Toxicity and Fetotoxicity of TCDD, TCDF and PCB Isomers in Rhesus Macaques (Macaca mulatta)

McNulty, Wilbur P.

doi:10.2307/3429947

Cited by 24 publications

(18 citation statements)

References 1 publication

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“…The difference in the prevalence of defects between the groups was mostly due to demarcated opacities and hypoplasia. The observation of induced enamel hypoplasia in exposed children is in accordance with studies on PCB-treated rats and nonhuman primates [Hashiguchi et al, 1985;McNulty, 1985], where selective toxic effects on ameloblasts and cells of stratum intermedium in the secretory stage of enamel development were reported. Hara [1985] found that an increased frequency of mottled enamel was reported in children born to occupationally exposed mothers, while contamination of PCBs with dioxins and furans cannot be definitely excluded.…”

Section: Discussionsupporting

confidence: 69%

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Polychlorinated Biphenyls Cause Developmental Enamel Defects in Children

Jan

Vrbic

2000

Caries Res

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The aim of this study was to evaluate the effects of long–term exposure to polychlorinated biphenyls (PCBs) on developing dental enamel. 202 8– to 14–year–old children who were pre– and post–natally exposed to PCBs in the contaminated region of Bela Krajina, Slovenia, were studied. 202 controls from Bršljin were matched for age and sex. Risk assessment was based on the concentrations of toxic PCB congeners in the diet. Levels of PCBs in dentine were used to validate exposure. PCB levels were analysed by high–resolution gas chromatography. The prevalence of developmental defects of enamel was assessed using the FDI Index. Developmental defects of enamel in permanent teeth were found in 71.3% of exposed children, compared to 49.5% in the control group. The enamel was abnormal in 21.9% of the permanent index teeth of exposed children and in 12.7% of the control children. The difference was statistically significant (χ² = 84.18; p = 0.0019), mostly on account of demarcated opacities and hypoplasia. The extent of the defects was also greater in the exposed group (χ² = 61.3; p = 0.0001). No significant correlations were found between PCB exposure and developmental defects in deciduous teeth. In conclusion, our results showed that long–term exposure to PCBs may cause developmental defects of enamel.

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Section: Discussionsupporting

confidence: 69%

“…Animal studies in several species have found that PCB exposure can lead to severe morphological changes in ameloblasts [Hashiguchi et al, 1985;McNulty, 1985]. There is strong evidence suggesting a common mechanism of action and also a number of common toxic responses similar to those observed for tetra-chloro-dibenzo-p-dioxin (TCDD) [Safe, 1994].…”

mentioning

confidence: 99%

Polychlorinated Biphenyls Cause Developmental Enamel Defects in Children

Jan

Vrbic

2000

Caries Res

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“…The irregular surface led McNulty to suggest that cysts lay beneath the gingival surface, as he has seen in postnatal monkeys poisoned with PCBs (11). Others have suggested that the gingiva may look unusual as it covers the first dentition just before it erupts.…”

Section: "Gingival Hyperplasia" and Natal Teethmentioning

confidence: 99%

“…In part this lack of movement may be due to a tendency to pass over the congenital findings, while concentrating on the effects among the large number of exposed children and adults. A notable new lead from this conference concerns dental problems (a) at birth (5), (b) subsequently (2, Kim brough, personal communication), and (c) in nonhuman primates (11). Prospective studies in Taiwan should include careful dental examinations.…”

Section: Congenital Yusho In Perspectivementioning

confidence: 99%

Congenital PCB Poisoning: A Reevaluation

Miller¹

1985

Environmental Health Perspectives

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A review of the literature reveals a need to clarify the pathologic physiology of congenital polychlorinated biphenyl (PCB) poisoning, which is characterized by intrauterine growth retardation, brown staining of the skin and mucous membranes, as in Addison's disease, natal teeth, widely open fontanelles and sagittal suture and apparent overgrowth of the gingiva. The skull abnormalities may represent irregular calcification, with natal teeth appearing because the bone of the mandible is penetrated more easily than usual. Some fetuses were poisoned at the time the mothers ingested the oil; others were affected in the subsequent years from residual contamination in the mothers' bodies. The misadventure in Japan was repeated in Taiwan in 1979. The seven congenital cases in Taiwan reported thus far seem to differ from those in Japan. In Taiwan the noses were somewhat black, two of the infants did not have low birth weight and the osseous abnormalities of the skull and gingival hyperplasia were not observed. Systematic followup studies should be made in Taiwan of the children born within 2 years of maternal poisoning with PCBs. Special attention should be given to age at first dentition and skull X-rays for spotty calcification, among other measures of physical, neurologic and intellectual development.

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“…In good agreement with these findings, deficits on tests of learning and changes in activity have been demonstrated as a result of PCB exposure in both rodents and monkeys. Adult monkeys chronically exposed to PCBs develop the classic signs of PCB toxicity in humans, including chloracne, hair loss, and swelling of the eyelids (82,83); however, whether PCB exposure in adult monkeys also produces the paresthesias and weakness reported in humans has not been addressed. Neurotoxicity has not been reported in adult rodents as a result of PCB exposure.…”

Section: Congruence Of Exposure Levels At Which Neurotoxicity Is Obsementioning

confidence: 99%