Developmental Dental Aberrations After the Dioxin Accident in Seveso

Abstract

Children’s developing teeth may be sensitive to environmental dioxins, and in animal studies developing teeth are one of the most sensitive targets of toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Twenty-five years after the dioxin accident in Seveso, Italy, 48 subjects from the contaminated areas (zones A and B) and in patches lightly contaminated (zone R) were recruited for the examination of dental and oral aberrations. Subjects were randomly invited from those exposed in their childhood and for whom frozen serum samples were available. The subjects were frequency matched with 65 subjects from the surrounding non-ABR zone for age, sex, and education. Concentrations of TCDD in previously analyzed plasma samples (zone ABR subjects only) ranged from 23 to 26,000 ng/kg in serum lipid. Ninety-three percent (25 of 27) of the subjects who had developmental enamel defects had been < 5 years of age at the time of the accident. The prevalence of defects in this age group was 42% (15 of 36) in zone ABR subjects and 26% (10 of 39) in zone non-ABR subjects, correlating with serum TCDD levels (p = 0.016). Hypodontia was seen in 12.5% (6 of 48) and 4.6% (3 of 65) of the zone ABR and non-ABR subjects, respectively, also correlating with serum TCDD level (p = 0.05). In conclusion, developmental dental aberrations were associated with childhood exposure to TCDD. In contrast, dental caries and periodontal disease, both infectious in nature, and oral pigmentation and salivary flow rate were not related to the exposure. The results support our hypothesis that dioxins can interfere with human organogenesis.

Fish oil rich in eicosapentaenoic acid protects against oxidative stress-related renal dysfunction induced by TCDD in Wistar rats

“…TCDD arises from a wide variety of sources, including municipal incinerators, sewage sludge and discharge from paper mills, forest fires, automobile exhaust and cigarettes (Whysner and Williams 1996). The hydrophobic structure of TCDD dictates it to be highly persistent, resistant to degradation, tending to accumulate in environment with an estimated half-life of 7.6 years (Alaluusua et al 2004). As a result the International Agency for Research on Cancer's classification, upgraded TCDD from possible human carcinogen to human carcinogen (IARC 1997).…”

From the Cover: Embryonic Exposure to TCDD Impacts Osteogenesis of the Axial Skeleton in Japanese medaka,Oryzias latipes

“…In humans, elevated exposure to polychlorinated dibenzo-p-dioxins and furans during breastfeeding has been strongly associated with hypomineralization of teeth (Alaluusua et al, 1996). Moreover, children living in the TCDD-contaminated zones in Seveso, Italy display an increased incidence of tooth enamel defects (Alaluusua et al, 2004). Cementoblasts, the osteoblast-like cells responsible for forming of mineralized tissue surrounding the tooth-root surface, are regulated by OSX/SP7 (Cao et al, 2012), suggesting a possible linkage between TCDD exposure and altered dentition and bone formation observed in humans.…”

Tooth Agenesis; Aetiological Factors

“…[52] The effect of dioxin on tooth development has been reported as an increase in prevalence of hypomineralisation of teeth in Kotka and Anjalankoski in Finland and as an increase in prevalence of tooth agenesis and hypomineralised enamel among people exposed to it in Seveso, Italy . [53]This has been verified in the laboratory in experimental animals . [54]Bailit believed that prenatal environmental factors such as nutrition and diseases have more influence than the postnatal factors on dental development .…”