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.
References
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.
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.
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.
Jensen NE, Walker AE. Chloracne: three cases. Proc R Soc Med
1972;65:687-8.
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.
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.
Reggiani G. Acute human exposure to TCDD in Seveso, Italy. J
Toxicol Environ Health 1980;6:27-43.
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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