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Chloracne is particularly linked to toxic exposure to dioxins (byproducts of many chemical processes, including the manufacture of herbicides such as Agent Orange)—so much so that it is considered a clinical sign of dioxin exposure. The severity and onset of chloracne may follow a typical asymptotic dose-response relationship curve.
The toxic effects have been attributed to dioxin-like PCBs and PCDFs. Their daily intake was up to 100,000 times higher than average intake presently. [1] There were many skin problems, chloracne, swelling of eyelids, and hypersecretion of Meibomian glands in the eyes. Babies born to Yusho and Yu-cheng mothers were smaller than normal, they had ...
Chlorine gas poisoning is an illness resulting from the effects of exposure to chlorine beyond the threshold limit value.Acute chlorine gas poisoning primarily affects the respiratory system, causing difficulty breathing, cough, irritation of the eyes, nose, and throat, and sometimes skin irritation.
The most toxic dioxin, 2,3,7,8-tetrachlorodibenzodioxin (TCDD), became well known as a contaminant of Agent Orange, a herbicide used in the Malayan Emergency and the Vietnam War. [11] Later, dioxins were found in Times Beach , Missouri [ 12 ] and Love Canal , New York [ 13 ] and Seveso , Italy . [ 14 ]
While little research has been done on the toxic effects of 2,2’,3,3’,4,4’-hexachlorobiphenyl, PCBs have been found to cause irritation in the eyes and when inhaled also in the airways. They may cause a rash when in contact with the skin and prolonged exposure can result in chloracne.
Toxic exposure is never a good thing, Kaden says, but “the dose makes the poison.” Groups like Valisure, she says, don’t always make that clear enough in their messaging to the public.
The halflife of heptachlorodibenzo-p-dioxin is calculated to be 3.6 years. This estimation was based on the analysis of fat tissue biopsies collected with an interval of 28 months from on 14-year-old girl who for a period of about 2–3 years had been exposed to technical pentachlorophenol.
TCDD and dioxin-like compounds act via a specific receptor present in all cells: the aryl hydrocarbon (AH) receptor. [6] [7] [8] This receptor is a transcription factor which is involved in the expression of genes; it has been shown that high doses of TCDD either increase or decrease the expression of several hundred genes in rats. [9]