Chemistry Reference
In-Depth Information
are the most vulnerable). The tools available for pre-
vention include exposure assessment, environmental
monitoring, biological monitoring, medical monitor-
ing, and a range of public health interventions. Medi-
cal examinations may sometimes be of use and can
pinpoint reasons for increased susceptibility that may
require additional action. Preventive interventions
should seek ways to target the source of the problem
and may require action to remove a subject from a dan-
gerous exposure. Treatment may be necessary as a last
resort when prevention has failed.
Five common principles guide all approaches to
prevention of toxicity caused by metals, whether in the
workplace or the general population: Hazard identi-
fi cation, reduction of exposure, monitoring, training,
and authority. The fi rst of these, and general guidelines
for the second, will be discussed in Section 2). The next
three will be discussed separately for the workplace and
general environments in Sections 2 and 3, respectively.
caused widespread toxicity. During the 1970s, sub-
clinical neurobehavioral defi cits were documented in
asymptomatic children with elevated lead concentra-
tions in blood (Landrigan
et al.,
1975; Needleman
et al.,
1979). Further studies from many countries confi rmed
these fi ndings. In response to these demonstrations
of low-dose toxicity, health agencies have serially
reduced the permissible concentration of lead in chil-
dren's blood. Current research on the developmental
neurotoxicity of lead focuses on the shape of the dose-
response curve at very low exposure levels, which
seem to cause surprisingly large functional decrements
(Canfi eld
et al.,
2003).
2.1.2 Methylmercury
Methylmercury was fi rst established as a neuro-
toxicant in men exposed occupationally (Hunter and
Russell
,
1954). The toxicity of methylmercury to the
developing fetal brain was fi rst recognized in the 1960s
in Minamata, Japan, where an epidemic of spasticity,
blindness, and profound mental retardation occurred
among infants whose mothers had consumed contami-
nated fi sh without being affected themselves (Harada
et al.,
1995). Recent studies have focused on the neu-
rodevelopmental effects of prenatal exposures to
methylmercury at doses insuffi cient to produce clini-
cally obvious symptoms. (Grandjean
et al.,
1997) (See
also Chapter 33 for more detailed discussion.) The US
National Academy of Sciences reviewed these studies
and concluded that strong evidence exists for the fetal
neurotoxicity of methylmercury, even at low-exposure
levels (National Academy of Sciences, 2002). These
fi ndings have led food safety and public health author-
ities in nations worldwide to issue dietary advisories
warning populations, especially women of child-bear-
ing ages, of the hazards of consuming predatory fi sh.
Substantial reductions have been achieved in mercury
use, as well as in its release from various sources, such
as hospitals and waste incinerators.
2.1 Hazard Identifi cation
First, the hazard must be recognized and routes of
exposure determined. This knowledge may be readily
available or may require substantial research. The his-
torical examples of lead, methylmercury, and arsenic
show that, as health hazard information becomes more
detailed, the range of effects that are uncovered increases
in extent and severity. Several examples demonstrate that
early warnings of toxicity have frequently been ignored.
2.1.1 Lead
The fi rst description of lead poisoning in young
children was presented in a report from Australia pub-
lished more than 100 years ago. The source of this out-
break was not immediately obvious and was discerned
only after several years of investigation. It was traced
to ingestion of lead-based paint by children playing
on painted verandas (Gibson, 1895). Further reports of
childhood lead poisoning from lead paint ingestion in
the United States followed over the next several decades
and resulted in bans in many nations on household use
of lead-based paint. Lead poisoning was, at that time,
considered an acute illness from which a child either
recovered or died. The realization that lead could cause
long-term neurological sequelae was fi rst documented
in the 1940s, when 19 of 20 survivors of acute lead poi-
soning in a clinical follow-up study conducted in Bos-
ton were found to have severe and persistent learning
and behavioral problems (Byers
et al.,
1943).
Despite those early warnings, extensive use of lead
in petrol, paints, ceramic glazes, and many other prod-
ucts continued through much of the 20
th
century and
2.1.3 Arsenic
Ingestion of arsenic-contaminated drinking water has
long been recognized to cause peripheral neuropathy in
adults (Landrigan, 1981). Dramatic documentation of
developmental neurotoxicity caused by arsenic was fi rst
reported from Japan, where, in 1955, consumption of
powdered infant milk contaminated with arsenic led to
more than 12,000 poisoning cases and 131 deaths (Yamas-
hita
et al.,
1972). Arsenic occurs in groundwater world-
wide and has been linked to various forms of cancers
(National Academy of Sciences, 2001). (See also Chap-
ter 19 for a detailed discussion of the effects of arsenic.)
As in the previous examples, continued research revealed
