Biomonitoring of possible human exposure to environmental genotoxic chemicals: Lessons from a study following the wreck of the oil tanker Braer

Cole, Jane; Beare, David; Waugh, Alastair P.W.; Capulas, Emily; Aldridge, Kay E.; Arlett, C.F.; Green, Michael H.L.; Crum, Jacqueline E.; Cox, Derek; Garner, R.C.; Dingley, Karen H.; Martin, Elizabeth; Podmore, Karen; Heydon, Robert T.; Farmer, Peter B.

doi:10.1002/(sici)1098-2280(1997)30:2<97::aid-em2>3.3.co;2-d

Cited by 7 publications

(12 citation statements)

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“…Vacek et al [2005] reported results of a human biomonitoring study in which mutation frequencies at the HPRT locus in lymphocytes of children whose siblings were included in the Dover Township pediatric cancer cluster were compared with frequencies in healthy nonexposed children; no difference in mutation frequencies were observed between the two groups of children. These results are consistent with several earlier reports showing no association between environmental chemical exposures and HPRT mutation frequencies in adult study populations [Cole et al, 1996[Cole et al, , 1997Becker et al, 2001;Kyrtopoulos et al, 2001]. Vacek et al [2005] speculated that the length of time from exposure to measurement of mutation frequencies may have contributed to the negative results.…”

Section: Introductionsupporting

confidence: 92%

Genotoxicity of styrene–acrylonitrile trimer in brain, liver, and blood cells of weanling F344 rats

Hobbs

Chhabra

Recio

et al. 2012

Environ and Mol Mutagen

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Styrene–acrylonitrile Trimer (SAN Trimer), a by-product in production of acrylonitrile styrene plastics, was identified at a Superfund site in Dover Township, NJ, where childhood cancer incidence rates were elevated for a period of several years. SAN Trimer was therefore tested by the National Toxicology Program in a 2-year perinatal carcinogenicity study in F344/N rats and a bacterial mutagenicity assay; both studies gave negative results. To further characterize its genotoxicity, SAN Trimer was subsequently evaluated in a combined micronucleus (MN)/Comet assay in juvenile male and female F344 rats. SAN Trimer (37.5, 75, 150, or 300 mg/kg/day) was administered by gavage once daily for 4 days. Micronucleated reticulocyte (MN-RET) frequencies in blood were determined by flow cytometry, and DNA damage in blood, liver, and brain cells was assessed using the Comet assay. Highly significant dose-related increases (P < 0.0001) in MN-RET were measured in both male and female rats administered SAN Trimer. The RET population was reduced in high dose male rats, suggesting chemical-related bone marrow toxicity. Results of the Comet assay showed significant, dose-related increases in DNA damage in brain cells of male (P < 0.0074) and female (P < 0.0001) rats; increased levels of DNA damage were also measured in liver cells and leukocytes of treated rats. Chemical-related cytotoxicity was not indicated in any of the tissues examined for DNA damage. The results of this subacute MN/Comet assay indicate induction of significant genetic damage in multiple tissues of weanling F344 male and female rats after oral exposure to SAN Trimer.

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Section: Introductionsupporting

confidence: 92%

Genotoxicity of styrene–acrylonitrile trimer in brain, liver, and blood cells of weanling F344 rats

Hobbs

Chhabra

Recio

et al. 2012

Environ and Mol Mutagen

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“…Braer Cole et al (1997) evaluated the possible genotoxicity as a consequence of the Braer tanker oil spill. They used blood samples to assess the primary damage in the DNA (DNA adducts in the mononuclear cell fraction by a modified 32 P-postlabeling method and mutations at the hprt locus in T lymphocytes).…”

Section: Epidemiological Studies On Genotoxicity and Endocrine Toxicitymentioning

confidence: 99%

Review on the effects of exposure to spilled oils on human health

Aguilera

Méndez

Pásaro

et al. 2010

J of Applied Toxicology

316

158

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Harmful effects of oil spills on diverse flora and fauna species have been extensively studied. Nevertheless, only a few studies have been compiled in the literature dealing with the repercussions of oil exposure on human health; most of them have focused on acute effects and psychological symptoms. The objective of this work was to gather all these studies and to analyze the possible consequences of this kind of complex exposure in the different aspects of human health. Studies found on this topic were related to the disasters of the Exxon Valdez, Braer, Sea Empress, Nakhodka, Erika, Prestige and Tasman Spirit oil tankers. The majority of them were cross-sectional; many did not include control groups. Acute effects were evaluated taking into account vegetative-nervous symptoms, skin and mucous irritations, and also psychological effects. Genotoxic damage and endocrine alterations were assessed only in individuals exposed to oil from Prestige. The results of the reviewed articles clearly support the need for biomonitoring human populations exposed to spilled oils, especially those individuals involved in the cleanup, in order to evaluate not only the possible immediate consequences for their health but also the medium- and long-term effects, and the effectiveness of the protective devices used.

