From March 1974 through July 1975, 76 (56%) of 133 persons who had worked at a pesticide plant that produced Kepone, a chlorinated hydrocarbon insecticide, contracted a previously unrecognized clinical illness characterized by nervousness, tremor, weight loss, opsoclonus, pleuritic and joint pain, and oligospermia. Illness incidence rates for production workers (64%) were significantly higher than for nonproduction personnel (16%). The mean blood Kepone level for workers with illness was 2.53 ppm and for those without disease 0.60 ppm (p less than 0.001). Blood Kepone levels in current workers (mean, 3.12 ppm) were higher than those in former employees (1.22 ppm). Blood Kepone levels for workers in nearby businesses and for residents of a community within 1.6 km of the plant ranged from undetectable to 32.5 ppb. Illness attributable to Kepone was found in two wives of Kepone workers; there was no apparent association between frequency of symptoms and proximity to the plant in the survey of the community population.
Recent animal and human studies suggest that prenatal exposure to carcinogens may increase the risk of childhood malignancy. The Texas Childhood Cancer Study (1976-1977) was designed to test the hypothesis that parental exposure to hydrocarbon-related occupations or industries increases this risk. The study subjects, parents of children with and without cancer, were questioned about their job histories. Parents of 296 children with cancer were not exposed to hydrocarbon-related occupations or industries more often than the uncles and aunts of these children, the parents of neighborhood children, or the parents of 283 children without cancer. During the year before birth, odds ratios for fathers of children seen at a hematology clinic with cancer relative to the uncles of these children (0.93), the fathers of neighborhood children (1.33), and the fathers of children seen at the clinic without cancer (0.50) were not statistically significantly different from 1.00 (p greater than 0.05). This lack of association persisted for the year after birth, the year before diagnosis, and the interval from the year before birth to the year of diagnosis; for different diagnoses; for different ages at diagnosis; and for the industries and occupations of female as well as male parents.
From September 1974 through November 1976, 13 adolescent patients with mucin-producing colorectal adenocarcinoma were treated at a Memphis, Tennessee, pediatric oncology center. Ten of these children were from rural areas of the Mississippi Delta, areas of high pesticide use. None of them had a family history of colorectal cancer, familial polyposis, or ulcerative colitis. Levels of pesticide residues, however, were not generally higher in blood samples from patients and their families than from controls.
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