Mercury, Vaccines, and Autism | AJPH | Vol. 98 Issue 2 https://ajph.aphapublications.org/doi/full/10.2105/AJPH.2007.

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Mercury, Vaccines, and Autism

One Controversy, Three Histories

Jeffrey P. BakerMD, PhD

[+] Author a�liations, information, and correspondence details

Accepted: May 08, 2007 Published Online: October 10, 2011

Abstract Full Text References PDF/EPUB

Abstract Section: Choose

The controversy regarding the once widely used mercury-containing preservative thimerosal in childhood vaccines has raised many historical questions
that have not been adequately explored. Why was this preservative incorporated in the �rst place? Was there any real evidence that it caused harm? And
how did thimerosal become linked in the public mind to the “autism epidemic”?

I examine the origins of the thimerosal controversy and their legacy for the debate that has followed. More speci�cally, I explore the parallel histories of
three factors that converged to create the crisis: vaccine preservatives, mercury poisoning, and autism.

An understanding of this history provides important lessons for physicians and policymakers seeking to preserve the public’s trust in the nation’s vaccine
system.

DESPITE THE REASSURANCE of no less than eight safety review panels conducted by the Institute of Medicine (IOM) since 2001, many parents continue to
fear that childhood vaccines can cause a host of adverse e�ects ranging from immune dysfunction to attention de�cit disorder and autism.1 Several trends
no doubt contribute to this anxiety: fading memory of vaccine-preventable diseases, adverse media coverage, misinformation on the Internet, and
litigation.2 Yet global explanations of this sort fail to do justice to the fact that controversies over vaccines have often followed quite disparate trajectories in
di�erent settings. For example, although the alleged relationship between childhood vaccines and autism has been the dominant controversy over child
immunization of recent years, British anxiety has centered on the measles-mumps-rubella vaccine, whereas Americans have focused much more on the
role of mercury in vaccine preservatives.3

I examine the origins of the American debate surrounding vaccines, mercury, and autism to illuminate how historical analysis can contribute to
understanding public attitudes toward vaccine safety. It is not my intent to answer whether mercury in vaccines explains the increasing prevalence of
autism; the IOM has already determined over the course of two reviews that available evidence fails to support such a conclusion.4 Instead, I examine the
historical questions that have been raised in the debate but only super�cially addressed by the IOM. Why was the mercury-containing preservative
thimerosal introduced in infant vaccines in the �rst place? Why was its use not questioned until the late 1990s, long after the toxic e�ects of mercury had
been recognized? Why was autism perceived to be “epidemic” in the 1990s, and how did it become linked to vaccines in the public’s mind?

I argue that the thimerosal story is best envisioned in terms of three historical “streams” dating back to the early 20th century that converged unexpectedly
and momentously in the summer of 1999. These three tributaries, corresponding to the histories of vaccine preservatives, mercury poisoning, and autism,
are examined successively to illuminate why various groups responded so di�erently to the debates beginning in that year.

THIMEROSAL AND VACCINES Section: Choose

Understanding why mercury was �rst incorporated into childhood vaccines leads back to the preantibiotic era, a time when physicians employed a variety
of compounds known as “germicides” to combat bacteria. Perhaps the best known was Joseph Lister’s carbolic acid, developed in the 1860s for surgical
antisepsis and later employed as a germicide and preservative known as phenol.5 Yet a variety of mercury compounds were also used for the same
purpose. No less an authority than Robert Koch championed the use of mercury chloride as an antiseptic, although the product’s propensity to cause tissue
irritation limited its use. In the early 20th century, investigators synthesized a new class of compounds they claimed to be both more e�ective and less
toxic, the organomercurials. Often brilliantly colored, these products soon found widespread usage, from operating suites to home medicine cabinets.6

Thimerosal was one of the most promising new organomercurials that excited the pharmaceutical industry after World War I. It was a white, crystalline
powder, approximately 50% mercury by weight, in the form of ethylmercury bound to thiosalicylate. The emerging pharmaceutical giant Eli Lilly and
Company provided grant support for its synthesis at the University of Chicago and in 1928 patented it under the trade name Merthiolate.7 Over the next
several years, Lilly’s investigators H.M. Powell and W.A. Jamieson conducted extensive in vitro testing, showing that thimerosal was 40 to 50 times as

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e�ective as phenol against Staphylococcus aureus. The two men evaluated toxicity by injecting the compound into over 300 rabbits and a variety of other
animals observed for a week’s time. The animals appeared to tolerate signi�cant doses—up to 20 mg per kg body weight in rabbits and still higher in rats—
without apparent injury.8

These encouraging results prompted the Lilly team in 1929 to o�er their product to the Indiana General Hospital during an epidemic of meningococcal
meningitis. Hospital physicians gave 22 patients as much as 180 mL of a 1% solution of thimerosal intravenously divided over �ve doses. From a
therapeutic standpoint, the trial was a failure, but investigators were struck by how well the patients seemed to tolerate such high doses.9 Combined with
the animal studies, the data further reinforced the impression that thimerosal was far more benign than earlier mercurials, preparing the way for its
incorporation at low concentrations into a wide range of biological products as a preservative. Vaccines would become an especially important niche.

One of the most troublesome safety issues a�icting early 20th-century child immunization was that of bacterial contamination. This could easily occur on a
sporadic basis, when general practitioners might have to draw vaccines from multidose vials under poor hygienic conditions. Contamination of entire lots
could be much more spectacular. In Columbia, South Carolina, in 1916, a tainted batch of typhoid vaccine stored at room temperature caused 68 severe
reactions, 26 abscesses, and 4 deaths. A still more disturbing incident took place in 1928 in Queensland, Australia, where 12 of 21 children inoculated with
contaminated diphtheria vaccine died of multiple staphylococcal abscesses and toxemia. The need for e�ective preservatives was readily apparent and
represented one of the most important safety issues for the promoters of new vaccines.10

In this context, Powell and Jamieson’s studies suggested that Merthiolate had an unexpected advantage. The problem with existing preservatives such as
phenol and cresol was that they often reduced the potency of the biological products they were intended to protect. By contrast, thimerosal not only
inhibited bacterial growth in vaccines and antisera at concentrations as low as 1:10000 but also had no such deleterious e�ects.11 A series of other
investigators con�rmed these �ndings over the next several years, and by 1940 thimerosal was incorporated into diphtheria toxoid, meningococcal serum,
pertussis vaccine, and a host of other biological products.12 Indeed, in 1938 Lilly’s assistant director of research listed Merthiolate along with insulin as one
of the �ve most important drugs ever developed by the company.13

