Changes in Congenital Anomaly Incidence in West Coast and Pacific States (USA) after Arrival of Fukushima Fallout

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Author(s)   Joseph Mangano^*, Janette D. Sherman

Affiliation(s) Radiation and Public Health Project, New York, USA.

ABSTRACT

Radioactive fallout after the March 2011 Fukushima nuclear meltdown entered the U.S. environment within days; levels of radioactivity were particularly elevated in the five western states bordering on the Pacific Ocean. The particular sensitivity of the fetus to radiation exposure, and the ability of radioisotopes to attach to cells, tissues, and DNA raise the question of whether fetuses/newborns with birth defects with the greater exposures suffered elevated harm during the period after the meltdown. We compare rates of five congenital anomalies for 2010 and 2011 births from April-November. The increase of 13.00% in the five western states is significantly greater than the 3.77% decrease for all other U.S. states combined (CI 0.030 – 0.205, p < 0.008). Consistent patterns of elevated increases are observed in the west (20 of 21 comparisons, 6 of which are statistically significant/borderline significant), by state, type of birth defect, month of birth, and month of conception. While these five anomalies are relatively uncommon (about 7500 cases per year in the U.S.), sometimes making statistical significance difficult to achieve, the consistency of the results lend strength to the analysis, and suggest fetal harm from Fukushima may have occurred in western U.S. states.

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Plutonium and environmental and health effects

 TOXICOLOGICAL PROFILE FOR PLUTONIUM , Agency for Toxic Substances and Disease Registry Division of Toxicology and Environmental Medicine/Applied Toxicology Branch,  Atlanta, Georgia“……….HOW CAN PLUTONIUM AFFECT MY HEALTH? Plutonium may remain in the lungs or move to the bones, liver, or other body organs. It generally stays in the body for decades and continues to expose the surrounding tissues to radiation. Lung, liver, and bone cancer You may develop cancer depending on how much plutonium is in your body and for how long it remains in your body. The types of cancers you would most likely develop are cancers of the lung, bones, and liver. These types of cancers have occurred in workers who were exposed to plutonium in air at much higher levels than is in the air that most people breathe. Affect ability to fight infections In laboratory animals, plutonium affected the animal’s ability to resist disease (immune system). More information on the health effects of plutonium is presented in Chapters 2 and 3………

  2.2 SUMMARY OF HEALTH EFFECTS Risks for adverse outcomes of plutonium exposures are strongly dependent on radiation doses received by specific tissues and organ systems. Most of the body burden of plutonium resides in the skeleton and liver, and following inhalation exposures, in the lung and lung-associated lymph nodes. As a result, these tissues receive relatively high radiation doses following exposures to plutonium. Radiation-induced toxicity to these tissues has been documented in human epidemiological studies and in animal models. The relatively high radiation doses received by bone, liver, and lung lend greater credibility to the epidemiological findings for these tissues than for outcomes in other tissues that receive much smaller radiation doses. All epidemiological studies that have reported adverse outcomes in these tissues have studied populations (i.e., workers in plutonium production and processing facilities) that experienced exposures and radiation doses that greatly exceed those experienced by the general public. Accordingly, risks for these outcomes in the general population are substantially lower than reported for these more highly exposed worker populations.

Death. Possible associations between exposure to plutonium and mortality have been examined in studies of workers at the U.S. plutonium production and/or processing facilities (Hanford, Los Alamos, Rocky Flats), as well as facilities in Russia (e.g., Mayak) and the United Kingdom (e.g., Sellafield). The Mayak studies provide relatively strong evidence for an association between cancer mortality (bone, liver, lung) and exposure to plutonium. Plutonium dose-response relationships for lung cancer mortality have been derived from studies of Mayak workers, who received much higher uptakes of plutonium compared to other epidemiological cohorts (i.e., mean body burdens 0.09–9.2 kBq, with much higher individual exposures [up to 470 kBq] in relatively large numbers of these workers). Excess relative risk (ERR) estimated in three studies (adjusted for smoking) were 3.9 per Gy (95% confidence interval [CI]: 2.6– 5.8) in males, and 19 per Gy (95% CI: 9.5–39) in females (attained age 60 years), 4.50 per Gy (95% CI: 3.15–6.10) in males, and 0.11 per Sv (95% CI: 0.08–0.17) or 0.21 per Sv (95% CI: 0.15–0.35), depending on the smoking-radiation interaction model that was assumed (these estimates per Sv correspond to 2.2 or 4.3 per Gy, respectively, assuming a radiation weighting factor of 20 for -radiation). The ERR per Gy in Mayak workers declined strongly with attained age. In a recent cohort mortality study of the Mayak workers, significant plutonium dose-response relationships (p<0.001) were found for deaths due to lung or liver cancer, and for deaths in which bone cancer was considered a contributing cause. At attained age of 60 years, ERRs for lung cancer were 7.1 per Gy (95% CI: 4.9–10) in males and 15 per Gy (95% CI: 7.6–29) in females. Averaged-attained age ERRs for liver cancer were 2.6 per Gy (95% CI: 0.7–6.9) for males and 29 per Gy (95% CI: 9.8–95) for females, and averaged-attained age ERRs for bone cancer were 0.76 per Gy (95% CI: <0–5.2) for males and 3.4 per Gy (95% CI: 0.4–20) for females. Elevated risks for bone cancer were observed only for workers with plutonium doses exceeding 10 Gy. For lung and bone cancer, the ERR declined with attained age, and for lung cancer, the ERR declined with age at first plutonium exposure.

Decreased survival was noted in beagle dogs exposed to plutonium aerosols (238PuO2, 239PuO2, or 239Pu(NO3)4) at levels resulting in initial lung burdens in the range of ≥1 kBq/kg body weight. Early deaths were attributed to radiation pneumonitis and decreased survival late in life was typically associated  with tumor development.

