Microwave sickness syndrome was first identified in the 1950s by Soviet researchers. Symptoms included headache, fatigue, ocular dysfunction, dizziness, and sleep disorders. The main clinical manifestations were dermographism, tumors, blood changes, reproductive and cardiovascular abnormalities, depression, irritability, and memory impairment. Later in the 1970s, American researchers reported similar findings. Electromagnetic radiation (EMR) from modern cellphone towers is largely comprised of high-frequency radio waves or microwaves. The adverse biological effects of EMR from cellphone towers have been observed in birds, bees, and humans. The associated decline in fruit-eating seed dispersers such as wild birds and in insect pollinators such as bees could have serious consequences for human food production. In addition to noting this possible indirect effect of microwave radiation, a direct effect on human health was evaluated. According to a new approach to cancer risk assessment, based on an apoptotic model of carcinogenesis, it was determined that proximity to EMR from cellphone towers may pose a potential cancer risk in humans since microwave radiation can induce various apoptotic pathways leading to cell death in transformed human cell lines. The stimulation of cellular apoptosis resulting in deregulated cell proliferation is being increasingly linked to cancer and may provide a possible mechanism for microwave radiation carcinogenesis.
Part of the book: Current Understanding of Apoptosis
Recently, it has become apparent that the pathogenesis of cancer is closely connected with aberrantly regulated apoptotic cell death and the resulting deregulation of cell proliferation. The loss of equilibrium between cell proliferation and cell death in a tissue may play a crucial role in tumor formation. In fact, the initiation of uncontrolled apoptosis in a tissue may serve as the trigger for carcinogenesis. Various laboratory studies on animals and certain human data are suggestive that tumor formation requires at least two discrete events to take place in response to a carcinogen according to this apoptotic model of carcinogenesis. The first involves an elevation of apoptosis in a particular tissue due to a genetic predisposition, stress, or mutation. The second confers resistance to apoptosis in that same tissue resulting in the formation of an abnormal growth due to a dysregulation of cell number homeostasis. The apoptotic response of each individual to any given carcinogenic or other environmental stimulus is determined by their unique double set of genes inherited from both parents. The singular genetic traits and biochemistry of each individual are attributable solely to this unique combination of genes and their specific regulation. A general example of genetic regulation, gene dose, and control is provided by β-thalassemia point mutations in the beta-globin gene, which confer a blood disease mainly in Mediterranean populations. This mutation (heterozygous and homozygous, at one or both genetic loci) can cause a hereditary red blood cell anemia. Specific examples in relation to cancer predisposition include various genetic models such as the elevated levels of skin cancer among those with certain polymorphisms or inherited mutations in their DNA repair genes like those associated with the disorder, Xeroderma pigmentosum (XP); the high rate of skin cancer observed in albinos with little or no melanin; and the high incidence of lymphomas occurring in patients with the inherited disorder, ataxia-telangiectasia (AT). The mutations associated with each of these conditions can result in an elevated level of apoptosis in the target tissues, either constitutively or in response to particular carcinogens such as UV rays, and can be linked to the initiation of cancer in those specific tissues.
Part of the book: Gene Expression Profiling in Cancer