Vol. 121, No. 1 (Supplement) 2016
Supplement abstract

Ultrastructural detection of environmental nanoparticles in circulating blood

Published 2017-10-06


  • ESEM,
  • environmental pollution,
  • nanoparticles,
  • circulating blood

How to Cite

Visani, G., Manti, A., Valentini, L., Canonico, B., Loscocco, F., Isidori, A., Gabucci, E., Gobbi, P., Montanari, S., Rocchi, M., Papa, S., & Gatti, A. M. (2017). Ultrastructural detection of environmental nanoparticles in circulating blood. Italian Journal of Anatomy and Embryology, 121(1), 105. Retrieved from https://oajournals.fupress.net/index.php/ijae/article/view/2243


The increase in the incidence of acute myeloid leukemia (AML) may suggest a possible environmental etiology. PM2.5 was declared by the International Agency for Research on Cancer (WHO organ) a Class I carcinogen. To date, no reports have focused on particulate environmental pollution together with AML. The study investigated the presence and composition of particulate matter in circulating blood with a Environmental Scanning Electron Microscope coupled with an Energy Dispersive Spectroscope for the elemental analysis of the samples. 38 peripheral blood samples, 19 AML cases and 19 healthy controls, were analysed. A significant overload of particulate matter-derived nanoparticles linked or aggregated to blood components was found in AML patients, while almost absent in matched healthy controls. Two tailed Student’s t-test, MANOVA and Principal Component Analysis indicated that the total numbers of aggregates and particles were statistically different between cases and controls (MANOVA, P<0.001 and P=0.009 respectively). The particles detected showed to contain highly reactive, non-biocompatible and non-biodegradable metals; in particular, micro- and nano-sized particles grouped in organic/inorganic clusters, with statistically higher frequency of a subgroup of elements in AML samples. The demonstration, of an overload of nanoparticles linked to blood components in AML patients suggests a possible, additional, pathogenetic mechanism for AML development.