Effects of Printer Emissions in Mice With Preexisting Allergic Airway Responses

PP-31-112 Background/Aims: Indoor air pollution in working places is widely recognized as one of the most serious environment risks to human health. With the advent of electronic technology, especially electronic equipment is now a potential source of indoor pollutants in office environment. To study the effects of printer emissions on the allergic responses, inflammation, and oxidative stress, an ovalbumin sensitized and challenged mouse model of allergic airways disease was utilized, along with the nonallergic mice. After the final challenge, both allergic and nonallergic mice were subjected to printer emissions. Physiological and inflammatory responses were measured after 30th day. Exposure to printer emissions has resulted in increased pulmonary responsiveness, BAL inflammatory cells, and oxidative stress Printer emissions exposure results in pulmonary effects that are more intense in mice with chronic allergic pulmonary inflammation. Methods: Female Balb/c mice aged 7 weeks (KOATECH, Korea) were acclimatized to laboratory conditions for a week. Mice that were sensitized and challenged with ovalbumin were referred to as allergic, whereas mice that did not undergo any sensitization or challenge were defined as nonallergic. Mice were divided into 4 groups, namely allergic (asthma induced), nonallergic, allergic + printer emissions, and nonallergic + printer emissions. After 24 hours of final exposure, BAL was performed and BAL cells were counted to analyze airway inflammation and lactate dehydrogenase activity in acellular BAL fluid, and histopathological evaluation of the lung was carried out to assess the lung injury. Results: Epidemiologic and experimental studies suggest that anthropogenic air pollutants in indoors are important cofactors in the development of respiratory health disorders (Destaillats et al, 2008). Previous studies have shown that chronic inhalation exposure to toner dust and volatile organic compounds VOC (which include printer emissions are studied separately) produces significant pulmonary response in normal rats (Muhle et al, 1991). Studies with regard to the direct exposure to printer emissions and the effects of printer emissions in populations with comprised airways are nil. This finding is related to acute inhalation exposure and the direct exposure to printer emissions via inhalation. Changes lactate dehydrogenase, and BAL cells represent significant increases in lung epithelial permeability, cytotoxicity, and lysosomal enzyme release, respectively. Increases in these biochemical indices of lung injury were associated with printer exposure, but the effect of printer emissions was significantly greater in allergic-sensitized mice. The results of this study showed that physiologic and inflammatory responses to ovalbumin challenge in sensitized mice were enhanced after exposure to printer emissions, an emission source particulate matter (PM) with a high content of VOC and toner dust. The overall toxicological effects in the current study might be attributed to the various chemicals released during the operation of the laser printer. Volatile organic compounds, semivolatile organic compounds, ozone, PM10, ultrafine aerosol particles, emitted from printer operation can cause airway epithelial injury and lung inflammation via oxidant injury. The toners used in laser printers contain a wide variety of chemicals in addition to fine, black carbon particles, or dyes and pigments for color toners. The study of Schnell et al (1992) reported that the concentration of black carbon aerosol produced by a photocopier is equivalent to black carbon levels observed in urban areas under moderate vehicle traffic and the respiratory health effects of black carbon aerosols are well documented which correlated with the increased particle concentration observed with the time of printer operation. The significant changes noted in the asthmatic mice exposed to printer emissions suggests the increased oxidative stress and inflammatory cells due to the exogenous and endogenous sources might have caused respiratory epithelial injury. Conclusion: The observed increased influx of inflammatory cells and lung injury might be due to the exposure to high VOCs and particle concentration generated during printer operation. In conclusion, exposure to printer emissions resulted in an increased pulmonary damage in nonsensitized mice and these responses were amplified in OVA-sensitized and challenged mice with greater than additive increase in pulmonary inflammatory cell infiltration and lung injury.