The document examines the health impacts of vaccine preservatives, particularly aluminum, highlighting controversies around vaccine safety and efficacy. It discusses the potential links between aluminum exposure and neurodevelopmental disorders, as well as its biological effects on various physiological systems. The review also evaluates research on aluminum's role in Alzheimer's disease and its toxicokinetics, emphasizing the need for further studies to understand its impact on human health.

1. Vaccine
Preservatives & Health Impact
Kimmer Collison-Ris
MSN, FNP-BC, WOCN, MS CAM

2. Abstract
• Vaccines are used to decrease disease in
humans and have been used for the past 100
years
• Controversy exists re: their necessity as
disease is less prevalent in developed nations
due to increased health & hygiene practices
• Many proponents say vaccine use is necessary
for public good
• Opponents question their safety & efficacy
• Many preservatives used in vaccines have links
to poor health outcomes & increased
mortality
• Does a reasonable doubt re: their safety in
certain populations exist?
• Could some of these preservatives increase
genetic mutations, autoimmune dysfunction,
& neurodevelopmental disorders in some
populations?
• Is the rising incidence of neuro-developmental
disorders related to a cumulative effect of
increased vaccines, multiple vaccine
ingredients, gene varients/susceptibility and
auto immune dysfunction?

4. Aluminum
• Aluminum is a trivalent cation found in its ionic form in most kinds of
animal and plant tissues and in natural waters everywhere.[1]
• It is the third most prevalent element and the most abundant metal in
the earth's crust, representing approximately 8% of total mineral
components.[2]
• Due to its reactivity, aluminum in nature is found only in combination
with other elements.
• Approximately 95% of an aluminum load becomes bound to transferrin
and albumin intravascularly and is then eliminated renally.
• In healthy subjects, only 0.3% of orally administered aluminum is
absorbed via the GI tract, and the kidneys effectively eliminate
aluminum from the human body.
• Only when the GI barrier is bypassed, such as by intravenous infusion or
in the presence of advanced renal dysfunction, does aluminum have the
potential to accumulate.
• example, IV infused aluminum, 40% is retained in adults and up to 75% is
retained in neonates.[4]
• Aluminum is absorbed from the GI tract in the form of oral phosphate-
binding agents (aluminum hydroxide), parenterally via immunizations,
via dialysate on patients on dialysis or total parenteral nutrition (TPN)
contamination, via the urinary mucosa through bladder irrigation, and
transdermally in antiperspirants. Lactate, citrate, and ascorbate all
facilitate GI absorption.
• If a significant aluminum load exceeds the body's excretory capacity, the
excess is deposited in various tissues, including bone, brain, liver, heart,
spleen, and muscle. This accumulation causes morbidity and mortality
through various mechanisms.[2]
– Jose F Bernardo (2014). Aluminum Toxicity. Medscape.
http://emedicine.medscape.com/article/165315-overview

5. Aluminum
• Injections of Al to animals produce behavioral,
neuropathological and neurochemical changes
that partially model Alzheimer’s Disease (AD).
• Aluminum has the ability to produce
neurotoxicity by many mechanisms.
– Excess, insoluble amyloid beta protein (A beta)
contributes to AD.
– Aluminum promotes formation and
accumulation of insoluble A beta and
hyperphosphorylated tau. To some extent, Al
mimics the deficit of cortical cholinergic
neurotransmission seen in AD.
– Al increases Fe-induced oxidative injury.
– The toxicity of Al to plants, aquatic life and
humans may share common mechanisms,
including disruption of the inositol phosphate
system and Ca regulation.
– Facilitation of Fe-induced oxidative injury and
disruption of basic cell processes may mediate
primary molecular mechanisms of Al-induced
neurotoxicity.

6. Aluminum
Abstract
• Aluminum is the most widely distributed metal in the environment
and is extensively used in modern daily life. Aluminum enters into
the body from the environment and from diet and medication.
However, there is no known physiological role for aluminum within
the body and hence this metal may produce adverse physiological
effects. The impact of aluminum on neural tissues is well reported
but studies on extraneural tissues are not well summarized. In this
review, the impacts of aluminum on humans and its impact on
major physiological systems are summarized and discussed. The
neuropathologies associated with high brain aluminum levels,
including structural, biochemical, and neurobehavioral changes,
have been summarized. In addition, the impact of aluminum on the
musculoskeletal system, respiratory system, cardiovascular system,
hepatobiliary system, endocrine system, urinary system, and
reproductive system are discussed. [1]

7. Aluminum…
Abstract
• The fact that aluminium (Al) and lead (Pb) are both toxic metals to
living organisms, including human beings, was discovered a long
time ago. Even when Al and Pb can reach and accumulate in almost
every organ in the human body, the central nervous system is a
particular target of the deleterious effects of both metals. Select
human population can be at risk of Al neurotoxicity, and Al is
proposed to be involved in the etiology of neurodegenerative
diseases. Pb is a widespread environmental hazard, and the
neurotoxic effects of Pb are a major public health concern. In spite
of the numerous efforts and the accumulating evidence in this area
of research, the mechanisms of Al and Pb neurotoxicity are still not
completely elucidated. This review will particularly address the
involvement of oxidative stress, membrane biophysics alterations,
deregulation of cell signaling, and the impairment of
neurotransmission as key aspects involved Al and Pb neurotoxicity.
[2]

8. Aluminum…
Abstract
• The strength of the evidence implicating aluminium as an important factor in the dementia of
Alzheimer's disease (AD) is reviewed. We submit that the weight of the epidemiological and
biological arguments is considerable. While a complete understanding has not been achieved, we
recommend lowering aluminium exposure in municipal drinking water to below 50 μg/l in at
least the province of Ontario. The Ministry of Energy and the Environment of Ontario maintains a
drinking water surveillance programme which has provided a database for more than 10 years.
This database has permitted assessment of the relative risk for AD using four independent
measures of disease prevalence: 1. weighted residential history as a measure of exposure in
autopsy-verified AD cases and controls; 2. first admission hospital discharge diagnoses of AD and
controls; 3. death certificate rates for AD and presenile dementia; 4. impairments in cognitive
function in elderly males. Taken together, many of the criticisms applied to epidemiological
studies conducted elsewhere and reaching similar conclusions have been met. A vast
experimental database on aluminium neurotoxicity, rapid advances in the understanding of the
molecular basis of AD, and comparison studies between human brains exposed to chronic low
dose aluminium exposure secondary to renal failure and AD, lend strong biological support to the
conclusions reached by the epidemiological studies. The factors initiating AD, how aluminium
gains access to the brain in AD, and the relative contributions of food, pharmaceuticals and skin
absorption, remain unknown. While a full understanding is not in hand, the devastating nature of
the disease, the lack of an effective treatment or prevention and the high cost to the health care
system, together with the human costs, weighed against the relative cost of moderately reducing
drinking water aluminium concentration to reduce exposure indicate that action is both
reasonable and timely.[3]