Thimerosal’s e�cacy was sometimes challenged during the �rst 50 years following its synthesis, but rarely its safety. In 1948, the American Medical
Association’s (AMA’s) Council on Pharmacy and Chemistry issued a report calling attention to a series of investigations asking whether organomercurials
were any more e�ective as germicides than inorganic mercury compounds had previously been.14 The AMA’s council, it should be noted, played an
important role before 1950 in providing independent assessments and approvals of drugs; the US Food and Drug Administration (FDA) did not require
manufacturers to submit prelicensure safety testing until 1938 or e�cacy testing until the 1960s.15 Despite these voices of dissent, thimerosal remained
popular in practice. Its defenders pointed to their own studies and the simple fact that contamination incidents had become exceedingly uncommon
following its introduction.16 Although Jonas Salk’s experience with inactivated polio vaccine in �eld trials from 1954 to 1955 suggested that in some cases
thimerosal, contrary to expectation, did in fact harm vaccine immunogenicity, this case was regarded as an exception to the rule.17

The �rst real questions regarding thimerosal’s safety were raised in the 1970s, provoked (as will be described in the next section) by rising awareness of the
dangers of organic mercury poisoning. Although the latter debate centered on the organomercurial methylmercury found in �sh and industrial pollution,
ethylmercury did not escape scrutiny. A series of case reports demonstrated the compound’s potential for neurotoxicity when given in large volumes, such
as when used as a topical antiseptic to “paint” large omphaloceles.18,19 These exposures exceeded those in vaccines, however, by many orders of
magnitude. Only one routine infant vaccine in the 1970s, the diphtheria-tetanus-pertussis combination, contained thimerosal. A formal review of
thimerosal by the FDA concluded in 1976 that no dangerous quantity of mercury was likely to be received from vaccines and other biological products over
a lifetime.20

Concerns over neurotoxicity in infants receiving thimerosal from vaccines were never raised by medical or governmental authorities before the late 1990s.
To be sure, some bacteriologists continued to question its e�cacy in the laboratory. As noted by dermatologists (and eventually the FDA), skin testing
revealed that contact with thimerosal caused hypersensitivity in many people. There was no evidence, however, that this phenomenon had any medical
signi�cance.21 Thimerosal’s toxicity at high doses was clearly established by the 1970s, but the comparatively miniscule exposures involved in vaccines were
well within all published guidelines for mercury exposure. The overwhelming consensus was that ethylmercury in low concentrations was safe and e�ective
in practice.

What broke this consensus was the convergence of the history of ethylmercury with the parallel history of methylmercury in the mid-1990s. This story,
known better to environmental scientists than vaccinologists, evolved in a direction that eventually suggested that even relatively low exposures to organic
mercury could be dangerous to the fetus and young infant.

METHYLMERCURY AND THE DEVELOPING BRAIN Section: Choose

Methylmercury, the form of mercury linked most closely in the public mind with environmental pollution, has a history as public and infamous as the
history of ethylmercury has been quiet and inconspicuous. Much in the thimerosal debate hinges on the alleged similarity, or dissimilarity, of ethylmercury
to methylmercury. The two compounds sound alike, di�er by only one methylated side chain in their structure, and tend to be mentioned interchangeably
in the popular press. Yet the chemical distinction is not trivial; it may be compared with that between ethanol (the form of alcohol in wine) and its highly
lethal counterpart methanol. Methylmercury was once used widely in developing countries as a fungicide as part of the “Green Revolution” that
transformed agriculture after 1945. It is also synthesized by bacteria living in mercury-polluted waters, where it is passed up the food chain and
concentrated in �sh. The dangers of methylmercury in both contexts have been vividly demonstrated in a series of environmental disasters.

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The �rst and best remembered of these took place in the �shing community of Minamata Bay, Japan. In the early 1950s, the Chisso chemical company
constructed a factory that began expelling large quantities of e�uent into the bay. The area’s inhabitants soon began witnessing a variety of disturbing
events. Seagulls fell from the sky, dead �sh washed ashore, and frenzied cats were seen whirling in a mad dance ending in death. Soon thereafter, doctors
began seeing patients with a staggering gait, numbness in the hands and feet, and more profound neurological impairments. A new form of viral
encephalitis was initially suspected. An investigation by Kumamoto University, however, pointed instead to the similarity of the symptoms to those
described in an obscure 1940 case report of four workers in a manufacturing plant producing methylmercury as a seed disinfectant. Bacteria in the bay, the
researchers concluded, had converted inorganic mercury discharged from the plant into methylmercury.22

The Minamata Bay disaster became one of the de�ning events in the rise of environmental awareness of the toxic e�ects of mercury. The Chisso company
long resisted pressure to improve its discharge system, and victims continued to appear in the 1960s both in Minamata and in Niigata, Japan, the site of a
second outbreak. Only in 1968 did the Japanese government release a formal statement implicating methylmercury in the outbreaks. A series of lawsuits
began shortly thereafter that would last until the end of the century. The magnitude of the disaster remains hard to determine, but as of 2003, over 2265
patients had been certi�ed to have had Minamata disease.23 The spectacle was brought to American eyes in the 1960s on the pages of Life magazine
through the poignant work of documentary photographer and activist W. Eugene Smith.24

Some of Smith’s most enduring images depicted children with mercury poisoning, some of whom, born to asymptomatic mothers, had been exposed in
utero. Here was the �rst indication that the fetus was more vulnerable than the adult. Infants with “congenital Minamata disease” manifested the hallmarks
of profound neurological injury: spasticity, seizures, deafness, and severe mental de�ciency. So great was the shame associated with the syndrome,
however, that investigators had a great deal of di�culty enrolling patients for formal studies.25

Tragically, a still greater disaster soon provided researchers another opportunity. In Iraq in 1971 and 1972, an estimated 6530 farmers and family members
were hospitalized for methylmercury poisoning, of whom 459 died. The source was homemade bread derived from seed wheat that had been
contaminated by fungicide.26 Extensive study of the Iraqi victims provided the basis for the �rst standards de�ning safe organic mercury exposure for
adults. Speci�cally, the FDA drew upon this data, as well as a variety of animal studies and reports from other mercury poisoning incidents, when it
proposed in the 1970s an acceptable daily intake of 0.4 μg per kg of body weight per day, based on the threshold at which paresthesia occurs in adults.27

