Pulmonary toxicity induced by intratracheal instillation of Asian yellow dust (Kosa) in mice

Oita University of Nursing and Health Sciences, Ōita, Ōita, Japan
Environmental Toxicology and Pharmacology (Impact Factor: 2.08). 07/2005; 20(1):48-56. DOI: 10.1016/j.etap.2004.10.009
Source: PubMed


Asian yellow dust (Kosa) causes adverse respiratory health effects in humans. The objective of this study was to clarify the lung toxicity of Kosa. ICR mice (5 weeks of age) were administered intratracheally with Kosa samples-two samples from Maowusu desert and Shapotou desert, one sample consisted of Shapotou Kosa plus sulfate, and natural Asian dust (NAD) from the atmosphere of Beijing-at doses of 0.05, 0.10 or 0.20mg/mouse at four weekly intervals. The four Kosa samples tested had similar compositions of minerals and concentrations of elements. Instillation of dust particles caused bronchitis and alveolitis in treated mice. The magnitude of inflammation was much greater in NAD-treated mice than in the other particles tested. Increased neutrophils, lymphocytes or eosinophils in bronchoalveolar lavage fluids (BALF) of treated mice were dose dependent. The number of neutrophils in BALF at the 0.2mg level was parallel to the content of β-glucan in each particle. The numbers of lymphocytes and eosinophils in BALF at the 0.2mg level were parallel to the concentration of SO(4)(2-) in each particle. Pro-inflammatory mediators-such as interleukin (IL)-12, tumor necrosis factor-(TNF)-α, keratinocyte chemoattractant (KC), monocyte chemotactic protein (MCP)-l and macrophage inflammatory protein-(MIP)-lα in BALF-were greater in the treated mice. Specifically, NAD considerably increased pro-inflammatory mediators at a 0.2mg dose. The increased amounts of MlP-lα and TNF-α at 0.2mg dose corresponded to the amount of β-glucan in each particle. The amounts of MCP-l or IL-12 corresponded to the concentration of sulfate (SO(4)(2-)) at a 0.2mg dose. These results suggest that inflammatory lung injury was mediated by β-glucan or SO(4)(2-), which was adsorbed into the particles, via the expression of these pro-inflammatory mediators. The results also suggest that the variations in the magnitude of inflammation of the tested Kosa samples depend on the amounts of these toxic materials.

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    • "Much of this concern has focussed more on the pulmonary toxicity and corresponding acute effects of PM inhalation, especially on asthmatic patients (e.g. Ichinose et al., 2005; Ueda et al., 2010; Watanabe et al., 2011), or on the potential transport of active bioaerosols between countries (e.g. Chen et al., 2010). "

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    • "Dust events are known to transport airborne microorganisms, thereby supporting the microbial immigration to downwind ecosystems (Griffin, 2007; Maki et al., 2010; Yamaguchi et al., 2012). In Asian regions, airborne microorganisms transported over long distances increase allergenic burden, consequently increasing the incidence of asthma (Ichinose et al., 2005) and contributing to the dispersion of diseases such as Kawasaki disease in humans (Rod o et al., 2011) and rust diseases in plants (Brown and Hovmøller, 2002). Some microorganisms isolated at high altitudes have been reported to induce allergy levels similar to that caused by Asian mineral dust particles (Liu et al., 2014). "

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    • "Asian dust particles contain chemical substances such as sulfates or nitrates derived from alkaline soil and microbiological materials [28] that may cause serious respiratory health problems in humans. Heat treatment of Asian dust particles has been reported to suppress allergic responses, which suggests that these adhered materials contribute to Asian dust particles-induced inflammation [29]. "
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    ABSTRACT: Asian dust is a springtime meteorological phenomenon that originates in the deserts of China and Mongolia. The dust is carried by prevailing winds across East Asia where it causes serious health problems. Most of the information available on the impact of Asian dust on human health is based on epidemiological investigations, so from a biological standpoint little is known of its effects. To clarify the effects of Asian dust on human health, it is essential to assess inflammatory responses to the dust and to evaluate the involvement of these responses in the pathogenesis or aggravation of disease. Here, we investigated the induction of inflammatory responses by Asian dust particles in macrophages. Treatment with Asian dust particles induced greater production of inflammatory cytokines interleukin-6 and tumor necrosis factor- α (TNF- α ) compared with treatment with soil dust. Furthermore, a soil dust sample containing only particles ≤10 μ m in diameter provoked a greater inflammatory response than soil dust samples containing particles >10 μ m. In addition, Asian dust particles-induced TNF- α production was dependent on endocytosis, the production of reactive oxygen species, and the activation of nuclear factor- κ B and mitogen-activated protein kinases. Together, these results suggest that Asian dust particles induce inflammatory disease through the activation of macrophages.
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