<abstract xml:lang="en" xmlns="http://www.w3.org/1999/xhtml">The term dioxins usually refers to polychlorinated dibenzo-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs). As 2,3,7,8-tetrachloro-dibenzo-p-dioxin (TCDD) has the highest toxic potential, the toxic potentials of other PCDDs and PCDFs are defined in comparison with it. Human exposure to dioxins can be environmental (background), occupational, or accidental pollution. In the human body, dioxins are in part metabolised and eliminated, and the rest is stored in body fat. People vary in their capacity to eliminate TCDD, but it is also dose-dependent; the elimination rate is much faster at higher than lower levels. The liver microsomal P4501A1 enzyme oxygenates lipophilic chemicals such as dioxins. It is encoded by the CYP1A1 gene. Cytosolic aryl hydrocarbon receptor (AhR) mediates their carcinogenic action. It binds to dioxin, translocates to nucleus and together with hydrocarbon nuclear translocator (ARNT) and xenobiotic responsive element (XRE) increases the expression of CYP1A1.Dioxins are classified as known human carcinogens, but they also cause noncancerous effects like atherosclerosis, hypertension, and diabetes. Long-term exposures to dioxins cause disruption of the nervous, immune, reproductive, and endocrine system. Short-term exposure to high levels impairs the liver function and causes chloracne. The most sensitive population to dioxin exposure are the foetuses and infants.A large number of health effects have been documented in the scientific literature, and they all place dioxins among the most toxic chemicals known to man.</abstract>

The term dioxins usually refers to polychlorinated dibenzo-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs). As 2,3,7,8-tetrachloro-dibenzo-p-dioxin (TCDD) has the highest toxic potential, the toxic potentials of other PCDDs and PCDFs are defined in comparison with it. Human exposure to dioxins can be environmental (background), occupational, or accidental pollution. In the human body, dioxins are in part metabolised and eliminated, and the rest is stored in body fat. People vary in their capacity to eliminate TCDD, but it is also dose-dependent; the elimination rate is much faster at higher than lower levels. The liver microsomal P4501A1 enzyme oxygenates lipophilic chemicals such as dioxins. It is encoded by the CYP1A1 gene. Cytosolic aryl hydrocarbon receptor (AhR) mediates their carcinogenic action. It binds to dioxin, translocates to nucleus and together with hydrocarbon nuclear translocator (ARNT) and xenobiotic responsive element (XRE) increases the expression of CYP1A1.Dioxins are classified as known human carcinogens, but they also cause noncancerous effects like atherosclerosis, hypertension, and diabetes. Long-term exposures to dioxins cause disruption of the nervous, immune, reproductive, and endocrine system. Short-term exposure to high levels impairs the liver function and causes chloracne. The most sensitive population to dioxin exposure are the foetuses and infants.A large number of health effects have been documented in the scientific literature, and they all place dioxins among the most toxic chemicals known to man.

Dioxins and Human Toxicity

Department of Chemistry and Biochemistry, Zagreb University School of Medicine

Medikol Outpatient Clinic, Zagreb, Croatia

Forensic Science Centre "Ivan Vučetić", General Police Directorate, Ministry of Interior, Zagreb, Croatia

Archives of Industrial Hygiene and Toxicology

{"article-title":"Dioxins and Human Toxicity"}

The term dioxins usually refers to polychlorinated dibenzo-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs). As 2,3,7,8-tetrachloro-dibenzo-p-dioxin...

Dioxins and Human Toxicity

Published Online: Dec 23, 2010

Page range: 445 - 453

DOI: https://doi.org/10.2478/10004-1254-61-2010-2024

Keywords
ARNT, CYP1A1, jetra, P4501A1, PCDD, PCDF, receptor arilnih ugljikovodika, TCDD, zdravstveni učinci

This content is open access.

Dioxins and Human Toxicity

Published Online: Dec 23, 2010

Page range: 445 - 453

DOI: https://doi.org/10.2478/10004-1254-61-2010-2024

KeywordsARNT, CYP1A1, jetra, P4501A1, PCDD, PCDF, receptor arilnih ugljikovodika, TCDD, zdravstveni učinci

This content is open access.

Keywords
ARNT, CYP1A1, jetra, P4501A1, PCDD, PCDF, receptor arilnih ugljikovodika, TCDD, zdravstveni učinci