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Risks to live in an industrialized world.

Risks to live in an industrialized world. Acute and Chronic Dioxin Poisoning. Acute Dioxin Toxicity. Seveso (1976) Yusho and Yucheng (1968 and 1978) Two Austrian secretaries (1997) Yushchenko (2004). Acute dioxin poisoning. Yushchenko autumn 2004, before and after.

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Risks to live in an industrialized world.

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  1. Risks to live in an industrialized world. Acute and Chronic DioxinPoisoning.

  2. Acute Dioxin Toxicity • Seveso (1976) • Yusho and Yucheng (1968 and 1978) • Two Austrian secretaries (1997) • Yushchenko (2004)

  3. Acute dioxin poisoning Yushchenko autumn 2004, before and after.

  4. Acute Dioxin Toxicity • Clinical Effects • Laboratory Effects

  5. Seveso 1976 a few days after.

  6. Exposure routes of humans after the Seveso accident. • Absorption from dermal contact with soil • Inhalation of contaminated dust • Contribution of drinkable water • Ingestion of vegetables grown in home gardens • Consumption of animal products (chickens and rabbits) from the area • Casual ingestion of soil

  7. Acute dioxin poisoning CLINICAL EFFECTS • Chloracne • Nausea • Vomiting • Epigastric pain • Appetite loss • Weight loss

  8. Acute dioxin poisoning • Abnormal liver function tests in Seveso children: increase in • γ-glutamyltransferase (GGT) • Alanine aminotransferase (ALT) • In induced abortions in the period 1976-78 the incidence of aberrant cytogenetic findings was increased as was the number of miscarriages in general.

  9. Acute dioxin poisoning Follow-up Seveso • Sex, distance from the accident site and meat consumption were significantly associated with an increased TCDD concentration. • Abnormal sex ratio (more girls) in relation to paternal exposure. • TCDD- concentration in breastmilk after 25 years still twice as high. • Increase in all cancers (rectum, lympho-hemopoietic, myeloid, thyroid gland and pleura)

  10. SEX RATIO after SEVESO

  11. Acute Dioxin Poisoning Coca-cola coloured baby stillborn after YUSHO Placental transfer of PCBs and Furans (1968)

  12. Acute Dioxin Poisoning Two secretaries in Austria 1997 Secretary nr. 1, 30 years old • TCDD-level: 144.000 pg/g fat in blood • Intake: 1,5 mg dioxin • Soon (few days) after moving in a new office in autumn 1997 : centro-facial chloracne and

  13. Acute Dioxin Poisoning Secretary nr 1: • Epigastric pain, gastritis, nausea • Chloracne auricular area, eyelids, genital region, limbs and trunk affected by hundreds of cysts and comedones, • Palmoplanar keratoderma • Secundary amenorrhoea

  14. Acute dioxin poisoning Secretary nr. 1

  15. Acute dioxin Poisoning Laboratory effects in secr. 1 : • Anemia, normochromic, normocytic • Trombocytopenia • Leucocytosis • Natural killer cells slightly lower • Triglycerides (7x increased) • Liver tests slightly abnormal • TSH normal, FT4: normal

  16. Acute dioxin poisoning Secretary nr.2: 27 years old • TCDD-level : 26.000 pg/g fat in blood, Intake: 0,4 mg dioxin • Gastro-intestinal symptoms during several months since autumn 1997 • Not so severe chloracne on the cheeks

  17. Acute dioxin poisoning Laboratory effects in nr.2 • Marginally elevated cholesterol • Triglycerides increased 2x • Anemia • Trombocytopenia • Leukocytosis • NK cells lower • TSH increased, FT4 normal

  18. Acute dioxin poisoning Two year Follow-up of both secretaries Nr 1: • Severe chloracne after one year on the back of the trunk • Big problems with chloracne in the face with inflammation • Depressed Nr 2: • Chloracne disappeared within one year year.

