Int. J. Environ. Res. Public Health 2011, 8 94 The data shows that each was stably resident, in different areas of the town up to 2009–2010, none of the parents were directly wounded or trapped under rubble and that, among them, only the male parent in Family 1 reported acute symptoms immediately after bombings. There is no obvious relationship to immediately adjacent bombing/burning of their houses or to the activity of cleaning/recovery of injured-dead people or to personal acute symptoms with them having a child with birth defect in the following years. This suggests that the birth defect in these families might not be due directly to acute exposure, but could be associated to their long term exposure and body accumulation of toxicants which are persistent in the environment. More efficaciously than chromosomal mutations or than multiple single gene mutations, epigenetic changes (alone or associated with other genetic changes) can account for the patterns and diversity of malformation which we see in families 107, 139 and 1. Epigenetic effectors can produce simultaneously different damages and multiple phenotypes, which vary depending on the specific agent(s), and on the timing and level of exposure during embryonic life. This possibility, per se, would fit the data. The novel presentation of sporadic and diverse birth defects, which can be caused uniquely or in composite fashion by epigenetic events, also suggest that agents capable of initiating these changes are still present in the environment and continue to induce novel effects. Teratogens in the postwar environment include metals and metal alloys which persist in the environment and in the body, and are potential risks to health (genotoxic, fetotoxic and epigenetic mechanisms of action). Metals are involved in regulating genome stability, in X chromosome inactivation, in gene imprinting, and in reprogramming gene expression. They act as metalloestrogens, inhibit DNA repair, alter DNA methylation, change transcriptome and microRNAs production, histone acetylation and methylation; all of which can lead to birth defects, whether translated into mutations or not [4]. As a consequence of internal radiation, some metals can induce sporadic gene mutations or oxidative DNA damage. In the case of depleted uranium (DU) it is unclear whether its radiation-derived mutational effects or its chemical toxic effects are more relevant. DU can induce epigenetic changes that are associated with leukemia via hypomethylation of the DNA. Exposure to teratogens of either father or mothers are potentially effective to induce birth defects at the epigenetic as well as the genetic level. In the cases we report here, the pattern of presentation does not exclude the contribution of either parent: the epigenetic changes are likely to behave as stochastic and not striclty deterministic events, and lack of effects in one of the two families branch with the same father cannot exclude his contribution to the occurrence of birth defects in the other family branch. Nonetheless, pregnant mothers' exposure to metal contaminants is potentially more relevant to the development of malformations in the case of Family 107, where both wives had deformed babies, but with different phenotypes, and where the daughter of one of the mothers, who herself delivered a child with atrophic and ectopic kidney, had a child with multiple skeletal and dermal abnormalities. There are no known candidate mutations governing both kidney and skeletal/dermal development, and it is likely that independent exposure to effectors in the environment during both pregnancies induced diverse epigenetic effects in the developing offspring. Prenatal exposure best explain, but also paternal exposure could account for, the cases in those families where only the progeny of one spouse presented birth defects which recurred in diverse phenotypes. Cases in point are the still births and ventricular septal defect (VDS) in Family 139 and multiple cases of child leukemia and TOF in Family 1.