Journal of Toxicology and Environmental Health, Part A, 74:1185–1194, 2011
Copyright © Taylor & Francis Group, LLC
ISSN: 1528-7394 print / 1087-2620 online
ANCESTRY OF PINK DISEASE (INFANTILE ACRODYNIA) IDENTIFIED AS A RISK
FACTOR FOR AUTISM SPECTRUM DISORDERS
Kerrie Shandley, David W. Austin
Swinburne Autism Bio-Research Initiative (SABRI), Brain and Psychological Sciences Research
Centre, Swinburne University of Technology, Hawthorn, Victoria, Australia
Pink disease (infantile acrodynia) was especially prevalent in the first half of the 20th century.
Primarily attributed to exposure to mercury (Hg) commonly found in teething powders, the
condition was developed by approximately 1 in 500 exposed children. The differential risk
factor was identified as an idiosyncratic sensitivity to Hg. Autism spectrum disorders (ASD)
have also been postulated to be produced by Hg. Analogous to the pink disease experience,
Hg exposure is widespread yet only a fraction of exposed children develop an ASD, sug-
gesting sensitivity to Hg may also be present in children with an ASD. The objective of this
study was to test the hypothesis that individuals with a known hypersensitivity to Hg (pink
disease survivors) may be more likely to have descendants with an ASD. Five hundred and
twenty-two participants who had previously been diagnosed with pink disease completed a
survey on the health outcomes of their descendants. The prevalence rates of ASD and a variety
of other clinical conditions diagnosed in childhood (attention deficit hyperactivity disorder,
epilepsy, Fragile X syndrome, and Down syndrome) were compared to well-established gen-
eral population prevalence rates. The results showed the prevalence rate of ASD among the
grandchildren of pink disease survivors (1 in 25) to be significantly higher than the compara-
ble general population prevalence rate (1 in 160). The results support the hypothesis that Hg
sensitivity may be a heritable/genetic risk factor for ASD.
Pink disease, or infantile acrodynia as it
was also known (primarily in Europe and
America), was an especially prevalent condi-
tion in Australia, North America, and Central
Europe in the first half of the 20th century
(Rocaz 1933). The first description of pink dis-
ease in the literature dates back to 1903 by
Selter, a German physician, although cases in
Australia predate this time by at least two
decades (Selter 1903; Wood and Wood 1935).
Pink disease remained in relative obscurity in
the greater medical community until 1914,
when it was again described, this time by Swift,
Received 29 January 2011; accepted 5 May 2011.
This study was funded by donations generously made to the Swinburne Autism Bio-Research Initiative (www.sabri.org.au). We
thank Di Farnsworth, the facilitator of the Pink Disease Support Group (www.pinkdisease.org), for her support of the study and role in the
recruitment of Pink Disease survivors. We also thank Sam Critchley for her assistance in entering the survey data and Dr. Denny Meyer
and Dr. Jahar Bhowmik for their statistical assistance.
Address correspondence to David W. Austin, Swinburne Autism Bio-Research Initiative (SABRI), Brain and Psychological
Sciences Research Centre, Swinburne University of Technology, Mail H29, PO Box 218, Hawthorn, Victoria 3122, Australia. E-mail:
an Australian-born physician, at an Australasian
medical congress in New Zealand (Swift 1914).
Case studies provided a comprehensive
clinical picture of pink disease long before
its etiology was established. The most com-
monly reported symptoms included: irritability,
neurosis, photophobia (light sensitivity), hyper-
hidrosis (excessive sweating), hypotonia (low
muscle tone), ataxia (lack of coordination),
digestive problems (including loss of weight,
loss of appetite, vomiting, and constipation),
anemia, excessive salivation, respiratory prob-
lems, lethargy, extreme misery, slurring/loss
1186 K. SHANDLEY AND D. W. AUSTIN
of speech, loosening/loss of teeth, swollen
extremities, and perhaps most famously (and
from which the name “pink disease” was
derived), marked reddening of the extremi-
ties, particularly the hands and feet (Rocaz
1933; Wood and Wood 1935; Leys 1950).
