Epidemiology and Pathology of a Tetrachlorodibenzodioxin Poisoning Episode

Kimbrough, Renate D.; Carter, Coleman D.; Liddle, John; Cline, Richard E.

doi:10.1080/00039896.1977.10667259

Cited by 89 publications

(25 citation statements)

References 24 publications

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“…In a larger study, Mocarelli et al (1986) tested liver enzyme levels yearly from 1977 to 1982 in male and female children from Seveso and from the unexpose d surrounding area. In the 1977In the , 1979In the , 1980 test series ALT, but not AST, was statistically signi® cantly (p < 0.05) elevated among male children in Seveso compared with unexposed comparisons. Female children had normal levels compared with controls for all years.…”

Section: Ast and Altmentioning

confidence: 85%

Human health effects after exposure to 2,3,7,8-TCDD

Sweeney¹,

Mocarelli²

2000

Food Additives and Contaminants

100

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In 1949, the first descriptions of human exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD)-contaminated chemicals were reported after a trichlorophenol reactor explosion in Nitro, West Virginia, USA. Reported non-cancer health effects included a range of conditions affecting most systems. Additional reports of the health consequences of exposure continued through the remainder of the century. The majority of effects have been reported among highly exposed groups including occupational populations, such as chemical production workers, pesticide applicators, and individuals who handled or were exposed to materials treated with 2,3,7,8-TCDD-contaminated pesticides, and among residents of communities contaminated with tainted waste oil (Missouri, USA) and industrial effluent (Seveso, Italy). For only six exposed populations were biological measurements of 2,3,7,8-TCDD-contaminated collected and used to examine the relationship between non-cancer health effects and exposure. Of the many non-cancer health effects thought to be associated with 2,3,7,8-TCDD exposure, only chloracne, elevations in GGT and triglyceride levels, and alterations in FSH and LH were related to serum 2,3,7,8-TCDD levels. Mortality from cardiovascular diseases also appeared to be elevated among cohorts of exposed chemical workers and Seveso residents. Continued surveillance of the health of exposed populations will be useful in identifying the long-term effects of both high and low 2,3,7,8-TCDD exposure.

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Section: Ast and Altmentioning

confidence: 85%

Human health effects after exposure to 2,3,7,8-TCDD

Sweeney¹,

Mocarelli²

2000

Food Additives and Contaminants

100

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“…These results are different both from the ones that indicate the presence of a polyneuropathy [5][6][7][8][9][10][11][12][13][14], also in the Seveso population [the cases of peripheral neuropathy reported were 22 and 26 in 1977 and 1978, respec tively; ref. 2,28], and from those that deny the existence of even a subclinical involve ment of peripheral nerves [17][18][19][20][21]. The dif ferent results obtained in previous investiga tions carried out on the Seveso population could be explained both by the different pe riods of time elapsed since the accident and by the selection of a control population liv ing in unpolluted areas and not in towns with a similar environmental pollution.…”

Section: Discussionmentioning

confidence: 49%

“…We decided to consider this particu lar population because chloracne is the most reliable indicator of marked dioxin ex posure [4], Reviewing the data reported in the litera ture, the presence of PNS involvement in subjects exposed to the toxin is controver sial. The majority of papers in which PNS functions have been investigated report the presence of an impairment ranging from few symptoms and mild signs of PNS damage to more evident signs of peripheral neuropathy [5][6][7][8][9][10][11][12][13][14], also confirmed by neurophysiologi cal studies [2,15,16], but there are other papers in which no toxic effects of dioxin on the PNS are reported [17][18][19][20][21],…”

Section: Introductionmentioning

confidence: 56%

Long-Term Effects of 2,3,7,8-Tetrachlorodibenzo-<i>p</i>-Dioxin on the Peripheral Nervous System

et al. 1987

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This work was set up to investigate the possible presence of peripheral nervous system involvement as a long-term effect of the exposure to dioxin in 152 subjects with chloracne from the Seveso area; 123 age- and sex-matched subjects living in nearby towns with similar environmental pollution formed the control group. The accident in Seveso took place in July, 1976, and this study was carried out from October, 1982, to May, 1983. Although a peripheral neuropathy was not found in any of the subjects, a significant increase of the number of individuals presenting at least two bilateral clinical signs (p < 0.05) or one abnormal electrophysiological parameter (p < 0.02) was found in the Seveso group. Principal component analysis did not show any subdivision between these two groups. The Fisher approach to discriminant analysis reveals a clear subdivision between the group of the most exposed subjects and randomly selected subgroups of control subjects. In conclusion, clinical and electrophysiological signs of peripheral nervous system involvement occur with a statistically increased frequency in the Seveso population 6 years after the accident, although a peripheral neuropathy was not evident in any of the chloracne patients using the World Health Organization diagnostic criteria.

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“…Part of the waste oil was obtained from a company in southwestern Missouri that manufactured 2,4,5-TCP as an intermediate for the production of hexachlorophene. Shortly after the application of waste oil to a horse arena in Moscow Mills, 43 horses in that arena died and exhibited intestinal colic, oral ulcers, severe weight loss, and other abnor-malities (31). There were 26 known abortions and many foals exposed in utero died.…”

Section: Human Evidence For Carcinogenicity Occupational Exposuresmentioning

confidence: 99%

Is 2,3,7,8-TCDD (dioxin) a carcinogen for humans?

Ayres¹,

Webb²,

Evans³

et al. 1985

Environ Health Perspect

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2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has suddenly become the focal point of controversy over the relationship of chemical waste to human health. Specific concern exists regarding its potential association with human malignancy. Subcellular, cellular, and whole-animal experiments suggest that TCDD exerts much of its activity by inducing enzymes that protect the intact organism from the assault of environmental contamination. TCDD is a potent inducer of aryl hydrocarbon hydroxylase, although wide variations between species do exist. Conventional tests for mutagenicity have produced conflicting results. Animal experiments have shown the development of tumors following chronic low level ingestion of TCDD. The human evidence regarding the potential carcinogencity of TCDD comes from occupational, military and environmental exposures. Several studies have come out of Sweden suggesting an association between sarcoma and exposure to herbicides. Although there is little solid evidence that 2,3,7,8-TCDD produces substantial chronic disability or premature death in man, a significant body of experimental evidence for its carcinogenicity makes it likely that a small number of human malignancies may be due to its action. Since 2,3,7,8-TCDD is an unwanted contaminant it could be eliminated with little measurable consequence.

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Epidemiology and Pathology of a Tetrachlorodibenzodioxin Poisoning Episode

Cited by 89 publications

References 24 publications

Human health effects after exposure to 2,3,7,8-TCDD

Human health effects after exposure to 2,3,7,8-TCDD

Long-Term Effects of 2,3,7,8-Tetrachlorodibenzo-<i>p</i>-Dioxin on the Peripheral Nervous System

Is 2,3,7,8-TCDD (dioxin) a carcinogen for humans?

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