9. Aluminum…
• Abstract
• Aluminium toxicity may act in two distinct ways, depending on the level of contamination. Relatively low
aluminium levels from environmental origin (mainly from drinking water poor in silica) have been shown
to be statistically associated with senile dementias of Alzheimer type (chronic intoxication). In addition,
high aluminium therapeutic levels (from phosphate binders, antacids, …) can induce different, more
rapid, symptoms (acute intoxication). In all cases, aluminium toxicity is largely conditioned by aluminium
bioavailability, which in turn hinges upon aluminium coordination chemistry in vivo. The highly
polarising power of the Al3+ ion dictates its particular affinity for oxygen donors that abound in essential
biomolecules and dietary substances. The influence of these substances on aluminium bioavailability,
metabolism and toxicity can be assessed through animal models. However, understanding the
mechanisms through which aluminium–ligand interactions may influence physiological processes on the
molecular level requires a knowledge of the speciation of the metal in the main biofluids. Access to this
critical information can a priori be gained through direct experimental analysis of relevant biological
samples. It is in this way that aluminium protein-bound fractions, involving essentially transferrin, have
been identified, but using such a direct approach to analyse the ultrafiltrable pool of the metal is a
virtually insurmountable task, hence the necessity to have recourse to computer-aided speciation
techniques based on simulation models. Following a previous review published in this journal on nearly
the same topic [Coord. Chem. Rev. 149 (1996) 241], this article updates the knowledge available on both
biological and chemical fronts. After a review of experimental investigations led on the roles of
aluminium–ligand interactions in aluminium bioavailability, metabolism and toxicity, contributions of
experimental and computer-aided speciation to the understanding of the relevant processes are then
analysed. Significant progress has been made in the diverse aspects of the biological field, in particular,
in relation to the role of dietary ligands on aluminium gastrointestinal absorption, excretion and tissue
distribution. Also, very intensive research has been pursued on the design of new aluminium
sequestering agents to treat acute intoxications. Some progress has also been made on the chemical
side relative to computer-aided speciation applications to gastrointestinal and blood plasma conditions.
However, the gap is increasing between the large body of observations made by physiologists and
toxicologists and the few data painfully obtained by coordination chemists to interpret the relevant
phenomena.[4]

10. Aluminum…
Abstract
• Information concerning developmental aluminum (Al) toxicity is available from
clinical studies and from animal testing. An Al toxicity syndrome including
encephalopathy, osteomalacia, and anemia has been reported in uremic children
receiving dialysis. In addition, some components of the syndrome, particularly
osteomalacia, have been reported in nondialyzed uremic children receiving Al-
based phosphate binders, nonuremic infants receiving parenteral nutrition with Al-
containing fluids, and nonuremic infants given high doses of Al antacids. The
number of children in clinical populations that are at risk of Al toxicity is not known
and needs to be determined. Work in animal models (rats, mice, and rabbits)
demonstrates that Al is distributed transplacentally and is present in milk. Oral Al
administration during pregnancy produces a syndrome including growth
retardation, delayed ossification, and malformations at doses that also lead to
reduced maternal weight gain. The severity of the effects is highly dependent on
the form of Al administered. In the postnatal period, reduced pup weight gain and
effects on neuromotor development have been described as a result of
developmental exposures. The significance of these findings for human health
requires better understanding of the amount and bioavailability of Al in food,
drinking water, and medications and from sources unique to infants and children
such as breast milk, soil ingestion, and medications used specifically by pregnant
women and children. We also need a better understanding of the unique
biological actions of Al that may occur during developmental periods, and unique
aspects of the developing organism that make it more or less susceptible to Al
toxicity.[5]

11. Aluminum…
Abstract
• Aluminium is a serious environmental toxicant and is inimical to biota.
Omnipresent, it is linked with a number of disorders in man including
Alzheimer's disease, Parkinson's dementia and osteomalacia. Evidence
supporting aluminium as an aetiological agent in such disorders is not
conclusive and suffers principally from a lack of consensus with respect to
aluminium's toxic mode of action. Obligatory to the elucidation of toxic
mechanisms is an understanding of the biological availability of
aluminium. This describes the fate of and response to aluminium in any
biological system and is thus an important influence of the toxicity of
aluminium. A general theme in much aluminium toxicity is an accelerated
cell death. Herein mechanisms are described to account for cell death
from both acute and chronic aluminium challenges. Aluminium
associations with both extracellular surfaces and intracellular ligands are
implicated. The cellular response to aluminium is found to be biphasic
having both stimulatory and inhibitory components. In either case the
disruption of second messenger systems is observed and GTPase cycles
are potential target sites. Specific ligands for aluminium at these sites are
unknown though are likely to be proteins upon which oxygen-based
functional groups are orientated to give exceptionally strong binding with
the free aluminium ion.[6]

12. Aluminum…
• Abstract
• Aluminum in the form of aluminum hydroxide, aluminum
phosphate or alum has been commonly used as an adjuvant in
many vaccines licensed by the US Food and Drug Administration.
Chapter 21 of the US Code of Federal Regulations [610.15(a)] limits
the amount of aluminum in biological products, including vaccines,
to 0.85 mg/dose. The amount of aluminum in vaccines currently
licensed in the US ranges from 0.85–0.125 mg/dose. Clinical studies
have demonstrated that aluminum enhances the antigenicity of
some vaccines such as diphtheria and tetanus toxoids. Moreover,
aluminum-adsorbed diphtheria and tetanus toxoids are distinctly
more effective than plain fluid toxoids for primary immunization of
children. There is little difference between plain and adsorbed
toxoids for booster immunization. Aluminum adjuvants have a
demonstrated safety profile of over six decades; however, these
adjuvants have been associated with severe local reactions such as
erythema, subcutaneous nodules and contact hypersensitivity. [7]

13. Aluminum…
Abstract
• This MiniReview updates and expands the MiniReview of aluminium toxicokinetics
by Wilhelm et al. published by this journal in 1990. The use of 26Al, analyzed by
accelerator mass spectrometry, now enables determination of Al toxicokinetics
under physiological conditions. There is concern about aluminium in drinking
water. The common sources of aluminium for man are reviewed. Oral Al
bioavailability from water appears to be about 0.3%. Food is the primary common
source. Al bioavailability from food has not been adequately determined.
Industrial and medicinal exposure, and perhaps antiperspirant use, can
significantly increase absorbed aluminium. Inhalation bioavailability of airborne
soluble Al appears to be about 1.5% in the industrial environment. Al may
distribute to the brain from the nasal cavity, but the significance of this exposure
route is unknown. Systemic Al bioavailability after single underarm antiperspirant
application may be up to 0.012%. All intramuscularly injected Al, e.g. from
vaccines, may eventually be absorbed. Al distributes unequally to all tissues.
Distribution and renal excretion appear to be enhanced by citrate. Brain uptake of
Al may be mediated by Al transferrin and Al citrate complexes. There appears to be
carrier-mediated efflux of Al citrate from the brain. Elimination half-lives of years
have been reported in man, probably reflecting release from bone. Al elimination
is primarily renal with ≤2% excreted in bile. The contribution of food to absorbed
Al needs to be determined to advance our understanding of the major
components of Al toxicokinetics. [8]

14. Mercury
• Mercury occurs in 3 different forms –
– elemental
– metallic,
– inorganic
– organic
• each with their own unique, toxicological characteristics and
primary sources of exposure
• Metallic mercury
– insoluble in water
– dissolves inorganic, lipophilic solvents
– found in dental amalgams, thermometers, electrical
switching and pressure-sensing devices, gauges, vacuum
pumps, etc.
– only metal that is in a liquid state at room temperature and
vaporizes easily.
– mercury vapor crosses the blood-brain barrier, where it
accumulates in the central nervous system (CNS), and
damages brain cells, particularly sensory and motor neurons
[2]
• Elemental mercury
– accumulates in the brain, kidneys, lungs and fatty tissues,
where it causes cellular dysfunction and acute and chronic
inflammation.
– poorly absorbed from the gastrointestinal (GI) tract
– Serious danger arises from exposure to mercury vapor.

