Vaccinazioni per l’infanzia ed autismo
Metalli tossici dei vaccini = Autismo vedi: PDF -  dott. M. Proietti

Sentenza 2012 - Trib. Rimini su Vaccini=Autismo

III.         MECHANISMS, SOURCES & EPIDEMIOLOGY OF EXPOSURE

a.   Exposure Mechanism
Vaccine injections are a known source of mercury (Plotkin and Orenstein, 1999), and the typical amount of mercury given to infants and toddlers in this manner exceeds government safety limits, according to Neal Halsey of the American Academy of Pediatrics (1999) and William Egan of the Biologics Division of the FDA (1999).
Most vaccines given to children 2 years and under are stored in a solution containing thimerosal, which is 49.6% mercury by weight. Once inside humans, thimerosal (sodium ethylmercurrithio–salicylate) is metabolized to ethylmercury and thiosalicylate (Gosselin et al, 1984). The vaccines mixed with this solution are DTaP, HIB, and Hepatitis B (Egan, 1999).  Thimerosal is not an integral component of vaccines, but is a preservative added to prevent bacterial contamination.  Many vaccine products are available without the thimerosal preservative; however, these alternatives have not been widely used (Egan, 1999). In addition, thimerosal is used during the manufacturing process for a number of vaccines, from which trace amounts are still present in the final injected product (FDA, personal communication; Smith-Kline press release on Hepatitis B, March 31, 2000).
Since at least 1977 clinicians have recognized thimerosal as being potentially dangerous, especially in situations of long term exposure (Haeney et al, 1979; Rohyans et al, 1984; Fagan et al, 1977; Matheson et al, 1980).  For nearly twenty years the US government has also singled out thimerosal as a potential toxin (FDA, 1982).  In response to the Food and Drug Administration (FDA) Modernization Act of 1997, which called for the FDA to review and assess the risk of all mercury containing food and drugs (MMWR, 1999, July 9), the FDA issued a final rule in 1998 stating that over-the-counter drug products containing thimerosal and other mercury forms “are not generally recognized as safe and effective” (FDA, 1998). 
In December 1998 and April 1999, the FDA requested US vaccine manufacturers to provide more information about the thimerosal content in vaccines (MMWR, 1999, July 9); and in July 1999, the CDC asked manufacturers to start removing thimerosal from vaccines and rescheduled the Hepatitus B vaccine so it is given at 9 months of age instead of at birth (CDC, July 1999).  In November 1999, the CDC repeated its recommendation that vaccine manufacturers move to thimerosal-free products (CDC, November 1999).
Importantly, based on the CDC’s own recommended childhood immunization schedule (and excluding any trace amounts), the amount of mercury a typically vaccinated two year old child born in the 1990s would receive is 237.5 micrograms; and a typical six month old might receive 187.5 micrograms (Egan, 1999). 
These amounts equate to 3.53 x 10¹⁷ molecules and 2.79 x 10¹⁷ molecules of mercury respectively (353,000,000,000,000,000 and 279,000,000,000,000,000 molecules). Since thimerosal is injected during vaccinations, the mercury is given intermittently in large, or ‘bolus’, doses:  at birth and at 2, 4, 6, and approximately 15 months (Egan, 1999).  The amount of mercury injected at birth is 12.5 micrograms, followed by 62.5 micrograms at 2 months, 50 micrograms at 4 months, another 62.5 micrograms during the infant’s 6-month immunizations, and a final 50 micrograms at about 15 months (Halsey, 1999).
Although infancy is recognized as a time of rapid neurological development, to the best of our belief and knowledge, there are no published studies on the effect of injected ethylmercury in intermittent bolus doses in infants from birth to six months or to 2 years (Hepatitis Control Report, 1999; Pediatrics, 1999; EPA, 1997, p.6-56).  In contrast, four government agencies have set safety thresholds for daily mercury exposure based on ingested fish or whale meat containing methylmercury.  Two of these guidelines are based on adult values and two are for pregnant women/fetuses (Egan, 1999).  Applying these guidelines to a bolus dose scenario (see Halsey, 1999 for bolus vs. daily dose discussion), the sum of Hg-doses given at 6 months of age or younger, correlated to infant weights, exceed all of the Hg-total guidelines for all infants. 
The 2 month dose is especially high relative to the typical infant body weight.  Halsey (1999) has calculated the 2 month dose to be over 30 times the recommended daily maximum exposure, with babies of the smallest weight category receiving almost three months worth of daily exposures on a single day.
Halsey’s observation is all the more important because even at doses which were not previously thought to be associated with adverse affects, mercury has resulted in some damage to humans (Grandjean et al, 1998).  Given that ethylmercury is equally neurotoxic as methylmercury (Magos et al, 1985), and that injected mercury is more harmful than ingested mercury (EPA, 1997,p.3-55; Diner and Brenner, 1998), the amount of injected ethylmercury given to young children is cause for concern.  The potential for Hg-induced harm is compounded by the special vulnerability of infants (Gosselin et al, 1984).  Mercury, which primarily affects the central nervous system, is most toxic to the developing brain (Davis et al, 1994; Grandjean et al, 1999; Yeates and Mortensen, 1994), and neonates exposed to methyl (organic) mercury have been shown to accumulate significantly more Hg in the brain relative to other tissues than do adults ( EPA, 1997, p.4-1). 
Mercury may also be more likely to enter the infant brain because the blood-brain barrier has not fully closed (Wild & Benzel, 1994).  In addition, infants under 6 months are unable to excrete mercury, most likely due to their inability to produce bile, the main excretion route for organic mercury (Koos and Longo, 1976; Clarkson, 1993).  Bakir et al (1973) have shown that those with the longest half-time of clearance are most likely to experience adverse sequelae, while Aschner and Aschner (1990) have demonstrated that the longer that organic mercury remains in neurons, the more it is converted to its inorganic irreversibly-bound form, which has greater neurotoxicity.

