Volume 28, Issue 2-3

Exposure to electrosmog generated by electric, electronic, and wireless technology is accelerating to the point that a portion of the population is experiencing adverse reactions when they are exposed. The symptoms of electrohypersensitivity (EHS), best described as rapid aging syndrome, experienced by adults and children resemble symptoms experienced by radar operators in the 1940s to the 1960s and are well described in the literature. An increasingly common response includes clumping (rouleau formation) of the red blood cells, heart palpitations, pain or pressure in the chest accompanied by anxiety, and an upregulation of the sympathetic nervous system coincident with a downregulation of the parasympathetic nervous system typical of the “fight-or-flight” response. Provocation studies presented in this article demonstrate that the response to electrosmog is physiologic and not psychosomatic. Those who experience prolonged and severe EHS may develop psychologic problems as a consequence of their inability to work, their limited ability to travel in our highly technologic environment, and the social stigma that their symptoms are imagined rather than real.

Persistent, bioaccumulative, and toxic (PBT) chemicals are a class of chemicals that resist degradation and persist in the environment for extensive periods. As a result of their persistence, when these chemicals are consumed, they bioaccumulate in the fat tissues, bones, and brain of organisms. Lead (Pb) is a PBT metal with the ability to bind irreversibly to neurons and to mimic natural minerals like calcium and zinc. The aim of this review is to examine the unique properties of a PBT, like Pb, as well as the analytic methods of detecting and characterizing PBTs. This review offers sections that explore Pb’s persistence in the environment, bioaccumulation in fish and birds, and toxic characteristics in the human body. It further examines how Pb’s effects on transcription factors could explain the observed Pb lines in Pb-poisoned individuals. This review also evaluates the relationship between the properties of persistence and bioaccumulation as a means to determine whether or not they are interconnected, interdependent, or independent of one another.

Background: Wireless phones, i.e., mobile phones and cordless phones, emit radiofrequency electromagnetic fields (RF-EMF) when used. An increased risk of brain tumors is a major concern. The International Agency for Research on Cancer (IARC) at the World Health Organization (WHO) evaluated the carcinogenic effect to humans from RF-EMF in May 2011. It was concluded that RF-EMF is a group 2B, i.e., a “possible”, human carcinogen. Bradford Hill gave a presidential address at the British Royal Society of Medicine in 1965 on the association or causation that provides a helpful framework for evaluation of the brain tumor risk from RF-EMF. Methods: All nine issues on causation according to Hill were evaluated. Regarding wireless phones, only studies with long-term use were included. In addition, laboratory studies and data on the incidence of brain tumors were considered. Results: The criteria on strength, consistency, specificity, temporality, and biologic gradient for evidence of increased risk for glioma and acoustic neuroma were fulfilled. Additional evidence came from plausibility and analogy based on laboratory studies. Regarding coherence, several studies show increasing incidence of brain tumors, especially in the most exposed area. Support for the experiment came from antioxidants that can alleviate the generation of reactive oxygen species involved in biologic effects, although a direct mechanism for brain tumor carcinogenesis has not been shown. In addition, the finding of no increased risk for brain tumors in subjects using the mobile phone only in a car with an external antenna is supportive evidence. Hill did not consider all the needed nine viewpoints to be essential requirements. Conclusion: Based on the Hill criteria, glioma and acoustic neuroma should be considered to be caused by RF-EMF emissions from wireless phones and regarded as carcinogenic to humans, classifying it as group 1 according to the IARC classification. Current guidelines for exposure need to be urgently revised.

This article discusses the impact of environmental factors on birth outcomes during the last two decades. It reiterates the correlation between air pollutants and adverse pregnancy including low birth weight (LBW) and infant mortality. Data sets are assembled for many OECD countries consisting of yearly air pollutants emissions including sulfur dioxide, nitrogen dioxide, carbon monoxide, and volatile organic compounds. Various health data are illustrated to suggest that countries with high emission levels of air pollutants seemed to increase with LBW and infant mortality. This article reports the association of pollutants, including particles and gases, on mortality in general and infant mortality in particular. To assess air pollution impact on infant mortality, Spearman’s correlation is used to summarize and interpret data. This statistical method is used to assess the relationship between air pollution and infant mortality in many OECD countries between 2000 and 2009 using a monotonic function. The results illustrate a positive correlation between air pollution and infant mortality, and in some cases, Spearman’s ρ-value is >0.9 and the p-value is <0.001. This article also backs up the association between some air pollutants and LBW and proposes the importance to design novel models for monitoring, controlling, and reducing air pollutants especially within cities and ultimately improving the well-being of communities worldwide.