Determining safe exposure for the fetus and newborn proved much more challenging.28 At an early point, investigators in Iraq identi�ed cases of severe
congenital mercury poisoning characterized by profound retardation and spasticity similar to those that had been described in Japan.29 Only gradually did it
become apparent that these infants represented the extreme of a continuum of toxicity. The �rst published studies of apparently asymptomatic Iraqi
infants exposed to intrauterine or postnatal (through breastmilk) methylmercury were reassuring, with tests revealing normal development at age 1 year.
As surveillance of these children continued into the 1980s, however, a disproportionate number began to show signs of delays in language acquisition.30
The probability that mercury might be analogous to lead, which was also shown to have more subtle yet real cognitive e�ects by researchers in the same
time period, was becoming more compelling.31

Two major longitudinal studies were launched during the 1980s in the hope of answering whether relatively low maternal methylmercury exposures could
result in any degree of neurological injury to the fetus. Both were conducted in isolated island populations consuming large quantities of �sh. The �rst,
based in the Seychelles in the Indian Ocean, used global measures such as overall IQ and the Denver Developmental Screening test, whereas the second,
based in the Faroe Islands in the North Atlantic, employed more-specialized, domain-related tests of function.

The two studies produced di�erent results. The Seychelles children did not appear to su�er any adverse outcomes. By contrast, the Faroe children
demonstrated de�cits in language, attention, and memory at age 7 years. It is unclear whether these di�erences re�ect testing strategies, di�erent genetic
vulnerabilities, or the source of mercury. The Faroe Islanders consumed mercury in more of a “bolus” fashion in the form of meals, including pilot whale
blubber, which is heavily contaminated with fat-soluble pollutants such as polychlorinated biphenyl (PCB) and pesticides. Still, the more-speci�c types of
testing in the Faroes led many environmental experts to give the results there precedence.32,33

The stage was now set for the confusing array of advisory recommendations on methylmercury that emerged in the 1990s. Agencies di�ered with respect
to directing recommendations at adults or pregnant women, balancing the con�icting data for the Seychelles and Faroes, and determining how much of an
uncertainty factor to take into account the extent to which individuals may metabolize mercury di�erently. As of 1999, the FDA continued to set its
acceptable daily intake at 0.4 μg per kg of body weight per day, the standard proposed for adults in the 1970s. It noted that this �gure should probably be
set lower for pregnant women. By contrast, the Environmental Protection Agency in 1994 lowered its reference dose for methylmercury exposure to 0.1 μg
per kg of body weight per day on the basis of the Iraqi data on women and children. To make the situation still more confusing, the Agency for Toxic
Substances and Disease Registry lowered its minimal risk level to 0.1 μg per kg of body weight per day in 1994, only to raise it back to 0.3 μg per kg of body
weight per day in 1999, prioritizing the Seychelles over the Faroes studies.34

Beyond the discrepancy between o�cial recommendations, two other points deserve emphasis. First, there was an emerging consensus among
environmental scientists that the fetus was indeed more sensitive to methylmercury than the adult and that this toxicity was better expressed as a
continuum than a clear-cut syndrome. The second point is that this concern had to do with relatively subtle cognitive and language delays, detectable in
older children through domain-speci�c testing. Autism was not even discussed. It was not described among either the profoundly injured children in
disasters such as Minamata Bay and Iraq or the milder delays described in the Faroes. Autism only entered the discourse in 1999, represented by a third
set of communities with their own historical memories.

AUTISM AND ITS HISTORIES Section: Choose

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The hypothesis that thimerosal-containing vaccines could explain the remarkable rise in the prevalence of autism arose not among environmental
scientists but among the communities that have emerged over the past 20 years of parents and professionals caring for autistic children.35 Speci�cally,
parents and clinicians who have framed autism in biomedical terms (such as immune or gastrointestinal dysfunction) have been critical agents in
promoting both the concept of the “autism epidemic” and the primacy of vaccines as its cause. The passion behind their arguments stems from a long
history of advocacy on behalf of their children, often in the face of psychiatric theories perceived as “parent blaming” and inadequately funded
developmental and educational resources in many communities.

The psychoanalyst Leo Kanner �rst coined the term “autistic” in a classic 1948 case report of 11 children exhibiting what he characterized as “an extreme
autistic aloneness” shutting out all social contact, as well as an “obsessive desire for the maintenance of sameness” in their play and daily routines. The
typical autistic child in his series eventually acquired language but used it in a mechanical way devoid of emotion, sometimes combined with striking rote
memory. One preschool child could recite 25 questions of the Presbyterian Catechism, another could distinguish 18 symphonies from one another. Kanner
(along with his contemporary Hans Asperger, who described a similar syndrome in 1944) was especially struck that all the children were born to highly
intelligent parents.36 Over the next two decades, autism researchers such as Bruno Bettelheim developed an explicitly Freudian explanation to account for
the association: autism arose in infancy in response to rejection by an emotionally distant (although typically well-educated) parent—a so-called
“refrigerator mother.”37

In 1965, psychologist Bernard Rimland (himself the father of an autistic child) rejected the psychogenic model of autism in his ground-breaking Infantile
Autism, proposing that the condition was instead rooted in biology.38 The collapse of the psychoanalytic model gave rise, however, to two rather di�erent
explanatory frameworks in its place. The ways in which these have diverged and have been embraced by di�erent communities of parents and
professionals is of critical importance to understanding the current debate over the existence of an autism epidemic.

