Effects Of Asian Sand Dust Research Articles

Effects of Fetal Exposure to Asian Sand Dust on Development and Reproduction in Male Offspring.

In recent experimental studies, we reported the aggravating effects of Asian sand dust (ASD) on male reproduction in mice. However, the effects of fetal ASD exposure on male reproduction have not been investigated. The present study investigated the effects of fetal ASD exposure on reproduction in male offspring. Using pregnant CD-1 mice, ASD was administered intratracheally on days 7 and 14 of gestation, and the reproduction of male offspring was determined at 5, 10, and 15 weeks after birth. The secondary sex ratio was significantly lower in the fetal ASD-exposed mice than in the controls. Histologic examination showed partial vacuolation of seminiferous tubules in immature mice. Moreover, daily sperm production (DSP) was significantly less in the fetal ASD-exposed mice than in the controls. DSP in the fetal ASD-exposed mice was approximately 10% less than the controls at both 5 and 10 weeks. However, both the histologic changes and the DSP decrease were reversed as the mice matured. These findings suggest that ASD exposure affects both the fetal development and the reproduction of male offspring. In the future, it will be necessary to clarify the onset mechanisms of ASD-induced male fetus death and male reproductive disorders.

Effects of Asian Sand Dust on Respiratory Health

Effects of Asian Sand Dust on Respiratory Health

Aggravating effects of Asian sand dust on lung eosinophilia in mice immunized beforehand by ovalbumin

Asian sand dust (ASD) event may result in a significant influence on an asthmatic patient. However, for obvious reasons, there is no experimental study in which asthmatic patients are exposed to ASD. This study was undertaken to clarify the effects of ASD on lung eosinophiliain mice immunized beforehand by ovalbumin (OVA). CD-1 mice were instilled intratracheally with OVA four times at 2-week intervals. Simultaneous intratracheal administration of OVA and ASD (OVA + ASD sim) at the last OVA treatment or intratracheal administration with ASD 1 day before (OVA + ASD pre) /after (OVA + ASD post) the last OVA treatment was performed to investigate the effects of OVA and ASD exposure timing. The three kinds of treatment (OVA + ASD pre; OVA + ASD sim; OVA + ASD post) aggravated allergic lung inflammation and proliferation of goblet cells in the airway epithelium in mice, as evidenced by the cellular profile of bronchoalveolar lavage fluid (BALF) and pathological examination. As an overall trend, these changes were paralleled with the expression of Th2-associated effecter molecules and eosinophil relevant cytokine chimokines in BALF as well as the production of OVA-specific IgG1 compared with OVA treatment alone. OVA + ASD sim aggravated lung eosinophilia remarkably compared with the other treatments. The order of the potency of the aggravation was OVA+ASD pre < OVA+ASD post <OVA+ASD sim. These results indicate that ASD has a potent effect in activating lung eosinopilia in mice immunized beforehand by OVA. The simultaneous exposure of asthmatic patients to ASD and its antigen may have serious consequences for such individuals.

Questionnaire Survey on the Effects of Asian Sand Dust on Human Health in Shimane Prefecture

Allergic rhinitis, especially Japanese cedar pollinosis, is a major problem in Japan. Recent research has revealed that the symptoms of allergic rhinitis are aggravated after the Asian sand dust (ASD) phenomenon which tends to occur concomitantly with the pollen season in Japan. Objectives: A questionnaire survey was conducted to investigate whether ASD is recognized as a factor which affects human health, and whether people are interested in information about the ASD phenomenon. The questionnaire survey was undertaken in cooperation with otolaryngologists in the eastern area of Shimane prefecture. Results: Three hundred and seventy-seven volunteers including 288 patients with allergic rhinitis and 89 without allergic rhinitis were enrolled. Two hundred and seventy-six of the 377 volunteers (73.2%) recognized ASD as a factor which may affect human health and 150 of the 377 volunteers felt that their own health condition changed after the ASD phenomenon. As symptoms, in addition to nasal symptoms, other symptoms such as sore throat, abnormal sensation, cough and eye symptoms developed in volunteers with/without allergic rhinitis. Two hundred and ninety-seven of the 377 volunteers answered that they were interested in information about ASD, such as the relationship between allergic rhinitis and ASD. Conclusion: The results of this survey suggest that clinicians who treat allergic diseases need to collect and provide information on not only pollen but also the ASD phenomenon for patients, especially those who have allergic rhinitis, to help them to maintain a good quality of life.

