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.

Analytical human biomonitoring method for the identification and quantification of the metabolite BDCPP originated from the organophosphate flame retardant TDCPP in urine.

Tris(1,3-dichloropropyl) phosphate (TDCPP, CAS 13674-87-8) is one of the most commonly used organophosphate flame retardants (OPFRs) in cars, residential furniture and other products containing polyurethane foam to meet the required flammability standards. For the tasks of the working group Analyses in Biological Material from the German Research Foundation (DFG), a human biomonitoring process for TDCPP is developed. The metabolism of TDCPP is described in different in vivo studies and it is already shown that Bis (1,3-dichloropropyl) phosphate (BDCPP, CAS 72236-72-7) is the primary compound specific metabolite of TDCPP which is often detectable in urine samples. BDCPP is also the most appropriate metabolite because it is unique to TDCPP since no other OPFR known today is transformed or hydrolyzed to BDCPP. A combined method by liquid chromatography-tandem mass spectrometry (LC-MS/MS) is implemented by optimizing atmospheric pressure chemical ionization (APCI) and Electron Spray Ionization (ESI) operating in negative ionization mode. Simultaneous, multiple reaction monitoring is studied to achieve the best performance with respect to selectivity, detectability and robustness of BDCPP. During an expanded validation assessment, the methodological performance characteristics are determined in details and the method is applied in a specific human biomonitoring study among non-occupationally exposed humans of randomly chosen volunteers from the Netherlands.

Standardisation of a European measurement method for the determination of anions and cations in PM2.5: results of field trial campaign and determination of measurement uncertainty.

European Committee for Standardisation (CEN) Technical Committee 264 'Air Quality' has recently produced a standard method for the measurements of anions and cations in PM2.5 within its Working Group 34 in response to the requirements of European Directive 2008/50/EC. It is expected that this method will be used in future by all Member States making measurements of the ionic content of PM2.5. This paper details the results of a field measurement campaign and the statistical analysis performed to validate this method, assess its uncertainty and define its working range to provide clarity and confidence in the underpinning science for future users of the method. The statistical analysis showed that, except for the lowest range of concentrations, the expanded combined uncertainty is expected to be below 30% at the 95% confidence interval for all ions except Cl-. However, if the analysis is carried out on the lower concentrations found at rural sites the uncertainty can be in excess of 50% for Cl-, Na+, K+, Mg2+ and Ca2+. An estimation of the detection limit for all ions was also calculated and found to be 0.03 µg m-3 or below.

Alveolar epithelial cells (A549) exposed at the air-liquid interface to diesel exhaust: First study in TNO's powertrain test center.

Air-liquid interface (ALI) exposures enable in vitro testing of mixtures of gases and particles such as diesel exhaust (DE). The main objective of this study was to investigate the feasibility of exposing human lung epithelial cells at the ALI to complete DE generated by a heavy-duty truck in the state-of-the-art TNO powertrain test center. A549 cells were exposed at the air-liquid interface to DE generated by a heavy-duty Euro III truck for 1.5h. The truck was tested at a speed of ∼70kmh(-1) to simulate free-flowing traffic on a motorway. Twenty-four hours after exposure, cells were analyzed for markers of oxidative stress (GSH and HO-1), cytotoxicity (LDH and Alamar Blue assay) and inflammation (IL-8). DE exposure resulted in an increased oxidative stress response (significantly increased HO-1 levels and significantly reduced GSH/GSSH ratio), and a decreased cell viability (significantly decreased Alamar Blue levels and slightly increased LDH levels). However, the pro-inflammatory response seemed to decrease (decrease in IL-8). The results presented here demonstrate that we are able to successfully expose A549 cells at ALI to complete DE generated by a heavy-duty truck in TNO's powertrain test center and show oxidative stress and cytotoxicity responses due to DE exposure.