Neurodevelopment & the Environment: Are Vaccines to Blame for Skyrocketing Childhood Illnesses?

Remarkable controversy exists on the safety and efficacy of vaccinations in the United States. Research supporting vaccine safety is scant yet crucial to the well being of every American citizen. Since 1980 the amount of vaccinations required for children began to rise quite dramatically. These vaccines contain various toxicants including thimerosal, a mercury (Hg) containing neurotoxicant, which may contribute to neurodevelopmental disorders such as sudden infant death syndrome (SIDS), autism, attention deficit hyperactivity disorder (ADHD), and Environmental Illness (EI) which are all on the rise. According to the U.S. Census Bureau autism, ADHD, and other neurodevelopmental disorders may affect as many as 1 in 6 children in the U.S. totaling over 12 million citizens (Ball, 2001). Many of these conditions developed or expanded around the time of increased vaccinations. Comparison of data on the increase of neurodevelopment disorders and the growth of synthetic chemical production show the data began to merge around 1970 (Colborn, 2004) much the same time the number of vaccines given to children began to increase. Both vaccines and increased chemicals in the environment warrant further investigation as possible causation of neurodevelopment disorders.

“Mercury in the thimerosal molecule is in the form of ethylmercury for which there is limited toxicologic information” (Clarkson, 2002). Thimerosal is the preservative commonly used in many vaccinations and given to children in amounts of ethylmercury that exceed the U.S. Environmental Protection Agency safety level for adults (Burbacher et al, 2005). Thimerosal has been withdrawn from many pediatric vaccines since 1999 as a result of concerns over the neurodevelopmental toxicity of organic mercury although it is still used in influenza, diphtheria, and pertussis vaccinations (Goth et al, 2006). It is plausible that the withdrawal of thimerosal is indicative of its potential as a neurotoxicant. Children vaccinated before 1990 time may have received cumulative doses of mercury exceeding 200µg/kg and because thimerosal is organic mercury there is suspicion among scientists that it acts as methylmercury does in the brain though the two forms vary in the way they are distributed and eliminated from the brain (Spzir, 2006). Health risk estimates from thimerosal in vaccines originally assumed that ethylmercury is toxicologically similar to methylmercury (Ball et al, 2001). Studies have since found this to be misleading as methylmercury is distributed differently than methylmercury (Burbacher et al, 2005).

Reports indicating infants can be given ethylmercury in the form of thimerosal above the guidelines for safe exposure set by the U. S. Environmental Protection Agency were challenged in an experiment (Burbacher et al, 2005) in which monkeys were exposed to methylmercury or thimerosal and tested at intervals to determine how long the mercury remained in the brains of the monkeys. Findings showed that methylmercury is not a proper reference for risk assessment from exposure to thimerosal-derived mercury as ethylmercury clears the brain faster than methylmercury (Burbacher et al, 2005). The deposition kinetics of the two forms of mercury varies greatly requiring further investigation into the safety and efficacy of ethylmercury from thimerosal as a vaccine preservative. “Although the initial distribution volume of total mercury is similar for the two groups, a biphasic exponential decline in total blood mercury is observed only after intramuscular injections of thimerosal. This suggests continual distribution into and localization in tissue sites over time” (Burbacher et al, 2005) where the mercury is stored and accumulated. More “knowledge of the toxicokinetics and developmental toxicity of thimerosal is needed to afford a meaningful assessment of the developmental effects of thimerosal-containing vaccines. We need knowledge of biotransformation of thimerosal to interpret the potential developmental effects of immunization with thimerosal-containing vaccines in infants. This information is critical if we are to respond to public concerns regarding the safely of childhood immunizations” (Burbacher et al, 2005).

Thimerosal also differs from methylmercury in that it causes kidney damage as well as damage to the nervous system at the same dose (Clarkson, 2002). In addition to disposition of mercury in the body a primary area of concern is the effects of mercury in the body and particularly the central nervous system. Clarkson (2002) emphasizes that the mature central nervous system is characterized by a latent period between mercury exposure and onset of symptoms of several weeks to months. Paresthesia, cerebellar ataxia, dysarthria, constriction of the visual fields, and loss of hearing are among the first symptoms of mercury toxicity often caused by loss of or damage to neuronal cells (Clarkson 2002). Damage by mercury also includes oxidative stress, lipid peroxidation, mitochondrial dysfunction, synaptic transmission disruption, microtubule formation, amino acid transport, and cellular migration, psychomotor retardation, seizures, mental retardation, and developmental delays (Schettler, 2001). There may conceivably be a correlation between the symptoms of mercury poisoning and the similar symptoms evident in neurodevelopment disorders. Clarkson (2002) ascertains “methylmercury is converted to inorganic mercury in the brain. It is possible that the inorganic ion is the proximate toxic agent responsible for the brain damage. However, experiments on rats comparing methyl and ethyl mercury compounds suggest that the intact methylmercury radical is the toxic agent. Ethylmercury converts to inorganic mercury more rapidly than methylmercury, but the latter products more serious brain damage. The toxicologic role of inorganic mercury remains a matter of debate.” What is clear is that safety of any mercury is highly questionable and requires further research before we continue to risk exposing children to thimerosal.

