Risks to live in an industrialized world. - PowerPoint PPT Presentation

barclay
slide1 n.
Skip this Video
Loading SlideShow in 5 Seconds..
Risks to live in an industrialized world. PowerPoint Presentation
Download Presentation
Risks to live in an industrialized world.

play fullscreen
1 / 35
Download Presentation
117 Views
Download Presentation

Risks to live in an industrialized world.

- - - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript

  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