Chemistry Reference
In-Depth Information
metals, the use of contraceptive pills should be taken
into account. Some of the drugs for the treatment
of hypertension, which essentially act as chelating
agents, also affect metal metabolism. Prolonged treat-
ment with some of these may increase zinc excretion,
but not cadmium excretion. Thus, such treatment may,
in the long run, cause changes in the cadmium/zinc
ratios. The use of chelating agents such as DMSA and
penicillamine in the treatment of metal poisoning is a
way of using interactions for therapeutic purposes (for
details, see Chapter 15). Attempts have also been made
to change the kinetics of methylmercury by the use of
resins that prevent the reabsorption of methylmercury
excreted through the bile (Chapter 15).
2.2 Infl uence of Age and Sex on
Metal Toxicity
2.2.1 Age
It has long been claimed that certain age groups are
at increased risk (i.e., young children and the elderly).
During the past decade, quantitative data have become
available to document these claims. Several investiga-
tions have dealt with young animals and children, and
data on elderly people are also forthcoming. The fetus is
regarded as especially vulnerable, because many func-
tions are not fully developed until after birth, and several
possibilities exist for contact between the fetus and toxic
metals. The toxic effects caused by metals on development
of the fetus are discussed in Chapter 12. Methylmercury
is known to cross the placental barrier and to accumulate
in the fetus. It is well documented that fetal exposure to
methylmercury can cause intrauterine methylmercury
poisoning (Chapter 33). Lead crosses the placental bar-
rier, and prenatal lead exposure may play a role for later
development. The fetal brain does not tolerate lead to the
same extent as the adult brain does (cf Chapters 16 and
31). Extensive animal studies have shown that newborn
and suckling animals have higher absorption of certain
toxic metals, like lead and cadmium, because of their
dependence on a milk diet. The neonate also has higher
whole-body retention, higher blood levels, and a much
higher accumulation in the brain compared with the
adult exposed to similar doses (cf Chapters 12 and 31).
Exposure of animals to lead in the early neonatal stages
can cause changes in behavior, learning defi cits, and
increased motor activity. There are also data demonstrat-
ing that children develop signs and symptoms at lower
blood-lead concentrations and have a higher absorption
of lead than adults. Because the calorie intake per person
increases rapidly during the period 6-20 years of age, it
follows that the daily intake of a metal (e.g., cadmium)
also increases during this time (cf Chapter 3). The uri-
nary excretion of cadmium has a peak in the age range
6-12 years, followed by a second peak at ages 50- 70.
The fi rst peak is explained by the increase in per person
intake in the mentioned age range and the growth rate
of the kidney, implying that a peak in kidney cadmium
concentration occurs. The later higher peak at age 50 is
explained by the gradual accumulation of cadmium by
age because of the long biological half-life of this metal in
the human kidney (Choudhury
et al.
, 2001).
2.1.2 Alcohol and Tobacco
Ethyl alcohol has been shown to cause an increase
in the absorption of lead. This might be of importance
when evaluating dose-effect relationships in people
exposed to lead in illicitly distilled alcohol. In cases of
lead poisoning caused by such consumption, the symp-
toms in the central nervous system (CNS) seem to be
more severe than what would be expected from lead
exposure alone. Thus, some synergistic action between
alcohol and lead might exist.
Consumption of large amounts of alcohol can tem-
porarily depress ALA-dehydratase activity, which is
also a sign of lead toxicity. However, it has also been
shown that ALA-dehydratase activity may increase
in animals exposed to both lead and alcohol. The
depression caused by either of the substances is par-
tially reversed when the two substances are combined
(Chapter 31).
Alcohol infl uences the metabolism of mercury after
exposure to mercury vapor. This is thought to be due
to the interference of alcohol with some of the enzymes
taking part in the conversion of mercury vapor to mer-
cury (II) (Nielsen-Kudsk, 1965; Chapter 33). Simultane-
ous exposure to cobalt and alcohol has caused so-called
beer drinker cardiomyopathy, where the effect was
greater than would be expected from the single action
of the compounds (see Chapter 25).
Smoking may affect the uptake and effects of metals
in several ways. A discussion in relation to carcinogen-
esis of arsenic compounds is given in Section 3. The
content of carbon monoxide, various organic com-
pounds, and a number of toxic metals (e.g., cadmium,
nickel, mercury, and lead) are probably of importance
in explaining the increased carcinogenicity of com-
bined exposures to carcinogenic metals/metalloids and
smoking, compared with single exposures, as show in
several studies performed in the working environment
(e.g., Lundstrom
et al.
, 2006).
2.2.2 Sex
When women are referred to as a high-risk group,
it is often meant that the exposure of pregnant women
results in the exposure of the fetus. Such aspects are
discussed in Chapter 12. The infl uences to be dealt
