Page 251 - Materials Chemistry, Second Edition

10 Life Cycle Impact Assessment 237

10.12 Human Toxicity

As explained in Sect. 10.11, both toxicity impact categories have a number of
things in common, like main emissions and sources, modelling principles, model
structure and even some of the models used in the characterisation are identical
between the human toxicity and ecotoxicity impact categories. Notably the fate
model used is the same in LCIA methods using mechanistic characterisation
modelling, which is the majority of existing methods. Therefore, only those parts
that are specific for human toxicity and different from ecotoxicity will be discussed
here. It is recommended to first read Sect. 10.11 in order to understand the main
underlying principles not repeated hereafter.

10.12.1 Problem

Human toxicity in LCA is based on essentially the same driving factors as eco-
toxicity: (1) emitted quantity (determined in the LCI), (2) mobility, (3) persistence,
(4) exposure patterns and (5) human toxicity, with the latter four considered by the
characterisation factor. The respective mechanisms and parameters are certainly
different and specific for human toxicity, notably for the exposure modelling, where
many factors capturing human behaviour, such as dietary habits, influence human
exposure pattern.
Chemical exposure of humans can result from emissions into the environment
which will affect the whole population, but also from the many chemical ingredients
in products released during their production, use, or end-of-life treatment and thus
affecting workers or consumers. Chemical emissions are responsible for, or con-
tribute to, many health impacts such as a wide range of non-cancer diseases as well
as increased cancer risks for those chemicals that are carcinogenic.

10.12.2 Environmental Mechanism

Modelling the toxicological effects on human health of a chemical emitted into the
environment, whether released on purpose (e.g. pesticides applied in agriculture), as
a by-product from industrial processes, or by accident, implies a cause–effect chain,
linking emissions and impacts through four consecutive steps as depicted in
Fig. 10.20.
The cause–effect chain links the emission to the resulting mass in the environ-
mental compartments (fate model) and on to the intake of the substance by the
overall population via food and inhalation exposure pathways (human exposure
model), and to the resulting number of cases of various human health risks by
comparison of exposure with the known dose-response relationship for the