15. Influencing Mercury Affects Factors
• Mercury exists in three chemical forms; each w/specific effects on
human health
– 1. Methylmercury
– 2. Elemental mercury
– 3. Other mercury compounds (inorganic and organic)
• Mercury poisoning symptoms are systemic; affecting every body
system
• Mercury overload inhibits the immune system causing other
diseases
• The severity of health effects re: mercury exposure include:
– the chemical form of mercury
– the dose
– the age of the person exposed (fetus most susceptible)
– duration of exposure;
– route of exposure
• inhalation, ingestion, dermal contact…
– health of the person exposed

16. Mercury
• For centuries, mercury was an essential part of many different medicines, such as diuretics, antibacterial
agents, antiseptics, and laxatives.
• Mercury in any form is poisonous, with mercury toxicity most commonly affecting the neurologic,
gastrointestinal (GI) and renal organ systems. Poisoning can result from mercury vapor inhalation, mercury
ingestion, mercury injection, and absorption of mercury through the skin. (See Etiology and Prognosis.)
• Mercury has 3 forms:
• (1) elemental mercury, (2) inorganic salts, and (3) organic compounds.
• Perhaps the most deadly form of mercury is methylmercury. Only 2-10% of the ingested mercury is
absorbed from the gut, and ingested elemental mercury is not absorbed at all; however, 90% of any
methylmercury ingested is absorbed into the bloodstream from the GI tract.
• In Wilson's classic textbook of neurology, published in 1940, Wilson concurred with Charcot's attribution of
tremors to mercury poisoning, but also described mercury-induced cognitive impairments, such as
inattention, excitement, and hallucinosis.[2]
• Severe poisoning eventually causes the patient to lie in a mute, semirigid posture that is broken only by
episodes of crying or primitive reflexive movements. (See Presentation.)
• Babies exposed in utero are the most severely affected. They are affected by low birth weight, seizure
disorders, profound developmental delay, incomplete visual loss (including tunnel vision) or total blindness,
and hearing loss.
• Neurologic damage in the form of diffuse and widespread neuronal atrophy is most severe in patients
exposed in utero. Long-term studies may indicate that even prenatal exposure at low concentrations can
cause subtle, but detectable, decrements in the areas of motor function, language, and memory.
• Children so affected may have long-term stigmata, including motor impairment, visual loss, hearing loss,
developmental delay, and seizure disorders.
– David A Olson (2014). Mercury Poisoning. Medscape. http://emedicine.medscape.com/article/1175560-overview

17. Mercury Exposure sx…
• Elemental mercury vapor symptoms:
– Constitutional: weight loss; anorexia or loss of appetite; anemia; drowsiness; insomnia;
excessive perspiration; cold, clammy skin, especially of the hands and feet;
– EENT: dizziness, tinnitus or noises in ears; dim or double vision; hearing loss;
– Mouth/Dental: bleeding gums; loosening of teeth; excessive salivation; halitosis or foul
breath; metallic taste in the mouth; leukoplakia or white patches of the oral mucosa;
gingivitis; stomatitis; ulceration of gingiva, palate and tongue; burning sensation in mouth
and throat;
– Resp: hypoxia (poor oxygenation of tissues); persistent cough; shallow and irregular
breathing; emphysema; asthma; rhinitis; sinusitis; allergies;
– GI: abdominal cramps; constipation or diarrhea; colitis;
– CV: arrhythmias (bradycardia, tachycardia); feeble and irregular pulse; alterations in blood
pressure; chest pain or pressure;
– Endo: subnormal body temperature; joint pains; Musk: alveolar (jaw) bone loss; muscle
weakness; fatigue;
– Blood/Lymph: lymphadenopathy or swollen glands, especially in the neck; peripheral
edema or swelling of limbs;
– Neuro: fine tremors of the hands, feet, eyelids, lips and tongue; parasthesias or abnormal,
unpleasant sensations; chronic or frequent headaches; short- and long-term memory loss;
– Psych: hallucinations; poor concentration; intellectual decline; irritability; fits of anger;
depression; anxiety or nervousness; shyness or timidity; loss of self-confidence;

18. Pediatric Mercury Exposure Manifestations
• Common neurological symptoms that occur in children are:
– decreased eye contact,
– flat affect,
– repeating certain actions over and over again,
– not responding to their name,
– not looking at an object that is being pointed at by another,
– poor concentration or attention,
– sensitivity to sensory stimulation.
• Common language or speech symptoms of mercury poisoning:
– loss of speech,
– delayed speech decreased understanding and articulating words,
– remembering certain words.
• Common are social problems:
– withdrawal,
– being irritated,
– aggressive behavior,
– night terrors and
– other sleep problems,
– mood swings.
• other symptoms include
– auto-immune disorders such as
– multiple sclerosis,
– juvenile diabetes,
– asthma,
– chromic ear infections,
– decreased immunity
• mercury can be a key trigger which sets these disorders in motion

19. Mercury…
• Abstract
• Today the most widespread human exposures to mercury are to
mercury vapor emitted from amalgam tooth fillings, to
ethylmercury as a preservative in vaccines, and to methylmercury in
edible tissues of fish. This review will focus on the mechanisms of
transport of these three species of mercury. All three species are
freely moveable throughout the body. Inhaled vapor in view of its
physical properties as an uncharged atomic gas is believed to be
transported by passive diffusion. Methylmercury and ethylmercury
also move freely in the body. Methylmercury, and presumably its
closely related chemical cousin ethylmercury, cross cell membranes
as complexes with small molecular weight thiol compounds,
entering the cell in part as a cysteine complex on the large neutral
amino acid carriers and exiting the cell in part as a complex with
reduced glutathione on endogenous carriers. The implications of
these mechanisms with regard to biological monitoring are
discussed.[9]

20. Mercury…
Abstract
• OBJECTIVES. Thimerosal is a mercurial preservative that was widely used in multidose
vaccine vials in the United States and Europe until 2001 and continues to be used in many
countries throughout the world. We conducted a pharmacokinetic study to assess blood
levels and elimination of ethyl mercury after vaccination of infants with thimerosal-
containing vaccines.
• METHODS. Blood, stool, and urine samples were obtained before vaccination and 12 hours
to 30 days after vaccination from 216 healthy children: 72 newborns (group 1), 72 infants
aged 2 months (group 2), and 72 infants aged 6 months (group 3). Total mercury levels were
measured by atomic absorption. Blood mercury pharmacokinetics were calculated by
pooling the data on the group and were based on a 1-compartment first-order
pharmacokinetics model.
• RESULTS. For groups 1, 2, and 3, respectively, (1) mean ± SD weights were 3.4 ± 0.4, 5.1 ±
0.6, and 7.7 ± 1.1 kg; (2) maximal mean ± SD blood mercury levels were 5.0 ± 1.3, 3.6 ± 1.5,
and 2.8 ± 0.9 ng/mL occurring at 0.5 to 1 day after vaccination; (3) maximal mean ± SD stool
mercury levels were 19.1 ± 11.8, 37.0 ± 27.4, and 44.3 ± 23.9 ng/g occurring on day 5 after
vaccination for all groups; and (4) urine mercury levels were mostly nondetectable. The
blood mercury half-life was calculated to be 3.7 days and returned to prevaccination levels
by day 30.
• CONCLUSIONS. The blood half-life of intramuscular ethyl mercury from thimerosal in
vaccines in infants is substantially shorter than that of oral methyl mercury in adults.
Increased mercury levels were detected in stools after vaccination, suggesting that the
gastrointestinal tract is involved in ethyl mercury elimination. Because of the differing
pharmacokinetics of ethyl and methyl mercury, exposure guidelines based on oral methyl
mercury in adults may not be accurate for risk assessments in children who receive
thimerosal-containing vaccines.