Fatality was reasonably high, with death result-
ing in 10–33% of cases (Rocaz 1933). For the
survivors, recovery was considered to be com-
plete, although research conducted in recent
decades revealed medical sequelae to be high
in this group, including Young’s syndrome
(infertility in men) and bronchiectasis (Hendry
et al. 1993; Williams and O’Reilly 1959).
In 1945, a critical study became the cata-
lyst that led to the discovery of the etiology of
pink disease. Upon noticing a similarity of pink
disease symptomatology to arsenic and thal-
lium poisoning, American physicians Warkany
and Hubbard (1948) undertook a quantitative
metal determination of 14 children diagnosed
with pink disease and found that 12 of the
14 children had elevated levels of urinary mer-
cury (Hg). A replication study by Warkany and
Hubbard (1951) consolidated the finding with
Hg levels elevated in 92% of 41 children diag-
nosed with pink disease in comparison to 15%
of controls. Although Hg was used in a wide
range of medicinal products at the time, the
primary culprit was determined to be teething
powders containing calomel (mercurous chlo-
ride). Following the removal of calomel from
most teething powders in 1954, pink dis-
ease essentially disappeared (Curtis et al.
1987). Interestingly, however, while millions of
teething powders were sold (some 7 million
annually in North England alone of one of
the most famous brands, Steedman’s Teething
Powder), only 1 in 500 exposed children devel-
oped pink disease (Emsley 2005). The differen-
tial risk factor was identified as an idiosyncratic
sensitivity to Hg (Warkany and Hubbard 1948;
Bivings 1949; Bivings and Lewis 1948).
It was postulated that autism spectrum dis-
orders (ASD), which are primarily comprised
of autistic disorder and Asperger’s disorder,
also have a pathogenesis stemming from Hg
exposure (Austin 2008; Bernard et al. 2001;
Mutter et al. 2005). The mounting evidence
is compelling. Behavioral changes, hyperactiv-
ity, and alterations in spontaneous and learned
behaviors have been observed in animals
exposed to Hg during the prenatal or early post-
natal period (Agency for Toxic Substances and
there were significant elevations of Hg in the
urine of children with autism in comparison to
controls, as well as in urinary markers of Hg
damage (Austin and Shandley 2008; Bradstreet
et al. 2003; Geier and Geier 2007; Nataf et al.
2006). Other investigations found the sever-
ity of autism to positively correlate with the
2009; Geier et al. 2009; Holmes et al. 2003). In
addition, some epidemiological studies demon-
strated an association between Hg exposure
and ASD prevalence (Gallagher and Goodman
2010; Geier and Geier 2006a; Palmer et al.
2006; 2009; Windham et al. 2006), but not all
studies confirmed this correlation (Hviid et al.
2003; Verstraeten et al. 2003).
Mercury contained in vaccines (as a
preservative under the tradename Merthiolate,
but more commonly known as thiomersal/
thimerosal), dental amalgams (silver fillings),
both in utero and in their early years (Austin
2008). However, not all children exposed to
such sources of Hg develop an ASD, suggesting,
as was the case with pink disease, that a hyper-
sensitivity to the adverse effects of Hg needs
to be present in addition to the Hg exposure
for the condition to manifest. Therefore, the
Hg–autism hypothesis is, in reality, a two-part
hypothesis that states that Hg exposure com-
bined with a genetic/physiological sensitivity to
Hg or a predisposition to impaired Hg excretion
capacity leads to a chronic elevation of Hg in
the brain and body (Bernard et al. 2001).
The purpose of the present study was to test
the Hg–autism hypothesis. If the hypothesis is
indeed correct, and a sensitivity to Hg is herita-
ble (genetic), the prevalence of ASD among the
descendants of a cohort confirmed as having a
hypersensitivity to Hg (pink disease survivors)
should be higher than a comparable general
ANCESTRY OF PINK DISEASE A RISK FACTOR FOR AUTISM 1187
MATERIALS AND METHODS
Participants and Study Design
Ethical approval to conduct the present
study was received from the Swinburne
University Human Research Ethics Committee.