What might be characterized as the “mainline” community of autism researchers has reconceptualized autism as a neurodevelopmental condition.39 Four
tenets have characterized most approaches by these researchers. First, the cause of autism is fundamentally biological and no more attributable to
parental behavior than is cerebral palsy or Down syndrome. Although the nature of the cause remains unknown, a variety of studies (ranging from
radiographic imaging to genetic twin studies and family pedigree analysis) have increasingly highlighted the importance of genetics.40 Second, autism is
conceptualized as a spectrum of disorders. In the 1970s, investigators modi�ed Kanner’s original restrictive diagnosis to encompass children with greater
intellectual and language impairment and then expanded it in the opposite direction to encompass higher-functioning children with labels such as
“pervasive developmental disorders” and “autistic spectrum disorders.”41

Third, if autism represents a spectrum disorder rooted in biology as pro�ered in the �rst two tenets, its treatment must be largely rehabilitative rather than
curative. For example, Eric Schopler of the University of North Carolina developed the in�uential TEACCH (Teaching and Education of Autistic and related
Communication-handicapped Children) program as a model combining parental education and therapy to assist parents in understanding their children
prior to setting realistic management approaches.42 Fourth, as with other developmental disorders, early referral and intervention o�er the greatest hope
for a positive outcome. Many autism researchers and parent allies have worked tirelessly to promote screening tools and special education programs in the
schools. In 1991, autism was o�cially added to the list of covered disabilities in the Individuals with Disabilities Education Act passed the preceding year,
providing a major boost to its diagnosis and early treatment.43

The essential point to understand is that the rise of autism diagnoses in the 1990s was exactly what the mainline researchers expected.44 It represented
the logical consequence of their ongoing e�orts to expand its de�nition and promote its recognition in developmental evaluation centers and the schools.
What perhaps was not expected, and certainly not welcome, was the gap that frequently appeared between the supply of and rising demand for autistic
services. All too often, parents confronted with their child’s diagnosis in the 1990s were met with long waiting lists and primary care doctors who seemed
barely familiar with the condition. Placed in this predicament, parents not surprisingly turned to one another and the Internet.

Parents frustrated by the mainline approach to autism were likely to meet what might be characterized as the “alternative” community of autism research.
This approach viewed autism in biomedical terms. Rather than viewing autism as a continuum of disability, it characterized the condition as a heterogenous
collection of discrete entities with di�erent etiologies sharing a common presentation. Most importantly, this viewpoint o�ered hope that at least some
forms of autism are not simply treatable, but curable. Many such cures have been proposed. Among the most popular were those focusing on special diets,
based on studies suggesting that an abnormality in intestinal permeability (a so-called “leaky gut”) may admit intestinal toxins or opioids a�ecting the
nervous system at an early age. Although promoted by researchers who viewed themselves as “dissident” with respect to mainline thinking, these theories
recast autism as biomedical in origin and potentially curable in ways that profoundly re�ected late 20th-century American hopes in the power of medical
technology.45

The most notable organization promoting this framework is the Autism Research Institute in San Diego, Calif, which through its Defeat Autism Now!
conferences and educational materials seeks to provide parents with the tools to understand and treat their own child. Parents provide much of the
leadership and energy in this and related organizations. A smaller cadre of professionals participate as well, some of whom are very prominent in their own
right. The Autism Research Institute was organized with the full support of psychologist Bernard Rimland, who had earlier played such a pivotal role in
dethroning the psychogenic approach.46

It was among these parental advocacy groups, not the medical or educational professions, that the notion of an autism “epidemic” �rst took root. These
organizations provided a context to bring parents out of isolation and into a realization that others—many others—shared their hopes and frustrations.
Against this background, an alarming possibility became more plausible: the cause of autism was not only biological but environmental, the consequence of
some new exposure faced by young children. Indeed, it seemed fair to speak of an autism epidemic as a means of summoning the sense of urgency the

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situation required.

In 1998, British gastroenterologist Andrew Wake�eld proposed a hypothesis linking the “leaky gut” etiologic framework of autism to a new environmental
factor explaining its rise. In that year, he published a report describing a small number of patients who developed autistic regression and diarrhea following
their measles-mumps-rubella immunization.47 Wake�eld’s study launched a major controversy in Britain, despite the failure of large epidemiological
studies to con�rm its results.48 Aided by the Internet, the controversy soon crossed the Atlantic and was viewed with concern by many parents of autistic
children as well as the parallel network of parent groups opposing compulsory immunization. Both groups gained a powerful ally when Congressman Dan
Burton (D, Ind) began a series of congressional hearings on autism and vaccine safety after his own grandchild was diagnosed with autism following the 12-
month vaccinations.49

By 1999, a growing body of articulate and well-organized parents of autistic children were set on a trajectory destined to collide with that of the vaccine
community. Their collective experience had taught them the importance of challenging conventional wisdom and expertise. Many were highly capable
individuals, such as Rick Rollens, an associate of California Governor Gray Davis (and, again, the father of an autistic child), who persuaded the legislature to
fund millions of dollars for autism research at the University of California at Davis, as well as a study examining the historical trend in children receiving
services for autism in the state’s public school system.50 Released on March 1, 1999, the report indicated that the rate of autism had increased 273% over
the past 10 years. Reported widely in the press, the California Department of Developmental Services study gave new urgency to calls for investigation of
an autism “epidemic” as the summer approached.51

CONFLUENCE Section: Choose

The events that would bring these three histories together began in 1997, when New Jersey Representative Frank Pallone, representing a district concerned
about environmental mercury poisoning, appended a rider to the FDA Modernization Act of that year to assess all of the agency’s products for mercury
content.52 In response, the Center for Biologics Evaluation and Research (CBER) at the FDA initiated a formal risk assessment of thimerosal in vaccines
beginning in April 1998. By this point, the vaccine schedule had expanded, and three of the vaccines routinely given to infants (diphtheria-tetanus-acellular
pertussis, Haemophilus in�uenzae type b conjugate, and hepatitis B) potentially contained thimerosal. The analysis was completed in the spring of 1999.
The actual cumulative exposure varied considerably, given that not all manufacturers used the preservative, but the CBER scientists calculated that a
minority of infants could receive as much as 187.5 mg of ethylmercury during the �rst 6 months of life. Lacking any standard for ethylmercury, the CBER
team compared this exposure to standards for methylmercury and discovered that it exceeded that set by the Environmental Protection Agency. Although
acknowledging the many uncertainties involved, the FDA responded by inviting vaccine advisory bodies for consultation in June 1999.53

There followed a rapid series of meetings and conference calls involving representatives of the American Academy of Pediatrics and the Centers for Disease
Control and Prevention (CDC), culminating in a joint statement released on July 9, 1999. Although noting that there was no evidence that the use of
thimerosal as a vaccine preservative had caused any true harm, the groups agreed that “thimerosal-containing vaccines should be removed as soon as
possible” given the concerns raised by the Environmental Protection Agency’s guidelines.54 The controversy was now out in the open.

