Particle emissions by office printers show differences between printer types, printers of the same type and a significant increase during working times [
5]. The average diameter of emitted particles from different printers was found to be in between 40-76 nm and well fitting to our results. The study checked up 62 different printers, but the type used in our case was not included [
5]. About a possible respiratory uptake of CNP in human office workers no systematic morphological investigations exist. A study about the respiratory health of workers handling printing toners showed a higher prevalence rate of thoracic radiographic abnormalities and a strong tendency towards a decline of lung function in long time exposed persons [
8]. In a case of granulomatous pneumonitis and mediastinal lymphadenopathy with photocopier toner dust exposure containing copper, this metal was detected in the tissue investigated by SEM and EDX [
10]. Metal oxides were detectable on the surface of toner particles in our case as well, but deposition in tissue has not been seen. In cases of anthracosilicosis dust deposits in the liver have been reported [
13]. This demonstrates that particle transport of inhaled dust via the blood stream with deposition in other organs can be found in humans [
11,
13]. Ultra fine carbon particles cause a strong down-regulating effect on the cytochrome P450 1B1 protein in monocytes. These data suggest that the induced reduction of gene expression may interfere with the activation and/or detoxification capabilities of inhaled toxic particles. In primary bronchial epithelial cells this effect showed remarkable inter-individual differences, which emphazises the role of polymorphisms [
14]. In the case reported here there were no obvious repiratory symptoms. Clinical studies revealed negative effects on respiratory health after toner exposure [
7,
8,
10], therefore further studies concerning morphology, genetics and clinical consequences are needed.