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“…The mutation spectrum was changed in newborns exposed to ETS (88); the mutation frequency was increased in tobacco smokers (90) as well as in marihuana smokers (100) and their newborns. No effect was seen in a population exposed to spilled crude oil (79) or in newborns exposed to ETS (87).…”

Section: Discussionmentioning

confidence: 88%

“…Our conclusion contradicts the recent evaluation by Dor et (65,66), in traffic policemen (74), and in smokers (16,91). Two studies found no effect of PAH exposure on DNA adduct levels (79,101). Immunologic methods such as competitive ELISA or immunohistochemistry use polyclonal and monoclonal antibodies to recognize PAH-DNA adducts (111).…”

Section: Discussionmentioning

confidence: 99%

Molecular Epidemiology Studies on Occupational and Environmental Exposure to Mutagens and Carcinogens, 1997-1999

Srám¹,

Binková²

2000

Environmental Health Perspectives

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Molecular epidemiology is a new and evolving area of research, combining laboratory measurement of internal dose, biologically effective dose, biologic effects, and influence of individual susceptibility with epidemiologic methodologies. Biomarkers evaluated were selected according to basic scheme: biomarkers of exposure-metabolites in urine, DNA adducts, protein adducts, and Comet assay parameters; biomarkers of effect-chromosomal aberrations, sister chromatid exchanges, micronuclei, mutations in the hypoxanthine-guanine phosphoribosyltransferase gene, and the activation of oncogenes coding for p53 or p21 proteins as measured on protein levels; biomarkers of susceptibility-genetic polymorphisms of genes CYP1A1, GSTM1, GSTT1, NAT2. DNA adducts measured by 32P-postlabeling are the biomarker of choice for the evaluation of exposure to polycyclic aromatic hydrocarbons. Protein adducts are useful as a biomarker for exposure to tobacco smoke (4-aminobiphenyl) or to smaller molecules such as acrylonitrile or 1,3-butadiene. Of the biomarkers of effect, the most common are cytogenetic end points. Epidemiologic studies support the use of chromosomal breakage as a relevant biomarker of cancer risk. The use of the Comet assay and methods analyzing oxidative DNA damage needs reliable validation for human biomonitoring. Until now there have not been sufficient data to interpret the relationship between genotypes, biomarkers of exposure, and biomarkers of effect for assessing the risk of human exposure to mutagens and carcinogens. Key words: air pollution, benzene, biomarkers, coke oven, genotypes, occupational exposure, PAHs, pesticides, tobacco smoke. -Envwron Health Perspect 1 08(suppl 1):57-70 (2000). http.//ehpnetl. niehs. nih.gov/docs/2000/suppl-1/57-70sram/abstract. html A new and evolving area of research termed molecular epidemiology attempts to merge sophisticated and highly sensitive laboratory methods (many of them developed during the recent revolution in molecular biology) with analytical epidemiologic methods. Molecular epidemiology bridges basic research in molecular biology and studies of human cancer causation by combining laboratory measurement of internal dose, biologically effective dose, biologic effects, and the influence of individual susceptibility with epidemiologic methodologies (1). The most common view is that the approach represents a natural convergence of molecular biology and epidemiology (2).The number of biomarkers available for evaluating genetic and cancer risk in humans is quite large. Their utility-for human biomonitoring is suggested by the well-known paradigm of environmentally induced cancer, which represents end points for assessing the entire spectrum of human-genotoxicant interactions (3). These biomarkers begin with exposure and include absorption, metabolism, distribution, critical target interaction (i.e., DNA damage and repair), genetic changes, and finally, disease, which is the province of traditional epidemiology. The development of biomarkers has given rise to the field of ...

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Biomonitoring of possible human exposure to environmental genotoxic chemicals: Lessons from a study following the wreck of the oil tanker Braer

Cited by 7 publications

References 0 publications

Genotoxicity of styrene–acrylonitrile trimer in brain, liver, and blood cells of weanling F344 rats

Genotoxicity of styrene–acrylonitrile trimer in brain, liver, and blood cells of weanling F344 rats

Review on the effects of exposure to spilled oils on human health

Molecular Epidemiology Studies on Occupational and Environmental Exposure to Mutagens and Carcinogens, 1997-1999

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