Many have criticized the process leading to the release of the joint statement, charging that it took place too rapidly and without proper consultation from
important parties.55 Its call to suspend the use of hepatitis B virus vaccine in infants younger than 6 months until thimerosal-free vaccine became widely
available was particularly contentious. Although the ban lasted only for several months, it resulted in considerable confusion and inconsistency in hepatitis
B virus vaccine delivery in some hospital nurseries.56 One study later found that the proportion of hospitals failing to vaccinate infants born to seropositive
mothers rose by over 6 times (from 1% to 7%) during the suspension.57 The consequences of this were harder to calculate but clearly worrisome given the
very high (up to 90%) chance that infants who acquire hepatitis B infection at birth will develop the infection in a chronic form, with a signi�cant (25%) risk
of liver cancer.58 By contrast, the statement’s defenders asserted the prime importance of preserving the public’s trust in the vaccine system, particularly
given the rising in�uence of populist “vaccine safety” groups since the 1970s. Manufacturers, moreover, did successfully mobilize to remove thimerosal
from their routine infant vaccines in a remarkably short time; the e�ort was largely complete by the summer of 2001.59,60

Meanwhile, the third of the historical streams, represented by parents within the “alternative” autism community, rapidly entered the debate. As detailed
by journalist David Kirby, it was in fact a group of parents of autistic children (rather than parental organizations critical of vaccination such as the National
Vaccine Information Center) who �rst seized upon thimerosal as an explanation for the autism epidemic. In keeping with their identity as participants in
shaping research, some spent long hours on the computer or in libraries researching studies on mercury. Eventually, their e�orts led to a published study
in Medical Hypotheses that compared the features of autism to various signs reported in past studies and case reports of mercury exposure.61 The
publication of this study in turn helped to legitimize the hypothesis and thereby reinforce a growing body of individual testimonies across the Internet and
in conferences.

Parents organized e�ectively in the political realm as well. The self-designated “Mercury Moms” created an advocacy organization, Safe Minds. They were
instrumental in persuading Congressman Burton to shift his focus from measles–mumps–rubella to thimerosal in his congressional hearings. And they
organized successfully to oppose a rider to the Homeland Security Bill in 2003 that would protect thimerosal’s manufacturer from legal action.62

These events are chosen among many that have taken place since 1999 that illustrate the polarization that soon characterized the entire debate. Although
a full analysis cannot be provided here, two themes deserve emphasis. One is the issue of trust. Physicians and public health leaders have generally turned
to the scienti�c process to sort out the controversy and have been reassured by the negative conclusions of the IOM reports. Vaccine opponents have
repeatedly rejected these studies, charging that the data have been manipulated for political reasons.63 The second factor has been the entry of personal
injury lawyers into the debate, accompanied by full-page advertisements in prominent newspapers and an infusion of �nancial support. Although hardly

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the primary agent in the story, litigation has without doubt fueled the polarization of the debate and further obscured scienti�c testimony through the
promotion of expert witnesses dissenting from the IOM position.64 Today, the mercury–autism hypothesis continues to be accepted widely among the
parents of autistic children.

CONCLUSION Section: Choose

At this point, it is fair to ask whether this narrative should more properly have focused on the story of the thimerosal controversy since 1999. Has not a new
group of actors, including members of Congress, professional groups, antivaccine organizations, and personal injury lawyers, assumed central relevance
since that time? Is it really that necessary to understand the long-term historical trends that converged just prior to the 1999 joint statement?

There are three answers, each corresponding to one of the historical streams already examined. The �rst is directed at the insinuation prevalent on the
Internet that thimerosal was a dubious product smuggled into vaccines by avaricious drug companies bent on pro�ts rather than the welfare of children. A
more sober assessment would suggest that thimerosal was the result of ethical scienti�c and corporate research in the 1920s and 1930s, speci�cally to
improve vaccine safety. Despite questions regarding its e�cacy, it has performed well in practice and posed toxicity so low as to be considered negligible
until recent years.

The second point concerns the history of mercury poisoning. Central to the public story of thimerosal has been a battle over the meaning of “mercury.”
Those in the scienti�c community take it as axiomatic that all forms of mercury are not created equal; in particular, there are good reasons to believe that
the ethylmercury used in vaccines is very di�erent from the methylmercury studied in environmental science. In public discourse, however, such
distinctions are subsumed under a single entity, mercury, with a long and very public history. Perhaps unfairly, history has endowed mercury in all of its
forms with a notoriety that is not easy to erase, as will quickly be discovered by any pediatrician trying to convince an anxious mother that a “trace” of
mercury in a vaccine is safe. One cannot simply brush aside this perception in constructing policy.

Finally, however important personal injury lawyers, vaccine skeptics, and their allies in Congress may have been in shaping the thimerosal controversy since
1999, they did not create it. Parents within the “alternative” wing of the autism community were the primary agents in popularizing the concepts that
autism had become epidemic and that vaccines were its cause. Jumping from the �rst to the second proposition may have been highly conjectural, but the
question of whether the rise in autism is real or de�ned (or both) remains open to reasonable debate. There is genuine anger in the autism community that
has fueled the polarization of the thimerosal debate, but this anger is best understood in terms of frustration with the medical and educational systems,
not the cynical manipulation of lawyers.

Although historical understanding may not readily translate into policy guidelines, it is essential for those responsible for conducting and implementing
such policy. A polarized debate both draws upon and contributes to polarized understandings of history. Participants within each of this story’s three
streams judged the same data using di�erent sets of assumptions, each shaped by history. Articulating and sharing these narratives represent a �rst step
toward transcending the powerful boundaries shaping today’s vaccine controversies.

This work was supported by a National Library of Medicine publication grant (#LM007898).