 Cancer. Possible associations between exposure to plutonium and cancer mortality and morbidity have been examined in studies of workers at the U.S. plutonium production and/or processing facilities (Hanford, Los Alamos, Rocky Flats), as well as facilities in Russia (Mayak) and the United Kingdom (e.g., Sellafield). Compared to studies of U.K. and U.S. facilities, the Mayak cohorts had relatively high uptakes of plutonium (i.e., mean body burdens as high as 9.2 kBq, with much higher individual uptakes [up to 470 kBq] in relatively large numbers of these workers). Collectively, the Mayak studies provide evidence for an association between cancer mortality (lung, liver, bone) and uptake of plutonium. Studies of U.K. and U.S. facilities have examined cohorts of workers who had substantially lower estimated plutonium uptakes and corresponding internal radiation doses than the Mayak cohorts (e.g., Sellafield: ≤1 kBq in 97% of the assessed workers; Los Alamos: mean body burden 0.970 kBq, range 0.05– 3.18 kBq). Although a significantly higher incidence of cancer mortality in certain groups of plutonium workers has been found in some studies, higher cancer incidence and/or risks for tissues that received the highest plutonium radiation doses (i.e., lung, liver, bone) have not been found, making causal connections of these outcomes to plutonium exposure more uncertain. The Sellafield study is by far the strongest of these studies and did not find associations between plutonium exposure and cancers to tissues receiving the highest radiation doses from plutonium.

  Plutonium dose-response relationships for lung cancer mortality and morbidity have been corroborated in four Mayak studies. Estimated excess relative risk in these four studies (adjusted for smoking) were as follows: (1) 3.9 per Gy (95% CI: 2.6–5.8) in males and 19 per Gy (95% CI: 9.5–39) in females; (2) 7.1 per Gy (95% CI: 4.9–10) in males and 15 per Gy (95% CI: 7.6–29) in females at attained age of 60 years; (3) 4.50 per Gy (95% CI: 3.15–6.10) in males; and (4) 0.11 per Sv (95% CI: 0.08–0.17) or 0.21 per Sv (95% CI: 0.15–0.35), depending on the smoking-radiation interaction model that was assumed (these estimates per Sv correspond to 2.2 or 4.3 per Gy, respectively, assuming a radiation weighting factor of 20 for “-radiation).

  The risks of mortality and morbidity from bone and liver cancers have also been studied in Mayak workers. Increasing estimated plutonium body burden was associated with increasing liver cancer mortality, with higher risk in females compared to males. Relative risk for liver cancer for a cohort of males and females was estimated to be 17 (95% CI: 8.0–26) in association with plutonium uptakes >7.4 kBq; however, when stratified by gender, the relative risk estimates for females was 66 (95% CI: 16–45) and higher than for males, 9.2 (95% CI: 3.3–23). Risk of bone cancer mortality in this same cohort (n=11,000) was estimated to be 7.9 (95% CI: 1.6–32) in association with plutonium uptakes >7.4 kBq (males and females combined). Risks of leukemia mortality, in the same cohort, were not associated with internal plutonium exposure. In a case control study of Mayak workers, the odds ratio for liver cancer was 11.3 (95% CI: 3.6–35.2) for subjects who received doses >2.0–5.0 Gy (relative to 0– 2.0 Gy) and the odds ratios for hemangiosarcomas were 41.7 (95% CI: 4.6–333) for the dose group >2.0– 5.0 Gy, and 62.5 (95% CI: 7.4–500) for the dose group >5.0–16.9 Gy; doses were estimated based on periodic urine sampling. A study reported averaged-attained age ERRs for liver cancer of 2.6 per Gy (95% CI: 0.7–6.9) for males and 29 per Gy (95% CI: 9.8–95) for females, and averaged-attained age ERRs for bone cancer of 0.76 per Gy (95% CI: <0–5.2) for males and 3.4 per Gy (95% CI: 0.4–20) for females. Elevated risks for bone cancer were observed only for workers with plutonium doses exceeding 10 Gy. For lung and bone cancer, the ERR declined with attained age, and for lung cancer, the ERR declined with age at first plutonium exposure. …….

Studies in Animals. Radiation pneumonitis has been observed following plutonium (primarily insoluble) aerosol exposure of dogs, nonhuman primates (monkeys and baboons), and rodents. As discussed in Section 3.2.1.1, radiation pneumonitis was identified as primary, major contributing, or incidental cause of death in some dogs and nonhuman primates that inhaled 238PuO2, 239PuO2, or 239Pu(NO3)4 aerosols.

Muggenburg et al. (2008) studied the effect of plutonium ILB and radiation dose on radiation pneumonitis in beagles as part of a plutonium lifespan composite study. The relationship between pneumonitis induction and the cause of death was reported to be a function of the plutonium ILB, the resulting cumulative radiation dose, and the particle size to some extent. Increased ILB and plutonium dose rate were associated with the fraction of animals with radiation pneumonitis as primary, major contributing, or incidental cause of death. A trend was observed for the induction of radiation pneumonitis at lower ILBs in the 0.75 and 1.5 µm AMAD groups than in the 3 µm AMAD group. At radiation doses sufficient to produce radiation pneumonitis, the resulting inflammation was a chronic symptom due to long-term retention of 239PuO2 in the lung.

