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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
http://www.vaccinationnews.com/DailyNews/July2001/AutismUniqueMercPoison.htm 2/5/2004
Autism: A Unique Type of Mercury Poisoning Page 38 of 62
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 to 1 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 [ Pobierz całość w formacie PDF ]

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