b.   Population Susceptibility
Nearly all children in the United States are immunized, yet only a small proportion of children develop autism.  The NIH (Bristol et al, 1996) estimates the current prevalence of autism to be 1 in 500. 
A pertinent characteristicof mercury is the great variability in its effects by individual.  At the same exposure level of mercury, some will be affected severely, while others will be asymptomatic or only mildly impaired (Dale, 1972; Warkany and Hubbard, 1953; Clarkson, 1997).  Aten-fold difference in sensitivity to the same exposure level has been reported (Koos and Longo, 1976; Davis et al, 1994; Pierce et al, 1972; Amin-Zaki, 1979). 
An example of variability in children is the mercury-induced disease called acrodynia.  In the earlier half of this century, from one in 500 to one in 1000 children exposed to the same chronic, low-dose of mercury in teething powders developed this disorder (Matheson et al, 1980; Clarkson, 1997), and the likelihood of developing the disease“appears to be dominated more by individual susceptibility and possibly age rather than the dose of the mercury” (Clarkson, 1992).  Given the documented inter-individual variability of responses to Hg, and the young age at which exposure occurs, the doses of mercury given concurrently with vaccines are such that only a certain percentage of children will develop overt symptoms, even as other children might have trait irregularities sufficiently mild as to remain unrecognized as having been induced by mercury.

c.   Sex Ratio
Autism is more prevalent among boys than girls, with the ratio generally recognized as approximately 4:1 (Gillberg & Coleman, 1992, p.90).  Mercury studies have consistently shown a greater effect on males than females, except in instances of kidney damage (EPA, 1997).  At the highest doses, both sexes are affected equally, but at lower doses only males are affected.  This is true of mice as well as humans (Sager et al, 1984; Rossi et al, 1997; Clarkson, 1992; Grandjean et al, 1998; McKeown-Eyssen et al, 1983; see also review in EPA, 1997, p.6-50).

