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
Radioactive waste from nuclear installations and nuclear reprocessing plants, nuclear accidents, and radioactive fallout from nuclear weapons testing constitute a serious problem facing future generations. Marine algae and phytoplanktons accumulate radionuclides from their surroundings and are used as bioindicators of radioactive pollution in the environment. In Northern Europe, the affected marine systems include the Irish Sea, the Baltic Sea, and the North Sea. The main sources of this radioactive contamination are global fallout from nuclear weapons tests, river transport from Siberia, and marine transport of discharges from Sellafield and Chernobyl. An increased leukemia incidence has been observed in young children at Seascale near Sellafield, and an elevated incidence of leukemia has been recorded among young people (0–24 years) in the French canton of Beaumont-Hague close to the Cap de la Hague nuclear reprocessing facility. In Scandinavia, scientists suspect that people in parts of Sweden are still dying from cancer caused by radiation from the Chernobyl accident. Moreover, the Baltic Sea is contaminated with man-made plutonium radionuclides from nuclear reprocessing. However, some experts are able to dismiss the above relationships due to important uncertainties over the estimation of radiation doses from environmental discharges based on a mutational theory of carcinogenesis. Consequently, it appears to be of paramount importance to reevaluate the current methods for cancer risk assessment in the case of radiation exposure within the context of an apoptotic model of carcinogenesis that could explain such a discrepancy. According to this new model, subtle differences in gene expression in response to a carcinogen can initiate cell death or apoptosis and act as a trigger for carcinogenesis. Simultaneously, future implications for human gene evolution are unavoidable.
Part of the book: Gene Expression and Phenotypic Traits
Cigarette smoke and air pollution have been associated with lung cancer and naso pharyngeal and laryngeal cancer, respectively. Significant concentrations of select heavy metals including lead and cadmium have been isolated in popular cigarette brands, and these heavy metals can be inhaled via smoking. Lead is able to mimic the activity of calcium in the human body, thereby leading to toxic effects in a variety of target organs. Lead perturbs and alters the release of intracellular calcium stores from organelles like the endoplasmic reticulum (ER) and mitochondria. A rise in mitochondrial calcium stimulates the generation of reactive oxygen species (ROS) and free fatty acids which can further promote calcium release and, ultimately, result in cell death. In the case of cadmium, the renal proximal tubule of the kidney accumulates freely filtered and metallothionein-bound metal, which is degraded in endosomes and lysosomes. This results in the release of free cadmium into the cytosol where it can generate reactive oxygen species and activate cell death pathways. In developing countries, indoor air pollution due to the domestic use of unprocessed biomass fuels such as wood, dung, and coal is another cause of respiratory tract cancers in humans. In some developed countries such as Australia and Canada, the alarming increase in forest fire frequency due to climate change and the associated smoke released into the environment is also likely to pose a future human health risk. Polycyclic organic particles in biomass and forest fire smoke can include carcinogens such as benzo[a]pyrene, which is also found in cigarette smoke. Benzo[a]pyrene can induce apoptosis in mammalian cells by initiating mitochondrial dysfunction, activating the intrinsic caspase pathway (caspase-3 and caspase-9), and via p53 activation. The constitutive activation of apoptotic pathways has been linked to carcinogenesis in a number of cancer models.
Part of the book: Heavy Metal Toxicity in Public Health