21. Mercury…
Abstract:
• Thimerosal is a preservative that has been used in manufacturing vaccines since
the 1930s. Reports have indicated that infants can receive ethylmercury (in the
form of thimerosal) at or above the U.S. Environmental Protection Agency
guidelines for methylmercury exposure, depending on the exact vaccinations,
schedule, and size of the infant. In this study we compared the systemic
disposition and brain distribution of total and inorganic mercury in infant monkeys
after thimerosal exposure with those exposed to MeHg. Monkeys were exposed to
MeHg (via oral gavage) or vaccines containing thimerosal (via intramuscular
injection) at birth and 1, 2, and 3 weeks of age. Total blood Hg levels were
determined 2, 4, and 7 days after each exposure. Total and inorganic brain Hg
levels were assessed 2, 4, 7, or 28 days after the last exposure. The initial and
terminal half-life of Hg in blood after thimerosal exposure was 2.1 and 8.6 days,
respectively, which are significantly shorter than the elimination half-life of Hg
after MeHg exposure at 21.5 days. Brain concentrations of total Hg were
significantly lower by approximately 3-fold for the thimerosal-exposed monkeys
when compared with the MeHg infants, whereas the average brain-to-blood
concentration ratio was slightly higher for the thimerosal-exposed monkeys (3.5 ±
0.5 vs. 2.5 ± 0.3). A higher percentage of the total Hg in the brain was in the form
of inorganic Hg for the thimerosal-exposed monkeys (34% vs. 7%). The results
indicate that MeHg is not a suitable reference for risk assessment from exposure
to thimerosal-derived Hg. Knowledge of the toxicokinetics and developmental
toxicity of thimerosal is needed to afford a meaningful assessment of the
developmental effects of thimerosal-containing vaccines. [11]

22. Mercury
Abstract
• Based on in vitro studies and short-term in vivo studies, all mercurials
were for a long time considered as prototypic immunosuppressive
substances. Recent studies have confirmed that organic mercurials such as
methyl mercury (MeHg) and ethyl mercury (EtHg) are much more potent
immunosuppressors than inorganic mercury (Hg). However, Hg interacts
with the immune system in the presence of a susceptible genotype to
cause immunostimulation, antinucleolar antibodies targeting fibrillarin,
and systemic immune-complex (IC) deposits, a syndrome called Hg-
induced autoimmunity (HgIA). Recent studies in mice with a susceptible
genotype has revealed that the immunosuppressive effect of MeHg and
EtHg will within 1–3 weeks be superseded by immunostimulation causing
an HgIA-like syndrome. At equimolar doses of Hg, MeHg has the weakest
immunostimulating, autoimmunogen, and IC-inducing effect, while the
effect of thimerosal is similar to that of inorganic mercury. The
immunosuppression is caused by the organic mercurials per se. Since they
undergo rapid transformation to inorganic Hg, studies are being
undertaken to delineate the importance of the organic substances per se
and the newly formed inorganic Hg for induction of autoimmunity.[12]

23. Mercury…
Abstract
• Inorganic mercury may aggravate murine systemic autoimmune diseases which are either spontaneous
(genetically determined) or induced by non-genetic mechanisms. Organic mercury species, the dominating
form of mercury exposure in the human population, have not been examined in this respect. Therefore, ethyl
mercury in the form of thimerosal, a preservative recently debated as a possible health hazard when present
in vaccines, was administered in a dose of 0.156–5 mg/L drinking water to female (NZB × NZW)F1 (ZBWF1)
mice. These mice develop an age-dependent spontaneous systemic autoimmune disease with high mortality
primarily due to immune-complex (IC) glomerulonephritis. Five mg thimerosal/L drinking water (295 μg Hg/kg
body weight (bw)/day) for 7 weeks induced glomerular, mesangial and systemic vessel wall IC deposits and
antinuclear antibodies (ANA) which were not present in the untreated controls. After 22–25 weeks, the
higher doses of thimerosal had shifted the localization of the spontaneously developing renal glomerular IC
deposits from the capillary wall position seen in controls to the mesangium. The altered localization was
associated with less severe histological kidney damage, less proteinuria, and reduced mortality. The effect
was dose-dependent, lower doses having no effect compared with the untreated controls. A different effect
of thimerosal treatment was induction of renal and splenic vessel walls IC deposits. Renal vessel wall deposits
occurred at a dose of 0.313–5 mg thimerosal/L (18–295 μg Hg/kg bw/day), while splenic vessel wall deposits
developed also in mice given the lowest dose of thimerosal, 0.156 mg/L (9 μg Hg/kg bw/day). The latter dose
is 3- and 15-fold lower than the dose of Hg required to induce vessel wall IC deposits in genetically
susceptible H-2s mice by HgCl2 and thimerosal, respectively. Further studies on the exact conditions needed
for induction of systemic IC deposits by low-dose organic mercurials in autoimmune-prone individuals, as well
as the potential effect of these deposits on the vessel walls, are warranted.[13]

24. Mercury…
Abstract
• Mercury has long been recognised as toxic, principally in relation to its effects on
humans following acute or prolonged high-level occupational exposures and, in the
latter half of the last century, from a number of environmental incidents. Recognised
target organs are the kidneys, central nervous system and thyroid glands. Recently
concern has grown about the potential risks to the human population from current
background environmental levels, leading bodies such as the World Health Organisation
to call for the reduction or, wherever possible, elimination of the use of mercury. This
review considers the strength of the epidemiological evidence on the effects of
prolonged low-level exposure to the various forms of mercury.
• The limited research base suggests that several of the potential targets of long-term
environmental exposure to mercury are similar to those occurring from occupational
exposure including the renal, cardiovascular and immune systems. However, the
evidence also suggests that, particularly in the case of organic mercury compounds, the
most sensitive endpoint is central nervous system toxicity, especially in relation to
exposure during the in utero period and childhood. It also appears that those human
populations which have traditionally consumed diets high in seafoods are at greatest
risk. While the extent of risk to the general population that may arise from existing
environmental exposure levels appears limited, this conclusion is based on an
incomplete dataset and therefore the general consensus view that exposure to mercury
in its various forms should be minimised where practical, appears to be justified. A
number of potential areas of further research are suggested as being pre-requisite to
the development of a more rigorous risk assessment. [17]

25. Mercury
Abstract
• Humans may be exposed to organic forms of mercury by either inhalation,
oral, or dermal routes, and the effects of such exposure depend upon both
the type of mercury to which exposed and the magnitude of the exposure.
In general, the effects of exposure to organic mercury are primarily
neurologic, while a host of other organ systems may also be involved,
including gastrointestinal, respiratory, hepatic, immune, dermal, and renal.
While the primary source of exposure to organic mercury for most
populations is the consumption of methylmercury-contaminated fish and
shellfish, there are a number of other organomercurials to which humans
might be exposed. The antibacterial and antifungal properties of
organomercurials have resulted in their long use as topical disinfectants
(thimerosal and merbromin) and preservatives in medical preparations
(thimerosal) and grain products (both methyl and ethyl mercurials).
Phenylmercury has been used in the past in paints, and dialkyl mercurials
are still used in some industrial processes and in the calibration of certain
analytical laboratory equipment. The effects of exposure to different
organic mercurials by different routes of exposure are summarized in this
article. [15]