d.   Exposure Levels & Autism Prevalence
Perhaps not coincidentally, autism’s initial description and subsequent epidemiological increase mirror the introduction and use of thimerosal as a vaccine preservative.  In the late 1930s, Leo Kanner, an experienced child psychologist and the“discoverer” of autism, first began to notice the type of child he would later label “autistic.”  In his initial paper, published in 1943, he remarked that this type of child had never been described previously:“Since 1938, there have come to our attention a number of children whose condition differs so markedly and uniquely from anything reported so far, that each case merits…a detailed consideration of its fascinating peculiarities.”  All these patients were born in the 1930s.  Thimerosal was introduced as a component of vaccine solutions in the 1930s (Egan, 1999).
Not only does the effect of mercury vary by individual, as noted above, it also varies in a dose-dependent manner, so that the higher the exposure level, the more individuals that are affected.  At higher dose levels, the most sensitive individuals will be more severely impaired, and the less sensitive individuals will be only moderately impaired, and the majority of individuals may still show no overt symptoms (Nielson and Hultman, 1999). 
The vaccination rate, and hence the rate of mercury exposure via thimerosal, has steadily increased since the 1930s.  In 1999 it was the highest ever, at close to 90% or above, depending on the vaccine (CDC, 1999, press release). The rate of autism has increased dramatically since its discovery by Kanner:  prior to 1970, studies showed an average prevalence of 1 in 2000; for studies after 1970, the average rate had doubled to1 in 1000 (Gillberg and Wing, 1999). In 1996, the NIH estimated occurrence to be 1 in 500 (Bristol et al, 1996). 
A large increase in prevalence, yet to be confirmed by stricter epidemiological analysis, appears to be occurring since the mid-1990s, as evidenced by several state departments of education statistics reflecting substantial rises in enrolment of ASD children (California, Florida, Maryland, Illinois, summarized by Yazbak, 1999). These increases have paralleled the increased mercury intake induced by mandatory innoculations:  in 1991, two vaccines, HIB and Hepatitis B, both of which generally include thimerosal as a preservative, were added to the recommended vaccine schedule (Egan, 1999).

e.   Genetic Factors
ASD is one of the most heritable of developmental and psychiatric disorders (Bailey et al, 1996). 
There is 90% concordance in monozygotic twins and a 3-5% risk of autism in siblings of affected probands (Rogers et al, 1999), a rate 50 to 100 times higher than would be expected in the general population (Smalley & Collins, 1996; Rutter, 1996).  From 2 to 10 genes are believed to be involved (Bailey et al, 1996).
Individual differences in susceptibility to mercury are said to arise from genetic factors and these too may be multiple in nature (Pierce et al, 1972; Amin-Zaki, 1979).  They include innate differences in (i) the ability to detoxify heavy metals, (ii) the ability to maintain balanced gut microflora, which can impair detoxification processes, and (iii) immune over-reactivity to mercury(Nielson and Hultman, 1999; Hultman and Nielson, 199; Johansson et al, 1998; Clarkson, 1992; EPA, review 1997, p.3-26). Many autistic children are described as having (i) difficulties with detoxification of heavy metals (Edelson & Cantor, 1998), possiblydue to low glutathione levels (O’Reilly and Waring, 1993), (ii) intestinal microflora imbalances that can impede excretion (Shattock, 1997), and (iii) autoimmune dysfunction (Zimmerman et al, 1993).  These characteristics might be reflective of the underlying “susceptibility genes” that predispose to mercury-induced sequelae and hence to autism.
As noted above, autism family studies show an exceptionally high concordance rate of 90% for identical twins.  Most environmental factors, such as a postnatal viral infection, tend not to be present at exactly the same time or at the same level or rate for each twin.  This would cause a difference in phenotype expression, and thus postnatal environmental influences in general reduce the concordance rate for identical twins. 
However, given the extremely high vaccination rate and the high likelihood of vaccination of one twin at the same time and with the same vaccines as the other twin, mercury-induced autism via vaccination injection, even though it is an environmental factor, would still lead to the high concordance rate seen in twins.
Furthermore, among identical twin pairs, the 90% concordance rate is for the milder phenotype:  if one twin has pure classic autism, there is (i) a 60% chance that the other twin will have pure classic autism; (ii) a 30% chance that the other twin will exhibit some type of impairment falling on the autism spectrum, but with less severe symptoms; and (iii) a 10% chance the other twin will be unimpaired.  The difference in symptom severity among the 40% of monozygotic pairs who do not exhibit classic autism may arise from either (i) a different vaccination history within pairs, or (ii) the tendency of thimerosal to “clump” or be unevenly distributed in solution, so that one twin might receive more or less mercury than the other.  One study found a 62% difference in the mercury concentration of ampoules drawn from the same container of immunoglabulin batches containing thimerosal (Roberts and Roberts, 1979).

