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Do laser printers cause cancer?
- Thread starter ginfreely
- Start date
Abstract
Incorporation of engineered nanomaterials (ENMs) into toners used in laser printers has led to countless quality and performance improvements. However, the release of ENMs during printing (consumer use) has raised concerns about their potential adverse health effects. The aim of this study was to use “real world” printer-emitted particles (PEPs), rather than raw toner powder, and assess the pulmonary responses following exposure by intratracheal instillation. Nine-week old male Balb/c mice were exposed to various doses of PEPs (0.5, 2.5 and 5 mg/kg body weight) by intratracheal instillation. These exposure doses are comparable to real world human inhalation exposures ranging from 13.7 to 141.9 h of printing. Toxicological parameters reflecting distinct mechanisms of action were evaluated, including lung membrane integrity, inflammation and regulation of DNA methylation patterns.
Results from this in vivo toxicological analysis showed that while intratracheal instillation of PEPs caused no changes in the lung membrane integrity, there was a pulmonary immune response, indicated by an elevation in neutrophil and macrophage percentage over the vehicle control and low dose PEPs groups. Additionally, exposure to PEPs upregulated expression of the Ccl5 (Rantes), Nos1 and Ucp2 genes in the murine lung tissue and modified components of the DNA methylation machinery (Dnmt3a) and expression of transposable element (TE) LINE-1 compared to the control group. These genes are involved in both the repair process from oxidative damage and the initiation of immune responses to foreign pathogens. The results are in agreement with findings from previous in vitro cellular studies and suggest that PEPs may cause immune responses in addition to modifications in gene expression in the murine lung at doses that can be comparable to real world exposure scenarios, thereby raising concerns of deleterious health effects.
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1. Introduction
The use of laser printers leads to exposure to various pollutants, including ozone, volatile organic compounds and particulate matter (PM), among other pollutants (He et al., 2007; Morawska et al., 2009; Wang et al., 2012). In particular, the release of a significant number of particles, the majority of which are nanoparticles, during the use of this growing technology has become a reason for concern. More recently, in order to assess the complex chemistry of printer emitted particles (PEPs) and their potential health hazards, a Printer Exposure Generation System (PEGS) was recently developed to generate and sample airborne PEPs for subsequent physicochemical, morphological and toxicological analyses (Pirela et al., 2014a). The PM emission profiles from commonly used printers were evaluated and further characterization was performed on both raw toner powder and PEPs. The detailed analysis showed that laser printers emit up to 1.3 million particles/cm3 with modal diameters of b200 nm (Pirela et al., 2014a). More importantly, Pirela et al. (2014b) found nanoscale materials used in the toner formulation that become airborne during the use of a printer, thus, classifying toners as nano-enabled products (NEPs). Additionally, the authors found that toner powders and PEPs share a complex chemistry and contain elemental and organic carbon, as well as inorganic compounds such as nanoscale metals and metal oxides.
While the physicochemical and morphological properties of PEPs have been studied in detail, their toxicological profiles remain largely unknown. In a series of recently published papers, several physiologically relevant cell lines (i.e., human small airway epithelial cells, microvascular endothelial cells, macrophages and lymphoblasts) were treated with various doses of PEPs using both mono- and co-culture exposure systems (Sisler et al., 2014; Pirela et al., 2015). In both studies, it was shown that PEPs triggered an unfavorable series of biological responses in macrophages, small airway epithelial cells and microvascular endothelial cells at doses comparable to approximately 8 h or more of consumer inhalation of PEPs. Specifically, cell treatment with PEPs led to significant changes in cell viability, hereditary genetic material changes, reactive oxygen species (ROS) generation and release of inflammatory mediators, among other adverse effects. Moreover, recent findings suggest that PEPs can also influence the cellular epigenome. Particularly, a 24-hour exposure to PEPs caused altered expression of DNA methylation machinery in small airway epithelial cells, in turn leading to changes in global DNA methylation and reactivation of transposable element (TE) LINE-1 and Alu(Pirela et al., 2015; Lu et al., 2015a).
Notably, the toxicity of PEPs remains poorly characterized in vivo with only a few published studies. Major discrepancy on those in vivo studies is the use of toner powders rather than the PM and gaseous pollutants emitted from laser printers. For example, Bai, Zhang (Bai et al., 2010) reported that mice exposed to printer toner particles showed significant pulmonary inflammation, damage to the epithelial-capillary barrier and enhanced cell permeability. Comparable inflammatory and fibrotic responses were also observed in rats exposed to toner powders (Morimoto et al., 2013). A historic rodent chronic inhalation exposure concluded that toner led to a substantial increase in lung weight, a chronic inflammatory response, pulmonary fibrosis and increased incidence of primary lung tumors in exposed rats (Muhle et al., 1991). However, as extensive as these studies were in identifying the biological response in the rodent lung following exposure to toner, they are limited by addressing only the toxicity of toner powder, which may be relevant to occupational settings and workers directly handling toner powders but is not applicable to consumers using laser printers.
Notably, the toxicity of PEPs remains poorly characterized in vivo with only a few published studies. Major discrepancy on those in vivo studies is the use of toner powders rather than the PM and gaseous pollutants emitted from laser printers. For example, Bai, Zhang (Bai et al., 2010) reported that mice exposed to printer toner particles showed significant pulmonary inflammation, damage to the epithelial-capillary barrier and enhanced cell permeability. Comparable inflammatory and fibrotic responses were also observed in rats exposed to toner powders (Morimoto et al., 2013). A historic rodent chronic inhalation exposure concluded that toner led to a substantial increase in lung weight, a chronic inflammatory response, pulmonary fibrosis and increased incidence of primary lung tumors in exposed rats (Muhle et al., 1991). However, as extensive as these studies were in identifying the biological response in the rodent lung following exposure to toner, they are limited by addressing only the toxicity of toner powder, which may be relevant to occupational settings and workers directly handling toner powders but is not applicable to consumers using laser printers.
In this study, we sought to further expand on the latest cellular toxicology studies performed by our group on PEPs (Sisler et al., 2014; Pirela et al., 2015; Lu et al., 2015b). Particularly, we present findings on the murine responses to intratracheal instillation exposures to various doses of PEPs. The endpoints evaluated included bronchoalveolar lavage (BAL) levels of lactate dehydrogenase, myeloperoxidase, cytokines and white blood cell differentials, as well as lung tissue expression of a number of genes involved in immune responses, cell survival and signaling, among other important biological processes.
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5. Conclusion
The study described here focuses on the assessment of toxicological potential of PEPs using an in vivo experimental animal model. Our data show that there may be an initiation of an immune response following the exposure to PEPs. Mice exposed to PEPs exhibited a variety of responses that translate into hallmarks of the initiation of an immune reaction due to the stress induced by PEPs. In toto, findings on lung injury, inflammation and changes in gene expression, point to possible adverse pulmonary effects. It is clear that these acute studies should be followed by more detailed sub-acute and chronic studies in order to have more conclusive evidence on deleterious effects from such a widely used nano-enabled product. Finally, this experimental approach used here linking exposures to particulate matter released across life cycle (called LCPM) could be used to study other NEPs for a more realistic risk assessment of nanomaterials and nano-enabled products.
Yes. You'll get cancer if you use it to print your imaginary hymen. You'll get vagina cancer.
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