As a result, 239PuO2-induced radiation pneumonitis was always associated with pulmonary fibrosis. The radiation pneumonitis/pulmonary fibrosis progressively impaired lung function, including alveolar-capillary gas exchange, resulting in increases in respiratory rate, minute volume, arterial CO2 pressure, and lung stiffness, along with decreases in tidal volume and arterial O2 pressure. Symptoms in order of decreasing frequency were tachypnea, increased breath sounds, body weight loss, anorexia, dyspnea, cyanosis, bradycardia, and discharge from the nose, eyes, or mouth. Increasing radiation dose and dose rate corresponded to progressively shorter times to onset of symptoms and increased severity of effects (Muggenburg et al. 2008). …….

Exposure of Dogs to 238PuO2. In the ITRI 238PuO2 dog studies, the first symptom of radiation pneumonitis (tachypnea) was observed at approximately 600 days after initial exposure (Muggenburg et al. 1996). …… Radiation pneumonitis was the primary cause of death in eight dogs with initial lung burdens of 8.3–45 kBq/kg (Muggenburg et al. 1996).

 Similar observations were reported in the PNL studies on 238PuO2, with chronic radiation pneumonitis observed in dogs with initial lung burdens ≥0.28 kBq/kg (Park et al. 1997). Exposure of Dogs to 239PuO2. Chronic radiation pneumonitis also was observed in the ITRI and PNL dogs exposed to 239PuO2 aerosols   ……  Radiation pneumonitis was observed in dogs dying from 0.3 to 11.7 years after inhaling 239PuO2, with the time to death inversely related to initial lung burden (Hahn et al. 1999; Muggenburg et al. 1999, 2008). The lowest initial lung burden causing fatal radiation pneumonitis was 1.0 kBq/kg (Muggenburg et al. 1999, 2008). The time to death from radiation pneumonitis was not different in ITRI dogs administered a single exposure (initial lung burden of 3.9 kBq/kg) or repeated exposures (7–10 semiannual exposures for a mean total lung burden of 5.3 kBq/kg) (Diel et al. 1992). Death due to radiation pneumonitis was observed in 239PuO2-exposed PNL dogs at mean initial lung burdens ≥1 kBq/kg (DOE 1988a; Weller et al. 1995b) …..

Exposure of Other Laboratory Animal Species. Baboons ….. Higher initial lung burdens resulted in earlier death from radiation pneumonitis accompanied by pulmonary edema. Radiation pneumonitis and pulmonary fibrosis were also reported in Rhesus monkeys…..

  Cardiovascular Effects. Epidemiological Studies in Humans. Possible associations between exposure to plutonium and cardiovascular disease have been examined in studies of workers at production and/or processing facilities in the United Kingdom (Sellafield) (McGeoghegan et al. 2003; Omar et al. 1999). These studies are summarized in Table 3-2 and study outcomes for mortality from cardiovascular disease are described in Section 3.2.1.1. Omar et al. (1999) compared mortality rates between plutonium workers and other radiation workers within a cohort of Sellafield workers and found that the mortality rate ratios were significantly elevated for cerebrovascular disease (1.27, p<0.05) in a cohort of Sellafield workers. The cumulative internal uptakes of plutonium in the cohort were estimated to range from 0 to 12 kBq, with approximately 75% of the cohort having cumulative uptakes ≤250 Bq. McGeoghegan et al. (2003) compared mortality rates between plutonium workers and other radiation workers within a cohort of Sellafield workers and found that morality rate ratios for plutonium workers were significantly elevated for deaths from circulatory disease (2.18, p<0.05) and ischemic heart disease (4.46, p<0.01). ….

Cancer.  Epidemiological Studies in Humans. Possible associations between exposure to plutonium and cancer mortality and morbidity have been examined in studies of workers at the U.S. plutonium production and/or processing facilities (Hanford, Los Alamos, Rocky Flats), as well as facilities in Russia (Mayak) and the United Kingdom (e.g., Sellafield). The most recent findings from these studies are summarized in Table 3-2. Compared to studies of U.K. and U.S. facilities, the Mayak cohorts had relatively high PLUTONIUM 55 3. HEALTH EFFECTS exposures to plutonium (i.e., mean body burdens ranging from 0.09 to 9.2 kBq, with individual exposures as high as 470 kBq (Krahenbuhl et al. 2005). Collectively, the Mayak studies provide evidence for an association between cancer mortality and exposure to plutonium. Plutonium dose-response relationships for lung cancer mortality have been corroborated in three Mayak studies (Gilbert et al. 2004; Jacob et al. 2005; Kreisheimer et al. 2003). ……

Collectively, the Mayak studies provide evidence for increased risk of cancer mortality (bone, liver, lung) in association with increased internal plutonium-derived radiation dose and/or body burden, with approximately 4-fold higher risks in females compared to males. Four studies estimated lung cancer mortality risk among Mayak workers and yielded similar estimates of excess relative risk per Gy of internal lung dose. Gilbert et al. (2004) estimated the excess lung cancer mortality risk (per Gy attained at age 60 years) for essentially the entire cohort of Mayak workers (n=21,790) to be approximately 4.7 per Gy (95% CI: 3.3–6.7) in males, and 19 per Gy (95% CI: 9.5–39) in females. Adjustment for smoking, based on risk estimates in subgroups for which smoking data were available, decreased these estimates only slightly: males, 3.9 per Gy (95% CI: 2.6–5.8); and females, 19 (95% CI: 7.7–51). Cancer mortality risk was linearly related to plutonium radiation dose. ……

Risks of mortality and morbidity from bone and liver cancers have also been studied in Mayak workers (Gilbert et al. 2000; Koshurnikova et al. 2000; Shilnikova et al. 2003; Sokolnikov et al. 2008; Tokarskaya et al. 2006). Increasing estimated plutonium body burden was associated with increasing cancer mortality, with higher risk in females compared to males. Gilbert et al. (2000) examined liver cancer mortality in a cohort of Mayak workers (n=11,000). …….