Individuals who had previously been diag-
nosed with pink disease were invited to
participate in this study by completing a sur-
vey either online, by mail, or via telephone
interview. In cases where the pink disease
survivor was incapacitated or deceased, fam-
ily members were able to complete the sur-
vey as a proxy. The Australian Pink Disease
Support Group (PDSG) estimated that approx-
imately 5000 survivors were still living at
the time of study commencement in July
2009 (D Farnsworth personal communication
19 November 2009).
Participants were recruited via the PDSG,
an Australian not-for-profit group dedicated to
providing support and information to pink dis-
ease survivors and their families—the only such
group in the world. The PDSG maintains a
membership database and sent out the sur-
vey to all of its past and present members, in
addition to advertising the study on its website
(www.pinkdisease.org). In order to minimize
response bias, the true purpose of the study
was not included on recruitment materials sent
out to potential participants; instead, recruit-
ment materials indicated that the purpose of
the study was to investigate the general health
outcomes of the descendants of pink disease
survivors. In total, 2600 surveys were sent,
2000 by mail and 600 by e-mail, with an antic-
ipated overlap of approximately 300 members
receiving the survey by both mail and e-mail. A
chance to win one of 10 shopping vouchers to
the value of $75 was offered as an incentive to
The survey included sociodemographic
questions regarding the pink disease survivor
(gender, date of birth, current place of res-
idence), the relationship of the respondent
to the survivor (if the survey was completed
by a proxy), and information pertaining to
the pink disease survivor’s descendants (chil-
dren and grandchildren). With respect to the
descendants, survey respondents were asked
to provide details regarding the number of
children and grandchildren, the gender and
age of each, and whether they had been
diagnosed with any of the following condi-
tions prior to the age of 16 years: autism,
Asperger’s disorder, attention deficit hyper-
activity disorder (ADHD), epilepsy, Fragile X
syndrome, mental retardation, and/or Down
The survey was commenced or returned by
531 people (a response rate of 23.1%); how-
ever, 9 surveys were removed from analysis, as
6 were repeated entries, and 3 surveys were
incomplete. This left a total of 522 surveys that
were included in the analysis. The character-
istics of the pink disease survivor cohort are
provided in Table 1.
TABLE 1. Characteristics of the Pink Disease Survivor Cohort
(n = 522)
(n = 105)
(n = 409) Parameter
Survey completion type
Survey respondent status
Current place of residencec
New South Wales
Australian Capital Territory
Note. PD = pink disease.
aGender was not provided by eight survey respondents; there-
fore, the total is not the sum of male and female in all cases.
bWhere the survey was completed by proxy the most common
person was the mother (n = 5), followed by the daughter (n = 4),
wife/widow (n = 3), and granddaughter (n = 1).
cPlace of residence was not provided by one survey
dWhere the survivor wasn’t located in Australia, the next most
common location was the United Kingdom (n = 38) followed by
New Zealand (n = 14) and Canada (n = 5).
1188 K. SHANDLEY AND D. W. AUSTIN
Descendants of Pink Disease Survivors
Pink disease survivors had a
cumulative total of 1103 children. Only live
births, biological children, and children surviv-
ing to at least 5 yr were included in the analy-
sis; therefore, 17 children were not included
for the following reasons: 7 children were
adopted, 4 stillborn, and 6 died at an early age
(cot death: n = 2, prematurity: n = 1, con-
genital heart disease: n = 1, immature lungs:
n = 1, unspecified: n = 1). Additionally, three
of the survey respondents stated that they had
children but failed to provide details and were
therefore not included in the analysis. This left
a total of 1086 children that were included. Of
the 522 survey respondents, 79.5% (n = 415)
stated that they had at least one child, with
the average being 2.2 children (range: 1–8).
