나노기술은 21세기 초반 첨단산업을 이끌어갈 핵심기술 중의 하나로 여러 나라들이 국가적인차원에서 전략적으로 개발하고 있다. 나노기술은 초정밀 가공기술, 원자 혹은 분자 단위의 조립(조합)기술, 소재공정기술 등의 기술 분야를 포함하며 나노스케일 영역에서 나노소재를 이용(제조 및 가공)하여 새로운 응용분야를 창출해내 거나 기존 산업을 더욱 고도화하는데 기여하는 기술이다. 나노소재는 금속, 세라믹, 고분자, 생체물질 등의 특정 물질 영역에 국한되지 않고 다양한 형태, 다양한 물성을 갖고 있으며 나노기술 구현에 있어서 직접적인 대상 혹은 중간매체에 해당한다. 따라서 나노소재기술은 대단히 광범위한 영역을 포함하는 나노기술의 바탕을 이루는 기반기술 또는 원천기술이라고 할 수 있다. 여러 형태의 나노소재 중에서 가장 저차원(0차원)의 물질에 해당하는 나노분말은 기술적으로 가장 실용화에 근접해 있으며 이미 많은 상용화 사례들이 나타나고 있다. 나노분말 기술은 기술 성숙도 측면에서 뿐만 아니라 확장성(유용성), 신규성(혁신성) 측면에서 대단한 가능성을 갖고 있기 때문에 향후 대단히 빠른 속도로 시장이 확대될 전망이다. 본 발표에서는 나노분말 기술의 개발 현황 및 전망에 대하여 언급하고자 한다.

To compare the pulmonary toxicity between ultrafine colloidal silica particles (UFCSs) and fine colloidal silica particles (FCSs), mice were intratracheally instilled with 3 mg of 14-nm UFCSs and 230-nm FCSs and pathologically examined from 30 mill to 24 hr post-exposure. Histopathologically, lungs exposed to both sizes of particles showed bronchiolar degeneration and necrosis, neutrophilic inflammation in alveoli with alveolar type II cell proliferation and particle-laden alveolar macrophage accumulation. UFCSs, however, induced extensive alveolar hemorrhage compared to FCSs from 30 min onwards. UFCSs also caused more severe bronchiolar epithelial cell necrosis and neutrophil influx in alveoli than FCSs at 12 and 24 hr post-exposure. Laminin positive immunolabellings in basement membranes of bronchioles and alveoli of UFCSs treated animals was weaker than those of FCSs treated animals in all observation times. Electron microscopy demonstrated UFCSs and FCSs on bronchiolar and alveolar wall surface as well as in the cytoplasm of alveolar epithelial cells, alveolar macrophages and neutrophils. Type I alveolar epithelial cell erosion with basement membrane damage in UFCSs treated animals was more severe than those in FCSs treated animals. At 12 and 24 hr post-exposure, bronchiolar epithelia cells in UFCSs treated animals showed more intense vacuolation and necrosis compared to FCSs treated animals. These findings suggest that UFCSs has greater ability to induce lung inflammation and tissue damages than FCSs.

Diesel exhaust Particles (DEPs) are known to induce allergic responses in airway epithelial cells, such as the production of various cytokines via nuclear factor-kappa B ($NF-{\kappa}B$). However. the intracellular signal transduction pathways underlying this phenomenon have not been fully examined. This study showed that DEP induced $NF-{\kappa}B$ activity via transforming growth factor-${\beta}$ activated kinase 1 (TAK1) and $NF-{\kappa}B$-inducing kinase (NIK) in L2 rat lung epithelial cells. DEP induced the $NF-{\kappa}B$ dependent reporter activity approximately two-to three-fold in L2 cells. However, this effect was abolished by the expression of the dominant negative forms of TAK1 or NIK. Furthermore, it was shown that DEP induced TAK1 phosphorylation in the L2 cells. These results suggest that TAK1 and NIK are important mediators of DEP-induced $NF-{\kappa}B$ activation.