2,3,7,8-Tetrachlordibenzo[b,e][1,4]dioxin Chemische Eigenschaften,Einsatz,Produktion Methoden
ERSCHEINUNGSBILD
FARBLOSE BIS WEISSE NADELARTIGE KRISTALLE.
CHEMISCHE GEFAHREN
Zersetzung beim Erhitzen auf 750-800°C und unter Einfluss von UV-Licht unter Bildung von Chlor.
ARBEITSPLATZGRENZWERTE
TLV nicht festgelegt (ACGIH 2005).
MAK: 10 ^-^8mg/m? (Einatembare Fraktion); Spitzenbegrenzung: überschreitungsfaktor II(8); Hautresorption; Krebserzeugend Kategorie 4; Schwangerschaft: Gruppe C; (DFG 2005).
AUFNAHMEWEGE
Aufnahme in den K?rper durch Inhalation des Staubes, über die Haut und durch Verschlucken.
INHALATIONSGEFAHREN
Verdampfung bei 20°C vernachl?ssigbar; eine gesundheitssch?dliche Partikelkonzentration in der Luft kann jedoch beim Dispergieren schnell erreicht werden.
WIRKUNGEN BEI KURZZEITEXPOSITION
WIRKUNGEN BEI KURZZEITEXPOSITION: Die Substanz reizt die Augen, die Haut und die Atemwege. M?glich sind Auswirkungen auf Herz-Kreislaufsystem, Magen-Darm-Trakt, Leber, Nervensystem und das endokrine System. Die Auswirkungen treten u.U. verz?gert ein.
WIRKUNGEN NACH WIEDERHOLTER ODER LANGZEITEXPOSITION
Wiederholter oder andauernder Hautkontakt kann Dermatitis hervorrufen. M?glich sind Auswirkungen auf Knochenmark, endokrines System, Immunsystem, Leberund Nervensystem. Krebserzeugend für den Menschen. Tierversuche zeigen, dass die Substanz m?glicherweise fruchtbarkeitssch?digend oder entwicklungssch?digend wirken kann.
LECKAGE
Gefahrenbereich verlassen! Fachmann zu Rate ziehen! Chemikalienschutzanzug mit umgebungsluftunabh?ngigem Atemschutzger?t.
R-S?tze Betriebsanweisung:
R11:Leichtentzündlich.
R38:Reizt die Haut.
R48/20:Gesundheitssch?dlich: Gefahr ernster Gesundheitssch?den bei l?ngerer Exposition durch Einatmen.
R63:Kann das Kind im Mutterleib m?glicherweise sch?digen.
R65:Gesundheitssch?dlich: kann beim Verschlucken Lungensch?den verursachen.
R67:D?mpfe k?nnen Schl?frigkeit und Benommenheit verursachen.
S-S?tze Betriebsanweisung:
S36/37:Bei der Arbeit geeignete Schutzhandschuhe und Schutzkleidung tragen.
S62:Bei Verschlucken kein Erbrechen herbeiführen. Sofort ?rztlichen Rat einholen und Verpackung oder dieses Etikett vorzeigen.
Chemische Eigenschaften
White Solid
Verwenden
A toxic polychlorinated dibenzo-p-dioxin detected in domestic meat and poultry.
Allgemeine Beschreibung
White crystals or tan crystalline powder.
Air & Water Reaktionen
Insoluble in water.
Reaktivit?t anzeigen
2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN reaacts when exposed to ultraviolet light in solution in isooctane or n-octanol. Undergoes catalytic perchlorination .
Health Hazard
Chlorinated dibenzo-p-dioxins
(CDDs) cause chloracne, may cause hepatotoxicity,
immunotoxicity, reproductive toxicity,
developmental toxicity, and central nervous
system toxicity, and are considered to be a
human carcinogen.
The most obvious health effect in humans
for exposure to CDDs is chloracne, a severe
skin disease characterized by follicular hyperkeratosis
(comedones) occurring with or without
cysts and pustules.2–4 Unlike adolescent acne,
chloracne may affect almost every follicle in an
involved area, and it may be more disfiguring
than adolescent acne.
Brandgefahr
Literature sources indicate that 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN is nonflammable.
