USEtox human exposure and toxicity factors for comparative assessment of toxic emissions in life cycle analysis: sensitivity to key chemical properties

PURPOSE: The aim of this paper is to provide science-based consensus and guidance for health effects modelling in comparative assessments based on human exposure and toxicity. This aim is achieved by (a) describing the USEtox™ exposure and toxicity models representing consensus and recommended modelling practice, (b) identifying key mechanisms influencing human exposure and toxicity effects of chemical emissions, (c) extending substance coverage. METHODS: The methods section of this paper contains a detailed documentation of both the human exposure and toxic effects models of USEtox™, to determine impacts on human health per kilogram substance emitted in different compartments. These are considered as scientific consensus and therefore recommended practice for comparative toxic impact assessment. The framework of the exposure model is described in details including the modelling of each exposure pathway considered (i.e. inhalation through air, ingestion through (a) drinking water, (b) agricultural produce, (c) meat and milk, and (d) fish). The calculation of human health effect factors for cancer and non-cancer effects via ingestion and inhalation exposure respectively is described. This section also includes discussions regarding parameterisation and estimation of input data needed, including route-to-route and acute-to-chronic extrapolations. RESULTS AND DISCUSSION: For most chemicals in USEtox™, inhalation, above-ground agricultural produce, and fish are the important exposure pathways with key driving factors being the compartment and place of emission, partitioning, degradation, bioaccumulation and bioconcentration, and dietary habits of the population. For inhalation, the population density is the key factor driving the intake, thus the importance to differentiate emissions in urban areas, except for very persistent and mobile chemicals that are taken in by the global population independently from their place of emission. The analysis of carcinogenic potency (TD50) when volatile chemicals are administrated to rats and mice by both inhalation and an oral route suggests that results by one route can reasonably be used to represent another route. However, we first identify and mark as interim chemicals for which observed tumours are directly related to a given exposure route (e.g. for nasal or lung, or gastrointestinal cancers) or for which absorbed fraction by inhalation and by oral route differ greatly. CONCLUSIONS: A documentation of the human exposu