Environmental Health Perspectives • volume 119 | number 4 | April 2011
Electronic waste (ewaste) has emerged as
a critical global environmental health issue
because of its massive production volume
and insufficient management policy in many
countries (Ogunseitan et al. 2009). Ewaste
includes waste cathode ray tube (CRT) tele
visions, desktops, laptops, CRT monitors,
liquid crystal display (LCD) monitors, cell
phones, keyboards, computer mice, print
ers, and copiers. Ewaste contains metals and
persistent organic pollutants (POPs); inap
propriate recycling processes occur in sev
eral developing countries and result in the
release of these toxicants into the environ
ment (LaDou and Lovegrove 2008; Robinson
2009). Although serious health concerns arise
from these primitive recycling activities, the
research needs are largely unaddressed. The
developing fetus and child are particularly
vulnerable to several known and suspected
developmental neurotoxicants in ewaste.
In this review, we survey the literature to
provide updated information about major toxi
cants in ewaste, potential neuro developmental
toxicity in children, and potential preventa
tive measures to reduce exposure. Because the
rate of ewaste accumulation is startling and
the combinatorial effects of toxicants are com
plex, this review addresses an urgent need to
evaluate potential adverse health effects of this
unprecedented exposure scenario.
Production and Management
Ewaste is the fastestgrowing stream of
municipal solid waste, but its management
is a significant environmental health con
cern. It is estimated that 20–50 million tons
of ewaste are produced annually worldwide;
the United States, Western Europe, China,
Japan, and Australia are the major produc
ers [Cobbing 2008; Davis and Herat 2010;
Robinson 2009; United Nations Environment
Programme (UNEP) 2005]. Figure 1 shows
an incomplete list of ewaste volume and
major informal recycling sites. According to a
U.S. Environmental Protection Agency (EPA)
estimate, the United States generated approxi
mately 2.5 million tons of ewaste in 2007,
which accounts for about 2% of municipal
solid waste and has a projected annual increase
of 3–5% (U.S. EPA 2008). In the United
States, only about 18% of ewaste is collected
for recycling, with the remaining 80% sent to
landfill and 2% for incineration (U.S. EPA
2007, 2008). Landfill can cause metal leaching
from the ewaste (Dagan et al. 2007). Burning
ewaste may produce extremely toxic dioxins
and furans (Li et al. 2007). Environmentally
friendly recycling has not been widely used,
although it is a promising approach to tackle
the ewaste problem (UNEP 2009). The
European Union has enacted two directives
to address the increasing concerns on ewaste:
the Restriction on the Use of Hazardous
Substances (RoHS) and the Waste Electrical
and Electronic Equipment (WEEE) (European
Union 1995, 1996; LaDou and Lovegrove
2008; Ogunseitan et al. 2009). The RoHS
directive restricts the use of lead (Pb), cad
mium (Cd), mercury (Hg), hexavalent chro
mium [Cr(VI)], polybrominated biphenyls,
and polybrominated diphenyl ethers (PBDEs)
in new electronic devices. The WEEE directive
requires the manufacturers to take responsibil
ity for collecting and recycling (“takeback”)
of the ewaste. In contrast, the United States
does not have legally enforceable federal poli
cies to regulate ewaste despite a patchwork of
legislation in about 25 states (e.g., mandating
statewide ewaste recycling or banning land
fill disposal of CRT monitors) [Electronics
Take Back Coalition (ETBC) 2010; LaDou
and Lovegrove 2008; Ogunseitan et al. 2009].
These include most coastal states, the Great
Lakes states, Oklahoma, and Texas. Japan has
an existing recycling system for limited home
electrical appliances, but it does not cover
all ewaste, and illegal dumping and transfer
still occur (Aizawa et al. 2008; LaDou and
Although the Basel Convention regulates
transboundary movement of hazardous waste,
significant amounts of ewaste have been
exported to developing countries and recycled
in local towns and villages, using primitive
technologies (LaDou and Lovegrove 2008). In
the biomedical literature, primitive recycling
of ewaste occurs in Guiyu, Taizhou, and
Jinghai, China (Huo et al. 2007; Wong et al.
2007), Bengaluru and Dehli, India (Chatterjee
2008; Ha et al. 2009), Lagos, Nigeria
(Osibanjo and Nnorom 2007; Schmidt 2006),
and Trang Minh, Dong Mai, and Bui Dau,
Vietnam (Tue et al. 2010) (see also Figure 1).
A recent report listed a few other countries
that may have smallscale informal ewaste
recycling (Brazil, Colombia, Kenya, Mexico,
Address correspondence to A. Chen, Division of
Epidemiology and Biostatistics, Department of
Environmental Health, University of Cincinnati
College of Medicine, P.O. Box 670056, Cincinnati,
OH 45267 USA. Telephone: (513) 5582129. Fax:
(513) 5584397. Email: firstname.lastname@example.org
This work is supported partly by National Institute
of Environmental Health Sciences grants P30
ES006096 and RC4ES019755.
The authors declare they have no actual or potential
competing financial interests.
Received 18 May 2010; accepted 20 October 2010.
Developmental Neurotoxicants in E-Waste: An Emerging Health Concern
Aimin Chen,1 Kim N. Dietrich,1 Xia Huo,2 and Shuk-mei Ho1
1Department of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA; 2Analytical Cytology
Laboratory and Key Immunopathology Laboratory of Guangdong Province, Shantou University Medical College, Shantou, Guangdong,
People’s Republic of China
oBjective: Electronic waste (e-waste) has been an emerging environmental health issue in both
developed and developing countries, but its current management practice may result in unintended
developmental neurotoxicity in vulnerable populations. To provide updated information about the
scope of the issue, presence of known and suspected neurotoxicants, toxicologic mechanisms, and
current data gaps, we conducted this literature review.
data sources: We reviewed original articles and review papers in PubMed and Web of Science
regarding e-waste toxicants and their potential developmental neurotoxicity. We also searched pub-
lished reports of intergovernmental and governmental agencies and nongovernmental organizations
on e-waste production and management practice.
data extraction: We focused on the potential exposure to e-waste toxicants in vulnerable popu-
lations—that is, pregnant women and developing children—and neurodevelopmental outcomes. In
addition, we summarize experimental evidence of developmental neurotoxicity and mechanisms.
data synthesis: In developing countries where most informal and primitive e-waste recycling
occurs, environmental exposure to lead, cadmium, chromium, polybrominated diphenyl ethers,
polychlorinated biphenyls, and polycyclic aromatic hydrocarbons is prevalent at high concentrations
in pregnant women and young children. Developmental neurotoxicity is a serious concern in these
regions, but human studies of adverse effects and potential mechanisms are scarce. The unprec-
edented mixture of exposure to heavy metals and persistent organic pollutants warrants further
studies and necessitates effective pollution control measures.
conclusions: Pregnant women and young children living close to informal e-waste recycling sites
are at risk of possible perturbations of fetus and child neurodevelopment.
key words: cadmium, chromium, developmental neurotoxicity, epigenetics, e-waste, lead, mercury,
polybrominated diphenyl ethers, toxicologic mechanisms. Environ Health Perspect 119:431–438
(2011). doi:10.1289/ehp.1002452 [Online 15 November 2010]
Chen et al.
volume 119 | number 4 | April 2011 • Environmental Health Perspectives
Morocco, Peru, Senegal, South Africa, and
Uganda) (UNEP 2009). Developing countries
are generating more and more ewaste in their
own territories and may also feed the recy
cling business (LaDou and Lovegrove 2008;
Robinson 2009).The purpose of recycling
activities in these developing countries is to
recover gold, silver, copper, zinc, iron, tin,
and other metals for profit (Huo et al. 2007;
Wong et al. 2007). However, because of a
lack of stringent environmental regulation and
worker protection, toxicants in ewaste cause
serious contaminations of local air, dust, soil,
and water (Ogunseitan et al. 2009; Schmidt
2006; Wong et al. 2007). The environmen
tal consequence is dire in these regions if the
activities remain uncontrolled. Further, infor
mal recycling processes (dismantling, cut
ting, heating, acid leaching, and burning) in
small town and village workshops expose the
workers and residents to dangerous mixtures
of metals and other pollutants (LaDou and
Electronic devices consist of a large number
of chemical elements and compounds. Even
a cell phone can contain > 40 elements from
the periodic table (UNEP 2009). The metals
in ewaste include steel (iron), copper, alu
minum, tin, Pb, nickel, silver, gold, arsenic,
Cd, Cr, indium, Hg, ruthenium, selenium,
vanadium, and zinc. The toxicity of these
chemicals in ewaste remains to be deter
mined. However, some chemicals are known
or suspected to have developmental neuro
toxicity. Neurodevelopmental deficits are a
serious concern of exposure to ewaste toxi
cants, because children living in ewaste recy
cling communities may have been exposed to
highlevel toxicant mixtures throughout their
lifetime. Infants and young children have
relatively smaller body weight than adults,
but their toxicant body load can be higher
because they have relatively low body weight
[American Academy of Pediatrics (AAP)
2003]. Developing fetuses and young children
are at critical windows of neuronal growth,
differentiation, migration, synaptogenesis,
and myelination. Disruption of these fine
tuned processes in human neurodevelopment
can have detrimental effects (Dietrich 2010).