26. Mercury
Abstract
• Background: Different chemical forms of mercury occur naturally in human milk.
The most controversial aspect of early post-natal exposure to organic mercury is
ethylmercury (EtHg) in thimerosal-containing vaccines (TCV) still being used in
many countries. Thus exclusively breastfed infants can be exposed to both, fish
derived methylmercury (MeHg) in maternal diets and to EtHg from TCV. The aim of
the study is to evaluate a new analytical method for ethyl and methyl mercury in
hair samples of breastfed infants who had received the recommended schedule of
TCV.
• Methods: The hair of infants (< 12 months) that had been exposed to TCV
(Hepatitis B and DTaP) was analysed. A method coupling isothermal gas
chromatography with cold-vapor atomic fluorescence spectrometry was used for
MeHg which can also speciate EtHg in biological matrices.
• Results: In 20 samples of infants' hair, all but two samples showed variable
amounts of MeHg (10.3 to 668 ng/g), while precise and reliable concentrations of
EtHg (3.7 to 65.0 ng/g) were found in 15 of the 20 samples. A statistically
significant inverse association (r = − 05572; p = 0.0384) was found between hair-
EtHg concentrations and the time elapsed after the last TCV shot.
• Conclusions: The analytical method proved sensitive enough to quantify EtHg in
babies' hair after acute exposure to thimerosal in vaccine shots. Provided that the
mass of hair was above 10 mg, organic-mercury exposure during early life can be
speciated, and quantified in babies' first hair, thus opening opportunities for
clinical and forensic studies.[16]

27. Mercury
• Abstract
• Because of increasing awareness of the potential neurotoxicity of even low
levels of organomercury compounds, analytical techniques are required for
determination of low concentrations of ethylmercury (EtHg) and
methylmercury (MeHg) in biological samples. An accurate and sensitive
method has been developed for simultaneous determination of
methylmercury and ethylmercury in vaccines and biological samples. MeHg
and EtHg were isolated by acid leaching (H2SO4–KBr–CuSO4), extraction of
MeHg and EtHg bromides into an organic solvent (CH2Cl2), then back-
extraction into Milli-Q water. MeHg and EtHg bromides were derivatized with
sodium tetrapropylborate (NaBPr4), collected at room temperature on Tenax,
separated by isothermal gas chromatography (GC), pyrolysed, and detected
by cold-vapour atomic fluorescence spectrometry (CV AFS). The repeatability
of results from the method was approximately 5–10% for EtHg and 5–15% for
MeHg. Detection limits achieved were 0.01 ng g−1 for EtHg and MeHg in
blood, saliva, and vaccines and 5 ng g−1 for EtHg and MeHg in hair. The
method presented has been shown to be suitable for determination of
background levels of these contaminants in biological samples and can be
used in studies related to the health effects of mercury and its species in
man. This work illustrates the possibility of using hair and blood as potential
biomarkers of exposure to thiomersal.[17]

28. Mercury
Abstract
• Acute or chronic mercury exposure can cause adverse effects during
any period of development. Mercury is a highly toxic element; there is
no known safe level of exposure. Ideally, neither children nor adults
should have any mercury in their bodies because it provides no
physiological benefit. Prenatal and postnatal mercury exposures occur
frequently in many different ways. Pediatricians, nurses, and other
health care providers should understand the scope of mercury
exposures and health problems among children and be prepared to
handle mercury exposures in medical practice. Prevention is the key to
reducing mercury poisoning. Mercury exists in different chemical
forms: elemental (or metallic), inorganic, and organic (methylmercury
and ethyl mercury). Mercury exposure can cause acute and chronic
intoxication at low levels of exposure. Mercury is neuro-, nephro-, and
immunotoxic. The development of the child in utero and early in life is
at particular risk. Mercury is ubiquitous and persistent. Mercury is a
global pollutant, bio-accumulating, mainly through the aquatic food
chain, resulting in a serious health hazard for children. This article
provides an extensive review of mercury exposure and children's
health. [18]

29. Mercury
Abstract
• Mercury (Hg) is considered one of the world’s most toxic metals. Current thinking suggests that exposure to
mercury occurs primarily from seafood contamination and rare catastrophic events. Recently, another
common source of exposure has been identified. Thimerosal (TMS), a preservative found in many infant
vaccines, contains 49.6% ethyl mercury (EtHg) by weight and typically contributes 25 μg. of EtHg per dose
of infant vaccine. As part of an ongoing review, the Food and Drug Administration (FDA) announced in 1999
that infants who received multiple TMS-preserved vaccines may have been exposed to cumulative Hg in
excess of Federal safety guidelines. According to the centers for disease control (CDC) recommended
immunization schedule, infants may have been exposed to 12.5 μg Hg at birth, 62.5 μg EtHg at 2 months,
50 μg EtHg at 4 months, 62.5 μg EtHg at 6 months, and 50 μg EtHg at approximately 18 months, for a total
of 237.5 μg EtHg during the first 18 months of life, if all TMS-containing vaccines were administered.
Neurobehavioral alterations, especially to the more susceptible fetus and infant, are known to occur after
relatively low dose exposures to organic mercury compounds. In effort, to further elucidate the levels of
ethyl mercury resulting from exposure to vaccinal TMS, we estimated hair Hg concentrations expected to
result from the recommended CDC schedule utilizing a one compartment pharmacokinetic model. This
model was developed to predict hair concentrations from acute exposure to methymercury (MeHg) in fish.
Modeled hair Hg concentrations in infants exposed to vaccinal TMS are in excess of the Environmental
Protection Agency (EPA) safety guidelines of 1 ppm for up to 365 days, with several peak concentrations
within this period. More sensitive individuals and those with additional sources of exposure would have
higher Hg concentrations. Given that exposure to low levels of mercury during critical stages of
development has been associated with neurological disorders in children, including ADD, learning
difficulties, and speech delays, the predicted hair Hg concentration resulting from childhood immunizations
is cause for concern. Based on these findings, the impact which vaccinal mercury has had on the health of
American children warrants further investigation. [19]

30. Formaldehyde
• Synonyms include formalin, formic aldehyde, methanal, methyl
aldehyde, methylene oxide, oxomethane, and paraform.
• colorless, highly toxic, and flammable gas at room temperature that
is slightly heavier than air. It has a pungent, highly irritating odor that
is detectable at low concentrations, but may not provide adequate
warning of hazardous concentrations for sensitized persons.
• It is used most often in an aqueous solution stabilized with methanol
(formalin).
• Most formaldehyde exposures occur by inhalation or by skin or eye
contact.
• Formaldehyde is absorbed well by the lungs, gastrointestinal tract,
and, to a lesser extent, skin. Systemic effects include metabolic
acidosis, CNS depression and coma, respiratory distress, and renal
failure.
• Formaldehyde reacts with strong oxidizers, alkalis, acids, phenols,
and urea.
• Children may be more susceptible than adults to the respiratory
effects
• potent sensitizer and a probable human carcinogen.
• interact with molecules on cell membranes and in body tissues and
fluids (e.g., proteins and DNA) and disrupt cellular functions. High
concentrations cause precipitation of proteins, which results in cell
death.
• Children do not always respond to chemicals in the same way that
adults do. Different protocols for managing their care may be
needed.

