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.

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