The commonly assessed neuro develop mental
end points include intelligence quotient (IQ),
memory, language, gross and fine motor skills,
attention, executive functions, and behavior.
Obviously, a focus on develop mental neuro
toxicity in this review does not exclude the
possibility of adverse effects on other organ
systems, but many previous human studies
of metal and POP exposure in community
settings revealed deficits in neurological func
tions in children (Dietrich 2010; Wright
and Baccarelli 2007). Table 1 summarizes
the developmental neurotoxicity and expo
sure routes of common ewaste toxicants. In
addition to exposure to ewaste, children are
exposed to these toxicants from other existing
sources (e.g., Pb and Hg from power plants
and other industrial emissions as well as diet)
Lead. Pb is arguably the moststudied
developmental neurotoxicant and unfor
tunately is also one of the major toxicants
in ewaste. An old CRT television contains
about 1.5–2 kg Pb, and a CRT computer
monitor contains about 0.5 kg Pb (U.S. EPA
2007, 2008). Pb has also been used in solder
in printed circuit boards and other compo
nents (Ramesh et al. 2007). In 1 to 6year
old children living in a primitive ewaste
recycling site, the mean blood Pb level
approaches 15 µg/dL, which is 50% higher
than the neighboring control site (~ 10 µg/dL)
(Huo et al. 2007; Zheng et al. 2008). Blood
Pb levels ≥ 10 µg/dL in early childhood are
detrimental to neurodevelopment, and the
recognized adverse effects include impaired
cognitive function, behavioral disturbances,
Figure 1. Estimated annual production of e-waste and major recycling sites. Estimates are from Robinson (2009), Davis and Herat (2010), and Cobbing (2008) and
may not reflect current production. In addition, the estimates are not complete for many regions, for example, Japan, Russia, and Canada. The number of recy-
cling sites is by no means complete but may represent major processing regions of e-waste.
~9 million tons
~2.5 million tons
~2.5 million tons
~0.33 million ton
~0.14 million ton
Country with estimated annual e-waste production
Known major e-waste recycling sites
E-waste toxicants and neurodevelopment
Environmental Health Perspectives • volume 119 | number 4 | April 2011
attention deficits, hyperactivity, and conduct
problems (Bellinger 2004). Newly identified
neuroanatomical changes in young adults
who are exposed to Pb in childhood include
reduced gray matter in the prefrontal region
and diffusivity changes in white matter that
indicate effects on myelination and axonal
integrity (Brubaker et al. 2009; Cecil et al.
2008). Childhood Pb exposure, especially
earlyschoolage blood Pb levels, strongly
predict neurologic deficits in children and
young adults (Hornung et al. 2009). There
is a considerable amount of evidence show
ing that every 10µg/dL increase of blood Pb
concentration is associated with a deficit of
2–3 IQ points (Pocock et al. 1994). Current
research suggests that a blood Pb concentra
tion < 10 µg/dL is also harmful for cogni
tive function (Canfield et al. 2003; Lanphear
et al. 2005). High Pb exposure in childhood
has been associated with delinquent behav
iors and criminal activities in adolescents and
young adults (Needleman et al. 2002; Wright
et al. 2008). In children, Pb exposure has also
been associated with increased risk of atten
tion deficit hyperactivity disorder (Braun et al.
2006). Ewaste exposure represents a situation
of continuous exposure, which raises concerns
about neurodevelopmental deficits in young
children and across the lifespan.
Mercury. Because Hg is used in laptop
monitors, cold cathode fluorescent lamps,
cell phones, and printed circuit boards (e.g.,
switches, relays), improper recycling of ewaste
may release Hg in its elemental vapor form
into the environment (Ramesh et al. 2007).
Each individual electronic device contains a
very small amount of Hg (< 1–2 g) (U.S. EPA
2007), but intensive processing of millions
of these devices could be highly problematic
for the environment. In bodies of water, bac
teria can transform inorganic Hg to organic
form [i.e., methylmercury (MeHg)], and
fish bio accumulate MeHg. Eating MeHg
contaminated fish is the primary route of
exposure in the general population, but people
living in ewaste recycling sites may be exposed
to both inorganic and organic Hg. So far,
there is a lack of studies investigating Hg lev
els in children who lived in ewaste recycling
sites. Currently, there is considerable debate
about neurodevelopmental effects of moder
ate MeHg levels (maternal hair Hg 4–6 µg/g)
or lowerlevel exposure because of conflicting
results from the research in the Faroe Islands
and Seychelles (Debes et al. 2006; Grandjean
et al. 1997; Myers et al. 2009). The study in
the Faroe Islands identified an association of
prenatal MeHg exposure [geometric mean
(GM) = 4 µg/g in maternal hair and 23 µg/L
in cord blood] and deficits in motor function,
attention, and verbal domains in children up
to 14 years of age but did not find associations
for postnatal exposure (GM = 3 µg/g in hair
and 9 µg/L in blood at 7 years of age) (Debes
et al. 2006). The research in Seychelles, how
ever, did not find a consistent pattern of asso
ciation between prenatal (mean = 7 µg/g in
maternal hair) or postnatal MeHg (mean =
6 µg/g in hair at 9 years of age) and neuro
develop mental end points (Davidson et al.
2010; Myers et al. 2009). An integrative analy
sis of three cohorts (Faroe island, Seychelles,
and another New Zealand study) found an
overall child IQ change of –0.18 points [95%
confidence interval (CI), –0.38 to –0.01] for
each microgram per gram increase of maternal
hair MeHg (Axelrad et al. 2007). A recent
study of U.S. background level MeHg expo
sure (~ 0.5 µg/L in whole blood at 2 years
of age) did not reveal significant associa
tions with neurodevelopmental outcomes in
children at ages 2, 5, and 7 years (Cao et al.
2010). For Hg vapor exposure from dental
amalgam, two recent large clinical trials did
not find adverse effects on cognitive function
in children (Bellinger et al. 2006; DeRouen
et al. 2006). In some Asian coastal regions,
the GM hair Hg levels can reach 1–2 µg/g in
women of reproductive age (Liu et al. 2008).
The exposure to Hg from ewaste recycling
needs to be characterized in pregnant women
and young children from ewaste recycling
sites, and if elevated, the neurodevelopmental
effects should be examined.
Cadmium. Cd is used in nickel–cadmium
(NiCd) batteries, surface mount devices chip
resistors, infrared detectors, and semiconduc
tor chips (Ramesh et al. 2007). Lithiumion
batteries have replaced NiCd batteries in
many electronic devices, but ewaste still con
tains old rechargeable batteries. Compared
with Pb and Hg, the adverse neurodevelop
mental effects of Cd are less well charac terized
in children. Cd levels in hair have been asso
ciated with deficits in cognition, learning,
behavior, and neuromotor skills in children
in earlier studies (Pihl and Parkes 1977;
Thatcher et al. 1982), but inadequate control
for Pb levels in the data analysis has been a
concern. A recent study indicates that current
background Cd exposure (~ 0.2 µg/L) in U.S.
children may not cause significant cognitive
and behavioral problems (Cao et al. 2009). In
a Chinese birth cohort study, however, higher
Cd exposure in cord blood (> 0.6 µg/L) was
associated with a 4point FullScale IQ deficit
at preschool age after adjustment for cord
blood Pb levels (Tian et al. 2009). The pla
centa limits the transfer of Cd from mother
to fetus after the first trimester, but high
cord blood Cd in infants may suggest high
maternal exposure. These infants may also be
postnatally exposed to Cd in the same mater
nal living environment (Osman et al. 2000).