31. Formaldehyde Exposure Sx
System Symptoms
Metabolism Absorption from the respiratory tract is very rapid; absorption from the gastrointestinal tract is
also rapid, but may be delayed by ingestion with food. Once absorbed, formaldehyde is
metabolized to formic acid, which may cause acid-base imbalance and a number of other
systemic effects. Accumulation of formic acid can cause an anion-gap acid-base imbalance.
Resp Fairly low concentrations of formaldehyde can produce rapid onset of nose and throat
irritation, causing cough, chest pain, shortness of breath, and wheezing. Higher exposures can
cause significant inflammation of the lower respiratory tract, resulting in swelling of the throat,
inflammation of the windpipe and bronchi, narrowing of the bronchi, inflammation of the
lungs, and accumulation of fluid in the lungs. Pulmonary injury may continue to worsen for 12
hours or more after exposure. Children may be more vulnerable because of relatively increased
minute ventilation per kg and failure to evacuate an area promptly when exposed.
GI Ingestion of aqueous solutions of formaldehyde can result in severe corrosive injury to the
esophagus and stomach. Nausea, vomiting, diarrhea, abdominal pain, inflammation of the
stomach, and ulceration and perforation of the oropharynx, epiglottis, esophagus, and stomach
may occur. Both formaldehyde and the methanol stabilizer are easily absorbed and can
contribute to systemic toxicity.
Immunologic In persons who have been previously sensitized, inhalation and skin contact may cause various
skin disorders, asthma-like symptoms, anaphylactic reactions and, rarely, hemolysis. The
immune system in children continues to develop after birth, and thus, children may be more
susceptible to certain chemicals.
ATSDR (2015). Toxic Portal: Formaldehyde, Medical Management Guideline for Formaldehyde. Retrieved from
http://www.atsdr.cdc.gov/mmg/mmg.asp?id=216&tid=39

32. Formaldehyde Exposure Sx…
System Symptoms
CNS Malaise, headache, sleeping disturbances, irritability, and impairment of dexterity, memory,
and equilibrium may result from a single, high level, exposure to formaldehyde. Increased
prevalence of headache, depression, mood changes, insomnia, irritability, attention deficit,
and impairment of dexterity, memory, and equilibrium have been reported to result from
long-term exposure. Chronic exposure may be more serious for children because of their
potential longer latency period.
Reproductive There have been reports of menstrual disorders in women occupationally exposed to
formaldehyde; Studies in experimental animals have reported some effects on
spermatogenesis; has been shown to have genotoxic properties in human and laboratory
animal studies producing sister chromatid exchange and chromosomal aberrations; Special
consideration regarding the exposure of pregnant women is warranted, since formaldehyde
has been shown to be a genotoxin; thus, medical counseling is recommended for the acutely
exposed pregnant woman.
Chronic
exposure:
The major concerns of repeated formaldehyde exposure are sensitization and cancer. In
sensitized persons, formaldehyde can cause asthma and contact dermatitis.
ATSDR (2015). Toxic Portal: Formaldehyde, Medical Management Guideline for Formaldehyde. Retrieved from
http://www.atsdr.cdc.gov/mmg/mmg.asp?id=216&tid=39

33. Formaldehyde
Abstract
• Formaldehyde, an economically important chemical, is classified as a
human carcinogen that causes nasopharyngeal cancer and probably
leukemia. As China is the largest producer and consumer of formaldehyde
in the world, the Chinese population is potentially at increased risk for
cancer and other associated health effects. In this paper we review
formaldehyde production, consumption, exposure, and health effects in
China. We collected and analyzed over 200 Chinese and English documents
from scientific journals, selected newspapers, government publications, and
websites pertaining to formaldehyde and its subsequent health effects.
• Over the last 20 years, China's formaldehyde industry has experienced
unprecedented growth, and now produces and consumes one-third of the
world's formaldehyde. More than 65% of the Chinese formaldehyde output
is used to produce resins mainly found in wood products — the major
source of indoor pollution in China. Although the Chinese government has
issued a series of standards to regulate formaldehyde exposure,
concentrations in homes, office buildings, workshops, public places, and
food often exceed the national standards. In addition, there have been
numerous reports of formaldehyde-induced health problems, including
poisoning and cancer. The lack of quality epidemiological studies and basic
data on exposed populations emphasizes the need for more extensive
studies on formaldehyde and its related health effects in China. [20]

34. Formaldehyde
Summary
• The aim of this study was to determine whether the inhalation of
formaldehyde has a neurotoxicological impact.
• Forty Wistar rats (Lew.1/K) were trained to find food in a maze within a
particular time. When all animals were at an equal level, 13 rats inhaled
2.6 ppm and 13 others inhaled 4.6 ppm formaldehyde 10 min/d, 7 d/week
for 90 d. The control group comprised 14 animals inhaling water steam
according to the same exposure pattern. During the exposure period and
the post-trial observation stage (30 d), the time required to find the food
and the number of mistakes made on the way were recorded.
• Between the animals exposed to formaldehyde and the control group a
statistically significant difference for both parameters was observed
(p<0.05). The animals exposed to formaldehyde needed more time and
made more mistakes than the animals of the control group while going
through the maze.
• The results underline the necessity for a systematic observance of
precautions in case of occupational or dwelling-related formaldehyde
exposure, and allow us to classify formaldehyde as “probably neurotoxic”.
Further investigations are required to assess the neurotoxicologic impact
of subchronic formaldehyde exposure.[21]

35. Formaldehyde
• Abstract
• Formaldehyde (FA) is a widely produced industrial chemical. Sufficient
evidence exists to consider FA as an animal carcinogen. In humans the
evidence is not conclusive. DNA-protein crosslinks (DPC) may be one
of the early lesions in the carcinogenesis process in cells following
exposures to carcinogens. It has been shown in in vitro tests that FA
can form DPC. We examined the amount of DPC formation in human
white blood cells exposed to FA in vitro and in white blood cells taken
from 12 workers exposed to FA and eight controls. We found a
significant difference (P = 0.03) in the amount of DPC among exposed
(mean ± SD 28 ± 5%, minimum 21%, maximum 38%) than among the
unexposed controls (mean ± SD 22 ± 6%, minimum 16%, maximum
32%). Of the 12 exposed workers, four (33%) showed crosslink values
above the upper range of controls. We also found a linear relationship
between years of exposure and the amount of DPC. We conclude that
our data indicate a possible mechanism of FA carcinogenicity in
humans and that DPC can be used as a method for biological
monitoring of exposure to FA. [22]

36. Formaldehyde (a)…
Abstract
• C-14 formaldehyde crosses the placenta and enters fetal tissues. The incorporated radioactivity is
higher in fetal organs (i.e., brain and liver) than in maternal tissues. The incorporation mechanism
has not been studied fully, but formaldehyde enters the single-carbon cycle and is incorporated as
a methyl group into nucleic acids and proteins. Also, formaldehyde reacts chemically with organic
compounds (e.g., deoxyribonucleic acid, nucleosides, nucleotides, proteins, amino acids) by
addition and condensation reactions, thus forming adducts and deoxyribonucleic acid-protein
crosslinks. The following questions must be addressed: What adducts (e.g., N-methyl amino acids)
are formed in the blood following formaldehyde inhalation? What role do N-methyl-amino adducts
play in alkylation of nuclear and mitochondrial deoxyribonucleic acid, as well as mitochondrial
peroxidation? The fact that the free formaldehyde pool in blood is not affected following exposure
to the chemical does not mean that formaldehyde is not involved in altering cell and
deoxyribonucleic acid characteristics beyond the nasal cavity. The teratogenic effect of
formaldehyde in the English literature has been sought, beginning on the 6th day of pregnancy
(i.e., rodents) (Saillenfait AM, et al. Food Chem Toxicol 1989, pp 545–48; Martin WJ. Reprod Toxicol
1990, pp 237–39; Ulsamer AC, et al. Hazard Assessment of Chemicals; Academic Press, 1984, pp
337–400; and U.S. Department of Health and Human Services. Toxicological Profile of
Formaldehyde; ATSDR, 1999 [references 1–4, respectively, herein]). The exposure regimen is
critical and may account for the differences in outcomes. Pregnant rats were exposed (a) prior to
mating, (b) during mating, (c) or during the entire gestation period. These regimens (a) increased
embryo mortality; (b) increased fetal anomalies (i.e., cryptochordism and aberrant ossification
centers); (c) decreased concentrations of ascorbic acid; and (d) caused abnormalities in enzymes of
mitochondria, lysosomes, and the endoplasmic reticulum. [23]…