f.    Course of Disease
Age of onset: Autism emerges during the same time period as infant and toddler thimerosal injections during vaccinations.  As noted above, the recommended childhood vaccination schedule from 1991 to 1999 has called for injections of thimerosal starting at birth and continuing at 2, 4, 6, and approximately 15 months (Halsey, 1999); a similar schedule occurred prior to this time but for DTP alone.  In the great majority of cases, the  more noticeable symptoms of autism emerge between 6 and 20 months old – and mostly between 12 and 18 months (Gillberg & Coleman, 1992).  Teitelbaum et al (1998), who have claimed the ability to detect subtle abnormalities at the youngest age so far, have observed these abnormalities at 4 months old at the earliest, the exception being a“Moebius mouth” seen at birth in a small number of subjects.
Symptoms of mercury poisoning do not usually appear immediately upon exposure, although in especially sensitive individuals or in cases of excessive exposure they can (Warkany and Hubbard, 1953; Amin-Zaki, 1978).  Rather, there is generally a preclinical“silent stage,” seen in both animals and humans, during which subtle neurological changes are occurring (Mattsson et al, 1981).  The delayed reaction between exposure and overt signs can last from weeks to months to years (Adams et al, 1983; Clarkson, 1992; Fagala & Wigg, 1992; Davis et al, 1994; Kark et al, 1971).  Consequently, mercury given in vaccines before age 6 months would not in most individuals lead to an observable or recognizable disorder, except for subtle signs, prior to age 6-12 months, and for some individuals, symptoms induced by early vaccinal Hg might not emerge until the infant had become a toddler (Joselow et al, 1972).
A few autism researchers have suggested a prenatal onset for autism (Rodier et al, 1997; Bauman & Kemper, 1994), which would preclude a vaccinal-mercury etiology.  Others, however, have evidence that suggest post-natal timings (Bailey, 1998; Courchesne, 1999; Bristol Power, NICHD, Dateline Interview, 1999).
The general consensus at this point is that the timing cannot be determined (Bailey et al, 1996; Bristol et al, 1996); and, further, that there is “little evidence” that prenatal or perinatal events “predict to later autism” (Bristol et al, 1996), even though clustering of adverse effects (suboptimality factors) are associated with autism (Prechtel, 1968; Bryson et al, 1988; Finegan and Quarrington, 1979).  There is also a general agreement that, in the great majority of cases, autistic signs emerge among infants and toddlers who had looked “normal”, developed normally, met major milestones, and had unremarkable pediatric evaluations (Gillberg & Coleman, 1992; Filipek et al, 1999; Bailey et al, 1996), so that autism presents as an obvious deterioration or regression, either before age two or before age three (Baranek, 1999; Bristol Power, NICHD, Dateline Interview, 1999; LeWine, 1999).
It is worthwhile to note that early and intensive educational and behavioral intervention can produce dramatic gains in function, and the gains made by these children “may be somewhat unique among the more severe developmental disabilities” (Rogers, 1996).  This phenomenon further suggests that autism arises from an environmental overlay rather than being purely an organic disease. Additionally, at least one study has reported that “re-education and physical treatment” can improve outcomes in mercurialism (Amin-zaki, 1978).
