Argumentation Analysis of Risk Assessments: The Case of Perfluorooctanoic Acid.

Risk assessment of chemicals can be based on toxicology and/or epidemiology. The choice of toxicological or epidemiological data can result in different health-based guidance values (HBGVs). Communicating the underlying argumentation is important to explain these differences to the public and policymakers. In this article, we explore the argumentation used to justify the use of toxicological or epidemiological data in the derivation of HBGVs in four different risk assessments for the chemical Perfluorooctanoic acid (PFOA). The pragma-dialectical argumentation theory (PDAT) is hereby applied. The argumentations to select relevant health endpoints or certain studies to infer causality appeared mainly based on "symptomatic relations," that is, study results are used as characteristic of what was claimed to be a causal relation without delving into the actual causal argumentation that preceded it. Starting points that are at the basis of the chain of arguments remained implicit. Argumentation to use epidemiological and/or toxicological data was only briefly mentioned and the underlying argumentative foundation that led to the conclusion was seldom found or not addressed at all. The decision to include/exclude information was made based on the availability of data, or the motives for the choice remained largely unclear. We conclude that more depth in argumentation and a subordinative chain of arguments is needed to better disclose the underlying reasoning leading to a certain health-based guidance value (HBGV). More explicit identification and discussion of starting points could be a valuable addition to general risk assessment frameworks for maximum use of toxicological and epidemiological data and shared conclusions of the assessment.

In vitro hazard characterization of simulated aircraft cabin bleed-air contamination in lung models using an air-liquid interface (ALI) exposure system.

Contamination of aircraft cabin air can result from leakage of engine oils and hydraulic fluids into bleed air. This may cause adverse health effects in cabin crews and passengers. To realistically mimic inhalation exposure to aircraft cabin bleed-air contaminants, a mini bleed-air contaminants simulator (Mini-BACS) was constructed and connected to an air-liquid interface (ALI) aerosol exposure system (AES). This unique "Mini-BACS + AES" setup provides steady conditions to perform ALI exposure of the mono- and co-culture lung models to fumes from pyrolysis of aircraft engine oils and hydraulic fluids at respectively 200 °C and 350 °C. Meanwhile, physicochemical characteristics of test atmospheres were continuously monitored during the entire ALI exposure, including chemical composition, particle number concentration (PNC) and particles size distribution (PSD). Additional off-line chemical characterization was also performed for the generated fume. We started with submerged exposure to fumes generated from 4 types of engine oil (Fume A, B, C, and D) and 2 types of hydraulic fluid (Fume E and F). Following submerged exposures, Fume E and F as well as Fume A and B exerted the highest toxicity, which were therefore further tested under ALI exposure conditions. ALI exposures reveal that these selected engine oil (0-100 mg/m3) and hydraulic fluid (0-90 mg/m3) fumes at tested dose-ranges can impair epithelial barrier functions, induce cytotoxicity, produce pro-inflammatory responses, and reduce cell viability. Hydraulic fluid fumes are more toxic than engine oil fumes on the mass concentration basis. This may be related to higher abundance of organophosphates (OPs, ≈2800 µg/m3) and smaller particle size (≈50 nm) of hydraulic fluid fumes. Our results suggest that exposure to engine oil and hydraulic fluid fumes can induce considerable lung toxicity, clearly reflecting the potential health risks of contaminated aircraft cabin air.

Health impact assessment of a skin sensitizer: Analysis of potential policy measures aimed at reducing geraniol concentrations in personal care products and household cleaning products.

A methodology to assess the health impact of skin sensitizers is introduced, which consists of the comparison of the probabilistic aggregated exposure with a probabilistic (individual) human sensitization or elicitation induction dose. The health impact of potential policy measures aimed at reducing the concentration of a fragrance allergen, geraniol, in consumer products is analysed in a simulated population derived from multiple product use surveys. Our analysis shows that current dermal exposure to geraniol from personal care and household cleaning products lead to new cases of contact allergy and induce clinical symptoms for those already sensitized. We estimate that this exposure results yearly in 34 new cases of geraniol contact allergy per million consumers in Western and Northern Europe, mainly due to exposure to household cleaning products. About twice as many consumers (60 per million) are projected to suffer from clinical symptoms due to re-exposure to geraniol. Policy measures restricting geraniol concentrations to <0.01% will noticeably reduce new cases of sensitization and decrease the number of people with clinical symptoms as well as the frequency of occurrence of these clinical symptoms. The estimated numbers should be interpreted with caution and provide only a rough indication of the health impact.