Effects of mercury on children show susceptibility for prenatal exposure to methylmercury as it passes though the placental barrier to the developing fetus from the mother (Bjornberg et al, 2005). Clarkson (2002) notes mothers with mild symptoms of mercury neurotoxicity often give birth to offspring with severe brain damage, delayed development, and other neurologic abnormalities. There is valid concern over the safety of the amount of additional mercury received in childhood vaccinations.

In the United States autism, once a rare condition (Goodman & Koduru, 2000), has increased from 4 – 5 per 10,000 children in the 1980’s to 30 – 60 per 10,000 children in the 1990’s, an increase of more than ten times, and the diagnosis of ADHD increased 250% between 1990 and 1998 (Szpir, 2006). The cause of these diseases is largely unknown at this time though some researchers are looking to phthalates, PCB’s, and other chemicals for which use has increased about the same time (Booker, 2001). A 2006 study concluded that there is a potential association between autism and estimated metal concentrations in the air (Windham et al, 2006). Another study postulates that thimerosal may be a potential triggering mechanism contributing to autism in susceptible individuals (Walker et al, 2006).

One of many studies examined and found correlation between sleep position and SIDS (Ostfeld et al, 2006) leaving unclear why a child would become vulnerable to a certain sleep position in recent years only when SIDS was unheard of before 1980. Another study suggests a strong link between metals in particulate air pollution and some forms of infant death (Glinianaia et al, 2004). Thimerosal being largely composed of the metal mercury is another likely culprit that requires additional research.

Also noteworthy is a study in which 33% of participants were found to be suffering from multiple chemical sensitivity, a form of EI (Meggs et al, 1996) that is caused by low molecular weight chemicals that bind to chemoreceptors on sensory nerve C-fibers leading to the release of inflammatory mediators (Meggs, 1999). With such a large percentage of the population suffering EI it is conceivable a common exposure such as thimerosal in vaccines could be the etiology behind turning on the CYP2D6 allele apparently responsible for genetically variable toxin pathways that may cause EI to surface (McKeown-Eyssen et al, 2004).

The effect of neurodevelopmental disorders reaches beyond the child to the parent, the social system, the work force, school curriculum, medical providers, care providers, the welfare system, and therefore affects the pocketbooks of every taxpaying citizen. Cumulative costs identified (Muir & Zegarac, 2001) for societal costs of exposure to toxic substances total between $568 billion and $793 billion dollars per year in Canada and the United States. Further at least 10% and as much as 50% of these costs are environmentally induced by toxicants (Muir & Zegarac, 2001). Neurodevelopment disorders cost the United States $81.5 to $167 billion annually and methylmercury induced toxicity alone is estimated to cost $8.7 billion dollars in lost productivity in the United States (Szpir, 2006). 67% of chemicals imported into the United States have not been examined for neurotoxicity (Szpir, 2006) and could also be a contributing factor. Children affected by neurodevelopment disorders will increasingly become burden to society for care as they age giving rise to the essentiality that scientists discover the etiology behind this alarming increase. The costs of reduced IQ in the United States alone in 1987 may have reached $327 billion (Muir & Zegarac, 2001).

What is absolutely clear is the evidence that pollution and toxicants affect the brain and central nervous system in a negative way. The symptoms of neurological disorders being similar to those of mercury poisoning will require additional research to determine if there is a connection between neurodevelopmental disorders and thimerosal in vaccines.