Because the halflife of Cd in kidneys and
bones is estimated to be 10–30 years (Jarup
and Akesson 2009), caution should be exer
cised to prevent Cd exposure in young chil
dren. The average blood Cd levels in children
from an ewaste recycling site in China was
1.6 µg/L, significantly higher than the con
trol site (1.0 µg/L) (Zheng et al. 2008). In
Asian countries where rice consumption and
environmental tobacco smoke are more com
mon, children already get higher Cd exposure
than those in Western countries (Jarup and
Akesson 2009). Living in an ewaste recy
cling site substantially increases exposure of
children to Cd, but the neurodevelopmental
effects remain to be determined.
Hexavalent chromium. Cr(VI) is used
in metal coatings of some electronic devices
for corrosion protection. It is a known
human carcinogen after occupational inha
lation exposure, but its toxicity in fetuses
and children after environmental exposure
is largely unknown (Pellerin and Booker
2000). Epidemiologic study of Cr expo
sure and child neurodevelopment is lacking.
One animal study reported motor activity
decrease in rats after chronic Cr exposure
Table 1. Characteristics of known and suspected neurotoxicants in e-waste and from its informal recy-
Potentially affected neuropsychological
functions in children
PbCognition (verbal and performance),
fine and gross motor skills, memory,
attention, executive function,
hyperactivity, academic achievement,
HgCognition, language, motor function,
Air, dust, water, soil,
leaded paint, leaded
gasoline (if not banned)
YesYesAir, seafood, Hg vapor
LimitedYes Air, dust, rice, vegetables,
Air, dust, water
Air, dust, food
Air, dust, seafood
Motor function (animal study only)
Cognition, visual–spatial function,
memory, attention, impulse control,
executive function, motor, behavior
Air, dust, soil, food
Air, dust, soil, food
Chen et al.
volume 119 | number 4 | April 2011 • Environmental Health Perspectives
(azMayans et al. 1986). Oxidative stress
in hypothalamus and anterior pituitary has
been reported in Crexposed animals (Nudler
et al. 2009). Increased urinary 8hydroxy2´
deoxyguanosine, a biomarker for oxidative
DNA lesions, was reported in children with
high urinary Cr (Wong et al. 2005). Ewaste
recycling can result in high Cr exposure in
fetuses, with one report of mean cord blood
Cr of 99 µg/L, significantly higher than the
controlsite mean of 32 µg/L (Li et al. 2008).
The reported Cr levels were very high com
pared with findings from a large U.K. study
(serum ~ 0.5 µg/L) and Italian Cr workers
(whole blood ~ 6.9 µg/L) (Davies et al. 1997;
Minoia and Cavalleri 1988).
PBDEs. PBDEs––a group of brominated
flame retardants––are used in electronic prod
ucts to reduce flammability. Animal studies
of PBDEs strongly suggest increased risk of
thyroid hormone disruption [PBDEs and thy
roxine (T4) are structurally similar], hyperactiv
ity, cognitive deficits, and impaired memory
(Costa and Giordano 2007). Susceptibility of
children to PBDEs is a major concern, because
children often have two to three times higher
serum concentrations than their parents (Toms
et al. 2009). A recent publication of prenatal
exposures to PBDEs and FullScale IQ deficits
[four points by interquartile range of BDE47
(20 ng/g lipid)] in preschool children raised the
concern of neurodevelopmental consequences
(Herbstman et al. 2010). This association
needs to be confirmed in other cohort studies.
Median serum ΣBDEs (BDE209 included)
of up to 600 ng/g lipid were detected in recy
cling workers (Bi et al. 2007), but most stud
ies found a mean or median of 100–400 ng/g
lipid in the sera of local residents in the recy
cling sites (Qu et al. 2007; Yuan et al. 2008;
Zhao et al. 2010). Breast milk from lactat
ing mothers in the recycling sites also contains
high PBDEs, with reported ΣBDEs of 84 ng/g
(BDE209 included) and 117 ng/g (BDE209
not included) lipid in two different small stud
ies in Vietnam and China, respectively (Leung
et al. 2010; Tue et al. 2010). In contrast, the
median serum ΣBDEs in the U.S. general
population is ~ 40–60 ng/g lipid (BDE209
not included), and that in Europe and Asia is
usually < 10 ng/g lipid (Sjodin et al. 2008; Zhu
et al. 2009). The ewaste recycling processes
release significant amounts of BDE209 that
are not often detected in the U.S. population
(Bi et al. 2007; Yuan et al. 2008). Although
BDE209 has a shorter halflife than less
brominated congeners in the environment,
it may be degraded to the latter compounds
and its toxicity remains to be determined
(Birnbaum and Staskal 2004).
Other toxicants: polychlorinated biphenyls,
dioxins/furans, polycyclic aromatic hydro-
carbons. Polychlorinated biphenyls (PCBs)
were present in old transformers and capacitors
before their ban in the 1970s, so ewaste recy
cling sites that deal with these devices may have
high PCBs levels. Contemporary comput
ers and cell phones do not contain PCBs. In
Taizhou, China, where two sites are involved
in ewaste recycling, Luqiao has higher serum
ΣPCBs levels in adults (median = 118 ng/g
lipid) than Wenling (median = 75 ng/g lipid),
presumably because of a focus on PCB
containing devices and longer recycling history
(Zhao et al. 2010). In another report, children
in Luqiao have mean ΣPCBs of 222 ng/g lipid
(boys) and 153 ng/g lipid (girls) (Ling et al.
2008). In contrast, adults in Guiyu, China,
did not have higher ΣPCBs levels than a non
recycling control site (median 52 vs. 63 ng/g
lipid, respectively) (Bi et al. 2007), probably
because Guiyu has been processing predomi
nantly obsolete computers and cell phones.
Informal ewaste recycling also produces
secondary emissions that are not chemicals in
the ewaste but reaction products from incin
eration or smelting processes. Polychlorinated
dibenzopdioxins and dibenzofurans (PCDD/
PCDFs) and polycyclic aromatic hydrocarbons
(PAHs) can result from open burning of the
ewaste (wires or plastics) to reduce volume or
to recover metals. Even in primitive recycling
sites, open burning of ewaste is usually pro
hibited. However, higher PCDD/PCDFs lev
els have been reported in breast milk, placenta,
and hair samples from ewaste processing sites
in Taizhou, China (Chan et al. 2007; Wen
et al. 2008). The reported PCDD/PCDFs
World Health Organization (WHO) toxic
ity equivalent (TEQ) level in breast milk was
21 pg/g lipid in Taizhou (Chan et al. 2007),
twice as high as the levels in the United States
and many European countries in a WHO
coordinated exposure study (van Leeuwen and
Malisch 2002). No human studies of PAHs
can be identified from ewaste recycling sites,
but environmental samples (air, soil, and sedi
ment) strongly suggest such contamination
exists. The sum of 16 PAHs concentrations in
PM2.5 (particulate matter with aerodynamic
diameter ≤ 2.5 µm) air samples was 102 ng/m3
in a location close to an open burning site in
Guiyu, China, much higher than average lev
els in Hong Kong (3–4 ng/m3) or Guangzhou
(22–58 ng/m3) (Deng et al. 2006).
PCBs are known developmental neuro
toxicants, and these compounds may affect
a variety of neuropsychological functions in
children, including general cognition, visual–
spatial function, memory, attention, execu
tive functions, and motor function (Boucher
et al. 2009; Schantz et al. 2003). Most birth
cohort studies of prenatal PCB exposure sug
gested a harmful role that was not accounted
for by other environmental exposures, socio
demographic factors, child rearing, and paren
tal IQ. The PCB levels in an ewaste recycling
site (Taizhou) were in the lowtomoderate
range of several international birth cohort
studies of PCBs (using CB153 as a criterion,
median 30–450 ng/g lipid) (Longnecker et al.
2003). PCDD/PCDFs are often heatdegraded
contaminants of PCBs; PCDFs in particular
have been indicated to contribute to the two
poisoning episodes in Japan and Taiwan (AAP
2003). The analytical testing of PCDD/PCDFs
is more difficult, and thus epidemiologic stud
ies are rare. However, in the Dutch PCB/
dioxin study, lactational exposure to dioxin
(median PCDD/Fs, WHO 1998 TEQ =
33 pg/g lipid in breast milk) was not associ
ated with child cognitive abilities at 42 months
of age (Patandin et al. 1999; Van den Berg
et al. 2006). Similarly, a recent Duisburg birth
cohort study in Germany (median PCDD/
PCDFs) [WHO 2005 TEQ = 11 pg/g lipid
in breast milk (Van den Berg et al. 2006)] did
not find an inverse association with mental
and psychomotor developmental indexes at
12 and 24 months of age (Van den Berg et al.
