Chronic upper airway inflammation and systemic oxidative stress from nanoparticles in photocopier operators: Mechanistic insights

Background Several recent studies have linked emissions from printing equipment with upper airway inflammation and systemic oxidative stress in healthy humans, lung inflammation in mice, and cytotoxicity, induction of inflammatory markers and epigenetic changes in human cell lines. Acute exposures have lead to upper airway inflammation and systemic oxidative stress, which for certain markers took longer than 24–36 h post-exposure to clear. Objective In this follow-up work, we determined: i) whether chronic exposures to nanoparticles from copiers lead to chronic upper airway inflammation and systemic oxidative stress; and ii) whether expression patterns of biomarkers for such stresses change during transition from acute to chronic exposures. Methods Six permanent employees from three copy centers and eleven controls participated in the study. Nasal lavage and urine samples were collected on Monday morning (pre-shift, Mo-AM) and evening (post-shift, Mo-PM), as well as at the end of the workweek (Fr-PM), over three random weeks. The matched controls were sampled over one week. Nasal lavage samples were analyzed for a panel of 14 pro-inflammatory cytokines/chemokines, inflammatory cells, and total protein. Urine samples were analyzed for 8-OH-dG , a biomarker of systemic oxidative stress. Detailed quantitative exposure assessment to airborne nanoparticles was conducted for a whole week, and included size distribution, size-fractionated aerosol collection, extensive chemical analysis, and lung burden estimates. Results The daily geometric mean total particle number concentration varied between 14,600–21,860 particles/cm 3 , 1.7–12.1 times greater than background, with maxima up to 143,000 particles/cm 3 . Mass concentration of the nanoscale fraction was in the 1–10 μg/m 3 range. Chemical composition of the nanoparticle fraction was comprised mostly of organic compounds, mixed with several engineered nanoparticles, which contributed a metal content ranging from 2 to 8% of the total particulate mass. Five out of the 14 inflammatory cytokines, namely IL-6, IL-8, TNFα, IL-1β and Eotaxin, were significantly elevated in the nasal lavage samples of the chronically exposed copier operators (p 8-OH-dG in (4.3 fold) in urine samples. Conclusion Chronic upper airway inflammation and systemic oxidative stress were documented in photocopier operators chronically exposed to nanoparticles. These findings agree with the recent toxicological literature on printer-emitted particles and medical case reports, and call for an industry-wide study of the health effects resulting from exposure to printer-emitted particles in chronically exposed workers. Inflammatory markers point to possible involvement of toll-like receptors, particularly TLR-4, oxidative stress, and the Nf-kB pathway in mediating airway tissue inflammation.