Environmental Health Criteria 214

HUMAN EXPOSURE ASSESSMENT
immediately following exposure (e.g., solvents in exhaled air, blood
and urine), the half-life reflects elimination from the central
compartment of blood and vessel-rich tissues. For samples taken days,
weeks or even years after exposure, the half-life corresponds to the
elimination from those compartments from which chemical clearance is
much slower; for example, lead from bone or lipophilic organic
chemicals from adipose tissue (Bernard, 1995).
Toxicokinetic data from animals and humans can aid in the
determination of the utility of biological markers in assessing
individual or population exposures. Fig. 30 illustrates how
toxicokinetic data could be utilized to select biological markers of
exposure based on the timing and concentration of exposure (IPCS,
1993). In order to interpret the extent of exposure, it is critical to
collect the biological sample after the exposure has reached an
equilibrium state. This can be especially important for chemicals with
short half-lives, such as benzene in exhaled air with a half-life of
22 h (Bernard, 1995). For example, in occupational settings,
biological monitoring has no advantages over environmental monitoring
for airborne chemicals with biological half-lives less than 10 h,
since the integration time for the marker is too short to allow
accurate representation of exposure (Droz, 1993).
10.3.2 Biological variability
The use of biological markers can also be affected by biological
parameters. Variation can depict true differences in individual
exposures, as represented for example by differing microenvironments
or differing behaviour. It may also represent inherent
inter-individual differences which affect the biological response to
exposure (Droz, 1992). Sources of biological variability include
demographic factors (e.g., age and sex), anthropometric
characteristics (e.g., body size and fat distribution), behaviour
(e.g., activity level or contaminant avoidance behaviours),
biological/circadian rhythms and toxicokinetic differences due to
genotype (Kompaore & Tsuruta, 1993), previous exposure, lifestyle
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