Pharmakologie
TCDD
and other chlorinated dibenzodioxins, dibenzofurans,
and planar PCBs are thought to operate through a
common mechanism. For humans and rodents, there
is an initial binding to the aryl hydrocarbon (Ah)
receptor. Binding to the receptor is a necessary (but
not sufficient) event for the biological response. TCDD
induces many responses, including induction of gene
expression, altered metabolism, altered cell growth and
differentiation, and disruption of steroid hormone and
growth factor signal transduction pathways. The very
diversity of tissue-selective and species-selective responses
elicited by TCDD requires that the receptor (Ah) is part
of a multicomponent system, and it is unlikely that
the differences in dose-response are related solely to
differences in Ah receptor concentrations or affinities in
various species or tissues (29). It is considered that there
is an inducible protein-binding site in the liver (30,31)
known as CYP1A1 (30–34) because TCDD was not
sequestered in the liver of transgenic mice that lack P450
1A2 gene.
Sicherheitsprofil
Confirmed carcinogen with experimental carcinogenic, neoplastigenic, tumorigenic, and teratogenic data. One of the most toxic synthetic chemicals. A deadly experimental poison by ingestion, skin contact, and intraperitoneal routes. Human systemic effects by skin contact: allergic dermatitis. Experimental reproductive effects. Human mutation data reported. An eye irritant. TCDD is the most toxic member of the 75 dioxins. It causes death in rats by hepatic cell necrosis. Death can follow a lethal dose by weeks. Acute and subacute exposure result in wasting, hepatic necrosis, thymic atrophy, hemorrhage, lymphoid depletion, chloracne. A by-product of the manufacture of polychlorinated phenols. It is found at low levels in 2,4,5-T, 2,4,5-trichlorophenol, and hexachlorophene. It is also formed during various combustion processes. Incineration of chemical wastes, including chlorophenols, chlorinated benzenes, and biphenyl ethers, may result in the presence of TCDD in flue gases, fly ash, and soot particles. It is immobile in contaminated soil and may be retained for years. TCDD has the potential for bio-accumulation in animals. An accident in Seveso, Italy, and inadvertent soil contamination in Mmouri have resulted in abandonment of the contaminated areas. When heated to decomposition it emits toxic fumes of Cl-.
m?gliche Exposition
TCDD is primarilly a research chemical. As noted above, TCDD is an inadvertent contaminant in herbicide precursors and thus in the herbicides themselves. It is also formed during various combustion processes including the incineration of chemical wastes (chlorophenols, chlorinated benzenes, and biphenyl ethers). It may be found in flue gases, fly ash, and soot particles. It is highly persistent in soil, and contamination may be retained for years. TCDD is the most toxic of all the dioxins, and has the potential for bio-accumulation in animals. Thus, it is applied in herbicide formulations, but is not used per se. It has been estimated that approximately 2 million acres in the United States have been treated for weed control on one or more occasions with approximately 15 million pounds of TCDD contaminated 2,4,5,-T, 2,4,-D, or combinations of the two.
Carcinogenicity
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is known to be a human carcinogen based on sufficient evidence of carcinogenicity from studies in humans, both epidemiological and on the mechanism of carcinogenesis. TCDD was first listed in the Second Annual Report on Carcinogens as reasonably anticipated to be a human carcinogen. Subsequently, a number of studies were published that examined cancer in human populations exposed to TCDD occupationally or through industrial accidents. A concerted research effort examined the molecular and cellular events that occur in tissues of humans and animals exposed to TCDD. Based on the new information, the listing was revised to known to be a human carcinogen in the January 2001 addendum to the Ninth Report on Carcinogens.
Stoffwechsel
Absorption. TCDD is retained in all tissues. The
highest retention is in fat and liver.
Penetration values into human skin are low. For example,
a dose of 6.5 ng/cm2 in acetone gave a rate of 5 g/cm2/h.
Transfer to the fetus has been observed (43).
Absorption rates after single dose in the diet were 50
to 70–90% (44–48). Rates in rats were lower (50–60%) when administered in the diet for more than 6 weeks (49),
compared with a single-dose absorption rate of 70% (46).
Distribution. The major storage sites are liver and
adipose tissue. The skin can act as an important storage
site, and high concentrations can also be found in the
adrenals (1). After one day of exposure for rats, mice,
hamsters and guinea pigs, 25–70% of the dose was stored
in the liver (41).
Excretion. Excretion is mostly fecal. Breast milk can be
a route of elimination. Whole body half-lives were from
17 to 31 days in rat studies (46–52). Mice had lower halflives
(53,54). Female rhesus monkeys with four years of
dietary exposure had a longer half-life (391 days) (55,56).
These half-lives are very fast considering human half-lives
of 5.8–11.3 years (cited earlier).
Inkompatibilit?ten
Decomposes in ultraviolet (UV) light.
2,3,7,8-Tetrachlordibenzo[b,e][1,4]dioxin Upstream-Materialien And Downstream Produkte
Upstream-Materialien
Downstream Produkte