Effects of Asian Sand Dust on Mucin Gene Expression and Activation of Nasal Polyp Epithelial Cells

Asian sand dust (ASD) contains a variety of chemical and microbiological materials such as lipopolysaccharide (LPS) and beta-glucan that can cause inflammation. The increase in the atmospheric concentration of ASD has been associated with asthma severity and adverse effects on respiratory function. The aim of this study was to evaluate the effect of ASD on the inflammatory process and mucin gene expression in nasal epithelial cells. Primary nasal polyp epithelial cells were exposed to ASD for 72 hours, and then the supernatants were collected. To determine the activation of the epithelial cells, IL-6, IL-8, and granulocyte-macrophage colony-stimulating factor were measured. In addition, the potential cytotoxic effects of ASD on the epithelial cells were evaluated. Quantitative reverse-transcription polymerase chain reaction for MUC4, MUC5AC, MUC5B, and MUC8 mRNA expression, in the nasal epithelial cells, was performed. ASD stimulated the production of chemical mediators in a time-dependent manner. The cytokine production was highest at 100 micrograms/mL of ASD. MUC4 and MUC5B mRNA expression was significantly increased at 10 and 50 micrograms/mL of ASD. Atomospheric exposure to various chemical species and microbiological materials carrying ASD may affect upper airway inflammation through the production of inflammatory cytokines and mucin.

Effects of Asian Sand Dust on Human Health and Allergic Symptom, Fukuoka, Japan

Effects of Asian Sand Dust on Human Health and Allergic Symptom, Fukuoka, Japan

Effects of Asian Sand Dust, Arizona Sand Dust, Amorphous Silica and Aluminum Oxide on Allergic Inflammation in the Murine Lung

The aggravating effects of Asian sand dust (SD) and related minerals on the allergic inflammation were examined in the murine lungs. The toxic materials adsorbed onto Asian SD, Arizona SD were inactivated by heat-treatment. ICR mice were administered mineral samples (0.1 mg/mouse) and/or ovalbumin (OVA) (1 μ g/mouse)—normal saline (control), Asian SD, Arizona SD, SiO2, Al2O3, OVA, OVA + Asian SD, OVA + Arizona SD, OVA + SiO2, and OVA + Al2O3—intratracheally four times at two-week intervals. All samples tested enhanced eosinophil recruitment induced by ovalbumin in the submucosa of the airway, which has a goblet cell proliferation in the bronchial epithelium. Arizona SD alone caused a slight increase of neutrophils in bronchoalveolar lavage fluids along with pro-inflammatory mediators, such as keratinocyte chemoattractant, but Asian SD alone or Al2O3 alone showed no effect. The test particles, except Al2O3, synergistically increased the numbers of eosinophils in BALF induced by ovalbumin. In particular, Arizona SD and SiO2 synergistically increased the eosinophil relevant cytokine and chemokine, such as IL-5 and monocyte chemotactic protein (MCP)-3. The aggravating effects of the samples were dependent on the SiO2 content. All samples tested also induced the adjuvant effects to specific IgG1 production by OVA. These results suggest that the aggravated allergic inflammation by mineral dusts may be due to the mineral elements (mainly SiO2). The enhancement by Arizona SD may be mediated, at least partially, by the increased expression of IL-5 and MCP-3 and also by the modulated expression of IL-5 and MCP-3.