  19. Back of secretary nr.1 shortly after (c) and one year after the intoxication (d)

  20. Acute Dioxin Poisoning Secr. 1 • more chloracne, more abnormal hematological effects • more abnormal lipid spectrum than nr. 2 • no effect on TSH-level Secr. 2 • less chloracne , • less abnormal hematological effects • less abnormal lipid spectrum • effect on TSH-level (increase)

  21. Acute dioxin poisoning Bone marrow • Anemia • Trombocytopenia, • NK cells decreased Lipid spectrum • Triglycerides increased • Cholesterol increased

  22. Acute Dioxin Poisoning, follow-up Chloracne in YUSHO-patient a:shortly after the incident b: after 25 years

  23. Acute and Chronic Dioxin Poisoning Trombocytopeniacharacteristic for dioxin poisoning • BASF workers 1953 • Japanese workers • Two secretaries 4. Dutch children perinatally exposed tobackground levels

  24. AcuteDioxin PoisoningIn the Long Run • Chloracne improves during 25 years • More cancer and 8 years earlier. • More diabetes and earlier in life. • More hypertension. • More miscarriages, prematurity, congenital malformations: congenital hydrocephalus and renal agenesis, and altered sex ratio. • More auto-antibodies to different tissues. • Earlier decline in cognitive functions.

  25. Therapy • There is no effective therapy. So primary prevention is warranted. • Acne therapy with isotretinoin creme may help to treat chloracne • Olestra, a resin that absorbs fat in the intestines, interferes with the entero-hepatic cycle and helps removing dioxin-molecules that are excreted in the gall • Antioxidants like vitamin C and vegetables high in antioxidants, like broccoli, olive oil, berries, tea, grapes, beats and green vegetables high in chlorophyl. • Lactation and liposuction are other possibilities to remove dioxins.

  26. Acute Dioxin Poisoning Conclusion • Clinical signs: chloracne, nausea and vomiting, gastro-intestinal effects.Weight loss. • Laboratory signs: anemia, trombocytopenia, leukocytosis, increased liver enzymes, dyslipidaemia,TSH increased (not at high dose), NK cells decreased.

  27. Chronic Dioxin poisoning • Background levels of dioxins are levels found in human milk in non-contaminated areas. • In Europe background levels of dioxins were and are a problem. • Dioxins are a collective of dioxins and furans and dioxinlike PCBs, expressed as Toxic Equivalent Quantities (TEQ’s).

  28. Chronic Dioxin Poisoning Background concentrations are levels in human milk in non-contaminated areas caused by: • Incineration of municipal waste (79% Netherlands) • By-products of chlorinated phenol production, • Other waste incineration, • Metal smelting, • Traffic

  29. Chronic toxicity of dioxins. • Thyroid Hormone Disruptors, • Estrogen/Androgen Disruptors, • Direct effects on cells.

  30. Chronic toxicity of dioxins. Effects in humans. • Liver function, • Brain function, • Adipose tissue, • Lung function, • Puberty. • Bone marrow, cancer • Longer follow-up is needed for reproductive effects.

  31. Chronic Dioxin Poisoning • In the Amsterdam-Zaandam region in the Netherlands a prospective study was started to effects of background levels of dioxins in the perinatal period in the years 1987-1991. • In the following slides a negative effect on neurofysiologic parameters is described.

  32. Chronic Dioxin Poisoning Characteristics of subjects. Amsterdam study started in 1987/1991 Follow-up:41 healthy 7-12 year old childrenoptimal pregnancies, single births.Dioxin-levels ( I-TEQ dioxin):prenatal exposure 8.74-88.8 ng postnatal exposure 4.34-384.51 ng

  33. Chronic Dioxin Poisoning MEG/EEG methods . • Cognitive functioning was assessed with help of a visual oddball paradigm. The subject has the task to count the times the oddball is seen, during a continuous presentation of a visual stimulus. ( about 60 times during a session) • Strongly associated with N200 (passive attention) and P300 (active attention), subdivided in P3a and P3b.N200 and P3b were analysed.

  34. Chronic Dioxin Poisoning Results The latencies of the N 200 and P3b component (pooled EEG- and MEG data) were significantly prolonged (p-value: 0.002) and the amplitude was decreased (p-value: 0.01) in relationto perinatal dioxin exposure

  35. Acute and Chronic Dioxin Poisoning Author: Janna G. Koppe CHEST-project. Leaders: Peter van den Hazel Moniek Zuurbier

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