BackgroundRecent reports have drawn attention to increases in congenital birth anomalies and cancer in Fallujah Iraq blamed on teratogenic, genetic and genomic stress thought to result from depleted Uranium contamination following the battles in the town in 2004. Contamination of the parents of the children and of the environment by Uranium and other elements was investigated using Inductively Coupled Plasma Mass Spectrometry. Hair samples from 25 fathers and mothers of children diagnosed with congenital anomalies were analysed for Uranium and 51 other elements. Mean ages of the parents was: fathers 29.6 (SD 6.2); mothers: 27.3 (SD 6.8). For a sub-group of 6 women, long locks of hair were analysed for Uranium along the length of the hair to obtain information about historic exposures. Samples of soil and water were also analysed and Uranium isotope ratios determined.ResultsLevels of Ca, Mg, Co, Fe, Mn, V, Zn, Sr, Al, Ba, Bi, Ga, Pb, Hg, Pd and U (for mothers only) were significantly higher than published mean levels in an uncontaminated population in Sweden. In high excess were Ca, Mg, Sr, Al, Bi and Hg. Of these only Hg can be considered as a possible cause of congenital anomaly. Mean levels for Uranium were 0.16 ppm (SD: 0.11) range 0.02 to 0.4, higher in mothers (0.18 ppm SD 0.09) than fathers (0.11 ppm; SD 0.13). The highly unusual non-normal Fallujah distribution mean was significantly higher than literature results for a control population Southern Israel (0.062 ppm) and a non-parametric test (Mann Whitney-Wilcoxon) gave p = 0.016 for this comparison of the distribution. Mean levels in Fallujah were also much higher than the mean of measurements reported from Japan, Brazil, Sweden and Slovenia (0.04 ppm SD 0.02). Soil samples show low concentrations with a mean of 0.76 ppm (SD 0.42) and range 0.1-1.5 ppm; (N = 18). However it may be consistent with levels in drinking water (2.28 μgL-1) which had similar levels to water from wells (2.72 μgL-1) and the river Euphrates (2.24 μgL-1). In a separate study of a sub group of mothers with long hair to investigate historic Uranium excretion the results suggested that levels were much higher in the past. Uranium traces detected in the soil samples and the hair showed slightly enriched isotopic signatures for hair U238/U235 = (135.16 SD 1.45) compared with the natural ratio of 137.88. Soil sample Uranium isotope ratios were determined after extraction and concentration of the Uranium by ion exchange. Results showed statistically significant presence of enriched Uranium with a mean of 129 with SD5.9 (for this determination, the natural Uranium 95% CI was 132.1 < Ratio < 144.1).ConclusionsWhilst caution must be exercised about ruling out other possibilities, because none of the elements found in excess are reported to cause congenital diseases and cancer except Uranium, these findings suggest the enriched Uranium exposure is either a primary cause or related to the cause of the congenital anomaly and cancer increases. Questions are thus raised about the characteristics a...

ObjectivesTo investigate the accuracy and scientific validity of the current very low risk factor for hereditary diseases in humans following exposures to ionizing radiation adopted by the United Nations Scientific Committee on the Effects of Atomic Radiation and the International Commission on Radiological Protection. The value is based on experiments on mice due to reportedly absent effects in the Japanese atomic bomb (Abomb) survivors.MethodsTo review the published evidence for heritable effects after ionising radiation exposures particularly, but not restricted to, populations exposed to contamination from the Chernobyl accident and from atmospheric nuclear test fallout. To make a compilation of findings about early deaths, congenital malformations, Down’s syndrome, cancer and other genetic effects observed in humans after the exposure of the parents. To also examine more closely the evidence from the Japanese A-bomb epidemiology and discuss its scientific validity.ResultsNearly all types of hereditary defects were found at doses as low as one to 10 mSv. We discuss the clash between the current risk model and these observations on the basis of biological mechanism and assumptions about linear relationships between dose and effect in neonatal and foetal epidemiology. The evidence supports a dose response relationship which is non-linear and is either biphasic or supralinear (hogs-back) and largely either saturates or falls above 10 mSv.ConclusionsWe conclude that the current risk model for heritable effects of radiation is unsafe. The dose response relationship is non-linear with the greatest effects at the lowest doses. Using Chernobyl data we derive an excess relative risk for all malformations of 1.0 per 10 mSv cumulative dose. The safety of the Japanese A-bomb epidemiology is argued to be both scientifically and philosophically questionable owing to errors in the choice of control groups, omission of internal exposure effects and assumptions about linear dose response.

After the Chernobyl reactor accident in April 1986, rainfall precipitation caused measurable radioactive contamination of Wales and Scotland. Using risk models developed by themselves and by the International Commission on Radiological Protection, the UK National Radiological Protection Board advised that no measurable increase in leukemia was predicted at exposures which they estimated from measurements of contamination. However, cancer registry data from both the Wales and Scotland registries show a sharp increase in cases of infant leukemia age 0–1 in the eighteen month period January 1st 1987 to June 30th 1988. This period is that in which the birth cohort who were in utero in the exposure period following the fallout would be in the age group 0–1. Compared with an ‘unexposed group’ consisting of the period 1975–1986 the Wales exposed group had a relative risk (RR) of 4.4 (p = 0.004), the Scotland group a RR of 3.7 (p = .001) and the combined Wales and Scotland group an RR of 3.87 (p = .0001). A second unexposed group, those aged 0–1 in 1989–91 had no significant increased risk although after 1991 rates increased slightly. This finding supports earlier reports of infant leukemia effects in Greece, Germany and the U.S. following Chernobyl. The data cannot entirely distinguish between pre-conception or in utero effects but also reported here are increases in very low birth-weight births in Wales following Chernobyl, suggesting a genetic component to both effects. The existence of good quality leukemia and exposure data makes it possible to calculate an error in the presently accepted risk factors for radiation induced leukemia following this kind of exposure of about 100-fold or more. The possibility of errors of this magnitude in the contemporary risk estimates of ionizing radiation effects suggests that a more cautious approach should be exercised to policy decisions about nuclear power options.

It is necessary to define and study groups of multiple stressors as in US EPA's Framework for Cumulative Risk Assessment (U.S. EPA 2003). Recent increased knowledge of the greater sensitivity of the unborn baby, the infant and the child, has led to general recognition that a higher degree of precaution is now needed in regulating for multiple stressors on the young. The more liberal permissive approach proceeding from established effects of the individual exposures is becoming less acceptable now that we know that there is much we do not understand about chronic effects of stressors during the early development phases. Conflicts over which approach to take may have to be resolved through engagement and negotiation with a wide community of stakeholders. This "community of interest" may include fundamental research scientists, practicing clinical paediatricians, patient groups, and others concerned with the health and wellbeing of infants and children.

Current legal frameworks for radiation exposure limits are based on the risk models of the International Commission on Radiological Protection (ICRP). In Publication 90 (2003), ICRP presents a safe (threshold) dose range of up to 100 mSv for radiogenic effects resulting from in utero exposure and bases this conclusion on the findings in Hiroshima and Nagasaki. However, a variety of observations of congenital malformations, fetal loss, stillbirths and infant deaths, as well as of Down's syndrome and other health defects in children after the Chernobyl accident exposures suggest that the A-bomb survivor data are incomplete. The Chernobyl findings are generally marginalized or even denied because of the low values of the estimated human exposures and the inconsistency of the results with the accepted risk models. One explanation for the observations is that physical dosimetric models have underestimated the effective exposure. This possibility is supported by biological dosimetry in the contaminated regions. The assumptions about effects after in utero exposure by incorporated radionuclides need to be revised.