ENDNOTES Section: Choose

References
1. The 8 reports are available at www.iom.edu/?ID=4705, accessed October 9, 2007. Google Scholar
2. James Colgrove and Ronald Bayer, “Could It Happen Here? Vaccine Risk Controversies and the Specter of Derailment,” Health A�airs 24 (2005): 729–739;
Christopher B. Wilson and Edgar K. Marcuse, “Vaccine Safety—Vaccine Bene�ts: Science and the Public’s Perception,” Nature Reviews Immunology 1 (2001):
160–165. Crossref, Google Scholar
3. Michael Fitzpatrick, MMR and Autism: What Parents Need to Know (London: Routledge, 2004); David Kirby, Evidence of Harm: Mercury in Vaccines and
the Autism Epidemic: A Medical Controversy (New York: St. Martin’s Press, 2005). Google Scholar
4. Institute of Medicine, Immunization Safety Review: Thimerosal-Containing Vaccines and Neurodevelopmental Disorders (Washington, DC: National
Academies Press, 2001); Institute of Medicine, Immunization Safety Review: Vaccines and Autism. (Washington, DC: National Academies Press, 2004).
Google Scholar
5. Roy Porter, The Greatest Bene�t to Mankind: A Medical History of Humanity (New York: W.W. Norton, 1997), 370–374. Google Scholar
6. John H. Brewer, “Mercurials as Antiseptics,” Annals of the New York Academy of Sciences 53 (1950): 211–219; Leonard J. Goldwater, Mercury: A History of
Quicksilver (Baltimore: York Press, 1972), 256–257. Crossref, Medline, Google Scholar
7. AMA Council on Pharmacy and Chemistry, “New and Nono�cial Remedies,” Journal of the American Medical Association 93 (1929): 1809. Crossref, Google
Scholar
8. H. M. Powell and W. A. Jamieson, “Merthiolate as a Germicide,” American Journal of Hygiene 13 (1931): 296–310. Google Scholar
9. K.C. Smithburn, G.E. Kempf, L.G. Zerfas, and L.H. Gilman, “Meningococcic Meningitis: A Clinical Study of One Hundred and Forty-Four Cases,” Journal of
the American Medical Association 95 (1930): 776–780; Powell and Jamieson, “Merthiolate as a Germicide,” 306–307. Crossref, Google Scholar
10. Graham S. Wilson, The Hazards of Immunization (London: Athalone Press, 1967), 75–84. Google Scholar
11. W.A. Jamieson and H.M. Powell, “Merthiolate as a Preservative for Biological Products,” American Journal of Hygiene 14 (1931): 218–224. Google Scholar
12. H.M. Powell and W.A. Jamieson, “On the E�cacy of ‘Merthiolate’ as a Biological Preservative After Ten Years’ Use,” Proceedings of the Indiana Academy

6 sur 10 23/02/2024, 20:04

Mercury, Vaccines, and Autism | AJPH | Vol. 98 Issue 2 https://ajph.aphapublications.org/doi/full/10.2105/AJPH.2007.113159

of Science 47 (1937): 65–70; Olga R. Povitsky and Minnie Eisner, “Merthiolate Versus Phenol as a Preservative for Diphtheria Toxoids,” Journal of
Immunology 28 (1935): 209–213. Google Scholar
13. James H. Madison, Eli Lilly: A Life, 1885–1977 (Indianapolis: Indiana Historical Society, 1989), 95. Google Scholar
14. AMA Council on Pharmacy and Chemistry, “Report to the Council: Organomercurial Compounds,” Journal of the American Medical Association 136
(1948): 36–41. Google Scholar
15. John P. Swann, “Food and Drug Administration,” in A Historical Guide to the US Government, ed. George Thomas Kurian (New York: Oxford University
Press, 1998), 248–254. Google Scholar
16. H.M. Powell, “Antibacterial Action of ‘Merthiolate’ Against Hemolytic Streptococci,” JAMA 137 (1948): 862–864; Brewer, “Mercurials as Antiseptics,” 211–
219. Robert Martenson’s analysis of the literature concluded that later investigators’ con�dence in thimerosal’s safety by the 1950s was grounded in their
own experience, not earlier publications from the Eli Lilly team; Robert L. Martenson, “Analysis Report in the Matter of Easter vs Eli Lilly and Company,”
November 1948 (unpublished). Crossref, Medline, Google Scholar
17. David Oshinsky, Polio: An American Story (Oxford: Oxford University Press, 2005), 205. Google Scholar
18. J.H.M. Axton, “Six Cases of Poisoning After a Parental Organic Mercurial Compound (Merthiolate),” Postgraduate Medicine 48 (1972): 417–421.
Crossref, Google Scholar
19. D.G. Fagan, J.S. Pritchard, T.W. Clarkson, and M.R. Greenwood, “Organ Mercury Levels in Infants With Omphaloceles Treated With Organic Mercurial
Antiseptic,” Archives of Disease in Children 52 (1977): 962–964. Crossref, Medline, Google Scholar
20. S. Gibson, memorandum from assistant director, Bureau of Biologics, FDA to director, Bureau of Biologics, “Use of Thimerosal in Biologics Production,”
February 27, 1976, quoted in Leslie K. Ball, Robert Ball, and R. Douglas Pratt, “An Assessment of Thimerosal Use in Childhood Vaccines,” Pediatrics 107
(2001): 1147–1154. Crossref, Medline, Google Scholar