Emergence of symptoms: The manner in which symptoms emerge in many cases of autism is consistent with a multiple low-dose vaccinal exposure model of mercury poisoning.  From a parent's and pediatrician's perspective, such an individual is a“normal” looking child who regresses or fails to develop after thimerosal administration.  Clinically relevant symptoms generally emerge gradually over many months, although there have been scattered parental reports of sudden onset (Filipek, et al, 1999).  The initial signs, occurring shortly after the first injections, are subtle, suggesting disease emergence, and consist of abnormalities in motor behavior and in sensory systems, particularly touch sensitivity, vision, and numbness in the mouth (excessive mouthing of objects) (Teitelbaum et al, 1998; Baranek, 1999). These signs persist and are followed by parental reports of speech and hearing abnormalities appearing before the child’s second birthday (Prizant, 1996; Gillberg & Coleman, 1992), that is, within several months of when additional and final injections are given.  Finally, in year two, there is a full blossoming of ASD traits and a continuing regression or lack of development, so that the most severe expression of symptoms occurs at approximately 3-5 years of age.
These symptoms then begin to ameliorate (Church & Coplan, 1995; Wing & Attwood, 1987; Paul, 1987). 
The exceptions are the subset of those with regression during adolescence or early adulthood, which may involve onset of seizures and associated neurodegeneration (Howlin, 2000; Paul, 1987; Tuunanen et al, 1996, 1997, 1999).
As in autism, onset of Hg toxicity symptoms is gradual in some cases, sudden in others (Amin-Zaki et al, 1979 & 1978; Joselow et al, 1972; Warkany and Hubbard, 1953).  In the case of organic poisoning, the first signs to emerge are abnormal sensation and motor disturbances; as exposure levels increase, these signs are followed by speech and articulation problems and then hearing deficits (Clarkson, 1992), just like autism. 
Once the mercury source is removed symptoms tend to ameliorate (though not necessarily disappear) except in instances of severe poisoning, which may lead to a progressive course or death (Amin-Zaki et al, 1978). 
As in autism, epilepsy in Hg exposure also predicts a poorer outcome (Brenner & Snyder, 1980).
Long term prognosis: The long term outcomes of ASD and mercury poisoning show the same wide variation.  Autism is viewed as a lifelong condition for most; historically, three-fourths of autistic individuals become either institutionalized as adults or are unable to live independently (Paul, 1987). 
There are, however, many instances of partial to full recovery, in which autistic traits persist in a much milder form or, in some individuals, disappear altogether once adulthood is reached (Rogers, 1996; Church & Coplan, 1994; Szatmari et al, 1989; Rimland 1994; Wing & Attwood, 1987).
Upon exposure, mercury entering the bloodstream tends to accumulate in tissues and organs, primarily the brain (Koos and Long, 1976; Lorscheider et al, 1995).  Once inside tissues, and particularly the brain, mercury will linger for years, as shown on X rays of a poisoned man 22 years after exposure (Gosselin et al, 1984), as well as autopsies of humans with known mercury exposure (Pedersen etal, 1999; Joselow et al, 1972) and primate studies (Vahter et al, 1994).  The continued presence of mercury in organs and the CNS in particualr would explain why autistic symptoms might persist, why researchers such as Zimmerman or Singh would detect an on-going immune reaction, why epilepsy might not emerge until adolescence, or why sulfate transporters in the intestine or kidney might continue to be blocked.
Nevertheless, despite the continued presence of Hg in tissue, the degree of recovery from mercurialism varies greatly.  Even in severe cases, there are reports of full or partial recovery (e.g., Adams et al, 1983; Vroom & Greer, 1972; Amin-Zaki et al, 1978).  In less severe cases, especially those in which exposure occurs early in life, the more severe symptoms may ameliorate over time, but milder impairments remain, especially neurological ones (Feldman, 1982; Yeates & Mortensen, 1994; Amin-Zaki, 1974 & 1978; Mathiesin et al, 1999; Vroom and Greer, 1972; EPA 1997, pp.3-10, 3-14, and 3-75). 
The widevariation in outcome is believed to be due, again, to individual sensitivity to mercury, in this case, the ability of some victims to develop “immunity” or a “tolerance” to Hg even when the metal is still present in tissue (Warkany & Hubbard, 1953).