U.K. Atomic Energy Authority and Atomic Weapons Establishment Workers. ………..The mortality rate ratio was significantly elevated for breast cancer (7.66, p<0.01) and cerebrovascular disease (1.27, p<0.05). McGeoghegan et al. (2003) examined cancer mortality in a cohort of female Sellafield workers (n=6,376), from which a subset (n=837) of women who had been monitored for plutonium exposure was identified as plutonium workers. This cohort overlapped considerably with that studied by Omar et al. 1999). Effective dose equivalents to the lung from plutonium were estimated to have ranged up to 178 mSv (mean: 3.45 mSv, 5th–95th percentile range: 0.36–8.89 mSv). Comparisons of mortality rates between plutonium workers and other radiation workers yielded significantly elevated mortality rate ratios for all deaths (2.20, p<0.01), all cancers (3.30, p<0.01), breast cancer (3.77, p<0.05), circulatory disease (2.18, p<0.05), and ischemic heart disease (4.46, p<0.01).

……p. 66   3.3 GENOTOXICITY Abundant information is available regarding the genotoxicity of ionizing radiation (refer to the Toxicological Profile for Ionizing Radiation for a detailed discussion of the genotoxic effects of various forms of ionizing radiation). The genotoxicity of alpha radiation from plutonium sources has been investigated in various groups of plutonium workers, as well as in vivo animal studies and a variety of in vitro test systems. Tables 3-4 and 3-5 present the results of in vivo and in vitro genotoxicity studies, respectively. Although epidemiological studies do not provide conclusive evidence that plutonium produces genetic damage in humans, results of some studies provide suggestive evidence of dose-related increases in chromosomal aberrations in plutonium workers with measurable internalized plutonium. For example, Livingston et al. (2006) examined relationships between external radiation dose, internal radiation dose, and frequencies of chromosomal aberrations and micronuclei in peripheral blood lymphocytes of a group of 30 retired plutonium workers with dosimetrically-estimated internal and external radiation doses >0.5 Sv, another 17 workers with predominantly external radiation doses <0.1 Sv, and 21 control subjects with no history of occupational radiation exposure. Frequency of chromosomal aberrations was positively correlated with the bone marrow dose (alpha radiation from internalized plutonium; 168 mSv  median dose to the bone marrow), but not with the external radiation dose. Frequency of micronuclei did not differ significantly among the three study groups.

Significantly increased frequencies of symmetrical and asymmetrical chromosomal aberrations were reported among workers at the Sellafield (United Kingdom) plutonium facility with internalized plutonium in excess of 20% of the maximum permissible body burden (Tawn et al. 1985). Frequencies of symmetrical aberrations were significantly higher at retesting 10 years later, although no significant external radiation exposure had occurred during the 10-year interim (Whitehouse et al. 1998). This finding is consistent with the hypothesis that internally-deposited plutonium irradiates hemopoietic precursor cells (Whitehouse et al. 1998).

  Internal plutonium dose-related increased frequencies in chromosomal aberrations have also been reported in peripheral blood lymphocytes of plutonium workers with estimated plutonium body burdens as high as 15.5 kBq from exposure at the Mayak plutonium facilities in Russia (Hande et al. 2003, 2005; Mitchell et al. 2004; Okladnikova et al. 2005). The increased frequencies of chromosomal aberrations in the Mayak workers persisted many years following the cessation of exposure (Hande et al. 2003, 2005; Mitchell et al. 2004).

 Significantly increased frequencies of chromosomal aberrations were observed among Rocky Flats (Colorado) plutonium workers with internal plutonium burdens >740 Bq (Brandom et al. 1990; IAEA 1979). Conversely, among Manhattan Project plutonium workers followed for up to 32 years, no apparent correlation was found between the frequency of chromosomal aberrations and plutonium body burdens in the range of 0.185–15.4 kBq (Hempelmann et al. 1973; Voelz et al. 1979).

Open wounds represent a significant route through which plutonium workers might be exposed to plutonium alpha particles. Chromosomal aberrations were observed in lymphocytes among eight plutonium workers in the United Kingdom occupationally exposed to plutonium with the primary routes of exposure through wounds, punctures, or abrasions (estimated plutonium body burdens from 0.78 to 1.5 kBq). In exposed individuals, the number of dicentric aberrations averaged 5 per 500 cells, while the natural population background frequency of this aberration is 1 per 4,000 cells (Schofield 1980; Schofield et al. 1974).

Results of in vivo genotoxicity studies in laboratory animals consistently reveal alpha radiation-induced dose-related increases in the frequency of chromosomal aberrations following internalization of   plutonium. Chromosomal aberrations were observed in monkeys and hamsters following inhalation exposure to plutonium. Increases in chromosomal aberrations in blood lymphocytes were seen in immature Rhesus monkeys exposed to 239PuO2 at concentrations resulting in initial lung burdens of 1.9– 19 kBq 239Pu/kg body weight (LaBauve et al. 1980) and Cynomolgus monkeys exposed to 239Pu(NO3)4 at a concentration resulting in a projected initial lung burden of 40 kBq (Brooks et al. 1992), but not at lower levels. ……

  Consistently positive genotoxicity results have been reported in various test systems exposed to the alpha radiation from plutonium compounds in vitro (see Table 3-5). Chromosomal aberrations were reported in human peripheral blood lymphocytes and lymphoblasts (DOE 1980h; Purrott et al. 1980)  ……https://www.atsdr.cdc.gov/toxprofiles/tp143.pdf?fbclid=IwAR1iffNMF8xj33aBhDW-zhtFzPejF0eNlQ5QUaIgxBhCcujUKU0XRC8NvMc     Agency for Toxic Substances and Disease Registry Division of Toxicology and Environmental Medicine/Applied Toxicology Branch 1600 Clifton Road NE Mailstop F-62 Atlanta, Georgia 30333

