Thimerosal has never undergone even one modern safety test. It was developed in 1927 and patented by Eli Lilly in 1928. It was first tested on small animals and killed a variety of mice, rabbits and chicks. After the animals died from exposure to Thimerosal, the decision was made to administer it to 22 patients suffering from bacterial meningitis during an epidemic in Indianapolis, Indiana in 1929.
Of the 22 persons given Thimerosal, all died, most within a day or two of administration. The doctor overseeing the trial, on stipend from Eli Lilly, declared that the patients had all died of meningitis and that Thimerosal was not observed to have caused any problem when administered to his patients. With that declaration, and a subsequent one by Eli Lilly staff that Thimerosal has a low order of toxicity for man, even though it killed small animals, Thimerosal was introduced into the drug supply. Yet, despite warnings in the published scientific literature that Thimerosal was toxic, and despite opposition to its use in every decade since, Thimerosal has remained in the drug supply. Ethyl Mercury Exposure Levels Based on Methyl Mercury Guidelines
A single Thimerosal-preserved flu vaccine contains 25 micrograms of ethylmercury. If the EPA RfD for ingested methylmercury is applied to this injected ethylmercury figure, an individual would have to weigh more than 250 kilograms (551 pounds) for the 25 microgram exposure to be considered safe.
Ethyl mercury is 50 times more toxic than methyl mercury (Guzzi et al, 2012) and twice as persistent in the brain (Burbacher et al, 2005). Both ethyl and methyl mercury cause DNA damage or impair DNA synthesis (Burke et al. 2006; Sharpe et al. 2012; Wu et al. 2008).
Both cause oxidative stress/creation of reactive oxygen species (Dreiem and Seegal 2007; Garg and Chang 2006; Myhre et al. 2003; Sharpe et al. 2012; Yin et al. 2007).
Both decrease glutathione activity, thus providing less protection from the oxidative stress caused by MeHg and EtHg (Carocci et al. 2014; Ndountse and Chan (2008); Choi et al. 1996; Franco et al. 2006; Mori et al. 2007; Muller et al. 2001; Ndountse and Chan 2008; Wu et al. 2008).
Both cause effects on cell division by damaging the spindle apparatus during mitosis (Burke et al. 2006; Castoldi et al. 2000; Gribble et al. 2005; Kim et al. 2007; Ou et al. 1999b; Machaty et al. 1999; Rodier et al. 1984).
Both MeHg and EtHg bind to the amino acid cysteine (Clarkson 1995; Wu et al. 2008).
Both MeHg and EtHg strongly inhibit the reacylation of arachidonic acid, thus inhibiting the reincorporation of this fatty acid into membrane phospholipids (Shanker et al. 2002; Verity et al. 1994; Zarini et al. 2006).
Both cause an increase in NOS, causing an overproduction of NO (Chen et al. 2003; Chuu et al. 2001; Shinyashiki et al. 1998).
Both disrupt glutamate homeostasis (Farina et al. 2003a, b; Manfroi et al. 2004; Mutkus et al. 2005; Yin et al. 2007).
Both alter intracellular calcium homeostasis (Elferink 1999; Hare et al. 1993;Kang et al. 2006; Limke et al. 2004b; Machaty et al. 1999; Marty and Atchison1997; Minnema et al. 1987; Peng et al. 2002; Sayers et al. 1993; Sirois and Atchison, 2000; Szalai et al. 1999; Tornquist et al. 1999; Zarini et al. 2006).
Both cause effects on receptor binding/neurotransmitter release involving one or more transmitters (Basu et al. 2008; Coccini et al. 2000; Cooper et al. 2003; Fonfria et al. 2001; Ida-Eto et al. 2011; Ndountse and Chan 2008; Yuan and Atchison 2003).
https://www.ncbi.nlm.nih.gov/books/NBK223724/