To date no studies have been performed to compare human populations vaccinated and populations unvaccinated. In the past the Centers for Disease Control (CC) has purported vaccines and autism to be unrelated or casually related (Institute of Medicine, 2004) though the CDC has recently announced the funding of a multi-agency study to determine the potential for environmental and genetic causes of autism which includes thimerosal (Centers for Disease Control and Prevention, 2006). Of further note is that studies have compared human populations vaccinated with thimerosal containing vaccinations to populations vaccinated with non-thimerosal containing alternatives. Do thimerosal containing vaccinations contribute to childhood developmental neurotoxicology resulting in neurodevelopment and neuropsychological disorders such as sudden infant death syndrome (SIDS), autism, attention deficit hyperactivity disorder (ADHD), and environmental illness in the United States?

Now we examine some of the most common neurodevelopmental and environmental disorders including autism, attention deficit hyperactivity disorder (ADHD), sudden infant death syndrome (SIDS), and multiple chemical sensitivities (MCS).

In the United States autism, once a rare condition (Goodman & Koduru, 2000), has increased from 4 – 5 per 10,000 children in the 1980’s to 30 – 60 per 10,000 children in the 1990’s, an increase of more than ten times (Szpir, 2006; Hertz-Picciotto et al, 2006). Autism spectrum disorder, which includes Asperger’s syndrome and pervasive developmental disorder (PDD), is defined by the American Psychiatric Association as a neurodevopmental disorder characterized by impairments in social interaction, verbal and nonverbal communication, and restricted, stereotyped interests and behaviors (Hertz-Picciotto et al, 2006).

Currently the cause and contributing factors to autism are poorly understood (Hertz-Picciotto et al, 2006). Originally thought to arise from a case of bad parenting, it is now widely accepted that aberrant brain development underlies autism as a mechanism of pathogenesis after several studies have shown structural changes and neurophysiologic differences in the brains of autistic children (Hertz-Picciotto et al, 2006). Genetic studies have linked certain genes to autism but no single gene has yet been reliably replicable (Hertz-Picciotto, et al, 2006). “Concordance in monozygotic twins suggests that a minimum of 40% of autism cases are likely to have an environmental cause” (Hertz-Picciotto, et al, 2006, p. 1119). Some researchers are looking to phthalates, PCB’s, and other chemicals for which use has increased about the same time as autism (Booker, 2001).

A 2006 study concluded that there is a potential association between autism and estimated metal concentrations in the air (Windham et al, 2006). Another study found a few specific environmental factors including prenatal exposure to thalidomide, valproic acid, and rubella though they are likely to play a negligible role in modern society (Hertz-Picciotto et al, 2006). Yet another study postulates that thimerosal may be a potential triggering mechanism contributing to autism in susceptible individuals (Walker et al, 2006). Other potential etiologies include neuroimmunomoduatory factors, lymphocyte activation, cytokine profiles, distribution of neuropeptides and neurotrophins at birth (Hertz-Picciotto, et al, 2006), and decreased levels of epidermal growth factor (Suzuki et al, 2006). As autism increases (Hertz-Picciotto, et al, 2006) it is becoming increasingly important to uncover the etiology behind this devastating and costly disorder (Szpir, 2006).

Attention deficit hyperactivity disorder (ADHD) is another common childhood disorder with prevalence estimated as high as 8% of the population (Braun et al, 2006). ADHD is characterized by an inability to organize complex sequences of behavior, focus in the face of distracting stimuli, and to respond appropriately to consequences (Rice, 2000). The person with ADHD may behave impulsively and be unable to pay attention to the task at hand (Rice, 2000). The diagnosis of ADHD has increased 250% between 1990 and 1998 (Szpir, 2006). Part of the large increase may be due to the fact that adults are being diagnosed with ADHD which was seldom diagnosed in the past, mainly because of the presence of comorbidities, and the failure to recognize ADHD as a real syndrome in adults by some researchers (Aparecida da Silva, 2006). The prevalence is three times higher among males than among females, possibly because males tend to externalize behaviors more than females (Braun et al, 2006). ADHD was shown by Adewuya & Famuyiwa (2006) to occur across cultures.

In early studies it was hypothesized that neuroanatomical abnormality of the prefrontal cortex may cause ADHD as this area of the brain is involved in the executive behaviors that ADHD produces a deficit in (Rice, 2000). More recently both genetic and environmental factors, including exposure to prenatal tobacco smoke and lead, have been implicated in ADHD (Braun et al, 2006). A study by Rice (2000) found parallels between the features of ADHD and the behavior of monkeys exposed developmentally to lead or polychlorinated biphenyls (PCBs). The deficits observed included discrimination reversal and spatial delayed alternation performance (Rice, 2000). Another study found high levels of lead were correlated with ADHD in children as well (Braun et al, 2006). Much like autism, ADHD is becoming increasingly costly and uncovering the etiology behind the condition is becoming increasingly critical (Szpir, 2006).