2006; Wilhelm et al. 2008). Additional studies
are needed to investigate the neurodevelop
mental effect of dioxins and furans at higher
exposure levels. Recent studies have suggested
that air pollutant PAHs may adversely affect
child neurodevelopment and lead to IQ defi
cits (Edwards et al. 2010; Perera et al. 2009a;
Tang et al. 2008). In the New York City and
Polish studies, prenatal PAH exposure above
the median (2.26 ng/m3 in New York City and
17.96 ng/m3 in Poland) was associated with an
IQ deficit of about 3–5 points at 5 years of age
(Edwards et al. 2010; Perera et al. 2009a).
Unique Characteristics of
E-Waste Toxicant Exposure
First, ewaste toxicants are released in uncon
trolled recycling processes as a mixture. It is
not uncommon that heavy metals and POPs
coexist in the environment in recycling work
shops and nearby neighborhoods. Second,
the ewaste toxicant exposure is not homo
geneous. The variability comes from several
sources: the type of ewaste, length of recy
cling history, quantity of recycling, speciali
zation in recycling processes, locations of
workshops, parental involvement in recycling,
and the daily activities of the child. Third,
the exposure to ewaste toxicants lasts a long
time. Many of the recycling sites have oper
ated for more than a decade, and cumulative
exposure in the local environment is typi
cally high. Pregnant women who grew up in
the recycling sites would have an even longer
exposure history and higher body burden in
physiologic deposits (e.g., bones and adipose
tissues) than in women who moved in at the
time of marriage. Transplacental and lacta
tional exposure is expected for most metals
and lipophilic organic pollutants in ewaste.
Infants and children are exposed from con
taminated indoor and outdoor air, dust, and
E-waste toxicants and neurodevelopment
Environmental Health Perspectives • volume 119 | number 4 | April 2011
soil. If the food and drinking water also come
from contaminated community, the exposure
will aggregate to a higher level.
Potential Mechanisms of
E-Waste Toxicants and
Toxicologic mechanisms of certain individual
developmental neurotoxicants, especially Pb,
have been investigated extensively, but data
are insufficient to address exposure mixtures
such as those in ewaste. Apparently several
toxicologic mechanisms may be involved in
this mixture of known and suspected neuro
toxicants, but more research is needed to
investigate the combinations of different
metals and POPs (Figure 2). These toxico
logic mecha nisms are very complicated and
may overlap, and other mechanisms related
to molecular biology and signal transduction
may be involved as well.
Oxidative stress. Heavy metals can induce
oxidative stress by increasing the production of
reactive oxygen species (ROS) and depletion
of antioxidant reserves (Wright and Baccarelli
2007). Neurons have limited capacity to
detoxify ROS and are particularly vulnerable
to oxidative stress. Pb exposure increases the
formation of superoxide anion (•O2–) and
hydrogen peroxide (H2O2) in the central ner
vous system (CNS), which may interact with
proteins, lipids, and DNA to induce apop
tosis (Sanders et al. 2009). MeHg affects the
mitochondria electron transport system and
causes overproduction of ROS (Johansson
et al. 2007). Cd induces oxidative stress in
cultured cells and animals and reduces anti
oxidant levels in humans (Joseph 2009; Lee
et al. 2006). Exposure to PBDEs increase the
generation of ROS, and different PBDEs con
geners (e.g., BDE47 and BDE99) may have
synergistic interactions in certain concentra
tions (Tagliaferri et al. 2010).
Neurotransmission and calcium
homeostasis. Many heavy metals can affect
neurotransmission and disrupt the calcium
signaling pathway and thus interfere with
synaptic functions. Pb ions (Pb2+) selectively
bind Nmethyldaspartate (NMDA) recep
tor, one subtype of glutamatergic receptors
(Toscano and Guilarte 2005). Glutamate is
the major excitatory neurotransmitter in the
brain tissues and is associated with learning
and memory by the establishment of long
term potentiation (LTP). Interaction of Pb
with the NMDA receptor increases Ca2+
influx, initiating cellular processes that lead to
cell dysfunction (Sanders et al. 2009). MeHg
exposure can increase Ca2+ levels in different
cell types, and it may cause disruptions in cell
cycles and migration (Johansson et al. 2007).
Cd exposure may modify calcium channels
and decrease the release of neurotransmit
ters glutamate and aspartate into the synaptic
clefts (Minami et al. 2001). A recent animal
study suggests that BDE209 exposure reduces
LTP and affects synaptic plasticity (Xing et al.
2009). The dopaminergic system is another
critical CNS neurotransmission pathway that
affects cognition, motivation and reward,
attention, and learning. Extensive evidence
on the role of environmental toxicants, such
as Pb, on synaptic dopamine release, its recep
tors and transporters, and metabolism has
emerged (Jones and Miller 2008).
Neuroendocrine disruption. Previous
research on heavy metals and neurotoxic
ity has suggested a similarity to the effects
of subtle hypothyroidism, but the evidence
is limited (Soldin et al. 2008; Wong et al.
1991). Thyroidstimulating hormone (TSH),
T4, and triiodothyronine (T3) could have
unique effects on the initiation and modula
tion of gene expressions for brain develop
ment (Porterfield 2000). Animal studies have
indicated potential disruption of transthyretin
levels in the cerebrospinal fluid and brain
deiodinase by Pb, Hg, or Cd (Mori et al.
2006; Soldin and Aschner 2007; Zheng et al.
2001). Pb exposure in occupational workers
reduced total T4 (TT4), free T4 (FT4), or total
T3 (TT3) (Lopez et al. 2000). Recent studies
suggest a reduced level of FT4 associated
with Pb exposure in pregnant women (Lamb
et al. 2008) and in adolescents (Dundar
et al. 2006), but the results are inconsistent
(Maervoet et al. 2007; Schell et al. 2008).
In one Canadian study, inorganic Hg was
associated with a reduction of FT4 (Takser
et al. 2005), but two other studies found non
significant associations in pregnant women
and children (Osius et al. 1999; Schell et al.
2008). Cd exposure was found to affect TSH
and FT4 levels in two recent studies (Iijima
et al. 2007; Osius et al. 1999), but not in
another (Maervoet et al. 2007). The animal
studies of PCBs or PBDEs and thyroid hor
mone disruption have shown strong correla
tions, mostly reducing circulating T4 or T3
levels, but human studies are still needed to
confirm the effects (Herbstman et al. 2008). A
recent epidemiologic study of PBDEs suggests
a slight decrease of TSH in exposed pregnant
women (Chevrier et al. 2010). One study
in ewaste recycling workers revealed higher
TSH levels than in controls, and the role of
PBDEs are suspected because of their struc
tural similarity to T4 (Yuan et al. 2008). A
recent larger study in ewaste recycling work
ers, however, found lower TSH levels than in
controls (Wang et al. 2010). Another study
suggested a lower TT4 level in maternal serum
in relation to exposure to PCDD/PCDFs and
PCBs (Zhang et al. 2010). Thyroid hormone
alteration warrants further study in the expo
sure to ewaste toxicants.
Epigenetic modifications. Epigenetic modi
fications are mitotically heritable changes of
gene function in the absence of alterations in
nucleotide sequence. These epigenetic changes
include DNA methylation, mostly in the
5´cytosine in the CpG dinucleo tides of the
gene promoter region, histone modifications,
and microRNAs that affect post transcriptional
regulation (Baccarelli and Bollati 2009).
Because nucleotide sequence is generally
static in somatic cells and epigenetic mark
ers are modifiable during the life course, the
Figure 2. Potential developmental neurotoxicants in e-waste and their adverse effects on neurodevelop-
ment in children. Solid lines represent more-studied links; dashed lines suggest possible links.
Chen et al.
volume 119 | number 4 | April 2011 • Environmental Health Perspectives
investigation of epigenetic changes induced
by environmental toxicants has received
increased attention (Baccarelli and Bollati
2009). Although examinations of these mecha
nisms in human neuro develop mental studies
are rare, several in vitro, in vivo, and human
studies suggest possible perturbations in DNA
methylation and histone modifications by Pb,
Hg, Cd, Cr, PAHs, and PBDEs (Benbrahim
Tallaa et al. 2007; Chen et al. 2010; Jiang
et al. 2008; Kondo et al. 2006; Onishchenko
et al. 2008; Perera et al. 2009b; Pilsner et al.
