Short-term tests for carcinogens and mutagens

Human internal and external exposure to PBDEs – A review of levels and sources

Damage to DNA appears to be the major cause of most cancer and genetic birth defects and may contribute to aging and heart disease as well. The agents that cause this damage must be identified. Many of these agents are natural chemicals present in the human diet as complex mixtures. The tens of thousands of man-made chemicals that have been introduced into the environment in the last few decades must also be tested for their ability to damage DNA. Existing animal tests and human epidemiology alone are inadequate for this task because of time, expense, and the difficulty of dealing with complex mixtures, Newly developed short-term tests, most of them assaying for mutagenicity, are discussed as key tools in identifying environmental mutagens and carcinogens.

https://science.sciencemag.org/content/sci/204/4393/587.full.pdf

Identifying Environmental Chemicals Causing Mutations and Cancer

Polybrominated diphenyl ethers (PBDEs) are a class of flame retardants used in a variety of consumer products. In the past 25 years, PBDEs have become ubiquitous environmental contaminants. They have been detected in soil, air, sediments, birds, marine species, fish, house dust, and human tissues, blood and breast milk. Diet and house dust appear to be the major sources of PBDE exposure in the general population, though occupational exposure can also occur. Levels of PBDEs in human tissues are particularly high in North America, compared to Asian and European countries, and have been increasing in the past 30 years. Concentrations of PBDEs are particularly high in breast milk, resulting in high exposure of infants. In addition, for toddlers, dust has been estimated to account for a large percentage of exposure. PBDEs can also cross the placenta, as they have been detected in fetal blood and liver. Tetra-, penta- and hexaBDEs are most commonly present in human tissues. The current greatest concern for potential adverse effects of PBDEs relates to their developmental neurotoxicity. Pre- or postnatal exposure of mice or rats to various PBDEs has been shown to cause long-lasting changes in spontaneous motor activity, mostly characterized as hyperactivity or decreased habituation, and to disrupt performance in learning and memory tests. While a reduction in circulating thyroid hormone (T4) may contribute to the developmental neurotoxicity of PBDEs, direct effects on the developing brain have also been reported. Among these, PBDEs have been shown to affect signal transduction pathways and to cause oxidative stress. Levels of PBDEs causing developmental neurotoxicity in animals are not much dissimilar from levels found in highly exposed infants and toddlers.

Developmental neurotoxicity of polybrominated diphenyl ether (PBDE) flame retardants

Polybrominated diphenyl ethers, PBDEs, are a class of brominated flame retardants that, like other persistent organic pollutants (POPs), have been found in humans, wildlife, and biota worldwide. Unlike other POPs, however, the key routes of human exposure are not thought to be food and fish, but rather are from their use in household consumer products, and to the high levels of PBDEs found in house dust. The exposure of Americans to PBDEs was systematically evaluated in this study. First, exposure media data on PBDE congeners were compiled. Then, an adult intake dose was derived using exposure factors in combination with these data. The exposure pathways evaluated included food and water ingestion, inhalation, and ingestion and dermal contact to house dust. These intakes were converted to a body burden using a simple pharmacokinetic (PK) model. The predicted body burdens were compared with representative profiles of PBDEs in blood and milk. The adult intake dose of total PBDEs was estimated to be 7.7 ng/kg body weight/day, and children's estimated intakes were higher at 49.3 ng/kg/day for ages 1–5, 14.4 ng/kg/day for 6–11, and 9.1 ng/kg/day for 12–19. The much higher dose for the child age 1–5 was due to the doubling of dust ingestion from 50 to 100 mg/day. The predicted adult body burden of total PBDEs was 33.8 ng/kg lipid weight (lwt), compared to representative measurements in blood and milk at 64.0 and 93.7 ng/g lwt, respectively Most of this apparent underprediction in total concentration was due to an underprediction of the key congener, BDE 47. The value for BDE 47 half-life in the body was identified as the variable most likely in error in this exercise. Other congener predictions compared well with measurements, suggesting general validity with the approach. An important finding from this assessment is that the food intake estimate of about 1.3 ng/kg/day (of the 7.7 ng/kg/day total) cannot explain current US body burdens; exposures to PBDEs in house dust accounted for 82% of the overall estimated intakes.

Exposure of Americans to polybrominated diphenyl ethers.

An international workshop reviewed 20 ongoing or recently completed studies of the effects of perinatal exposures to dioxins, dibenzofurans, and PCBs on the reproductive, endocrine, neurodevelopmen...

Workshop on perinatal exposure to dioxin-like compounds. I. Summary.

Bruce Ames and Kim Hooper reply to a recent criticism of their inquiry into the relation between mutagenic potency in the Ames test and carcinogenic potency.

Does carcinogenic potency correlate with mutagenic potency in the Ames assay

This paper describes four assays that detect somatic gene mutations in humans: the hypoxanthine-guanine phosphoribosyl transferase assay, the glycophorin A assay, the HLA-A assay, and the sickle cell hemoglobin assay. Somatic gene mutation can be considered a biomarker of carcinogenesis, and assays for somatic mutation may assist epidemiologists in studies that attempt to identify factors associated with increased risks of cancer. Practical aspects of the use of these assays are discussed.

/pdf/human-somatic-mutation-assays-as-biomarkers-of-5f287exn3s.pdf

Human somatic mutation assays as biomarkers of carcinogenesis

PBDEs in the San Francisco Bayarea : Measurements in fish

Studies of perinatal exposures to dioxin-like compounds (DLCs), coplanar polycyclic halogenated aromatics whose prototype is 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), have employed a variety of o...

Workshop on perinatal exposure to dioxin-like compounds. VI. Role of biomarkers.

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