Genetic changes in children of soldiers who were exposed to ionising radiation

Typical mutations in children of radar soldiers https://www.sciencedaily.com/releases/2018/10/181005111447.htm, October 5, 2018 Source: University of Bonn Summary: The offspring of radar soldiers exposed to high doses of radiation during their service experience more genetic alterations than families without radiation exposure. The offspring of radar soldiers exposed to high doses of radiation during their service experience more genetic alterations than families without radiation exposure. This has been demonstrated in a pilot study by the research team involving Charité-Universitätsmedizin Berlin, the Berlin Institute of Health (BIH), the Max Delbrück Centre for Molecular Medicine, Radboud University Nijmegen (Netherlands) and the University Hospital Bonn, which has now been published in the journal Scientific Reports. The results of this pilot study will be reviewed in a larger scale study. Until the 1980s, military radar systems were often inadequately shielded against spurious radiation emitted by radar amplifier tubes. Such rays can cause radiation damage to service and maintenance personnel. The persons involved have joined forces in the ‘Association for the support of persons harmed by radar beams’. In 2003, a commission of experts made recommendations on compensatory payments. Since some children of former radar soldiers suffer from physical disabilities attributed to the radiation exposure of their fathers, their offspring are now in the spotlight. Whether radiation led to genotype damage in these children is debated. A research team from Charité-Universitätsmedizin Berlin, the Berlin Institute of Health (BIH), the Max Delbrück Center for Molecular Medicine, Radboud University Nijmegen (Netherlands) and the University Hospital Bonn have now investigated this question in a pilot study. ‘Through the latest methods of high-throughput sequencing, the complete genomes of parents and their children can now be studied within a short time. This allows us to determine the mutation rates after radiation exposure much more accurately than before’ says first author Dr. med. Manuel Holtgrewe of the Core Unit Bioinformatics (CUBI) of the Berlin Institute of Health (BIH) and Charité-Universitätsmedizin Berlin. Researchers studied the genomes of twelve families The scientists studied the genomes of twelve families of radar soldiers. The entire genomes of 18 offspring and their parents were sequenced. The exact radiation exposure of the soldiers cannot be determined retroactively. Researchers estimate, however, that a ‘high dose’ of radiation emanated from the radar systems, especially because radar soldiers very frequently became ill, many from cancer. Scientists compared the mutation rates in the genomes of radar soldier families with that of 28 offspring of parents who were not exposed to radiation. The focus was on so-called ‘multisite de novo mutations’ (MSDN), which have already been demonstrated in mice because of radiation. An MSDN is present when two or more defects in DNA strands occur adjacently to each other in a line of 20 base pairs. While in the families without radiation exposure, only every fifth offspring had an MSDN, in the radar soldier families this was two out of three offspring. Twelve MSDNs were found in the 18 offspring of radar soldiers, in one family indeed six MSDNs in three offspring. In addition, in two offspring, chromosomal alterations were also detected that had serious clinical consequences. The origin of these mutations could also be traced back to the paternal germ line and only rarely occurs by chance. ‘The results of our pilot study suggest that an accumulation of certain genotype damage by radiation can basically be demonstrated in the next generation,’ says Prof. Dr. med. Peter Krawitz from the Institute for Genomic Statistics and Bioinformatics at the University Hospital Bonn. How pronounced the accumulation of genotype damage by radiation is must be demonstrated by even larger studies, the results of which rely on a much broader database. A team involving Krawitz is currently planning such a follow-up study together with the Institute of Human Genetics of the University Hospital Bonn, the Charité-Universitätsmedizin Berlin and the Berlin Institute of Health (BIH), who are funding it. The researchers thank the Government Organisation in Support of Radar Victims (BzUR) and its members for supporting the current study. The investigation was facilitated by a private donation of 50,000 euros by Dr. Gisela Sperling. Story Source: Materials provided by University of Bonn. Note: Content may be edited for style and length. Journal Reference: Manuel Holtgrewe, Alexej Knaus, Gabriele Hildebrand, Jean-Tori Pantel, Miguel Rodriguez de los Santos, Kornelia Neveling, Jakob Goldmann, Max Schubach, Marten Jäger, Marie Coutelier, Stefan Mundlos, Dieter Beule, Karl Sperling, Peter Michael Krawitz. Multisite de novo mutations in human offspring after paternal exposure to ionizing radiation. Scientific Reports, 2018; 8 (1) DOI: 10.1038/s41598-018-33066-x

Tritium was identified as the primary culprit in damaging fetuses and mothers’ rapidly diving cells.

Paul Richards Nuclear Fuel Cycle Watch South Australia, 6 Oct 18, 
This information was tabled in December 2007; as these were the findings of the German KiKK Study,
‘‘Epidemiologische Studie zu Kinderkrebs in der Umgebung von Kernkraftwerken’’  ‘‘Epidemiological Study of Childhood Cancer in the Vicinity of Nuclear Power Stations”^ and then subsequently was made public this decade.To date, no studies with NRC oversight have attempted to replicate the same methodology used in the 2007 KiKK Study.

Nonetheless, there have been plenty of opinion pieces in response to the study, pontificating why these results exist, how they are wrong, or even claiming the results are inconclusive. Which interestingly, are written by those affiliated with vested interest groups in the nuclear industry.

Where just claiming multiple epidemiology studies prior to this demonstrate contrary data. Unfortunately, this carries little, if any scientific weight.

Furthermore, the effect measured, quantified and subsequently published in Germany has never been discredited by peer review on the basis of replicating the study methods anywhere.

The outcome is the German KiKK Study^ stands alone unchallenged as a new benchmark verifying rapidly dividing cells in the womb and in mothers are actually affected detrimentally by tritium created in nuclear reactors. Creating leukaemia and birth defects in unborn babies.

