-rich ash. In the winter months while the CCA-treated plywood was being burned, we would have anticipated even greater contamination. With the increased popularity of burning wood for household heating purposes, the environmental health hazard of burning CCA-treated wood needs recognition and evaluation. The role of chromium and copper in contributing to these health problems is conjectural. We would suggest that all three elements could be responsible for this kaleidoscopic clinical pattern. Joy Savides Felker provided advice and secretarial aid and Lee Sjouik, MS, contributed technical assistance. References 1. Oettingen WF: Poisoning—A Guide to Clinical Diagnosis and Treatment, ed 2. Philadelphia, WB Saunders Co, 1958, pp 239–242. 2. Woolson E, Ahronson N: Separation and detection of arsenicals pesticides residues and some of their metabolites by high pressure liquid chromatography-graphite furnace atomic absorption spectro. J Assoc Off Anal Chem 1980;63:523–528. 3. Boylen GW, Hardy NL: Distribution of arsenic in nonexposed persons (hair, liver, and urine). Am Ind Hyg Assoc J 1967;28:148–150. 4. Mees RA: The nails with arsenical polyneuritis. JAMA 1919;72:1337. 5. Biologic and economic assessment of pentachlorophenol inorganic arsenicals, and creosote, in Wood Preservatives, Technical Bulletin No. 1658–1, US Dept of Agriculture, 1980, vol 1, pp 31–192. 6. Tseng WP: Effects and dose-response relationships of skin cancer and blackfoot disease with arsenic. Environ Health Perspect 1977; 19:109–119. 7. Stewart CP, Stolman A: Toxicology—Mechanisms and Analytical Methods. New York, Academic Press Inc, 1960, vol 1, pp 202–206. 8. Moeschlin S: Poisoning—Diagnosis and Treatment New York, Grune & Stratton Inc, 1965, pp 162–169. 9. Creason JP, Hinners TA, Bumgarner SE, et al: Trace elements in hair as related to exposure in metropolitan New York. Clin Chem 1975; 21:603–612. 10. Harrison WW, Yurachek JP, Benson CA: The determination of trace elements in human hair by atomic absorption spectroscopy. Clin Chim Acta 1969;23:83–91. 11. Harrison WW, Clemena GG: Survey analysis of trace elements in human fingernails by spark source mass spectrometry. Clin Chim Acta 1971;36:485–492. 12. Harrison WW, Tyree AB: The determination of trace elements in human fingernails by atomic absorption spectroscopy. Clin Chim Acta 1971;31:63–73. 13. Casarett LJ, Doull J: The Basic Science of Poisons Toxicology. New York, Macmillan Publishing Co Inc, 1975, pp 464–465. 14. Ginsburg JM: Renal mechanism for excretion and transformation of arsenic in the dog. Am J Physiol 1965;208:832–840. 15. Feldman RG, Niles CA, Kelly-Hayes M, et al: Peripheral neuropathy in arsenic smelter workers. Neurology 1979;29:939–944. 16. International Agency for Research on Cancer (IARC): Arsenic and Arsenic Compounds, IARC monographs on the evaluation of the carcinogenic risk of chemicals to humans. Lyon, France, World Health Organization, IRAC, vol 23, pp 39–141. 17. Woolson EA: Fate of arsenicals in different environmental substrates. Environ Health Perspect 1977;19:73–81. 18. Fowler BA: International conference on environmental arsenic: An overview. Environ Health Perspect 1977;19:239–242.
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