37. Formaldehyde(b)…
Abstract (cont)
• The alterations in enzymatic activity persisted 4 mo following birth. In addition, formaldehyde
caused metabolic acidosis, which was augmented by iron deficiency.
• However, either changing the endpoints for measurement or exposing neonates during
periods of neurogenesis (days 1–14 following birth) and during subsequent developmental
periods produced adverse effects. These effects included neuroapoptosis, decreased
deoxyribonucleic acid and ribonucleic acid synthesis, abnormalities in adenylyl cyclase
cascade, and neurobehavioral effects (Johnson DE, et al. Brain Res Bull 1998, pp 143–47;
Lassiter TL, et al. Toxicol Sci 1999, pp 92–100; Chakraborti TK, et al. Pharmacol Biochem
Behav 1993, pp 219–24; Whitney KD, et al. Toxicol Appl Pharm 1995, pp 53–62; Chanda SM,
et al. Pharmacol Biochem Behav 1996, pp 771–76; Dam K, et al. Devel Brain Res 1998, pp 39–
45; Campbell CG, et al. Brain Res Bull 1997, pp 179–89; and Xong X, et al. Toxicol Appl Pharm
1997, pp 158–74 [references 8–15, respectively, herein]). Furthermore, the terata caused by
thalidomide is a graphic human example in which the animal model and timing of exposure
were key factors (Parman T, et al. Natl Med 1999, pp 582–85; and Brenner CA, et al. Mol
Human Repro 1998, pp 887–92 [references 16 and 17, respectively, herein]). Thus, it appears
that more sensitive endpoints (e.g., enzyme activity, generation of reactive oxygen species,
timing of exposure) for the measurement of toxic effects of environmental agents on
embryos, fetuses, and neonates are more coherent than are gross terata observations. The
perinatal period from the end of organogenesis to the end of the neonatal period in humans
approximates the 28th day of gestation to 4 wk postpartum. [23]…

38. Formaldehyde(c)…
Abstract (cont)
• Furthermore, newborns exposed to formaldehyde in utero had abnormal performances in open-
field tests. Disparities in teratogenic effects of toxic chemicals are not unusual. For example,
chlorpyrifos has not produced teratogenic effects in rats when mothers are exposed on days 6–
15 (Katakura Y, et al. Br J Ind Med 1993, pp 176–82 [reference 5 herein]) of gestation (Breslin WJ,
et al. Fund Appl Toxicol 1996, pp 119–30; and Hartley TR, et al. Toxicol Sci 2000, pp 100–08
[references 6 and 7, respectively, herein]). Therefore, researchers must investigate similar stages
of development (e.g., neurogenesis occurs in the 3rd trimester in humans and neonatal days
occur during days 1–14 in rats and mice, whereas guinea pigs behave more like humans). Finally,
screening for teratogenic events should also include exposure of females before mating or
shortly following mating. Such a regimen is fruitful inasmuch as environmental agents cause
adverse effects on ovarian elements (e.g., thecal cells and ova [nuclear-deoxyribonucleic acid and
mitochondrial deoxyribonucleic acid]), as well as on zygotes and embryos before implantation.
Mitochondrial deoxyribonucleic acid mutations and deletions occur in human oocytes and
embryos (Parman T, et al. Natl Med 1999, pp 582–85; and Brenner CA, et al. Mol Human Repro
1998, pp 887–92 [references 16 and 17, respectively, herein]). Thus, it is likely that xenobiotics
directly affect n-deoxyribonucleic acid and/or mitochondrial deoxyribonucleic acid in either the
ovum or the zygote/embryo or both (Thrasher JD. Arch Environ Health 2000, pp 292–94
[reference 18 herein]), and they could account for the increasing appearance of a variety of
mitochondrial diseases, including autism (Lomard L. Med Hypotheses 1998, pp 497–99; Wallace
EC. Proc Natl Acad Sci 1994, pp 8730–46; and Giles RE, et al. Proc Natl Acad Sci 1980, pp 6715–19
[references 19–21, respectively, herein]). Two cases of human birth defects were reported in
formaldehyde-contaminated homes (Woodbury MA, et al. Formaldehyde Toxicity 1983; pp 203–
11 [reference 22 herein]). One case was anencephalic at 2.76 ppm, and the other defect at 0.54
ppm was not characterized. Further observations on human birth defects are recommended.
[23]

39. Formaldehyde…
Abstract
• Background: Formaldehyde levels were measured in 80 houses in the Latrobe Valley,
Victoria, Australia. An association between exposure to formaldehyde and
sensitization to common aeroallergens has been suggested from animal trials, but no
epidemiologic studies have tested this hypothesis.
• Methods: A total of 148 children 7–14 years of age were included in the study, 53 of
whom were asthmatic. Formaldehyde measurements were performed on four
occasions between March 1994 and February 1995 with passive samplers. A
respiratory questionnaire was completed, and skin prick tests were performed.
• Results: The median indoor formaldehyde level was 15.8 μg/m3(12.6 ppb), with a
maximum of 139 μg/m3 (111 ppb). There was an association between formaldehyde
exposure and atopy, and the adjusted odds ratio was 1.40 (0.98–2.00, 95% CI) with
an increase in bedroom formaldehyde levels of 10 μg/m3. Furthermore, more severe
allergic sensitization was demonstrated with increasing formaldehyde exposure. On
the other hand, there was no significant increase in the adjusted risk of asthma or
respiratory symptoms with formaldehyde exposure. However, among children
suffering from respiratory symptoms, more frequent symptoms were noted in those
exposed to higher formaldehyde levels.
• Conclusions: Low-level exposure to indoor formaldehyde may increase the risk of
allergic sensitization to common aeroallergens in children. [24]

40. Formaldehyde
Abstract
• Six patients with multiple subjective health complaints, which have been
correlated with chronic exposure to formaldehyde during the course of their
education and occupations, were tested for the existence of antibodies (IgE,
IgM, and IgG) to formaldehyde (F) conjugated to human serum albumin (F-
HSA). In addition, the percentage and absolute numbers of peripheral
lymphocyte subpopulations as determined by surface markers were
investigated. Antibody titers to F-HSA were present as follows: IgE (2
patients), IgM (3 of 4 tested patients), and IgG (5 patients). Analysis of
lymphocyte subpopulations showed T-helper/suppressor (H/S) ratios ranging
from 0.8 to 3.3. All 6 patients had elevated Tal cells (antigen memory cells),
whereas interleuken 2 receptor positive cells were within expected values.
Following formaldehyde exposure, 5 of the patients complained of an initial
flulike illness from which they have not completely recovered. The sixth
individual had a history of recurrent respiratory infections and surgical
removal of hyperplastic ethmoid sinus tissue. The common occurrence of
anti-F-HSA antibodies, flulike illness, and Tal cells are interpreted as
suggestive of a chronic antigenic stimulation of the immune system in these 6
patients. Further immunological work-up of additional subjects and immune
parameters with similar history of formaldehyde exposure and subjective
health complaints is warranted.[25]

41. Laboratory Analysis
• Mercury and other toxic heavy metals are primarily
measured in hair, blood cells and urine samples.
– hair analysis is a useful screening tool but does not provide
information about the actual amount of mercury in the body
• Red blood cell analysis gives somewhat more information
about tissue levels, but misses mercury bound in brain,
bone and fatty tissues.
• Most accurate, clinical measurement of the relative total
body burden of mercury is obtained via provocative, 24-
hour elemental urine analysis.
– Procedure: a dose of DMSA and glycine is taken the evening
before beginning the urine test, thereby extracting mercury and
other toxic heavy metals from their hiding places deep in the
tissues, which is then collected in the urine, thus giving a more
accurate measure of total body burden.

