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Fukushima and the Politics of Risk by Majia Nadesan. Presentation to ASU's New College as part of SBS's Lecture Series September, 2014.
Abstract
Fukushima politics are examined by comparing competing accounts of the March 2011 nuclear disaster and through an examination of the biopolitics of radiation health effects research.
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OBJECTIVES: To examine whether there is a continued increase in neurological deaths in the major developed countries over the period 1979-2010.
STUDY DESIGN: Analyzes changing patterns of neurological deaths and Total Mortality of people aged 55-74 years by sex.
METHODS: Baseline WHO 3-year average mortality for 1979-81 were compared with changes in 2008-10, for Total Mortality and the neurological categories Nervous Disease, and Alzheimer & other Dementias deaths in rates per million. To control for different diagnostic practice, the focus is upon Total Neurological Deaths in relation to Total Mortality and Odds ratios are calculated. UK Motor Neuron Disease, Parkinson's disease and variant CJD are explored as possible constituent categories of Nervous Disease for other countries.
RESULTS: Total Mortality fell substantially in every country, conversely, Nervous Disease and Alzheimer's rose in seven and six countries respectively. Total Neurological Deaths for males and females increased significantly in Australia, Canada, England & Wales, Italy, the Netherlands and especially the USA. Unlike motor neurone disease, variant CJD' deaths in England and Wales did not contribute substantially to the overall neurological increases found. Odds ratios indicated that neurological deaths differentially increased significantly in every country compared to Total Mortality.
CONCLUSIONS: These results pose a major public health problem, as the epigenetic contribution to these changes, rather than longevity, have serious implications indicating earlier onset of neurological morbidity pressurizing families, health and social care services, with resource implications especially for Australia, Canada, Italy, Netherlands, Spain, the UK and the USA.
Mutations generate sequence diversity and provide a substrate for selection. The rate of de novo mutations is therefore of major importance to evolution. Here we conduct a study of genome-wide mutation rates by sequencing the entire genomes of 78 Icelandic parent-offspring trios at high coverage. We show that in our samples, with an average father's age of 29.7, the average de novo mutation rate is 1.20 × 10(-8) per nucleotide per generation. Most notably, the diversity in mutation rate of single nucleotide polymorphisms is dominated by the age of the father at conception of the child. The effect is an increase of about two mutations per year. An exponential model estimates paternal mutations doubling every 16.5 years. After accounting for random Poisson variation, father's age is estimated to explain nearly all of the remaining variation in the de novo mutation counts. These observations shed light on the importance of the father's age on the risk of diseases such as schizophrenia and autism.
Recent research has discovered that a number of genetic risk factors for autism are de novo mutations. Advanced parental age at the time of conception is associated with increased risk for both autism and de novo mutations. We investigated the hypothesis that other environmental factors associated with increased risk for autism might also be mutagenic and contribute to autism by causing de novo mutations. A survey of the research literature identified 9 environmental factors for which increased pre-conceptual exposure appears to be associated with increased risk for autism. Five of these factors--mercury, cadmium, nickel, trichloroethylene, and vinyl chloride--are established mutagens. Another four--including residence in regions that are urbanized, located at higher latitudes, or experience high levels of precipitation--are associated with decreased sun exposure and increased risk for vitamin D deficiency. Vitamin D plays important roles in repairing DNA damage and protecting against oxidative stress--a key cause of DNA damage. Factors associated with vitamin D deficiency will thus contribute to higher mutation rates and impaired repair of DNA. We note how de novo mutations may also help explain why the concordance rate for autism is so markedly higher in monozygotic than dizygotic twins. De novo mutations may also explain in part why the prevalence of autism is so remarkably high, given the evidence for a strong role of genetic factors and the low fertility of individuals with autism--and resultant selection pressure against autism susceptibility genes. These several lines of evidence provide support for the hypothesis, and warrant new research approaches--which we suggest--to address limitations in existing studies. The hypothesis has implications for understanding possible etiologic roles of de novo mutations in autism, and it suggests possible approaches to primary prevention of the disorder, such as addressing widespread vitamin D deficiency and exposure to known mutagens.
We tested the hypothesis that de novo copy number variation (CNV) is associated with autism spectrum disorders (ASDs). We performed comparative genomic hybridization (CGH) on the genomic DNA of patients and unaffected subjects to detect copy number variants not present in their respective parents. Candidate genomic regions were validated by higher-resolution CGH, paternity testing, cytogenetics, fluorescence in situ hybridization, and microsatellite genotyping. Confirmed de novo CNVs were significantly associated with autism (P = 0.0005). Such CNVs were identified in 12 out of 118 (10%) of patients with sporadic autism, in 2 out of 77 (3%) of patients with an affected first-degree relative, and in 2 out of 196 (1%) of controls. Most de novo CNVs were smaller than microscopic resolution. Affected genomic regions were highly heterogeneous and included mutations of single genes. These findings establish de novo germline mutation as a more significant risk factor for ASD than previously recognized.