Which in turn, is one of the central reasons for the phase-out of nuclear reactors in Germany, as most readers here are well aware many other nations have taken the lead on.
____________
^ https://onlinelibrary.wiley.com/doi/epdf/10.1002/ijc.23330

German : http://www.kinderkrebsregister.de/…/pID8_20110808_DE.pdf

https://www.bfs.de/…/ergebnisse/kikk/kikk-studie.html         https://www.facebook.com/groups/1021186047913052/

THE HIGH TOXICITY AND RADIOTOXICITY OF TRITIUM

Ken Raskin, Tritium is mostly what the Japanese want to dump from Fukushima. Millions of tons of water with tritium in it. Massive amounts of nuclear waste from Fukushima.

Tritium bombards, and even attaches to tissue covalently. There is usually a lot of UNACCOUNTED FOR RADIONUCLIDE-TRITIUM, around nuclear reactors. That is because the nucleoapes that run the reactors are psychopaths. They have little value for life, human or otherwise. Like radioactice Carbon 14 can, Tritium, binds to tissue. TRITIUM then permanently bombards the heck out of surrounding tissue, with beta rays!

There was a large study, that showed tritium increases cancer 20 times.  It is teratogenic. There are several case studies, of workers with increased rates of granulomas and lymphomas who were chronically exposed for years.
The pronukers go on and on, about k40 which is a nonstart. Even the gaslighters do it. It is Irrelevent, then they trurn around and lie their asses off about the extreme radiotoxicity and biological toxicity of tritium!

The nuclearists encourage the myth of how harmless tritium is. It does not just mostly pass through the body in water. Another blatant lie. It biocumulates in worse ways than radioactive, iodine, cesium, uranium because it becomes a part of the human body. It impairs and destroys reproductive capabilities. There is a comprehensive study done showing it increased cancer several times. It can covalently take the place of hydrogen in the body, in tissue.

https://www.scientificamerican.com/article/is-radioactive-hydrogen-in-drinking-water-a-cancer-threat/

Cancers in children near nuclear sites , and the risks to embryos

Ian Fairlie  London N8 https://www.lrb.co.uk/v40/n07/thomas-jones/diary  Vol. 40 No. 8 · 26 April 2018

Thomas Jones digs up Carol Barton’s research article from 2001, in which she relayed her findings that, between 1972 and 1996, the risk of child leukaemia within ten kilometres of Aldermaston and Burghfield was double the rate for the UK as a whole (LRB, 5 April). Barton was then a consultant haematologist at the Royal Berkshire Hospital. ‘Until the cause of cancer is fully understood, and what the part of radiation in the process could be,’ she wrote, ‘no firm measures can be taken to redress the balance.’

Research has moved on since then. More than sixty epidemiological studies worldwide have examined the incidence of cancer in children near nuclear power plants (NPPs): most indicate increases in leukaemia. These include the landmark 2008 KiKK study commissioned by the German government, which found relative risks of 1.6 in total cancers and 2.2 in leukaemias among infants living within five kilometres of all German NPPs.

A number of hypotheses have been proposed to explain these findings. One is that the increased cancers arise from the exposure of pregnant women near NPPs to radiation. However, any theory has to account for the greater than a thousand-fold discrepancy between official estimates of radiation doses from nuclear emissions and the observed increases in cancer risk. It may be that radiation exposures from spikes in NPP radionuclide emissions are significantly larger than the averages recorded in official estimates. In addition, the risks to embryos and foetuses from radiation exposure are much greater than to adults, and the blood-forming tissues in embryos and foetuses are even more radiosensitive.

 

Deaths of newborns increased in areas irradiated by Fukushima nuclear disaster

Academic paper: “Increases in perinatal mortality in prefectures contaminated by the Fukushima nuclear power plant accident in Japan”  Source Institute: 医療問題研究会

エビデンスに基づく保健・医学・薬学（EBM）の実践的研究を

Institute link : http://ebm-jp.com

Link to full text pdf: http://ebm-jp.com/wp-content/uploads/media-2016002-medicine.pdf

Authors and copyright:  Hagen Heinrich Scherb, Dr rer nat Dipl-Matha,∗, Kuniyoshi Mori, MDb, Keiji Hayashi, MDcEditor: Roman Leischik.

Abstract:

Descriptive observational studies showed upward jumps in secular European perinatal mortality trends after Chernobyl.

The question arises whether the Fukushima nuclear power plant accident entailed similar phenomena in Japan. For 47 prefectures representing 15.2 million births from 2001 to 2014, the Japanese government provides monthly statistics on 69,171 cases of perinatal death of the fetus or the newborn after 22 weeks of pregnancy to 7 days after birth.

Employing change-point methodology for detecting alterations in longitudinal data, we analyzed time trends in perinatal mortality in the Japanese prefectures stratified by exposure to estimate and test potential increases in perinatal death proportions after Fukushima possibly associated with the earthquake, the tsunami, or the estimated radiation exposure.

Areas with moderate to high levels of radiation were compared with less exposed and unaffected areas, as were highly contaminated areas hit versus untroubled by the earthquake and the tsunami. Ten months after the earthquake and tsunami and the subsequent nuclear accident, perinatal mortality in 6 severely contaminated prefectures jumped up from January 2012 onward: jump odds ratio 1.156; 95% confidence interval (1.061, 1.259), P-value 0.0009.

There were slight increases in areas with moderate levels of contamination and no increases in the rest of Japan.

In severely contaminated areas, the increases of perinatal mortality 10 months after Fukushima were essentially independent of the numbers of dead and missing due to the earthquake and the tsunami. Perinatal mortality in areas contaminated with radioactive substances started to increase 10 months after the nuclear accident relative to the prevailing and stable secular downward trend. These results are consistent with findings in Europe after Chernobyl. 

