The Relationship of Thyroid Cancer with Radiation Exposure from Nuclear Weapon Testing in the Marshall Islands.
Department of Public Health, Yamagata University, Ямагата, Yamagata, Japan Journal of Epidemiology
(Impact Factor: 3.02).
04/2003; 13(2):99-107. DOI: 10.2188/jea.13.99
The US nuclear weapons testing program in the Pacific conducted between 1946 and 1958 resulted in radiation exposure in the Marshall Islands. The potentially widespread radiation exposure from radio-iodines of fallout has raised concerns about the risk of thyroid cancer in the Marshallese population. The most serious exposures and its health hazards resulted from the hydrogen-thermonuclear bomb test, the Castle BRAVO, on March 1, 1954. Between 1993 and 1997, we screened 3,709 Marshallese for thyroid disease who were born before the BRAVO test. It was 60% of the entire population at risk and who were still alive at the time of our examinations. We diagnosed 30 thyroid cancers and found 27 other study participants who had been operated for thyroid cancer before our screening in this group. Fifty-seven Marshallese born before 1954 (1.5%) had thyroid cancer or had been operated for thyroid cancer. Nearly all (92%) of these cancers were papillary carcinoma. We derived estimates of individual thyroid dose proxy from the BRAVO test in 1954 on the basis of published age-specific doses estimated on Utirik atoll and 137Cs deposition levels on the atolls where the participants came from. There was suggestive evidence that the prevalence of thyroid cancer increased with category of estimated dose to the thyroid.
Available from: Raid Amin
- "The main environmental risk factor for thyroid cancer reported in the literature is exposure of the thyroid gland to radiation. Potential sources that have been studied include radiation that comes from the atmosphere, ground water, energy plants, and medical procedures [14, 18–23]. It appears that younger age increases susceptibility to the effects of radiation on the thyroid gland. "
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Thyroid cancer is a common cancer in adolescents and young adults ranking 4th in frequency. Thyroid cancer has captured the interest of epidemiologists because of its strong association to environmental factors. The goal of this study is to identify thyroid cancer clusters in Florida for the period 2000-2008. This will guide further discovery of potential risk factors within areas of the cluster compared to areas not in cluster.
Thyroid cancer cases for ages 15-39 were obtained from the Florida Cancer Data System. Next, using the purely spatial Poisson analysis function in SaTScan, the geographic distribution of thyroid cancer cases by county was assessed for clusters. The reference population was obtained from the Census Bureau 2010, which enabled controlling for population age, sex, and race.
Two statistically significant clusters of thyroid cancer clusters were found in Florida: one in southern Florida (SF) (relative risk of 1.26; P value of <0.001) and the other in northwestern Florida (NWF) (relative risk of 1.71; P value of 0.012). These clusters persisted after controlling for demographics including sex, age, race.
In summary, we found evidence of thyroid cancer clustering in South Florida and North West Florida for adolescents and young adult.
Available from: David Orlo Carpenter
- "There is other evidence that early life exposure to radiation elevates risk for cancer later in life. Prepubertal children exposed to ionizing radiation from atomic bomb tests in the Marshall Islands from 1946 to 1958 developed thyroid cancer 15 to 29 years after exposure, but exposed adults had little or no increased risk  . Similarly, after the accident at the Chernobyl nuclear reactor in 1986, an increased risk for thyroid cancer was found among individuals who were younger than 18 at the time of exposure, and their risk remained elevated for more than 2 decades. "
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ABSTRACT: Many chemical carcinogens are in food, water, air, household products, and personal care products. Although genetic susceptibility is an important factor in how an individual responds to exposure to a carcinogen, heritable genetic factors alone account for only a minor portion of cancer rates.
We review the evidence that early life exposure to carcinogenic chemicals and ionizing radiation results in elevations in cancer later in life.
Because cells are rapidly dividing and organ systems are developing during childhood and adolescence, exposure to carcinogens during these early life stages is a major risk factor for cancer later in life. Because young people have many expected years of life, the clinical manifestations of cancers caused by carcinogens have more time in which to develop during characteristically long latency periods. Many chemical carcinogens persist in the body for decades and increase risk for all types of cancers. Carcinogens may act via mutagenic, nonmutagenic, or epigenetic mechanisms and may also result from disruption of endocrine systems. The problem is magnified by the fact that many chemical carcinogens have become an integral part of our food and water supply and are in air and the general environment.
The early life onset of a lifelong exposure to mixtures of multiple environmental chemical carcinogens and radiation contributes significantly to the etiology of cancer in later life.
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ABSTRACT: In the tumor tissue of papillary thyroid carcinoma (PTC) developed in an externally irradiated patient, we identified an undescribed yet structural mutation which comprised the juxtapositioning of the 5′ portion of an rfp gene upstream of the fragment encoding the tyrosine kinase domain of RET. At the genomic level, the formation of a chimeric gene occurred as a result of balanced chromosomal translocation of the short arm of chromosome 6 and long arm of chromosome 10, t(6;10)(p21.3;q11.2). The presence of the mutation was confirmed by extensive molecular, cytogenetic, and functional analysis. The product of the fusion gene, termed Δrfp/RET, was able to form homodimers as demonstrated by a yeast two-hybrid system, thus being in compliance with an essential condition of the constitutive activation of ret/PTC tyrosine kinases. In addition, the newly revealed rearrangement was shown to be tumorigenic, as NIH 3T3 cells stably transfected with a mammalian expression vector encoding full-length cDNA of the Δrfp/RET yielded rapidly growing tumors in immunocompromised mice. The finding provides an additional line of evidence of facilitated susceptibility of the ret protooncogene to structural mutations in irradiated human thyroid cells and pathogenic role of the ret rearrangements in human papillary thyroid cancer.
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