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S.3 TOXIOTY AND RISKS INDUCED BY OCCUPATIONAL EXPOSURE TO CHEMICAL COMPOUNDS 277

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rIGUKt 5.42 Responses of the immune system to exposure to some chemicals. (Used with
permission,)

potential interactions, the no-interaction assumption is the most common
premise. Finally, it is also possible that some constituents reduce the effects of
other exposures; however, there are no well-demonstrated examples of this
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kind of antagonistic action between occupational exposures. >57,85-87
The interactions may be physicochemical without the participation of bio-
logical mechanisms; for example, deep lung exposure to highly soluble irrita-
tive gases, such as sulfur dioxide, may become enhanced due to adsorption of
the gas onto fine particles. Biological interactions may occur at all stages and
body sites. For example, toxicity is increased when adverse effects are due to
some reactive metabolic intermediate and exposure to another agent stimu-
lates its metabolic activation (enzyme induction).
5.3.4.3 Mechanisms of Toxicity
Paracelsus, a Swiss physician of the sixteenth century, stated that every-
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thing is toxic, it is just the dose that matters. This statement still holds true
500 years after Paracelsus developed it to defend the use of toxic compounds
such as lead and mercury in the treatment of serious diseases such as syphilis.
Chemical compounds cause their toxic effects by inducing changes in cell
physiology and biochemistry, and an understanding of cellular biology is a
prerequisite if one wishes to understand the nature of toxic reactions.
Toxic reactions occur by several mechanisms: activation of metabolism,
production of reactive intermediates and subsequent reactions with ceil mac-
romolecules, changing receptor responses, or through abnormal defence reac-
tions. Several compounds cause toxicity by mimicking the organism's own
hormones or neurotransmitters, or activating the body's endogenous receptors
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in some non-physiological way.