Since observational studies as the one presented here may suggest but cannot prove causality because of unknown and uncontrolled factors or confounders, intensified research in various scientific disciplines is urgently needed to better qualify and quantify the association of natural and artificial environmental radiation with detrimental genetic health effects at the population level….. more https://nuclearexhaust.wordpress.com/2017/11/27/academic-paper-increases-in-perinatal-mortality-in-prefectures-contaminated-by-the-fukushima-nuclear-power-plant-accident-in-japan

 

Congenital abnormalities due to ionising radiation

The first documented excesses of congenital anomalies were among children of survivors of the Hiroshima and Nagasaki bombings.

The 1986 meltdown at Chernobyl produced numerous reports of certain congenital anomalies among populations subject to fallout from the stricken reactor

Open Journal of Pediatrics
Vol.05 No.01(2015), Article ID:54828,13 pages
10.4236/ojped.2015.51013

Changes in Congenital Anomaly Incidence in West Coast and Pacific States (USA) after Arrival of Fukushima Fallout   Joseph Mangano*, Janette D. Sherman

Radiation and Public Health Project, New York, USA 

ABSTRACT

Radioactive fallout after the March 2011 Fukushima nuclear meltdown entered the U.S. environment within days; levels of radioactivity were particularly elevated in the five western states bordering on the Pacific Ocean. The particular sensitivity of the fetus to radiation exposure, and the ability of radioisotopes to attach to cells, tissues, and DNA raise the question of whether fetuses/newborns with birth defects with the greater exposures suffered elevated harm during the period after the meltdown.

We compare rates of five congenital anomalies for 2010 and 2011 births from April-November. The increase of 13.00% in the five western states is significantly greater than the 3.77% decrease for all other U.S. states combined (CI 0.030 – 0.205, p < 0.008). Consistent patterns of elevated increases are observed in the west (20 of 21 comparisons, 6 of which are statistically significant/borderline significant), by state, type of birth defect, month of birth, and month of conception.

While these five anomalies are relatively uncommon (about 7500 cases per year in the U.S.), sometimes making statistical significance difficult to achieve, the consistency of the results lend strength to the analysis, and suggest fetal harm from Fukushima may have occurred in western U.S. states.

1. Introduction

The harmful effects of radiation exposure to chromosomes have been known for nearly a century, starting with the discovery of chromosomal deformities in irradiated fruit flies [1] . Experiments with mice [2] [3] and rats [4] confirmed this knowledge, and documented elevated risk for congenital defects, at relatively low doses of exposure. Populations exposed to pre-conception X-rays have been shown to have higher congenital anomalies [5] as were those living in areas with relatively high background radiation [6] [7] .

One form of radiation, byproducts of uranium or plutonium fission, was first introduced into the environment from weapons and reactors seven decades ago [8] -[10] . These isotopes bind with cells, tissues, and DNA of the unborn, and thus risks of congenital defects in irradiated populations have been studied. The first documented excesses of congenital anomalies were among children of survivors of the Hiroshima and Nagasaki bombings. [8] -[10] . During the 1950s, reports of various defects among newborns in the Marshall Islands, the site of 67 large-scale U.S. nuclear weapons tests, were made public. Other studies found links with between atmospheric tests and elevated birth defects, including a high rate of Down Syndrome in northwest England in 1963-1964, the peak period of global fallout from tests [11] . Another report documented elevated birth defect incidence near the Hanford nuclear weapons plant in Washington state (USA) [12] .

The 1986 meltdown at Chernobyl produced numerous reports of certain congenital anomalies among populations subject to fallout from the stricken reactor. One documented a doubling of congenital developmental anomalies among infants born to fathers who worked as liquidators to contain the meltdown [13] . Various analyses presented elevated congenital anomaly rates in various parts of the Belarus region, which received the greatest doses of radioactivity from the meltdown, in the years following Chernobyl [14] -[22] . Other research also found high birth defect rates in the Ukraine [23] [24] , Bulgaria [25] , Croatia [26] , and Germany [27] -[30] including areas with fallout levels well below those Belarussian sites closest to the reactor.

Post-Chernobyl studies also identified elevated rates of specific anomalies, the most-analyzed of which was Down syndrome (Trisomy-21), mostly in Germany [31] -[39] . Other conditions included neural tube defects in Turkey [40] -[43] , cleft lip/palate in Germany [44] [45] , and anencephaly in Turkey [46] . Meta-analyses concluded that a pattern of elevated congenital anomaly rates was associated with exposure to the Chernobyl meltdown [47] -[49] .

No published reports exist on the change in congenital defects rates in Japan after the March 2011 meltdown at Fukushima. However, at least one report examines morphological abnormality rates in aphids in the first sexual reproduction period after the meltdown, and found a 13.2% rate close to Fukushima vs. 3.8% in seven control areas [50] .

Changes in the rate of one type of birth defect, congenital hypothyroidism, have been reported. In the five U.S. states bordering on the Pacific Ocean, with the most elevated levels of environmental radiation after the meltdown, a 16% increase in incidence of the disorder was observed in the nine months following the meltdown, compared to a 3% decrease in 36 other U.S. states [51] . The gap was particularly large (28% increase vs. a 4% decrease) in the first 14 weeks after the arrival of fallout. In addition, the rate of California newborns with a Thyroid Stimulating Hormone score of 19 micro international units per milliliter of blood during initial screening, was 27% greater in the nine months after the meltdown compared to other periods in 2011-2012 [52] . The known affinity for radioactive iodine to attack cell membranes and DNA in the thyroid gland indicates a potential link between Fukushima fallout and congenital hypothyroidism.

