TiO2 Nanomaterials Non-Controlled Contamination Could Be Hazardous for Normal Cells Located in the Field of Radiotherapy.

Among nanomaterials (NMs), titanium dioxide (TiO2) is one of the most manufactured NMs and can be found in many consumers' products such as skin care products, textiles and food (as E171 additive). Moreover, due to its most attractive property, a photoactivation upon non-ionizing UVA radiation, TiO2 NMs is widely used as a decontaminating agent. Uncontrolled contaminations by TiO2 NMs during their production (professional exposure) or by using products (consumer exposure) are rather frequent. So far, TiO2 NMs cytotoxicity is still a matter of controversy depending on biological models, types of TiO2 NMs, suspension preparation and biological endpoints. TiO2 NMs photoactivation has been widely described for UV light radiation exposure, it could lead to reactive oxygen species production, known to be both cyto- and genotoxic on human cells. After higher photon energy exposition, such as X-rays used for radiotherapy and for medical imaging, TiO2 NMs photoactivation still occurs. Importantly, the question of its hazard in the case of body contamination of persons receiving radiotherapy was never addressed, knowing that healthy tissues surrounding the tumor are indeed exposed. The present work focuses on the analysis of human normal bronchiolar cell response after co-exposition TiO2 NMs (with different coatings) and ionizing radiation. Our results show a clear synergistic effect, in terms of cell viability, cell death and oxidative stress, between TiO2 NMS and radiation.

Attempted validation of ICRP 30 and ICRP 66 respiratory models.

The validation of human biological models for inhaled radionuclides is nearly impossible. Requirements for validation are: (1) the measurement of the relevant human tissue data and (2) valid exposure measurements over the interval known to apply to tissue uptake. Two lung models, ICRP 30(1) and ICRP 66(2), are widely used to estimate lung doses following acute occupational or environmental exposure. Both ICRP 30 and 66 lung models are structured to estimate acute rather than chronic exposure. Two sets of human tissue measurements are available: (210)Po accumulated in tissue from inhaled cigarettes and ingested in diet and airborne global fallout (239,240)Pu accumulated in the lungs from inhalation. The human tissue measurements include pulmonary and bronchial tissue in smokers, ex-smokers and non-smokers analysed radiochemically for (210)Po, and pulmonary, bronchial and lymph nodes analysed for (239,240)Pu in lung tissue collected by the New York City Medical Examiner from 1972 to 1974. Both ICRP 30 and 66 models were included in a programme to accommodate chronic uptake. Neither lung model accurately described the estimated tissue concentrations but was within a factor of 2 from measurements. ICRP 66 was the exception and consistently overestimated the bronchial concentrations probably because of its assumption of an overly long 23-d clearance half-time in the bronchi and bronchioles.