Dioxinlike properties of a trichloroethylene combustion-generated aerosol.
Male
dioxin-response element binding
Biomedical and clinical sciences
incomplete combustion by-products
trichloroethylene
Guinea Pigs
Pollution and Contamination
dioxin-like toxicity
Oryzias
Incineration
liver
Toxicology
Dioxins
Medical and Health Sciences
03 medical and health sciences
Animals
embryo cardiovascular toxicity
complex mixture
Aerosols
0303 health sciences
Biomedical and Clinical Sciences
Molecular Structure
Liver Disease
500
Health sciences
DNA
Trichloroethylene
3. Good health
Environmental sciences
Liver
Oncorhynchus mykiss
Ah receptor
antiestrogen
Biological Assay
Female
Generic health relevance
Digestive Diseases
vitellogenin
Environmental Sciences
DOI:
10.1289/ehp.96104734
Publication Date:
2011-03-16T19:17:56Z
AUTHORS (10)
ABSTRACT
Conventional chemical analyses of incineration by-products identify compounds of known toxicity but often fail to indicate the presence of other chemicals that may pose health risks. In a previous report, extracts from soot aerosols formed during incomplete combustion of trichloroethylene (TCE) and pyrolysis of plastics exhibited a dioxinlike response when subjected to a keratinocyte assay. To verify this dioxinlike effect, the complete extract, its polar and nonpolar fractions, some containing primarily halogenated aromatic hydrocarbons, were evaluated for toxicity using an embryo assay, for antiestrogenicity using primary liver cell cultures, and for the ability to transform the aryl hydrocarbon receptor into its DNA binding form using liver cytosol in a gel retardation assay. Each of these assays detect dioxinlike effects. Medaka (Oryzias latipes) embryos and primary liver cell cultures of rainbow trout (Oncorhynchus mykiss) were exposed to concentrations of extract ranging from 0.05 to 45 micrograms/l. Cardiotoxicity with pericardial, yolk sac, and adjacent peritoneal edema occurred after exposure of embryos to concentrations of 7 micrograms/l or greater. These same exposure levels were associated with abnormal embryo development and, at the higher concentrations, death. Some of the fractions were toxic but none was as toxic as the whole extract. In liver cells, total cellular protein and cellular lactate dehydrogenase activity were not altered by in vitro exposure to whole extract (0.05-25 micrograms/l). However, induction of cytochrome P4501A1 protein and ethoxyresorufin O-deethylase activity occurred. In the presence of whole extract, estradiol-dependent vitellogenin synthesis was reduced. Of the fractions, only fraction 1 (nonpolar) showed a similar trend, although vitellogenin synthesis inhibition was not significant. The soot extract and fractions bound to the Ah receptor and showed a significantly positive result in the gel retardation/DNA binding test. Chemical analyses using GC-MS with detection limits for 2,3,7,8-tetrachlorodibenzo-p-dioxin and dibenzofuran in the picomole range did not show presence of these compounds. Our results indicate that other chemicals associated with TCE combustion and not originally targeted for analysis may also pose health risks through dioxinlike mechanisms.
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