“Sudden infant death syndrome (SIDS) is the unexpected death of an infant under the age of 1 year, where a complete autopsy, including scene investigation, fails to reveal a cause of death” (Losiniecki, 2006). SIDS is diagnosed by exclusion of all other possible causes of death (Losiniecki, 2006). Prior to sudden death, victims of sudden infant death syndrome (SIDS) are described as having less reactions to environmental stimuli, being less physically active, having faster heart rate and decreased movement during sleep, and experiencing more breathlessness and exhaustion during feeding (Reid, 2006).

Many studies examined and found correlation between sleep position, bed sharing, and SIDS (Ostfeld et al, 2006; Alder et al, 2006; Thompson et al, 2006). However it is unclear why a child would become vulnerable to a certain sleep position or why there has been a sudden increase in SIDS since 1980 though some postulations include problems with the airway and brain stem (Ostfeld et al, 2006; Alder et al, 2006; Thompson et al, 2006). One study by Thompson et al (2006) cited several potential confounders including younger infant age, Maori ethnicity, low birth weight, prone sleep position, use of a sheepskin, and pillow use that were associated with an increased risk of SIDS. Another study suggests a strong link between metals in particulate air pollution and some forms of infant death (Glinianaia et al, 2004) that may explain the etiology behind the confounders found by other researchers. Recently researchers have turned to environmental factors in attempts to explain SIDS. One study found a correlation between environmental tobacco smoke and SIDS (Bonham et al, 2001). Wasley et al (2002) found an association between exposure to methyl parathion, an organophosphate pesticide, and SIDS. Though the association was not statistically significant, Wasley et al (2002) concluded that more studies were necessary on the basis of the association. Additional studies will be required to replicate these studies and perhaps isolate the etiology of SIDS.

Multiple chemical sensitivity (MCS) is an environmental illness (EI) in which negative health effects including fatigue, headache, nausea, cognitive dysfunction, heart arrhythmia, respiratory distress, and seizures are experienced in multiple organ systems from exposure to low levels of common chemicals normally deemed as safe (Gibson, 2003). In 1999 a consensus criteria was established for the diagnoses and definition of MCS (Joffres et al, 2005). The criteria states that symptoms are reproducible with repeated chemical exposure, the condition is chronic, levels of exposure lower than previously tolerated elicit symptoms, symptoms improve or resolve when incitants are removed, symptoms appear in response to multiple chemically unrelated substances, and symptoms involve multiple organ systems commonly the cardiac, pulmonary, and neurological systems (Joffres et al, 2005). . The prevalence of MCS ranges from 16% (Gibson, 2005) to 33% (Meggs et al, 1996). Sixteen percent is generally accepted as the most accurate figure for prevalence in the United States (Gibson, 2005).

One of the first studies on MCS focused on possible long term potentiation in the hippocampus and neural sensitization as a central mechanism in MCS (Pall, 2003). Later studies examined the role of the inflammatory process and found that brain inflammation is correlated with symptoms of MCS (Pall, 2003). Meggs (1999) concluded that MCS is potentially caused by low molecular weight chemicals that bind to chemoreceptors on sensory nerve C-fibers leading to the release of inflammatory mediators. Another study concluded the CYP2D6 allele was apparently responsible for genetically variable toxin pathways that may cause MCS to surface (McKeown-Eyssen et al, 2004). Pall (2003) more recently identified a pattern of evidence that suggests elevated nitric oxide and peroxynitrite (NO/ONOO) may be the etiology behind the symptoms for MCS as well as several other related conditions including fibromyalgia, post traumatic stress disorder, gulf war syndrome, and chronic fatigue syndrome. Pall has identified viral infection, bacterial infection, carbon monoxide exposure, physical trauma, organophosphate poisoning, severe psychological stress, ciguatoxin poisoning, and ionizing radiation exposures as initiating stressors that begin the NO/ONOO cycle of biochemistry leading to MCS (Pall, 2006). With such a large percentage of the population suffering from MCS (Gibson, 2005) and a large amount of toxicants that may initiate the NO/ONOO cycle (Pall, 2006) it is conceivable that nearly any environmental toxicant could also be a common exposure that may initiate or exacerbate MCS.

It is plausible that a single toxicant or a combination of toxicants may be linked to the etiology of autism, ADHD, SIDS, and MCS. Only time and research will tell.

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Originally posted on American Chronicle

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