Parental exposure to ionizing radiation increases the frequency of germline
mutations detectable in the next generation1. Parental exposure
can also increase the rate of mutation in somatic cells2, 3
and confer a predisposition to cancer4, 5, 6 in offspring, suggesting
that there could be an indirect effect of radiation on somatic genome stability
that is transmissible through the germ line of the irradiated parents. We
have found that this indirect effect extends to the germ line of unexposed
first-generation offspring in mice, as revealed by an increased instability
of repeat-DNA sequences in their descendants.
In this review we will evaluate evidence that altered gene dosage and structure impacts neurodevelopment and neural connectivity through deleterious effects on synaptic structure and function, and evidence that the latter are key contributors to the risk for autism. We will review information on alterations of structure of mitochondrial DNA and abnormal mitochondrial function in autism and indications that interactions of the nuclear and mitochondrial genomes may play a role in autism pathogenesis. In a final section we will present data derived using Affymetrix SNP 6.0 microarray analysis of DNA of a number of subjects and parents recruited to our autism spectrum disorders project. We include data on two sets of monozygotic twins. Collectively these data provide additional evidence of nuclear and mitochondrial genome imbalance in autism and evidence of specific candidate genes in autism. We present data on dosage changes in genes that map on the X chromosomes and the Y chromosome. Precise analyses of Y located genes are often difficult because of the high degree of homology of X- and Y-related genes. However, continued efforts to analyze the latter are important, given the consistent evidence for a 4:1 ratio of males to females affected by autism. It is also important to consider whether environmental factors play a role in generating the nuclear and mitochondrial genomic instability we have observed. The study of autism will benefit from a move to analysis of pathways and multigene clusters for identification of subtypes that share a specific genetic etiology.
• The government now says it is clear that 300 tons (71,895 gallons/272,152 liters) are pouring into the sea each day, enough to fill an Olympic-size swimming pool every eight days
• The government now says it is clear that 300 tons (71,895
gallons/272,152 liters) are pouring into the sea each day,
enough to fill an Olympic-size swimming pool every eight
days. Patrick J. Kiger (2013, Aug 7) Fukushima's Radioactive
Water Leak: What You Should Know
http://news.nationalgeographic.com/news/energy/2013/0
Canopy-Forming Kelps as California's Coastal Dosimeter: 131I from Damaged Japanese Reactor Measured in Macrocystis Pyrifera
- S Manley
- C Lowe
• Manley, S. and C. Lowe (6 March 2012) 'Canopy-Forming Kelps as California's Coastal
Dosimeter: 131I from Damaged Japanese Reactor Measured in Macrocystis Pyrifera',
Environmental Science & Technology,
http://pubs.acs.org/doi/abs/10.1021/es203598r?journalCode=esthag.
Genome Stability: Transgenerational mutation by radiation
- W Wertelecki
- M A Xu-Friedman
- W G Regehr
- E Yuri
- M Plumb
- B Gutierrez
- E Emma Boulton
- A J Kinney
- D K Barch
- D H Chayka
- B Napoleon
- S Munir
"Text of Genetics Committee Report Concerning Effects of Radioactivity on Heredity" (13 July 1956), The
New York Times, p. 18.-Wertelecki, W. (2010). Malformations in a Chornobyl-impacted region. Pediatrics 125(4), e836-e843;
published ahead of print March 22, 2010.-Xu-Friedman, M. A., & Regehr, W G. (1999, April). Presynaptic strontium dynamics and synaptic
transmission. Biophys J., 76(4), 2029-2042.
Additional References-CHERNOBYL IMAGE Paul Fusko Chernobyl Legacy,
http://www.magnumphotos.com/C.aspx?VP3=SearchResult&ALID=2K7O3RSPPMM
also
http://www.paulfuscophoto.com/index.php#mi=2&pt=1&pi=10000&s=0&p=1&a=0&
at=0-Callaway, E. (2013, Aug ) Fathers bequeath more mutations as they age. Nature,
http://www.nature.com/news/fathers-bequeath-more-mutations-as-they-age1.11247-Dubrova, Yuri E., Plumb, M., Gutierrez, B., Emma Boulton, E., & A. J. Jeffreys (2000,
May 4). Genome Stability: Transgenerational mutation by radiation. Nature, 405, 37
http://www.nature.com/nature/journal/v405/n6782/abs/405037a0.html-Kinney, D. K., Barch, D. H., Chayka, B., Napoleon, S., Munir, K. M. (2010)
Environmental risk factors for autism: Do they help cause do novo genetic mutations
that contribute to the disorder? Medical Hypotheses, 74, 102-106.