Ultrafine particles (UfPs, PM <0.1 ) are constituents of urban ambient air aerosol. We have reviewed literature on UfPs in urban ambient air and their health perspectives. Generally traffic-linked and of anthropogenic origin, these are toxicants and a health risk factor for urban subjects. UfPs occur in single and agglomerate forms. Studies on the number concentrations of UfPs show tens of thousand times greater levels in urban aerosol than in nonurban aerosol. These nanosize pollutants seem to have more aggressive implications than other respirable fractions of urban aerosol. In literature, it is hypothesized that a chronic exposure to their high number concentrations and their vast surface area, transporting various toxicants, injure tissues or cells and induce inflammation or, eventually, adverse health effects. UfPs are deposited deep in the tissues, translocate, and skip the innate clearance mechanisms. After retention for a long time, these can infiltrate into the interstitium and permeate cells. Traffic-linked UfPs have been found to be toxic to the respiratory, cardiovascular, and nervous systems. At the molecular level, UfPs influence signaling cascade, actin-cytoskeleton pathway, immunoregulation, reactive oxygen species generation to trigger histaminic response, mast cell activation, and pro-inflammatory changes; their mutagenic and carcinogenic effects are also tacit in view of the carcinogenic potential of diesel exhaust in humans. The molecular changes are proposed to be the subclinical effects that manifest disease exacerbations or the predisposition of subjects to pathologies after exposure to UfP. A legislatively regulated monitoring of UfP-contaminated urban ambient air environment is also endorsed to reduce the disease load or its exacerbation that is growing in diesel exhaust (a human carcinogen)-polluted urban areas.

Fish provide healthy protein as well as recreational and cultural benefits, but can also contain mercury (Hg), polychlorinated biphenyls (PCBs), and other contaminants that have adverse effects on humans and other organisms, particularly developing fetuses. Recently, some authors have suggested that a molar excess of selenium (Se) [e.g., selenium/mercury (Se/Hg) molar ratio >1] confers protection from Hg toxicity derived from fish consumption. Herein, we review our studies of Hg and Se in freshwater, marine, and commercial fish (mainly marine), examining the following: (1) whether and how Se/Hg molar ratios vary among species; (2) whether and how the molar ratios vary within species; (3) whether the molar ratios differ between freshwater and saltwater fish; (4) whether mean molar ratio values provide a reliable indication of potential risk to fish consumers; and (5) whether mean Se/Hg molar ratios are sufficiently constant (e.g., low variation) to allow for use in risk assessment, risk management, or risk communication. In saltwater fish, mean Se/Hg molar ratios varied from 0.3 in mako shark to 68.1 in whiting. For freshwater fish, the mean ratios varied from 0.68 in bowfin to 20.8 in black crappie. Commercial seafood (mainly saltwater) showed great variation in ratios; shrimp and scallops had very high ratios. There was somewhat less variability in the ratios for freshwater fish compared with the fish from saltwater, but there was no overall predictable difference in variation in Se/Hg molar ratios. For both saltwater and freshwater fish, some species with mean molar ratios above 1 had a significant proportion of individual fish with molar ratios below 1. Overall, this indicates great variation in measures of central tendencies and in measures of dispersion. We suggest that relying on the Se/Hg molar ratio as a method of predicting reduced risk from Hg toxicity is problematic because of the great variation among and within fish species, and the variation is not predictable because Hg varies by season, size of the fish, and location of the fish (which is not available for commercial fish). With the high variation in ratios, and low predictability, the ratios are currently not useful for risk assessment and risk management, and vulnerable individuals cannot rely on mean Se/Hg molar ratios for protection from Hg toxicity.