Course of Disease:
Typical Autism & Ingested Organic Mercury

g.      Thimerosal Interaction with Vaccines
As noted above, for most ASD children symptom onset is gradual, but for a significant minority it is sudden. Additionally, many parents believe there is a connection between their child’s autism and his or her immunizations.  The Cure Autism Now Foundation, for example, reports that half the parents who call its hotline mention such a connection (Portia Iversen, CAN president, personal communication).  The association extends not only to the mercury-containing vaccines – DTP/DTaP, HIB, and Hepatitis B – but also to those without thimerosal, particularly the MMR (Bernard Rimland, president, Autism Research Institute, personal communication).  Parents may describe a variety of post-vaccine scenarios:  a fever followed by a short recovery period and then a more gradual symptom onset; onset of symptoms immediately and suddenly after inoculation with or without fever; or even a mildly impaired child whose condition worsened after vaccination (CAN Parent Advisory Board Internet list; St. John’s Autism Internet list).
While it is possible that any temporal association between vaccination and emergence of autism is due to chance, Warkany and Hubbard, who successfully proved the connection between acrodynia and mercury poisoning to the medical community 50 years ago,offer alternate explanations. 
In their 1953 article in Pediatrics, they made the following points:
(a)                 They noted that high fever accompanied by a rash after mercury administration can be signs of a “typical, acute, mercurial reaction,” and “acrodyniamay follow, immediately or after short intervals, acute idiosyncratic reactions to mercury.” This reaction was independent of hypersensitivity to mercury, as detected from skin tests, as they reported that only 10% of acrodynia victims responded positively to Hg on patch tests.
Thus in ASD, the fevers and deteriorations seen by parents immediately after a thimerosal-containing vaccine injection may be a systemic reaction (and not a hypersensitivity response) to the mercury content, and this reaction may subsequently progress to the emergence of autism, just as topical mercury administration produced fever and then acrodynia over 50 years ago.
(b)                 Warkany and Hubbard provided some tentative observations that the administration of a vaccine, irrespective of whether or not it contains thimerosal, can set off a reaction to any mercuric compound that may also be given to a child, which in the case of acrodynia, would be topical mercury in powders or rinses.  This inter-reactivity might explain the pronounced effects from the MMR among subsequently-diagnosed autistic children:
“[One patient] underwent a fourteen day course of antirabies injections six weeks before outbreak of acrodynia. Ten days after completion of the therapy she was treated with ammoniated mercury ointment and subsequently acrodynia developed...[In another case] antirabies treatment preceded the disease by three months. In several children various immunization procedures preceded the onset of acrodynia in addition to [topical] mercurial exposure. This could be purely coincidental or the vaccination material may play a role as an accessory factor. It is noteworthy that many vaccines andsera contain small amounts of mercury as preservatives which are injected together with the biologic material.
These small amounts of mercurial compounds could act as sensitizing substances. In several instances vaccination against smallpox preceded the development of acrodynic symptoms, and some patients were exposed to bismuth, arsenic, lead, and antimony in addition to mercury.
Such observations deserve attention.”
(c)                 Finally, these two researchers observed that some individuals would react to mercury and then, upon re-exposure, not show any effects, i.e., they had acquired an unexplained tolerance to it. In other cases, Hg sensitivity would be maintained. Rarely, though, would reactivity occur with the first dose: “more often the patient tolerates several” before the reaction occurs.
“The organism can harbor appreciable amounts of mercury while remaining in perfect health, and then, for unknown reasons, these innocuous stores of mercury become toxic. It seems in such cases as if the barriers which held the mercury in check break down without provocation, or as if the mercury had been converted from a nontoxic to a toxic form...”
In ASD, this delayed sensitivity would explain why some might develop autism later, not after the first few vaccines, andit would also explain in part why the more vaccines that are given, the more likely it is that a given individual will develop a reaction since there are more “sensitizing” opportunities.  Importantly, in susceptible individuals, the reactions described by Warkany and Hubbard are likely to occur if mercury's presence occurred via injected thimerosal.

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