2009, 2010; Sun et al. 2009; Takiguchi et al.
2003) (summarized in Table 2). Epigenetic
changes may affect gene expression in specific
tissues (e.g., brain regions) and subsequently
modify neuro development in a critical win
dow of development, but the role of neuro
toxicants needs to be determined.
Data Gaps in E-Waste
Toxicants and Developmental
Lack of comprehensive exposure assess-
ment. Comprehensive exposure assessment
is urgently needed to characterize the pro
files of chemicals and their concentrations,
especially in countries where informal ewaste
recycling exists on a large scale but exposure
assessment is scarce, for example, in India
(Ha et al. 2009). Exposure assessment should
include both environmental and biological
sampling in the recycling sites and control
sites to determine the extent of exposure.
Exposure of children needs to be examined
from in utero to adolescence —in pregnant
women (blood, urine, hair), neonates (meco
nium, cord blood, breast milk), and children
(blood, urine, hair). Toxicant profiles includ
ing metals and POPs should be determined in
the same study subjects to reflect a realworld
exposure scenario of ewaste recycling.
Lack of evaluation of adverse develop-
mental effects. The demonstration of adverse
health effects has historically preceded effec
tive pollution control measures. Even though
the precautionary principle has gained increas
ing attention in developed countries, in devel
oping countries observed detrimental health
effects are more likely to be a turning point in
public opinion and policy making. Research is
clearly needed to investigate the health effects
of ewaste toxicants resulting from informal
recycling activities. These health effects may
include fetal development (birth weight, birth
length, head circumference, gestational age,
thyroid function) and child growth and neuro
development (cognition, memory, learning,
motor function, executive functions, behavior).
Lack of toxicologic mechanistic research.
Ewaste toxicant mixtures have not been exam
ined for their potential mechanisms of human
developmental toxicity. Even in in vitro or
in vivo studies, investigation of mixture toxic
ity is rare. In the case of primitive ewaste recy
cling, there is a need—and indeed a unique
opportunity—to integrate human exposure
assessment, adverse health effects, and toxi
cologic mechanisms, because such exposure
is unprecedented and complex. Mechanistic
research that involves new advancements in
genomics, epigenetics, and proteomics may
provide novel understanding of these known
and suspected neurotoxicants. Potential effect
modification and synergistic interactions of
these toxicants can also be determined in this
complex exposure. Mechanistic research can
also elucidate the pathway from exposure to
internal dose and to biological markers of
early adverse effects. Biomarkers including
biochemical and epigenetic changes can be
reliably assessed in various biospecimens
such as blood, urine, buccal swab, and saliva.
Integrating mechanistic research into human
studies will supplement the findings of ani
mal studies with direct evidence of modifiable
molecular changes in exposed populations.
Lack of investigation of preventive meas-
ures. Although informal ewaste recycling has
occurred in developing countries for more
than a decade, and high toxicant exposures
in vulnerable population have been reported,
few attempts have been made to intervene and
reduce exposures in the local communities.
Research can further determine the major con
tributing factors to high toxicant exposures
that can be prevented or mitigated. Such fac
tors could include locations of recycling work
shops relative to residential communities,
using houses as recycling workshops or storage,
specific recycling processes and technical pro
cedures, lack of personal and environmental
protection during recycling, lack of additional
protection for pregnant women and young
children, and nutritional and behavioral factors
(iron and zinc deficiency, insufficient vitamin
intake, environmental tobacco smoke). These
risk factors can be reduced at either a personal
or community level and could reduce the expo
sures and adverse health effects even if the recy
cling activities do not cease immediately.
Investigations. Ewaste is an emerging issue in
environmental health, and its potential signifi
cance is now being recognized by both scien
tists and policy makers. However, serious data
gaps exist in the quantification of exposures and
health effects. In communities where informal
recycling occurs, biomonitoring of exposures,
especially in vulnerable pregnant women and
young children, provide critical information
for epidemiologic investigations, environmental
policy making, and informed plans for interven
tion. Studies that use sensitive neuro develop
mental end points are particularly important
in this complex exposure. Other potential tox
icities in humans—for example, cancer, respira
tory diseases, reproductive functions, and renal
effects—should also be examined.
Prevention. A systematic approach guided
by exposure assessment and health effect
research is needed to prevent toxicant expo
sures in ewaste. Engineers, environmental sci
entists, and other professionals can participate
in the research to minimize exposure to these
toxicants. Restricting the use of toxic chemi
cals in manufacturing of electronic devices
will surely be the upstream of prevention
efforts. Appropriate recycling technologies
should be the mainstay of ewaste recycling
practices. Informal and primitive recycling
practices need to be significantly reduced or
eliminated. Exposure of children to excessive
Table 2. Potential epigenetic modifications by environmental toxicants in e-waste.
Pb Pilsner et al. 2009 Human cord blood leukocytes
Maternal exposure associated with
Brain Hg associated with brain genomic
Hypermethylation in brain-derived
neurotropic factor gene
Initial DNA hypomethylation,
subsequent DNA hypermethylation
after prolonged exposure
hypermethylation in RASSF1A and
Hypermethylation in p16 gene
Increased global histone H3
lysine 9 (H3K9) and H3K4 di- and
trimethylation, decreased H3K27
trimethylation and histone H3 arginine
2 (H3R2) dimethylation
Hypermethylation of ACLS3 gene
Global DNA hypomethylation
Hg Pilsner et al. 2010Polar bear brain
Onishchenko et al.
Takiguchi et al.
Rat liver cells
et al. 2007
Jiang et al. 2008
Kondo et al. 2006
Sun et al. 2009
Human embryo lung fibroblast cells
Human lung cancer
Human lung A549 cells
PAHs Perera et al. 2009bHuman cord blood leukocytes
PBDEsChen et al. 2010 Neonatal rat hippocampal neurons
E-waste toxicants and neurodevelopment
Environmental Health Perspectives • volume 119 | number 4 | April 2011
ewaste toxicants should be minimized at both
household and community levels.
Environmental health policies. Effective
environmental regulations in ewaste manage
ment are needed to prevent excessive exposure
to toxicants. Both developed and developing
countries share joint responsibility in regu
lating electronic device manufacturing and
ewaste transboundary movement. In coun
tries where primitive recycling processes
exist, human health, especially the health of
children, needs to drive the regulation and
manage ment of recycling activities.
AAP (American Academy of Pediatrics). 2003. Pediatric
Environmental Health. Elk Grove Village, IL:American
Academy of Pediatrics.
Aizawa H, Yoshida H, Sakai SI. 2008. Current results and future
perspectives for Japanese recycling of home electrical
appliances. Resour Conservat Recycl 52:1399–1410.
Axelrad DA, Bellinger DC, Ryan LM, Woodruff TJ. 2007. Dose-
response relationship of prenatal mercury exposure and
IQ: an integrative analysis of epidemiologic data. Environ
Health Perspect 115:609–615.
az-Mayans J, Laborda R, Nunez A. 1986. Hexavalent chromium
effects on motor activity and some metabolic aspects of
Wistar albino rats. Comp Biochem Physiol C 83:191–195.
Baccarelli A, Bollati V. 2009. Epigenetics and environmental
chemicals. Curr Opin Pediatr 21:243–251.
Bellinger DC. 2004. Lead. Pediatrics 113:1016–1022.
Bellinger DC, Trachtenberg F, Barregard L, Tavares M,
Cernichiari E, Daniel D, et al. 2006. Neuropsychological
and renal effects of dental amalgam in children: a random-
ized clinical trial. JAMA 295:1775–1783.
Benbrahim-Tallaa L, Waterland RA, Dill AL, Webber MM,
Waalkes MP. 2007. Tumor suppressor gene inactivation
during cadmium-induced malignant transformation of
human prostate cells correlates with overexpression of
de novo DNA methyltransferase. Environ Health Perspect
Bi X, Thomas GO, Jones KC, Qu W, Sheng G, Martin FL, et al.
2007. Exposure of electronics dismantling workers to poly-
brominated diphenyl ethers, polychlorinated biphenyls,
and organochlorine pesticides in South China. Environ Sci
Birnbaum LS, Staskal DF. 2004. Brominated flame retardants:
cause for concern? Environ Health Perspect 112:9–17.