The mean age of the children was 37.1 yr
(SD = 8.81), ranging from 3 to 61 yr.
Pink disease survivors had
a cumulative total of 1380 grandchildren. As
was the case for children, only live births, bio-
logical grandchildren, and grandchildren sur-
viving to at least 5 yr were included in the
analysis. Therefore, 14 grandchildren were not
included, as 8 grandchildren were stillborn and
6 died at an early age (Potter’s syndrome:
n = 1, Werdnig Hoffmann’s disease: n = 1,
stroke in the womb: n = 1, congenital heart
defect: n = 1, unspecified: n = 1). This left a
total of 1366 grandchildren that were included
in the analysis. Of the 522 survey respondents,
60.7% (n = 317) stated that the pink disease
survivor had at least one biological grandchild,
with an average of 4.3 grandchildren (range:
1–15). The mean age of the grandchildren
was 11.3 yr (SD = 7.65), ranging from <1
to 38 yr.
The numbers of children and grandchildren
diagnosed with autism, Asperger’s disorder,
ADHD, epilepsy, fragile X syndrome, mental
retardation or Down syndrome are presented
in Table 2.
The general population ASD prevalence
rates used as the comparison group for this
study were taken from a report commis-
sioned by the Australian Advisory Board on
Autism Spectrum Disorders (MacDermott et al.
2007). ASD prevalence is well understood
to be difficult to measure, due, in part,
to changing diagnostic criteria and databases
of variable quality (Charman et al. 2009).
The Australian Advisory Board data, however,
were largely immune from these confound-
ing variables as they were gathered over a
period of time when diagnostic criteria for
autism and Asperger’s disorder did not change.
Data were collected from multiple sources
across health, disability, and education sec-
tors in addition to Australian state and terri-
tory autism associations, allowing for the vast
TABLE 2. Frequency of Self-Reported Clinical Conditions Among the Descendants of Pink Disease Survivors
(n = 1086)
(n = 1366)
(n = 545)
(n = 513)
(n = 638)
(n = 567)
Fragile X syndrome
Note. ADHD = attention deficit hyperactivity disorder.
aGender was not provided for all children and grandchildren, therefore the total is not the sum of male
and female in all cases.
ANCESTRY OF PINK DISEASE A RISK FACTOR FOR AUTISM1189
majority of Australian ASD cases to be cap-
tured. Furthermore, the reported rates were
highly consistent with other ASD prevalence
studies conducted internationally around that
same time (Centers for Disease Control and
This study presents the comparative rates
for two age groups used in the Australian
Advisory Board report (6–12 and 13–16 yr) for
the most recent year for which data is available,
2005. The Australian Advisory Board calcu-
lated its ASD prevalence rates from Centrelink
data. Centrelink is an Australian federal gov-
ernment social service agency and is consid-
ered the most comprehensive single source
of Australian ASD data. Figures 1 and 2 pro-
vide a graphical comparison of the preva-
lence rates of autism and Asperger’s disor-
der, respectively, among the general population
reported by the Australian Advisory Board and
the age-matched grandchildren of pink dis-
ease survivors. Only data for grandchildren are
reported here, as the children of the pink dis-
ease cohort were mainly born in the 30-year
period from 1950 to 1980, a period for which
no reliable Australian ASD population preva-
lence rates are available. The most recent
Australian ASD prevalence rate for children
6–12 years is 1 in 160, 13–16 years 1 in 272,
and for 6–16 years, 1 in 189 (MacDermott
et al. 2007). This figure is a combination of the
autism and Asperger’s disorder rates in 2005.
The comparative ASD prevalence rate for the
grandchildren of pink disease survivors aged
6–12 years is 1 in 25 (n = 398), 13–16 years
1 in 35 (n = 141), and for 6–16 years, 1 in 27
(n = 539).