42. Preservative Summary
• Aluminum, Mercury, & Formaldehyde are standard vaccine
preservatives
• Formaldehyde is carcinogenic, immunosuppressive, &
mutanogenic
• Aluminum is neurotoxic, mutanogenic & immunosuppressive
• Mercury is neurotoxic, mutanogenic, & immunosuppressive
• All preservatives demonstrate increased absorption in utero
& in early developmental phases
• Children’s developing systems are more systemically
vulnerable to Aluminum, Mercury, & Formaldehyde
• Individuals w/vulnerable immune systems & genetic
variations should be protected from the systemic threats
these preservatives possess
• Each individual responds differently
• Multiple simultaneous preservative exposure poses a
significant threat to vulnerable populations
• No objective clinical research has studied the simultaneous
impact of these preservatives on vulnerable populations
• The increase in proven vaccine injuries warrants further
comprehensive analysis
• There is enough evidence to question the safety & efficacy of
current vaccine schedule upon vulnerable populations

43. Vaccine Ingredients
Name/Company Vaccine Ingredients
Acel-Immune DTaP
Wyeth-Ayerst #800.934.5556
diphtheria - tetanus - pertussis diphtheria and tetanus toxoids and acellular pertussis adsorbed
plus: formaldehyde, aluminum hydroxide, aluminum phosphate,
thimerosal, and polysorbate 80 (Tween-80) and gelatin
Act HIB-Haemophilus influenza
Type B
Connaught Laboratories
800.822.2463
Haemophilus influenza Type B Haemophilus influenza Type B
Plus: polyribosylribitol phosphate, ammonium sulfate, formalin, and
sucrose
Attenuvax-
Merck & Co., Inc. 800-672-6372
measles measles live virus
Plus: neomycin sorbitol hydrolized gelatin, chick embryo
Biavax-
Merck & Co., Inc. 800-672-6372
rubella rubella live virus
Plus: neomycin, sorbitol, hydrolized gelatin, human diploid cells from
aborted fetal tissue
DPT (diphtheria - tetanus –
pertussis)
GlaxoSmithKline 800.366.8900
X 5231
diphtheria - tetanus - pertussis diphtheria and tetanus toxoids and acellular pertussis adsorbed
plus: formaldehyde, aluminum phosphate, ammonium sulfate, and
thimerosal washed sheep RBCs
Engerix-B
GlaxoSmithKline 800.366.8900
X 5231
recombinant hepatitis B genetic sequence of the hepatitis B virus that codes for the surface
antigen (HbSAg), cloned into GMO yeast
plus: aluminum hydroxide, and thimerosal
Fluvirin
Medeva Pharmaceuticals
888.MEDEVA 716.274.5300
Flu influenza virus
Plus: neomycin, polymyxin beta-propiolactone chick embryonic fluid
FluShield
Wyeth-Ayerst 800.934.5556
Flu trivalent influenza virus types A&B
Plus: gentamicin sulphate, formadehyde, thimerosal, and polysorbate
80 (Tween-80)

44. Vaccine Ingredients
Name/Company Vaccine Ingredients
Havrix
GlaxoSmithKline
800.366.8900 X 5231
hepatitis A hepatitis A virus
plus: formalin, aluminum hydroxide, 2-phenoxyethanol, and polysorbate 20 residual MRC5
proteins -human diploid cells from aborted fetal
Haemophilus influenza Type B
Wyeth-Ayerst 800.934.5556
HiB Titer tissue Haemophilus influenza Type B
Plus: polyribosylribitol phosphate, yeast ammonium sulfate, thimerosal, and chemically
defined yeast-based medium
MMR-
Merck & Co., Inc.
800.672.6372
measles - mumps -
rubella
measles, mumps, rubella live virus
plus: neomycin, sorbitol, hydrolized gelatin, chick embryonic fluid, and human diploid cells
from aborted fetal tissue
Menomune
Connaught Laboratories
800.822.2463
-meningococcal freeze-dried polysaccharide antigens from Neisseria meningitidis bacteria
Plus: thimerosal lactose
ProQuad
Merck & Co., Inc.
800.672.6372
measles, mumps,
rubella & varicella
live measles (Enders' attenuated Edmonston), mumps (Jeryl LynnTM), rubella (Wistar RA
27/3), and varicella (oka/Merck) strains of viruses Proquad (cont.)
Plus: neomycin, monosodium L-glutamate (MSG), potassium chloride, potassium phosphate
monobasic, potassium phosphate dibasic, sodium bicarbonate, sodium phosphate dibasic,
sorbitol, and sucrose human albumin, human diploid cells, residual components of MRC-5
cells including DNA and proteins, bovine serum, hydrolized gelatin, and chicken embryo
Recombivax
Merck & Co., Inc.
800.672.6372
recombinant
hepatitis B
genetic sequence of the hepatitis B virus that codes for the surface antigen (HbSAg), cloned
into GMO yeast
Plus: aluminum hydroxide, and thimerosal
Tripedia
Aventis Pasteur USA
800.VACCINE
-diphtheria - tetanus
- pertussis
Corynebacterium diphtheriae and Clostridium tetani toxoids and acellular Bordetella
pertussis adsorbed
Plus: aluminum potassium sulfate, formaldehyde, thimerosal, and polysorbate 80 (Tween-
80)

45. Vaccine Ingredients
Name/Company Vaccine Ingredients
Typhim
Aventis Pasteur USA SA
800.VACCINE
Vi-typhoid cell surface Vi polysaccharide from Salmonella typhi Ty2 strain
Plus: aspartame, phenol, and polydimethylsiloxane (silicone)
Varivax-
Merck & Co., Inc.
800.672.6372
chickenpox varicella live virus
Plus: neomycin phosphate, sucrose, and monosodium glutamate (MSG) processed gelatin, fetal
bovine serum, guinea pig embryo cells, albumin from human blood, and human diploid cells
from aborted fetal tissue
Chemicals commonly used in the production of vaccines include a suspending fluid (sterile water, saline, or fluids containing protein);
preservatives and stabilizers (for example, albumin, phenols, and glycine); and adjuvants or enhancers that help improve the vaccine's
effectiveness. Vaccines also may contain very small amounts of the culture material used to grow the virus or bacteria used in the
vaccine, such as chicken egg protein. http://www.cdc.gov/vaccines/vac-gen/additives.html
Vaccines contain ingredients, called antigens, which cause the body to develop immunity. Vaccines also contain very small amounts of
other ingredients--all of which play necessary roles either in making the vaccine, or in ensuring that the vaccine is safe and effective.
These types of ingredients are listed below.

46. Bibliography
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http://www.sciencedirect.com/science/article/pii/S0013935102943525
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• [3] McLachlan DRC (1995). Aluminium and the risk for alzheimer's disease. Environmetrics, Special
Issue: Aluminium and Alzheimer's Disease. Volume 6, Issue 3, pages 233–275, May/June 1995.
Retrieved from http://onlinelibrary.wiley.com/doi/10.1002/env.3170060303/abstract
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and toxicity. Coordination Chemistry Reviews Volume 228, Issue 2, 3 June 2002, Pages 319–341.
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• [5] Golub MS and Domingo JL (1996). WHAT WE KNOW AND WHAT WE NEED TO KNOW ABOUT
DEVELOPMENTAL ALUMINUM TOXICITY. Journal of Toxicology and Environmental Health Volume
48, Issue 6, 1996. Retrieved from
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