Background About one-fifth of people in industrialised countries are tattooed, potentially putting them at risk of exposure to possible carcinogenic or otherwise harmful substances. Health risks are directly correlated with the amounts of substances introduced, yet reliable data on the systemic exposure to tattoo inks are lacking.

Objectives This study aims to determine the exposure to soluble tattoo ink ingredients and their excretion within 24 hours after tattooing. Comparative in vivo and in vitro experiments were conducted to determine the change in metabolite exposure between tattooing and oral exposure.

Methods In a clinical study, 24 subjects were tattooed with black or red tattoo ink to which the tracer substances potassium iodide, 4-aminobenzoic acid (PABA) and 2-phenoxyethanol (PEtOH) had been added to mimic known hazardous substances found in tattoo inks. Tracers and their metabolites were quantified in blood, urine, ink, and consumables pre- and post-tattooing. Tattooed skin area was determined using picture analysis. PABA metabolism upon tattooing was compared to peroral administration. Skin fibroblasts and macrophages were tested in vitro for their ability to metabolise PABA.

Results All tracers or their metabolites were identified in urine; iodide and the PABA metabolite 4-acetamidobenzoic acid (ACD) were identified in plasma. The worst-case scenario for systemic ink exposure was estimated to be 0.31 g of ink per tattoo session (75th percentile). Peroral administration resulted in lower levels of ACD than tattooing. Fibroblasts and macrophages were capable of converting PABA into ACD.

Discussion Our results are the first human in vivo data on soluble tattoo ink ingredients and suggest that the overall exposure might be lower than the estimates previously used for regulatory purposes. In addition, the first-pass effect by skin metabolism leads to an altered metabolite profile compared to oral exposure. Skin metabolism might also contribute to detoxification of certain carcinogenic substances through N-acetylation.

The authors have declared no competing interest.

DRKS00026022

This work was supported by the intramural research projects SFP 1323-103, SFP 1322-808 and the externally funded project (60-0102-02.P600) at the German Federal Institute for Risk Assessment (BfR).

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Ethics committee of the Charite Universitaetsmedizin Berlin (Berlin, Germany) gave ethical approval for this work

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