Elke Rauscher-Gabernig

Human studies involving exposure to trifluoroacetic acid (TFA) and the associated clinical outcomes are typically not considered in standard chemical toxicity assessments. This review aimed to identify and synthesize all available human data on TFA exposure, regardless of study design or context. Given TFA’s long-standing use and its formation as a degradation product of various compounds, a wide range of exposure scenarios was considered, including post-anesthesia monitoring, environmental assessments, and chemical incidents. The database searches in MEDLINE (PubMed) and EMBASE (Scopus) were conducted on 28 and 29 April 2025. A total of 17 studies met the inclusion criteria: 4 case reports, 3 case series, 5 observational studies, and 5 pharmacokinetic studies. All studies documented clear human exposure to TFA and reported at least one TFA-related outcome. Some acute exposures exceeded the currently proposed threshold values. However, no study demonstrated clinically relevant effects attributable to TFA. As a strong acid, TFA can cause typical corrosive injuries upon direct contact, but no additional systemic or organ-specific toxic effects were observed.

Due to their extensive usage, organophosphorus flame retardants (OPFRs) have been detected in humans and in the environment. Human are exposed to OPFRs via inhalation of indoor air, dust uptake or dietary uptake through contaminated food and drinking water. Only recently, few studies addressing dietary exposure to OPFRs were published. In this study, we used human biomonitoring (HBM) data of OPFRs to estimate how much the dietary intake may contribute to the total exposure. We estimated by reverse dosimetry, the daily intake of tris (2-chloroethyl) phosphate (TCEP), tris (1-chloro-2-propyl) phosphate (TCIPP), tris (1,3-dichloro-2-propyl) phosphate (TDCIPP) for children using HBM data from studies with sampling sites in Belgium, Denmark, France, Germany, Slovenia and Slovakia. For estimating the dietary exposure, a deterministic approach was chosen. The occurrence data of selected food categories were used from a published Belgium food basket study. Since the occurrence data were left-censored, the Lower bound (LB)—Upper bound (UB) approach was used. The estimated daily intake (EDI) calculated on the basis of urine metabolite concentrations ranged from 0.03 to 0.18 µg/kg bw/d for TDCIPP, from 0.05 to 0.17 µg/kg bw/d for TCIPP and from 0.02 to 0.2 µg/kg bw/d for TCEP. Based on national food consumption data and occurrence data, the estimated dietary intake for TDCIPP ranged from 0.005 to 0.09 µg/kg bw/d, for TCIPP ranged from 0.037 to 0.2 µg/kg bw/d and for TCEP ranged from 0.007 to 0.018 µg/kg bw/d (summarized for all countries). The estimated dietary intake of TDCIPP contributes 11–173% to the EDI, depending on country and LB-UB scenario. The estimated dietary uptake of TCIPP was in all calculations, except in Belgium and France, above 100%. In the case of TCEP, it is assumed that the dietary intake ranges from 6 to 57%. The EDI and the estimated dietary intake contribute less than 3% to the reference dose (RfD). Therefore, the estimated exposure to OPFRs indicates a minimal health risk based on the current knowledge of available exposure, kinetic and toxicity data. We were able to show that the dietary exposure can have an impact on the general exposure based on our underlying exposure scenarios.

Tryptamine acts as a neuromodulator and vasoactive agent in the human body. Dose–response data on dietary tryptamine are scarce and neither a toxicological threshold value nor tolerable levels in foods have been established so far. This paper reviews dose–response characteristics and toxicological effects of tryptamine as well as tryptamine contents in food, estimates dietary exposure of Austrian consumers, and calculates risk-based maximum tolerable limits for food categories. A dose without effect of 8 mg kg⁻¹ body weight day⁻¹ was derived from literature data. Dietary exposure via fish/seafood, beer, cheese and meat products was estimated for Austrian schoolchildren, female and male consumers, based on 543 food samples analysed in Austria 2010–15 and on food consumption data from 2008. Even worst-case estimates based on very high tryptamine contents reported in the literature did not exceed 5.9 mg kg⁻¹ body weight day⁻¹, and thus were below the dose without effect. Maximum tolerable levels for food commodities were calculated for high-consumption scenarios (95th percentile of female Austrian consumers). For fresh/cooked fish, preserved fish, cheese, raw sausage, condiments, sauerkraut and fermented tofu, maximum tolerable levels were 1650, 3200, 2840, 4800, 14,120, 1740 and 2400 mg kg⁻¹, respectively. For beer, the maximum tolerable limit of 65 mg kg⁻¹ included an uncertainty factor of 10. None of the Austrian occurrence data exceeded these levels (in fact, only 3.3% of samples demonstrated measurable amounts of tryptamine), and just one report was found in the literature on a raw fish sample exceeding the respective tolerable level. In sum, dietary intake of tryptamine should not cause adverse health effects in healthy individuals. The assessment did not take into account the combined effects of simultaneously ingested biogenic amines, and increased susceptibility to tryptamine, e.g., due to reduced monoamine oxidase activity.

Human exposure to polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) and dioxin-like PCBs (dl-PCBs) should be assessed regularly. In order to evaluate the contamination levels in various food products on the Austrian market and to assess the dietary exposure of the Austrian population for the first time, a national monitoring programme was conducted from 2005 to 2011. The 235 food products comprised meat, poultry, game and offal, fish and fish products, milk and dairy products, eggs, animal fats and vegetable oils. To estimate the dietary intakes of PCDD/Fs and dl-PCBs, mean concentrations in food were combined with the respective food consumption data from the Austrian food consumption survey. Estimated dietary intakes were expressed as toxic equivalents (WHO-TEQs 1998). The mean intakes for PCDD/Fs and dl-PCBs were estimated as 0.77, 0.75 and 0.61 pg WHO-TEQ kg⁻¹ bw day⁻¹ for children, women and men, respectively. The main contributors to total intake were milk and dairy products followed by fish and fish products for children and women, and meat, poultry, game and offal for men (65% and 15% for children, 67% and 14% for women, and 63% and 19% for men, respectively). Comparison of the estimated dietary intakes with the toxicological reference values shows that both children and adults are well below those values.