Historical reports linking exposure to ionizing radiation with congenital anomaly risk, plus the initial reports on congenital hypothyroidism in the western U.S. suggest further analysis be conducted on other birth defects.

The U.S. Centers for Disease Control and Prevention (CDC) publishes national data collected by state health departments on incidence of five congenital anomalies in the nation. These include Anencephaly, Cleft Lip/Pa- late, Down Syndrome, Omphalocele/Gastroschisis, and Spina Bifida/Meningocele [53] . Approximately 7500 cases of these five defects occur in the U.S. each year. As of mid-2014, the CDC web site contained complete birth defect data for the years 2007 to 2012.

These five specific anomalies to be addressed in this report, merit some discussion, including their suspected link with radiation exposure………http://file.scirp.org/Html/13-1330400_54828.htm

Chernobyl’s toll of radiation induced deformities in children

Fukushima Not Even Close To Being Under Control, Oil Price, By ZeroHedge Sun, 28 June 2015 “……..As an example of how media fails to deal with disaster blowback, here are some Chernobyl facts that have not received enough widespread news coverage: Over one million (1,000,000) people have already died from Chernobyl’s fallout.

Additionally, the Rechitsa Orphanage in Belarus has been caring for a very large population of deathly sick and deformed children. Children are 10 to 20 times more sensitive to radiation than adults.

Zhuravichi Children’s Home is another institution, among many, for the Chernobyl-stricken: “The home is hidden deep in the countryside and, even today, the majority of people in Belarus are not aware of the existence of such institutions” (Source: Chernobyl Children’s Project-UK).

One million (1,000,000) is a lot of dead people. But, how many more will die? Approximately seven million (7,000,000) people in the Chernobyl vicinity were hit with one of the most potent exposures to radiation in the history of the Atomic Age.

The exclusion zone around Chernobyl is known as “Death Valley.” It has been increased from 30 to 70 square kilometres. No humans will ever be able to live in the zone again. It is a permanent “dead zone.”

Additionally, over 25,000 died and 70,000 disabled because of exposure to extremely dangerous levels of radiation in order to help contain Chernobyl. Twenty percent of those deaths were suicides, as the slow agonizing “death march of radiation exposure” was too much to endure……..http://oilprice.com/Latest-Energy-News/World-News/Fukushima-Not-Even-Close-To-Being-Under-Control.html

The story of Malaysia’s thorium caused leukaemias and birth defects was quietly covered up

Mitsubishi Quietly Cleans Up Its Former Refinery  http://www.nytimes.com/2011/03/09/business/energy-environment/09rareside.html?_r=0 By KEITH BRADSHER : March 8, 2011 BUKIT MERAH, Malaysia — Hidden here in the jungles of north-central Malaysia, in a broad valley fringed with cave-pocked limestone cliffs topped with acacia and durian trees, lies the site of the largest radiation cleanup yet in the rare earth industry.

Residents blamed a rare earth refinery for birth defects and eight leukemia cases within five years in a community of 11,000 — after many years with no leukemia cases. Seven of the leukemia victims have since died.

The Bukit Merah case is little known even elsewhere in Malaysia, and virtually unknown in the West, because Mitsubishi Chemical quietly agreed to fix the problem even without a legal order to do so. Local protesters had contacted Japanese environmentalists and politicians, who in turn helped persuade the image-conscious company to close the refinery in 1992 and subsequently spend an estimated $100 million to clean up the site.

Image-burnishing was important because the company is part of the Mitsubishi Group of Companies, which has long made Malaysia the cornerstone of its southeast Asian operations. The group has dominant positions in manufacturing a range of products, including air-conditioners and cars.

Mitsubishi Chemical also reached an out-of-court settlement with residents here by agreeing to donate $164,000 to the community’s schools, while denying any responsibility for illnesses.

Osamu Shimizu, the director of Asian Rare Earth, the Mitsubishi Chemical subsidiary that owns the mine, declined to discuss details of the factory’s operation before it closed in 1992. But he said that the company was committed to a safe and complete cleanup.

Workers in protective gear have already removed 11,000 truckloads of radioactively contaminated material, hauling away every trace of the old refinery and even tainted soil from beneath it, down to the bedrock as much as 25 feet below, said Anthony Goh, the consultant overseeing the project for one of Mitsubishi’s contractors, GeoSyntec, an Atlanta-based firm.

To dispose of the radioactive material, engineers have cut the top off a hill three miles away in a forest reserve, buried the material inside the hill’s core and then entombed it under more than 20 feet of clay and granite.

The toughest part of the Bukit Merah cleanup will come this summer, when robots and workers in protective gear are to start trying to move more than 80,000 steel barrels of radioactive waste from a concrete bunker. They will mix it with cement and gypsum, and then permanently store it in the hilltop repository.

The refinery processed slag from old tin mines — material rich in rare earth ore. The company and Malaysian regulators said that it was statistically possible that the leukemia cases were a coincidence because tin mining towns tend to have above-average levels of background radiation. But an academic study of another tin mining town suggested that communities of Bukit Merah’s size should only have one leukemia case every 30 years.

Lai Kwan, aged 69, still recalls how she cheerfully moved in the 1980s from a sawmill job to a better-paying position in the refinery that involved proximity to radioactive materials. She remembers that while pregnant, she was told to take an unpaid day off only on days when the factory bosses said that a particularly dangerous consignment of ore had arrived.

She has spent the last 29 years washing, dressing, feeding and otherwise taking care of her son from that pregnancy, who was born with severe mental and physical disabilities. She and other local residents blame the refinery for the problems, although birth defects can have many causes.

“We saw it as a chance to get better pay,” Ms. Lai recalled. “We didn’t know what they were producing.”