An outbreak of subacute poisoning occurred among nine members of a family; eight were ill with gastrointestinal symptoms, four developed encephalopathy, and two died. Abnormal liver function tests and leukopenia were common laboratory findings. Epidemiologic and environmental investigations traced the source of arsenic exposure to a farm well with water containing 108 ppm arsenic. The soil adjacent to the well was also contaminated with arsenic, possibly from waste pesticide. Presumably, arsenic gained access to the well through obvious leaks in the well's casing. To our knowledge, this is only the second reported outbreak of fatal arsenic poisoning from contaminated drinking water and one of few instances where illness followed exposure to a toxic substance which was disposed of, or possibly disposed of, in an indiscriminate manner.

In September 1982, two Charlottesville, Virginia, residents were found by their dentists to have general erosion of dental enamel consistent with exposure to acid. Both patients were competitive swimmers at the same private club pool. No other common exposure could be determined. An epidemiologic survey was made of 747 club members. Symptoms compatible with dental enamel erosion were reported by 3% of nonswimmers (9/295), 12% of swimmers who were not members of the swim team (46/393), and 39% of swim team members (23/59). All four swimmers with clinically verified dental enamel erosion had trained regularly in the pool for competitive swimming meets, compared with one of eight matched swimmers without enamel erosion. Examination of the implicated swimming pool revealed a gas-chlorinated pool with corrosion of metal fixtures and etching of cement exposed to the pool water. A pool water sample had a pH of 2.7, i.e., an acid concentration approximately 100,000 times that recommended for swimming pools (pH 7.2-8.0). A review of pool management practices revealed inadequate monitoring of pool water pH. Acid erosion of dental enamel--"swimmer's erosion"--is a painful, costly, irreversible condition which can be caused by inadequately maintained gas-chlorinated swimming pools.

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To determine risk factors for infection of hyperalimentation catheters, we prospectively studied 169 catheter systems (88 patients) by using a semiquantitative culture technique. Infection occurred in 24 (14%) catheters (16 patients), was inversely proportional to the number of previous catheters inserted by the operator (P less than .02), and was proportional to the interval between admission and catheter insertion (P less than .0005). Catheter replacement over a guidewire was no more likely to be associated with infection than was a de novo percutaneous insertion at another site (P = .6). Using a proportional hazards model, we estimated the risk of infection per day to be 1.3 times greater for a catheter if the patient had been hospitalized 50 days instead of seven days, and 3.8 times greater if the patient had a Swan-Ganz catheter at the time of insertion.

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