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Results of a Pilot Study of Health Effects due to 2,3,7,8- Tetrachlorodibenzodioxin Contamination -- Missouri

In 1971, waste oils containing 2,3,7,8-tetrachlorodibenzodioxin (TCDD) were sprayed on residential, recreational, and work areas in Missouri to control dust. In several of these areas, the extent of environmental contamination did not become apparent until late 1982 and into 1983. Starting in January 1983, the Missouri Division of Health and CDC administered approximately 800 Health Effect Survey screening questionnaires to individuals initially solicited because of potential exposures at residential areas in eastern Missouri. In February, a group of 68 persons considered to have a high probability of exposure (i.e., who lived in, worked at, or recreated at these areas) and a group of 36 persons considered to have no exposure were selected after reviewing these questionnaires. These 104 persons received detailed medical examinations and a series of laboratory tests focused on detecting subclinical effects in key, target-organ systems (i.e., hepatic, dermatologic, immunologic, and neurologic systems).

Comparisons of these two groups produced no consistent indications of increased disease prevalence directly related to the putative exposures; no cases of chloracne, overt porphyria cutanea tarda (PCT)* or precursor conditions of PCT, or soft-tissue sarcomas were seen. An apparent trend of urinary-tract abnormalities was indicated by an increased prevalence of self-reported kidney/urinary problems, a higher proportion of leukocyturia, and a greater prevalence of microscopic hematuria in the group at high risk of exposure. None of the findings from the medical histories or the immune-function assays demonstrated statistically significant differences. There was, however, an indication of an increased prevalence of T((4))/T((8))-cell ratios less than 1.0 in the high-risk group. No significant differences in standard and specialized liver-function test results were detected.

This pilot study of a group of individuals presumed to be at high risk of exposure was intended to provide a perspective on the types and degrees of abnormalities likely to be seen in such TCDD exposures. The results appear negative, but no overall definitive conclusion should be based solely on this initial study. The insights provided need to be examined in more refined epidemiologic studies using different designs and strategies (especially in larger, more homogeneous population groups in which exposure status can be better characterized). These studies should be focused primarily, but not exclusively, on discerning any effects on the immune and neurologic systems and the urinary tract and liver. Reported by K Webb, S Ayres, R Slavin, A Knutsen, S Roodman, St. Louis University, WB Gedney, St. Joseph Hospital, Kirkwood, W Schramm, RL Hotchkiss, R Miller, HD Donnell, State Epidemiologist, Missouri Div of Health; Special Studies Br, Chronic Diseases Div, Clinical Chemistry Div, Center for Environmental Health, CDC.

Editorial Note

Editorial Note: Animal toxicity studies are commonly used to predict health effects in humans (although the existence of species-specific and even organ-specific effects of TCDD make extrapolations tenuous). The organ systems most prominently affected in animals are the liver (acute toxicity and hepatocarcinogenesis), the immune system (thymic atrophy and decreased cell-mediated immunity), and the skin (chloracne-like changes); effects on reproduction have also been noted (1,2).

Most direct knowledge of TCDD effects on human health has been obtained from workers exposed to dioxin during the production or subsequent handling of 2,4,5-trichlorophenol (2,4,5-TCP) or 2,4,5-trichlorophenyoxyacetic acid (2,4,5-T) (3). In some workplaces, exposed persons had chloracne but no systemic illnesses; other reports have noted that workers fatigued easily and experienced weight loss, myalgias, insomnia, irritability, and decreased libido. The liver has been shown to become tender and enlarged, and sensory changes, particularly in the lower extremities, have been reported. Total serum lipids may be increased, and the prothrombin times may be prolonged (4). PCT has also been observed (5). The most specific of the dioxin-related findings are chloracne (which can also be caused by other structurally similar compounds, such as polychlorinated biphenyls (PCBs) and chlorinated naphthalenes) and PCT (which also has a variety of potential causes). A number of studies addressing the association of TCDD exposures to soft-tissue sarcoma have been conducted in the industrial setting. These include two case-control studies in Sweden in which investigators reported a sixfold increase in the risk of soft-tissue sarcomas among persons exposed to chlorphenols and phenoxy herbicides (6).

Information on health effects involving nonoccupational environmental exposure is sparse. In 1976, after an explosion at a Seveso, Italy, chemical plant, chloracne developed in exposed children; some elevated liver-function test results were detected in the exposed population, and the incidence of abnormal nerve conduction tests was reported significantly elevated in subjects with chloracne (7). In Missouri, after playing in dirt in a riding arena contaminated with up to 33 parts per million TCDD, a child had hemorrhagic cystitis (8).

Public health policy in situations such as this environmental contamination with TCDD must continue to focus on the prevention of any potential health effects (particularly delayed or long-term), even if effects are not demonstrated in a pilot study. For this reason, appropriate efforts to prevent human exposure must continue, in this and other similar situations, until a more complete understanding of public health risks is obtained.


  1. Gupta BN, Vos JG, Moore JA, Zinkl JG, Bullock BC. Pathologic effects of 2,3,7,8-Tetrachlorodibenzo-p-dioxin in laboratory animals. Environ Hlth Per 1973;5:125-40.

  2. Kociba RJ, Keyes DG, Beyer JE, et al. Results of a two-year chronic toxicity and oncogenicity study of 2,3,7,8-Tetrachlorodibenzo-p-dioxin in rats. Toxicol Appl Pharmacol 1978;46:279-303.

  3. Kimbrough RD, ed. Topics in environmental health. Volume 4. Halogenated biphenyls, terphenyls, naphthalenes, dibenzodioxins and related products. Amsterdam, The Netherlands: Elsevier/North Holland Biomedical Press, 1980.

  4. Jensen NE, Walker AE. Chloracne: three cases. Proc R Soc Med 1972;65:687-8.

  5. Poland AP, Smith D, Metter G, Possick P. A health survey of workers in a 2,4-D and 2,4,5-T plant with special attention to chloracne, porphyria cutanea tarda, and psychologic parameters. Arch Environ Health 1971;22:316-27.

  6. Eriksson M, Hardell L, Berg NO, Moller T, Axelson O. Soft-tissue sarcomas and exposure to chemical substances: a case-referent study. Br J Ind Med 1981;38:27-33.

  7. Reggiani G. Acute human exposure to TCDD in Seveso, Italy. J Toxicol Environ Health 1980;6:27-43.

  8. Carter CD, Kimbrough RD, Liddle JA, et al. Tetrachlorodibenzodioxin: an accidental poisoning episode in horse arenas. Science 1975;188:738-40. *An acquired form of porphyria characterized by chronic skin lesions and other symptoms.

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