21. Neil H. Cox and Angela Forsyth, “Thimerosal Allergy and Vaccination Reactions,” Contact Dermatitis 18 (1988): 229–233; Halvor Moller, “All These Positive
Tests to Thimerosal,” Contact Dermatitis 31 (1994): 209–213. Hypersensitivity concerns prompted the FDA to propose rules on the use of thimerosal as a
preservative on 2 occasions; see Department of Health, Education, and Welfare, Food and Drug Administration, “Skin Test Antigens: Proposed
Implementation of E�cacy Review,” Federal Register 42 (September 30, 1977): 52719–52721; Idem, “Mercury-Containing Drug Products for Topical
Antimicrobial Over-the-Counter Human Use: Establishment of a Monograph,” Federal Register 47 (January 5, 1982): 436–442. Crossref, Medline, Google
Scholar
22. Masazumi Harada, “Minamata Disease: Methylmercury Poisoning in Japan Caused by Environmental Pollution,” Critical Reviews in Toxicology 25 (1995):
1–24. For the original description of the symptoms of methylmercury poisoning, see Donald Hunter, Richard Bromford, and Dorothy Russell, “Poisoning by
Methyl Mercury Compounds,” Quarterly Journal of Medicine 9 (1940): 193–214. Crossref, Medline, Google Scholar
23. Masazumi Harada, Minamata Disease, translated by Tsushima Sachie and Timothy S. George (Tokyo: Iwanami Shoten, 2004), 85–112, 205–219. Google
Scholar
24. W. Eugene Smith and Aileen M. Smith, Minamata (New York: Holt, Rinehart, and Winston, 1975). Google Scholar
25. Masazumi Harada, “Congenital Minamata Disease: Intrauterine Methylmercury Poisoning,” Teratology 18 (1978): 285–288. Crossref, Medline, Google
Scholar
26. F. Bakir, S.F. Damluji, L. Amin-Zaki, et al., “Methylmercury Poisoning in Iraq,” Science 181 (1973): 230–241. Crossref, Medline, Google Scholar
27. Kathyryn R. Maha�ey, “Methylmercury: A New Look at the Risks,” Public Health Reports 114 (1999): 403, 407. Google Scholar
28. For a review of the state of knowledge in the 1970s, see Brian J. Koos and Lawrence D. Longo, “Mercury Toxicity in the Pregnant Woman, Fetus, and
Newborn Infant,” American Journal of Obstetrics and Gynecology 126 (1976): 390–409. Crossref, Medline, Google Scholar
29. Laman Amin-Zaki, Sami Elhassani, Mohammed A Majeed, et al., “Intra-Uterine Methylmercury Poisoning in Iraq,” Pediatrics 54 (1974): 587–595.
Medline, Google Scholar
30. Laman Amin-Zaki, Sami Elhassani, Mohammed A Majeed, et al., “Studies of Infants Postnatally Exposed to Methylmercury,” Journal of Pediatrics 85
(1974): 81–84; Laman Amin-Zaki, S.B. Elhassani, M.A. Majeed, et al., “Methylmercury Poisoning in Mothers and Their Suckling Infants,” Developments in
Toxicology and Environmental Science 8 (1980): 75–78; David O. Marsh, Thomas W. Clarkson, Christopher Cox, et al., “Fetal Methylmercury Poisoning:
Relationship Between Concentration in Single Strands of Hairs and Child E�ects,” Archives of Neurology 44 (1987): 1017–1022. Crossref, Medline, Google
Scholar
31. A. Fowler, D.C. Bellinger, R.L. Bornschein, et al., Measuring Lead Exposure in Infants, Children, and Other Sensitive Populations (Washington, DC:
National Academy of Sciences Press, 1993). Google Scholar
32. P. Grandjean, P. Weihe, R.F. White, et al., “Cognitive De�cit in 7-year-old Children with Prenatal Exposure to Methylmercury,” Neurotoxicology and
Teratology 19 (1997): 417–428. Crossref, Medline, Google Scholar
33. Philip W. Davidson, Gary J. Myers, Christopher Cox, et al., “E�ects of Prenatal and Postnatal Methylmercury Exposure From Fish Consumption on
Neurodevelopment: Outcomes at 66 Months of Age in the Seychelles Child Development Study,” Journal of the American Medical Association 280 (1998):
701–707. Crossref, Google Scholar
34. Maha�ey, “Methylmercury,” 403, 407–411. Google Scholar
35. On the role of parental communities in shaping the diagnosis and treatment of autism, see Chloe Silverman, A Disorder of A�ect: Love, Tragedy,
Biomedicine, and Citizenship in American Autism Research, 1943–2003 [PhD dissertation] (Philadelphia: University of Pennsylvania, 2004). Google Scholar
36. Leo Kanner, “Autistic Disturbances of A�ective Contact,” Nervous Child 2 (1943): 217–250. Asperger’s paper was published in German during wartime
and “re-discovered” later by Anglo-American autism researchers; see Uta Frith, “Asperger and His Syndrome,” in Autism and Asperger Syndrome, ed. Uta
Frith (Cambridge: Cambridge University Press, 1991), 1–36. Google Scholar
37. Bruno Bettelheim, The Empty Fortress: Infantile Autism and the Birth of the Self (New York: Free Press, 1967). Google Scholar
38. Bernard Rimland, Infantile Autism: The Syndrome and Its Implications for a Neural Theory of Behavior (London: Methuen, 1965). Google Scholar