Boucher O, Muckle G, Bastien CH. 2009. Prenatal exposure to
polychlorinated biphenyls: a neuropsychologic analysis.
Environ Health Perspect 117:7–16.
Braun J, Kahn RS, Froehlich T, Auinger P, Lanphear BP. 2006.
Exposure to environmental toxicants and attention deficit
hyperactivity disorder in U.S. children. Environ Health
Brubaker CJ, Schmithorst VJ, Haynes EN, Dietrich KN,
Egelhoff JC, Lindquist DM, et al. 2009. Altered myelination
and axonal integrity in adults with childhood lead expo-
sure: a diffusion tensor imaging study. Neurotoxicology
Canfield RL, Henderson CR Jr., Cory-Slechta DA, Cox C,
Jusko TA, Lanphear BP. 2003. Intellectual impairment in
children with blood lead concentrations below 10 microg
per deciliter. N Engl J Med 348:1517–1526.
Cao Y, Chen A, Jones RL, Radcliffe J, Caldwell KL, Dietrich KN,
et al. 2010. Does background postnatal methyl mercury
exposure in toddlers affect cognition and behavior?
Cao Y, Chen A, Radcliffe J, Dietrich KN, Jones RL, Caldwell KL,
et al. 2009. Postnatal cadmium exposure, neurodevelop-
ment, and blood pressure in children at 2, 5, and 7 years of
age. Environ Health Perspect 117:1580–1586.
Cecil KM, Brubaker CJ, Adler CM, Dietrich KN, Altaye M,
Egelhoff JC, et al. 2008. Decreased brain volume in
adults with childhood lead exposure. PLoS Med 5:e112;
doi:10.1371/journal.pmed.0050112 [Online 27 May 2008].
Chan JK, Xing GH, Xu Y, Liang Y, Chen LX, Wu SC, et al.
2007. Body loadings and health risk assessment of
polychlorinated dibenzo-p-dioxins and dibenzofurans at an
intensive electronic waste recycling site in China. Environ
Sci Technol 41:7668–7674.
Chatterjee P. 2008. Health costs of recycling. BMJ 337:a296.
Chen J, Liufu C, Sun W, Sun X, Chen D. 2010. Assessment of the
neurotoxic mechanisms of decabrominated diphenyl ether
(PBDE-209) in primary cultured neonatal rat hippocampal
neurons includes alterations in second messenger signal-
ing and oxidative stress. Toxicol Lett 192:431–439.
Chevrier J, Harley KG, Bradman A, Gharbi M, Sjodin A,
Eskenazi B. 2010. Polybrominated diphenylether (PBDE)
flame retardants and thyroid hormone during pregnancy.
Environ Health Perspect 118:1444–1449.
Cobbing M. 2008. Toxic Tech: Not in Our Backyard. Uncovering
the Hidden Flows of E-Waste. Report from Greenpeace
International, Amsterdam. Available: http://www.green-
our-backyard.pdf [accessed 18 October 2010].
Costa LG, Giordano G. 2007. Developmental neurotoxicity of
polybrominated diphenyl ether (PBDE) flame retardants.
Dagan R, Dubey B, Bitton G, Townsend T. 2007. Aquatic toxic-
ity of leachates generated from electronic devices. Arch
Environ Contam Toxicol 53:168–173.
Davidson PW, Leste A, Benstrong E, Burns CM, Valentin J,
Sloane-Reeves J, et al. 2010. Fish consumption, mer-
cury exposure, and their associations with scholastic
achievement in the Seychelles Child Development Study.
Davies S, McLaren Howard J, Hunnisett A, Howard M. 1997.
Age-related decreases in chromium levels in 51,665 hair,
sweat, and serum samples from 40,872 patients—impli-
cations for the prevention of cardiovascular disease and
type II diabetes mellitus. Metabolism 46:469–473.
Davis G, Herat S. 2010. Opportunities and constraints for
developing a sustainable e-waste management system
at local government level in Australia. Waste Manag Res
Debes F, Budtz-Jorgensen E, Weihe P, White RF, Grandjean P.
2006. Impact of prenatal methylmercury exposure on
neurobehavioral function at age 14 years. Neurotoxicol
Deng WJ, Louie PKK, Liu WK, Bi XH, Fu JM, Wong MH. 2006.
Atmospheric levels and cytotoxicity of PAHs and heavy
metals in TSP and PM2.5 at an electronic waste recycling
site in southeast China. Atmos Environ 40:6945–6955.
DeRouen TA, Martin MD, Leroux BG, Townes BD, Woods JS,
Leitao J, et al. 2006. Neurobehavioral effects of dental
amalgam in children: a randomized clinical trial. JAMA
Dietrich KN. 2010. Environmental toxicants. In: Pediatric
Neuropsychology, 2nd ed. (Yeates KO, Ris MD, Taylor HG,
Pennington BF, eds). New York:Guilford Press, 211–264.
Dundar B, Oktem F, Arslan MK, Delibas N, Baykal B, Arslan C,
et al. 2006. The effect of long-term low-dose lead exposure
on thyroid function in adolescents. Environ Res 101:140–145.
Edwards SC, Jedrychowski W, Butscher M, Camann D,
Kieltyka A, Mroz E, et al. 2010. Prenatal exposure to air-
borne polycyclic aromatic hydrocarbons and children’s
intelligence at age 5 in a prospective cohort study in
Poland. Environ Health Perspect 118:1326–1331.
ETBC (Electronics Take Back Coalition). 2010. State Legislation.
tion/state_legislation.htm [accessed 28 July 2010].
European Union. 1995. European Union Directive 2002/95/EC.
Restriction of the Use of Certain Hazardous Substances in
Electrical and Electronic Equipment. Available: www.rohs.
eu [accessed 18 October 2010].
European Union. 1996. European Union Directive 2002/96/EC.
Waste Electrical and Electronic Equipment. Available:
www.weee.eu [accessed 18 October 2010].
Grandjean P, Weihe P, White RF, Debes F, Araki S, Yokoyama K,
et al. 1997. Cognitive deficit in 7-year-old children with
prenatal exposure to methylmercury. Neurotoxicol Teratol
Ha NN, Agusa T, Ramu K, Tu NP, Murata S, Bulbule KA, et al.
2009. Contamination by trace elements at e-waste recy-
cling sites in Bangalore, India. Chemosphere 76:9–15.
Herbstman JB, Sjodin A, Apelberg BJ, Witter FR, Halden RU,
Patterson DG, et al. 2008. Birth delivery mode modifies the
associations between prenatal polychlorinated biphenyl
(PCB) and polybrominated diphenyl ether (PBDE) and
neonatal thyroid hormone levels. Environ Health Perspect
Herbstman JB, Sjodin A, Kurzon M, Lederman SA, Jones RS,
Rauh V, et al. 2010. Prenatal exposure to PBDEs and
neuro development. Environ Health Perspect 118:712–719.
Hornung RW, Lanphear BP, Dietrich KN. 2009. Age of greatest
susceptibility to childhood lead exposure: a new statistical
approach. Environ Health Perspect 117:1309–1312.
Huo X, Peng L, Xu X, Zheng L, Qiu B, Qi Z, et al. 2007. Elevated
blood lead levels of children in Guiyu, an electronic
waste recycling town in China. Environ Health Perspect
Iijima K, Otake T, Yoshinaga J, Ikegami M, Suzuki E, Naruse H,
et al. 2007. Cadmium, lead, and selenium in cord blood and
thyroid hormone status of newborns. Biol Trace Elem Res
Jarup L, Akesson A. 2009. Current status of cadmium as an
environmental health problem. Toxicol Appl Pharmacol
Jiang G, Xu L, Song S, Zhu C, Wu Q, Zhang L, et al. 2008. Effects
of long-term low-dose cadmium exposure on genomic
DNA methylation in human embryo lung fibroblast cells.
Johansson C, Castoldi AF, Onishchenko N, Manzo L, Vahter M,
Ceccatelli S. 2007. Neurobehavioural and molecular
changes induced by methylmercury exposure during
development. Neurotox Res 11:241–260.
Jones DC, Miller GW. 2008. The effects of environmental neu-
rotoxicants on the dopaminergic system: a possible role in
drug addiction. Biochem Pharmacol 76:569–581.
Joseph P. 2009. Mechanisms of cadmium carcinogenesis.
Toxicol Appl Pharmacol 238:272–279.
