Wildlife has often presented and suggested the effects of endocrine disrupting chemicals (EDCs). Animal studies have given us an important opportunity to understand the mechanisms of action of many chemicals on the endocrine system and on neurodevelopment and behaviour, and to evaluate the effects of doses, time and duration of exposure. Although results are sometimes conflicting because of confounding factors, epidemiological studies in humans suggest effects of EDCs on prenatal growth, thyroid function, glucose metabolism and obesity, puberty, fertility, and on carcinogenesis mainly through epigenetic mechanisms. This manuscript reviews the reports of a multidisciplinary national meeting on this topic.

Exposure to low frequency and radiofrequency electromagnetic fields at low intensities poses a significant health hazard that has not been adequately addressed by national and international organizations such as the World Health Organization. There is strong evidence that excessive exposure to mobile phone-frequencies over long periods of time increases the risk of brain cancer both in humans and animals. The mechanism(s) responsible include induction of reactive oxygen species, gene expression alteration and DNA damage through both epigenetic and genetic processes. In vivo and in vitro studies demonstrate adverse effects on male and female reproduction, almost certainly due to generation of reactive oxygen species. There is increasing evidence the exposures can result in neurobehavioral decrements and that some individuals develop a syndrome of "electro-hypersensitivity" or "microwave illness", which is one of several syndromes commonly categorized as "idiopathic environmental intolerance". While the symptoms are non-specific, new biochemical indicators and imaging techniques allow diagnosis that excludes the symptoms as being only psychosomatic. Unfortunately standards set by most national and international bodies are not protective of human health. This is a particular concern in children, given the rapid expansion of use of wireless technologies, the greater susceptibility of the developing nervous system, the hyperconductivity of their brain tissue, the greater penetration of radiofrequency radiation relative to head size and their potential for a longer lifetime exposure.

No abstract

Obesity is becoming an epidemic health problem. During the last years not only genetic but also, and primarily, environmental factors have been supposed to contribute to the susceptibility to weight gain or to develop complications such as type 2 diabetes. In spite of the intense efforts to identify genetic predisposing variants, progress has been slow and success limited, and the common obesity susceptibility variants identified only explains a small part of the individual variation in risk. Moreover, there is evidence that the current epidemic of obesity and diabetes is environment-driven. Recent studies indicate that normal metabolic regulation during adulthood besides requiring a good balance between energy intake and energy expenditure, can be also affected by pre- and post-natal environments. In fact, maternal nutritional constraint during pregnancy can alter the metabolic phenotype of the offspring by means of epigenetic regulation of specific genes, and this can be passed to the next generations. Studies focused on epigenetic marks in obesity found altered methylation and/or histone acetylation levels in genes involved in specific but also in more general metabolic processes. Recent researches point out the continuous increase of "obesogens", in the environment and food chains, above all endocrine disruptors, chemicals that interfere with many homeostatic mechanisms. Taken into account the already existing data on the effects of obesogens, and the multiple potential targets with which they might interfere daily, it seems likely that the exposure to obesogens can have an important role in the obesity and diabesity pandemic.

The wide spectrum of unique needs and strengths of Autism Spectrum Disorders (ASD) is a challenge for the worldwide healthcare system. With the plethora of information from research, a common thread is required to conceptualize an exhaustive pathogenetic paradigm. The epidemiological and clinical findings in ASD cannot be explained by the traditional linear genetic model, hence the need to move towards a more fluid conception, integrating genetics, environment, and epigenetics as a whole. The embryo-fetal period and the first two years of life (the so-called ‘First 1000 Days’) are the crucial time window for neurodevelopment. In particular, the interplay and the vicious loop between immune activation, gut dysbiosis, and mitochondrial impairment/oxidative stress significantly affects neurodevelopment during pregnancy and undermines the health of ASD people throughout life. Consequently, the most effective intervention in ASD is expected by primary prevention aimed at pregnancy and at early control of the main effector molecular pathways. We will reason here on a comprehensive and exhaustive pathogenetic paradigm in ASD, viewed not just as a theoretical issue, but as a tool to provide suggestions for effective preventive strategies and personalized, dynamic (from womb to adulthood), systemic, and interdisciplinary healthcare approach.

No abstract

Mobile phones and other wireless devices that produce electromagnetic fields (EMF) and pulsed radiofrequency radiation (RFR) are widely documented to cause potentially harmful health impacts that can be detrimental to young people. New epigenetic studies are profiled in this review to account for some neurodevelopmental and neurobehavioral changes due to exposure to wireless technologies. Symptoms of retarded memory, learning, cognition, attention, and behavioral problems have been reported in numerous studies and are similarly manifested in autism and attention deficit hyperactivity disorders, as a result of EMF and RFR exposures where both epigenetic drivers and genetic (DNA) damage are likely contributors. Technology benefits can be realized by adopting wired devices for education to avoid health risk and promote academic achievement.

We reviewed available evidence in medical literature concerning experimental models of exposure to ionizing radiations (IR) and their mechanisms of producing damages on living organisms. The traditional model is based on the theory of “stochastic breakage” of one or both strands of the DNA double helix. According to this model, high doses may cause the breaks, potentially lethal to the cell by damaging both DNA strands, while low doses of IR would cause essentially single strands breaks, easily repairable, resulting in no permanent damages. The available evidence makes this classical model increasingly less acceptable, because the exposure to low doses of IR seems to have carcinogenic effects, even after years or decades, both in the exposed individuals and in subsequent generations. In addition, the cells that survived the exposure to low doses, despite being apparently normal, accumulate damages that become evident in their progeny, such as nonclonal chromosomal aberrations, which can be found even in cells not directly irradiated due to the exchange of molecular signals and complex tissue reactions involving neighboring or distant cells. For all these reasons, a paradigm shift is needed, based on evidence and epigenetics.