To determine whether the difference in
ASD prevalence rate between the pink disease
grandchildren and the general population is sig-
nificant and, furthermore, whether there is an
elevated risk for disease generally among pink
disease descendants (for the clinical condi-
tions captured in our survey: ADHD, epilepsy,
Fragile X syndrome, and Down Syndrome),
one-sided Poisson probabilities were calcu-
lated, the results of which are presented
in Table 3. Ninety-five percent confidence
intervals were calculated using Byar’s approx-
imation. Well-established population preva-
lence rates were used as a comparison for
fragile X syndrome (Fragile X Association of
Australia 2009) and Down syndrome (Down’s
Syndrome Association of Victoria 2009). For
ADHD, there is no definitive agreement regard-
ing an accepted prevalence rate, with fig-
ures ranging from 1.7 to 6%; consequently,
the midpoint (3.85%) was used as the com-
parison rate (Buckmeister 2004). In Australia,
there have been no apparent studies under-
taken to determine the prevalence of epilepsy
in childhood. Consequently, for this study,
Years of age
FIGURE 1. Autism prevalence rates for children aged 6–12 and 13–16 years among the Australian population and the grandchildren of
pink disease survivors.
1190 K. SHANDLEY AND D. W. AUSTIN
Years of age
FIGURE 2. Asperger’s disorder prevalence rates for children aged 6–12 and 13–16 years among the Australian population and the
grandchildren of pink disease survivors.
TABLE 3. Comparison of Observed and Expected Cases of Clinical Conditions Among the Grandchildren of
Pink Disease Survivors Aged 6–16 Years at 2005 (n = 539)
Fragile X syndrome
Note. SIR = Standardized incidence ratios; ASD = autism spectrum disorder; ADHD = attention deficit
hyperactivity disorder; Asterisk indicates lower limit for fragile X males and down syndrome not calculable;
Data for males and females were pooled unless otherwise stated.
the Australian adult epilepsy prevalence rate
was used for comparison (0.68%) (Australian
Bureau of Statistics 1998). This figure is broadly
equivalent to international studies reporting
both childhood and adult prevalence rates for
epilepsy (Sridharan 2002; Oka et al. 2006).
Mental retardation was not included in this
analysis as an accepted prevalence rate is not
available due to complications in measuring
intellectual disability among school-aged chil-
dren (Wen 1997). As is shown in Table 3,
the elevated risk for an ASD among pink dis-
ease grandchildren was significant. There were
no significant elevations in prevalence among
the grandchildren on any of the non-ASD
The prevalence of ASD was found to
be significantly higher among the grandchil-
dren of pink disease survivors in comparison
to the general population, providing support
for the hypothesis that Hg sensitivity may
be a heritable/genetic risk factor for ASD.
Furthermore, an examination of the prevalence
rates of a group of non-ASD clinical condi-
tions (ADHD, epilepsy, Fragile X syndrome,
and Down syndrome) among the pink disease
descendants and the general population indi-
cates there is not a general elevated risk for
disease among this cohort, but rather a specific
risk for ASD. An alternative explanation for the
ANCESTRY OF PINK DISEASE A RISK FACTOR FOR AUTISM1191
findings may relate to the higher body burden
of Hg in a parent being passed to their off-
spring. It is difficult to conceptualize how this
may occur in terms of paternal transfer, but the
phenomenon of Hg preferentially distributing
to the developing fetus via the umbilical cord
in Hg-exposed mothers is well documented
(Sakamoto et al. 2010).
As identified earlier, numerous studies
demonstrated a relationship between ASD
and Hg (Agency for Toxic Substances and
Disease Registry 1999; Austin and Shandley
2008; Bradstreet et al. 2003; Geier and Geier
2006a; 2007; Nataf et al. 2007; Adams et al.
2009; Geier et al. 2009; Holmes et al. 2003;
Gallagher and Goodman 2010; Palmer et al.