Kondo K, Takahashi Y, Hirose Y, Nagao T, Tsuyuguchi M,
Hashimoto M, et al. 2006. The reduced expression and
aberrant methylation of p16(INK4a) in chromate workers
with lung cancer. Lung Cancer 53:295–302.
LaDou J, Lovegrove S. 2008. Export of electronics equipment
waste. Int J Occup Environ Health 14:1–10.
Lamb MR, Janevic T, Liu X, Cooper T, Kline J, Factor-Litvak P.
2008. Environmental lead exposure, maternal thyroid func-
tion, and childhood growth. Environ Res 106:195–202.
Lanphear BP, Hornung R, Khoury J, Yolton K, Baghurst P,
Bellinger DC, et al. 2005. Low-level environmental lead expo-
sure and children’s intellectual function: an inter national
pooled analysis. Environ Health Perspect 113:894–899.
Lee DH, Lim JS, Song K, Boo Y, Jacobs DR Jr. 2006. Graded
associations of blood lead and urinary cadmium concentra-
tions with oxidative-stress-related markers in the U.S. pop-
ulation: results from the third National Health and Nutrition
Examination Survey. Environ Health Perspect 114:350–354.
Leung AO, Chan JK, Xing GH, Xu Y, Wu SC, Wong CK, et al.
2010. Body burdens of polybrominated diphenyl ethers
in childbearing-aged women at an intensive electronic-
waste recycling site in China. Environ Sci Pollut Res Int
Li H, Yu L, Sheng G, Fu J, Peng P. 2007. Severe PCDD/F and
PBDD/F pollution in air around an electronic waste dis-
mantling area in China. Environ Sci Technol 41:5641–5646.
Li Y, Xu X, Liu J, Wu K, Gu C, Shao G, et al. 2008. The hazard
of chromium exposure to neonates in Guiyu of China. Sci
Total Environ 403:99–104.
Ling B, Han G, Xu Y. 2008. PCB levels in humans in an area of
PCB transformer recycling. Ann NY Acad Sci 1140:135–142.
Liu X, Cheng J, Song Y, Honda S, Wang L, Liu Z, et al. 2008.
Mercury concentration in hair samples from Chinese peo-
ple in coastal cities. J Environ Sci (China) 20:1258–1262.
Longnecker MP, Wolff MS, Gladen BC, Brock JW, Grandjean P,
Jacobson JL, et al. 2003. Comparison of polychlori-
nated biphenyl levels across studies of human neuro-
development. Environ Health Perspect 111:65–70.
Lopez CM, Pineiro AE, Nunez N, Avagnina AM, Villaamil EC,
Roses OE. 2000. Thyroid hormone changes in males
exposed to lead in the Buenos Aires area (Argentina).
Pharmacol Res 42:599–602.
Maervoet J, Vermeir G, Covaci A, Van Larebeke N, Koppen G,
Schoeters G, et al. 2007. Association of thyroid hormone
concentrations with levels of organochlorine compounds
in cord blood of neonates. Environ Health Perspect
Minami A, Takeda A, Nishibaba D, Takefuta S, Oku N. 2001.
Cadmium toxicity in synaptic neurotransmission in the
brain. Brain Res 894:336–339.
Minoia C, Cavalleri A. 1988. Chromium in urine, serum and
red blood cells in the biological monitoring of workers
exposed to different chromium valency states. Sci Total
Chen et al. Download full-text
volume 119 | number 4 | April 2011 • Environmental Health Perspectives
Mori K, Yoshida K, Hoshikawa S, Ito S, Yoshida M, Satoh M,
et al. 2006. Effects of perinatal exposure to low doses
of cadmium or methylmercury on thyroid hormone
metabolism in metallothionein-deficient mouse neonates.
Myers GJ, Thurston SW, Pearson AT, Davidson PW, Cox C,
Shamlaye CF, et al. 2009. Postnatal exposure to methyl
mercury from fish consumption: a review and new
data from the Seychelles Child Development Study.
Needleman HL, McFarland C, Ness RB, Fienberg SE, Tobin MJ.
2002. Bone lead levels in adjudicated delinquents. A case
control study. Neurotoxicol Teratol 24:711–717.
Nudler SI, Quinteros FA, Miler EA, Cabilla JP, Ronchetti SA,
Duvilanski BH. 2009. Chromium VI administration induces
oxidative stress in hypothalamus and anterior pituitary
gland from male rats. Toxicol Lett 185:187–192.
Ogunseitan OA, Schoenung JM, Saphores JD, Shapiro AA.
2009. Science and regulation. The electronics revolution:
from e-wonderland to e-wasteland. Science 326:670–671.
Onishchenko N, Karpova N, Sabri F, Castren E, Ceccatelli S.
2008. Long-lasting depression-like behavior and epigenetic
changes of BDNF gene expression induced by perinatal
exposure to methylmercury. J Neurochem 106:1378–1387.
Osibanjo O, Nnorom IC. 2007. The challenge of electronic waste
(e-waste) management in developing countries. Waste
Manag Res 25:489–501.
Osius N, Karmaus W, Kruse H, Witten J. 1999. Exposure to
polychlorinated biphenyls and levels of thyroid hormones
in children. Environ Health Perspect 107:843–849.
Osman K, Akesson A, Berglund M, Bremme K, Schutz A, Ask K,
et al. 2000. Toxic and essential elements in placentas of
Swedish women. Clin Biochem 33:131–138.
Patandin S, Lanting CI, Mulder PG, Boersma ER, Sauer PJ,
Weisglas-Kuperus N. 1999. Effects of environmental expo-
sure to polychlorinated biphenyls and dioxins on cognitive
abilities in Dutch children at 42 months of age. J Pediatr
Pellerin C, Booker SM. 2000. Reflections on hexavalent chro-
mium: health hazards of an industrial heavyweight. Environ
Health Perspect 108:A402–A407.
Perera F, Li Z, Whyatt R, Hoepner L, Wang S, Camann D, et al.
2009a. Prenatal airborne polycyclic aromatic hydrocarbon
exposure and child IQ at age 5 years. Pediatrics 124:e195–
Perera F, Tang WY, Herbstman J, Tang D, Levin L, Miller R,
et al. 2009b. Relation of DNA methylation of 5’-CpG island
of ACSL3 to transplacental exposure to airborne poly-
cyclic aromatic hydrocarbons and childhood asthma. PLoS
One 4:e4488; doi: 10.1371/journal.pone.0004488 [Online
16 February 2009].
Pihl RO, Parkes M. 1977. Hair element content in learning dis-
abled children. Science 198:204–206.
Pilsner JR, Hu H, Ettinger A, Sanchez BN, Wright RO,
Cantonwine D, et al. 2009. Influence of prenatal lead expo-
sure on genomic methylation of cord blood DNA. Environ
Health Perspect 117:1466–1471.
Pilsner JR, Lazarus AL, Nam DH, Letcher RJ, Sonne C, Dietz R,
et al. 2010. Mercury-associated DNA hypomethylation in
polar bear brains via the LUminometric Methylation Assay:
a sensitive method to study epigenetics in wildlife. Mol
Pocock SJ, Smith M, Baghurst P. 1994. Environmental lead and
children’s intelligence: a systematic review of the epide-
miological evidence. BMJ 309:1189–1197.
Porterfield SP. 2000. Thyroidal dysfunction and environmen-
tal chemicals—potential impact on brain development.
Environ Health Perspect 108(suppl 3):433–438.
Qu W, Bi X, Sheng G, Lu S, Fu J, Yuan J, et al. 2007. Exposure
to polybrominated diphenyl ethers among workers at an
electronic waste dismantling region in Guangdong, China.
Environ Int 33:1029–1034.
Ramesh BB, Parande AK, Ahmed BC. 2007. Electrical and
electronic waste: a global environmental problem. Waste
Manag Res 25:307–318.
Robinson BH. 2009. E-waste: an assessment of global production
and environmental impacts. Sci Total Environ 408:183–191.
Sanders T, Liu Y, Buchner V, Tchounwou PB. 2009. Neurotoxic
effects and biomarkers of lead exposure: a review. Rev
Environ Health 24:15–45.
Schantz SL, Widholm JJ, Rice DC. 2003. Effects of PCB expo-
sure on neuropsychological function in children. Environ
Health Perspect 111:357–576.
Schell LM, Gallo MV, Denham M, Ravenscroft J, DeCaprio AP,
Carpenter DO. 2008. Relationship of thyroid hormone levels
to levels of polychlorinated biphenyls, lead, p,p’-DDE, and
other toxicants in Akwesasne Mohawk youth. Environ
Health Perspect 116:806–813.