7 sur 10 23/02/2024, 20:04

Mercury, Vaccines, and Autism | AJPH | Vol. 98 Issue 2 https://ajph.aphapublications.org/doi/full/10.2105/AJPH.2007.113159

39. Prominent exponents of this approach have included Eric Schopler in the United States and Michael Rutter and Lorna and John Wing in Britain. See
Early Childhood Autism: Clinical, Educational, and Social Aspects, ed. John K. Wing (Oxford: Pergamon Press, 1966); E. Schopler, S.S. Brehm, M. Kinsbourne,
and R.J. Reichler, “E�ect of Treatment Structure on Development in Autistic Children,” Archives of General Psychiatry 24 (1971): 415–421. Google Scholar
40. S. Folstein and M. Rutter, “Infantile Autism: A Genetic Study of 21 Twin Pairs,” Journal of Child Psychology and Psychiatry 18 (1977): 297–321; Peter
Szatami, “The Causes of Autism Spectrum Disorders,” British Medical Journal 326 (2003): 173–174. Crossref, Medline, Google Scholar
41. Michael Rutter added impaired language to Kanner’s 2 criteria of impaired social relationships and preoccupation with sameness, developing the
autistic triad underlying most de�nitions ever since; Rutter, “Diagnosis and De�nition of Childhood Autism,” Journal of Autism and Childhood Schizophrenia
8 (1978): 139–161. On the concept of an autistic spectrum, see Lorna Wing, The Autistic Spectrum (London: Constable, 1996). In the United States, both
developments are re�ected in successive revisions of Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition (Washington, DC:
American Psychiatric Association, 1987) and Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (Washington, DC: American Psychiatric
Association, 1994). Crossref, Medline, Google Scholar
42. E. Schopler and R.J. Reichler, “Parents as Cotherapists in the Treatment of Psychotic Children,” Journal of Autism and Childhood Schizophrenia 1 (1971):
87–102. Behavioral therapy ranges from the primarily rehabilitative approach exempli�ed by Schopler to the more optimistic claims of applied behavioral
analysis and similar methodologies; see O.I. Lovass, “Behavioral Treatment and Normal Educational and Intellectual Functioning in Young Autistic Children,”
Journal of Consulting and Clinical Psychology 55 (1987): 3–9; M.G. Aman, “Treatment Planning for Parents with Autism Spectrum Disorders,” Journal of
Clinical Psychiatry 66 (suppl 10) (2005): 38–45. Crossref, Medline, Google Scholar
43. Judith S. Palfrey and John S. Rodman, “Legislation for the Education of Children With Disabilities,” in Developmental-Behavioral Pediatrics, 3rd edition,
ed. Melvin D. Levine, Willam B. Carey, and Allen C. Crocker (Philadelphia: W.B. Saunders, 1999), 869–872. Google Scholar
44. Lorna Wing, “Autistic Spectrum Disorders: No Evidence for or Against an Increase in Prevalence,” British Medical Journal 312 (1996): 327–328; Eric
Fombonne, “Is There an Epidemic of Autism?” Pediatrics 107 (2001): 411–413. Crossref, Medline, Google Scholar
45. Silverman, “A Disorder of A�ect,” 360–451. Google Scholar
46. J. Pangorn and S. Baker, Autism: E�ective Biomedical Treatments (Have We Done Everything We Can for This Child?): Individuality in an Epidemic (San
Diego: Autism Research Institute, 2005). Google Scholar
47. A.J. Wake�eld, S.H. Murch, A. Anthony, et al., “Ileal–Lymphoid–Nodular Hyperplasia, Non-Speci�c Colitis, and Pervasive Developmental Disorder in
Children,” Lancet 351 (1998): 637–641. Crossref, Medline, Google Scholar
48. Fitzpatrick, MMR and Autism. Google Scholar
49. Autism: Present Challenges, Future Needs—Why the Increased Rates? Hearing Before the Committee on Government Reform, House of
Representatives, 106th Cong, 2nd Sess (April 6, 2000); Brian Vastag, “Congressional Autism Hearings Continue: No Evidence MMR Vaccine Causes Disorder,”
Journal of the American Medical Association 285 (2001): 2567–2568. Google Scholar
50. Kirby, Evidence of Harm, 89–90. Google Scholar
51. Changes in the Population of Persons With Autism and Pervasive Developmental Disorders in California’s Developmental Services System: 1987
Through 1998: A Report to the Legislature (Sacramento: California Department of Developmental Services, March 1, 1999). Google Scholar
52. Arthur Allen, “The Not-So-Crackpot Autism Theory,” New York Times Magazine, November 10, 2002. Medline, Google Scholar
53. Leslie K. Ball, Robert Ball, and R. Douglas Pratt, “An Assessment of Thimerosal Use in Childhood Vaccines,” Pediatrics 107 (2001): 1147–1154. Crossref,
Medline, Google Scholar
54. “Joint Statement of the American Academy of Pediatrics (AAP) and the United States Public Health Service (USPHS),” Pediatrics 104 (1999): 568–569.
Crossref, Medline, Google Scholar
55. For details on the negotiations leading to the joint statement, see Gary L. Freed, Margie C. Andrae, Anne E. Cowan, and Samuel L. Katz, “The Process of
Public Policy Formation: The Case of Thimerosal in Vaccines,” Pediatrics 109 (2002): 1153–1159; “Uproar Over a Little-Known Preservative, Thimerosal,
Jostles US Hepatitis B Vaccination Policy,” Hepatitis Control Reports 4 (Summer 1999): 1–10. Crossref, Medline, Google Scholar
56. J.B. Seal and R.S. Daum, “What Happened to Primum non Nocere?” Pediatrics 201 (2001): 1177–1179. Crossref, Google Scholar
57. Sarah J. Clark, Michael D. Cabana, Tasneem Malik, Hussain Yusuf, and Gary L. Freed, “Hepatitis B Vaccination Practices in Hospital Nurseries Before and
After Changes in Vaccine Recommendations,” Archives of Pediatrics and Adolescent Medicine 135 (2001): 915–920; “Impact of the 1999 AAP/USPHS Joint
Statement on Thimerosal in Vaccine on Infant Hepatitis B Vaccination Practices,” MMWR Morbidity and Mortality Weekly Report 50 (2001): 94–97. Google
Scholar
58. Francis J. Mahoney and Mark Kane, “Hepatitis B Vaccine,” in Vaccines, 3rd edition, ed. Stanley A. Plotkin and Walter A. Orenstein (Philadelphia: W.B.
Saunders, 1999), 159–160. Google Scholar
59. Neal Halsey, “Limiting Infant Exposure to Thimerosal and Other Sources of Mercury,” JAMA 282 (1999): 1763–1765; American Academy of Pediatrics
Committee on Infectious Diseases and Committee on Environmental Health, “Thimerosal in Vaccines—An Interim Report to Clinicians,” Pediatrics 104
(1999): 570–574; Neal Halsey and Lynn Goldman, “Balancing Risks and Bene�ts: Primum non Nocere Is Too Simplistic,” Pediatrics 108 (2001): 466–467.
Crossref, Medline, Google Scholar
60. On the modern revival of vaccine resistance, see James Colgrove, State of Immunity: The Politics of Vaccination in Twentieth-Century America (Berkeley:
University of California Press, 2006), 186–252; Je�rey P. Baker, “The Pertussis Vaccine Controversy in Great Britain, 1974–1986,” Vaccine 21 (2003): 4003–
4010; Robert D. Johnston, “Contemporary Anti-Vaccination Movements in Historical Perspective,” in The Politics of Healing: Histories of Alternative Medicine
in Twentieth-Century North America, ed. Robert D. Johnston (New York: Routledge, 2004), 259–286. Google Scholar
61. S. Bernard, A. Enyati, L. Redwood, H. Roger, and T. Binstock, “Autism: A Novel Form of Mercury Poisoning,” Medical Hypotheses 56 (2001): 462–471;
Kirby, Evidence of Harm, 46–78. Crossref, Medline, Google Scholar
62. Kirby, Evidence of Harm, 1–7. Google Scholar
63. One reason that many parents have not accepted the IOM Report’s conclusion is their belief that the CDC deliberately manipulated data in early

8 sur 10 23/02/2024, 20:04

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analyses of the Vaccine Safety Datalink, a charge that the primary researchers have patently denied. See Kirby, Evidence of Harm, 270–299; T. Verstraeten,
R.L. Davis, F. deStefano, et al., “Safety of Thimerosal-Containing Vaccines: A Two-Phased Study of Computerized Health Maintenance Organization
Databases,” Pediatrics 112 (2003): 1039–1048. Google Scholar
64. Among many examples, see David A. Geier and Mark R. Geier, “An Assessment of the Impact of Thimerosal on Childhood Neurodevelopmental
Disorders,” Pediatric Rehabilitation 6 (2003): 97–102. Crossref, Medline, Google Scholar

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