2006; 2009; Windham et al. 2006), and our
results add further compelling evidence in sup-
port of this relationship. The unique contribu-
tion of this study is that, to our knowledge,
it is the first to examine the “individual sus-
ceptibility” variable inherent in the Hg–autism
hypothesis. Our results suggest that this variable
may have a heritable component and there-
fore, of course, a genetic basis. What our results
do not do, however, is enable an understand-
ing of the degree to which the susceptibility is
inheritable and the mechanism by which this
may occur. This is clearly an important focus
for future research.
A possible mechanism for Hg-induced
autism was proposed by James et al. (2004) and
Geier and Geier (2006b), who demonstrated
that oxidative stress is high and glutathione
(GSH) levels are low in children with autism.
This is entirely consistent with an etiology of
autism based on a gene–Hg interaction, as low
GSH predisposes an individual to damage from
Hg exposure by limiting the body’s capacity to
both minimize oxidative damage produced by
the metal and excrete the toxin.
Of additional note is the gender ratio
in which the descendants of the pink dis-
ease cohort were diagnosed with ASD. ASD is
reported to occur more commonly in males;
typically the quoted ratio is four males to one
female (MacDermott et al. 2007). Interestingly,
the present study replicates this pattern, with
male descendants approximately fourfold more
likely to be reported as diagnosed with an
ASD in comparison to female descendants.
Unfortunately, data are not available to con-
firm (or disconfirm) whether males were more
likely to be stricken with pink disease, as the
condition was never mandated as a reportable
The Hg–autism hypothesis engenders pas-
sionate debate on both sides; however, the
cumulative science in this field is now of
such depth and breadth that it is difficult, if
not impossible, to be completely dismissive of
the Hg–autism link. Furthermore, our findings
clearly suggest that individuals with a fam-
ily history of pink disease are at significantly
greater risk of having a grandchild with an ASD
than the general population. Irrespective of
the Hg–autism hypothesis, this has implications
for public and environmental health, fields of
genetic counseling and family planning, and
autism research generally.
The present study design had several
response biases and maximize the validity of
the data, the true purpose of the study was
not included on recruitment materials sent
out to potential participants (i.e., informa-
tion statement); instead, recruitment materi-
als merely stated that the researchers were
investigating the health outcomes of their
descendants. Recruitment was maximized by
obtaining the assistance of the Australian Pink
Disease Support Group, which sent out sur-
vey packs to its members, both past and
present, and publicized the study online. In
addition, pink disease survivors were provided
with a variety of response format options
(online, telephone, mail). This is especially
important as we were largely dealing with an
elderly cohort. A further strength was that our
comparison groups (grandchildren and general
population) were matched for age and birth
A challenge encountered with this study
was findingan appropriate
ADHD. As mentioned earlier, no agreement
has been reached regarding a definitive preva-
lence rate for ADHD with estimates ranging
1192 K. SHANDLEY AND D. W. AUSTIN
from 1.7 to 6%. Therefore, the difference
between the observed and expected cases
displayed in Table 3 for ADHD needs to be
viewed with caution. Weaknesses of this study
include the fact that independent assessments
of the pink disease survivors’ descendents
were not conducted in order to validate
the accuracy of the self-reported diagnoses.
Information on other variables hypothesized
to play a role in the development of ASD,
such as birth weight, breastfeeding history, or
maternal and paternal age, was not collected.
Nevertheless, the results shed significant light
on the gene–environment interaction hypothe-
sized to underpin the etiology of ASD. The role
that accessory factors such as birth weight and
breastfeeding history may play in the etiology
warrants further research.
Given that Hg is well established as a potent
young children), and that the findings from this
study show that individuals with a confirmed
hypersensitivity to Hg are at significantly greater
risk of having a descendant with an ASD, it
health professionals and health policy makers
to minimize Hg exposure (particularly for preg-
nant and nursing mothers and their children).
Furthermore, there is an urgent need to fund
research programs designed to build upon our
understanding of the gene–environment patho-
genesis (and possibly pathogeneses) of ASD.
in nature so as to facilitate research into multi-
focus on environmental triggers (i.e., Hg) and
heritable (genetic) risk factors.
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