Schmidt CW. 2006. Unfair trade: e-waste in Africa. Environ
Health Perspect 114:A232–A235.
Sjodin A, Wong LY, Jones RS, Park A, Zhang Y, Hodge C, et al.
2008. Serum concentrations of polybrominated diphenyl
ethers (PBDEs) and polybrominated biphenyl (PBB) in the
United States population: 2003–2004. Environ Sci Technol
Soldin OP, Aschner M. 2007. Effects of manganese on thyroid
hormone homeostasis: potential links. Neurotoxicology
Soldin OP, O’Mara DM, Aschner M. 2008. Thyroid hormones
and methylmercury toxicity. Biol Trace Elem Res 126:1–12.
Sun H, Zhou X, Chen H, Li Q, Costa M. 2009. Modulation of his-
tone methylation and MLH1 gene silencing by hexavalent
chromium. Toxicol Appl Pharmacol 237:258–266.
Tagliaferri S, Caglieri A, Goldoni M, Pinelli S, Alinovi R, Poli D,
et al. 2010. Low concentrations of the brominated flame
retardants BDE-47 and BDE-99 induce synergistic oxidative
stress-mediated neurotoxicity in human neuro blastoma
cells. Toxicol In Vitro 24:116–122.
Takiguchi M, Achanzar WE, Qu W, Li G, Waalkes MP. 2003.
Effects of cadmium on DNA-(cytosine-5) methyltransferase
activity and DNA methylation status during cadmium-
induced cellular transformation. Exp Cell Res 286:355–365.
Takser L, Mergler D, Baldwin M, de Grosbois S, Smargiassi A,
Lafond J. 2005. Thyroid hormones in pregnancy in relation
to environmental exposure to organochlorine compounds
and mercury. Environ Health Perspect 113:1039–1045.
Tang D, Li TY, Liu JJ, Zhou ZJ, Yuan T, Chen YH, et al. 2008.
Effects of prenatal exposure to coal-burning pollutants on
children’s development in China. Environ Health Perspect
Thatcher RW, Lester ML, McAlaster R, Horst R. 1982. Effects of
low levels of cadmium and lead on cognitive functioning in
children. Arch Environ Health 37:159–166.
Tian LL, Zhao YC, Wang XC, Gu JL, Sun ZJ, Zhang YL, et al.
2009. Effects of gestational cadmium exposure on preg-
nancy outcome and development in the offspring at age
4.5 years. Biol Trace Elem Res 132:51–59.
Toms LM, Sjodin A, Harden F, Hobson P, Jones R, Edenfield E,
et al. 2009. Serum polybrominated diphenyl ether (PBDE)
levels are higher in children (2–5 years of age) than in
infants and adults. Environ Health Perspect 117:1461–1465.
Toscano CD, Guilarte TR. 2005. Lead neurotoxicity: from
exposure to molecular effects. Brain Res Brain Res Rev
Tue NM, Sudaryanto A, Minh TB, Isobe T, Takahashi S, Viet PH,
et al. 2010. Accumulation of polychlorinated biphenyls and
brominated flame retardants in breast milk from women
living in Vietnamese e-waste recycling sites. Sci Total
UNEP (United Nations Environment Programme). 2005. E-Waste,
the Hidden Side of IT Equipment’s Manufacturing and Use.
Environment Alert Bulletin. Available: http://www.grid.unep.
23 January 2010].
UNEP (United Nations Environment Programme and United
Nations University). 2009. Sustainable Innovation and
Technology Transfer Industrial Sector Studies. Recycling—
From E-waste to Resources. Available: http://www.unep.
FINALVERSION-sml.pdf [accessed 18 October 2010].
U.S. EPA (U.S. Environmental Protection Agency). 2007.
Management of Electronic Waste in the United States:
Approach 2. EPA530-R-07-004b. Washington, DC:Office of
Solid Waste, U.S. EPA.
U.S. EPA (U.S. Environmental Protection Agency). 2008.
Electronics Waste Management in the United States:
Approach 1. EPA530-R-08-009. Washington, DC:Office of
Solid Waste, U.S. EPA.
Van den Berg M, Birnbaum LS, Denison M, De Vito M,
Farland W, Feeley M, et al. 2006. The 2005 World Health
Organization reevaluation of human and mammalian toxic
equivalency factors for dioxins and dioxin-like compounds.
Toxicol Sci 93:223–241.
van Leeuwen FX, Malisch R. 2002. Results of the third round
of the WHO-coordinated exposure study on the levels of
PCBs, PCDDs and PCDFs in human milk. Organohalogen
Wang H, Zhang Y, Liu Q, Wang F, Nie J, Qian Y. 2010. Examining
the relationship between brominated flame retardants
(BFR) exposure and changes of thyroid hormone levels
around e-waste dismantling sites. Int J Hyg Environ Health
Wen S, Yang FX, Gong Y, Zhang XL, Hui Y, Li JG, et al. 2008.
Elevated levels of urinary 8-hydroxy-2’-deoxyguanosine
in male electrical and electronic equipment dismantling
workers exposed to high concentrations of polychlorinated
dibenzo-p-dioxins and dibenzofurans, poly brominated
diphenyl ethers, and polychlorinated biphenyls. Environ
Sci Technol 42:4202–4207.
Wilhelm M, Wittsiepe J, Lemm F, Ranft U, Kramer U, Furst P,
et al. 2008. The Duisburg birth cohort study: influence
of the prenatal exposure to PCDD/Fs and dioxin-like
PCBs on thyroid hormone status in newborns and neuro-
development of infants until the age of 24 months. Mutat
Wong MH, Wu SC, Deng WJ, Yu XZ, Luo Q, Leung AO, et al.
2007. Export of toxic chemicals—a review of the case of
uncontrolled electronic-waste recycling. Environ Pollut
Wong RH, Kuo CY, Hsu ML, Wang TY, Chang PI, Wu TH, et al.
2005. Increased levels of 8-hydroxy-2-deoxyguanosine
attributable to carcinogenic metal exposure among
schoolchildren. Environ Health Perspect 113:1386–1390.
Wong VC, Ng TH, Yeung CY. 1991. Electrophysiologic study in
acute lead poisoning. Pediatr Neurol 7:133–136.
Wright JP, Dietrich KN, Ris MD, Hornung RW, Wessel SD,
Lanphear BP, et al. 2008. Association of prenatal and
childhood blood lead concentrations with criminal arrests
in early adulthood. PLoS Med 5:e101; doi:10.1371/journal.
pmed.0050101 [Online 27 May 2008].
Wright RO, Baccarelli A. 2007. Metals and neurotoxicology.
J Nutr 137:2809–2813.
Xing T, Chen L, Tao Y, Wang M, Chen J, Ruan DY. 2009. Effects
of decabrominated diphenyl ether (PBDE 209) exposure
at different developmental periods on synaptic plastic-
ity in the dentate gyrus of adult rats in vivo. Toxicol Sci
Yuan J, Chen L, Chen D, Guo H, Bi X, Ju Y, et al. 2008. Elevated
serum polybrominated diphenyl ethers and thyroid-stimu-
lating hormone associated with lymphocytic micronuclei
in Chinese workers from an e-waste dismantling site.
Environ Sci Technol 42:2195–2200.
Zhang J, Jiang Y, Zhou J, Wu B, Liang Y, Peng Z, et al. 2010.
Elevated body burdens of PBDEs, dioxins, and PCBs on
thyroid hormone homeostasis at an electronic waste recy-
cling site in China. Environ Sci Technol 44:3956–3962.
Zhao XR, Qin ZF, Yang ZZ, Zhao Q, Zhao YX, Qin XF, et al.
2010. Dual body burdens of polychlorinated biphenyls
and polybrominated diphenyl ethers among local resi-
dents in an e-waste recycling region in Southeast China.
Zheng L, Wu K, Li Y, Qi Z, Han D, Zhang B, et al. 2008. Blood
lead and cadmium levels and relevant factors among
children from an e-waste recycling town in China. Environ
Zheng W, Lu YM, Lu GY, Zhao Q, Cheung O, Blaner WS. 2001.
Transthyretin, thyroxine, and retinol-binding protein in
human cerebrospinal fluid: effect of lead exposure. Toxicol
Zhu L, Ma B, Hites RA. 2009. Brominated flame retardants in
serum from the general population in northern China.
Environ Sci Technol 43:6963–6968.