Summary

Canada’s economy, like that of many other industrialized countries, is benefitting from the development of nanotechnologies, with their rich potential that can be put to work in many different industries. A growing number of Québec companies are already producing nanoparticles (NPs) and there is good reason to believe that others will follow in their footsteps in the years ahead. As a result, not only will the number of workers employed in the manufacture and synthesis of NPs grow substantially, so will the number of worker who will have to handle and process them in nanotechnologies in general. One consequence of this situation is an increase in the number of people who may be exposed to NPs. The scientific literature includes numerous studies reporting inflammatory effects caused by inhaling NPs, with the respiratory system being the most probable NP exposure pathway. It has been demonstrated, for example, that NPs such as zine oxides (ZnO) and copper induce recruitment of eosinophil immune cells (EOs) in the lungs of rodents. Such cells are well known to cause a variety of lung disorders and diseases, including asthma. Despite this, there were no data on interactions between NPs and human EOs available before this project was undertaken. In other words, the mode of action of NPs on EO biology was unknown. Furthermore, people can be exposed to NPs not only through airways but also through the skin and even by ingestion, allowing NPs to make their way through the bloodstream or other tissue.

Given the above, it was hypothesized that NPs could alter the biology of human EOs, and this study was undertaken with the primary goal of filling in the knowledge gap. To expand the field of knowledge and get a better understanding of the mode of action of NPs, EOs from consenting healthy donors were freshly isolated and then exposed to a given NP to assess the modulatory capacities of several functions related to the inflammatory process, including the capacity of NPs to affect production of reactive oxygen species (ROS), chemotaxis, adhesion, apoptosis and production of certain cytokines by EOs.

Using an experimental approach, it was possible to demonstrate the differential effects of NPs on the biology of human EOs. For example, cerium dioxide (CeO₂) NPs cause the biggest increase in ROS production but do not affect apoptosis, and titanium dioxide (TiO₂) NPs cause the greatest increase in EO adhesion to cell substrates but have little or no effect on ROS production or apoptosis.

The results clearly demonstrate that it is difficult to classify NPs solely on the basis of their potential to modify any one of the functions studied. It is best to provide a more nuanced picture showing the effects provoked by a given NP on the biology of in vitro human EO that must be considered to understand its mode of action. In other words, the effects of NPs are extremely varied and the aim of this study is to demonstrate that they do not all act in the same way.

The impacts of this research project involving isolated healthy cells are many. The results show that it is worthwhile to use the cells of workers who have may have been exposed to NPs (including researchers, students and technical staff) to study EO functions that could have disproportionate functional responses or, conversely, little response. The results and observations of this study, together with those that will be described by other teams studying different facets of NP toxicity, will help in making certain decisions regarding the management of risks related to occupational exposure to nanoparticles.