immune activation of splenocytes following exposure to tar from Asian sand dust.

Air pollution, especially that initiated by particulate matter (PM), has been implicated as a risk factor for several inflammatory diseases. Previously, it was reported that PM enhances immune responses. PM includes the tar fraction that contains polycyclic aromatic hydrocarbons (PAHs), which produce adverse health effects in exposed individuals.

Long term trends in atmospheric concentrations of polycyclic aromatic hydrocarbons and nitropolycyclic aromatic hydrocarbons: A study of Japanese cities from 1997 to 2014.

Total suspended particulate matter (TSP) was collected during the summer and winter in five Japanese cities spanning Hokkaido to Kyushu (Sapporo, Kanazawa, Tokyo, Sagamihara and Kitakyushu) from 1997 to 2014. Nine polycyclic aromatic hydrocarbons (PAHs) with four to six rings, including pyrene (Pyr) and benzo[a]pyrene (BaP), were identified using high-performance liquid chromatography (HPLC) with fluorescence detection. Two nitropolycyclic aromatic hydrocarbons (NPAHs), 1-nitropyrene (1-NP) and 6-nitrobenzo[a]pyrene (6-NBaP), were identified by HPLC with chemiluminescence detection.

Urban PM2.5 exacerbates allergic inflammation in the murine lung via a TLR2/TLR4/MyD88-signaling pathway.

Nevertheless its mechanism has not been well explained yet, PM2.5 is recognized to exacerbate asthma. In the present study, the roles of toll-like receptor (TLR) 2, TLR4 and MyD88, in exacerbation of allergen-induced lung eosinophilia caused by urban PM2.

PM2.5-induced lung inflammation in mice: Differences of inflammatory response in macrophages and type II alveolar cells.

Particulate matter 2.5 ( View Article and Find Full Text PDF

Differences in allergic inflammatory responses in murine lungs: comparison of PM2.5 and coarse PM collected during the hazy events in a Chinese city.

Urban particulate matter (PM) is associated with an increase in asthma. PM2.5 ( View Article and Find Full Text PDF

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.

PM2.5 collected in China causes inflammatory and oxidative stress responses in macrophages through the multiple pathways.

Air pollution continues to increase in East Asia, particularly in China, and is considered to cause serious health problems. In this study, we investigated the toxicological properties of particulate matter ≤2.5mm (PM2.

Differences in allergic inflammatory responses between urban PM2.5 and fine particle derived from desert-dust in murine lungs.

The biological and chemical natures of materials adsorbed onto fine particulate matter (PM2.5) vary by origin and passage routes. The exacerbating effects of the two samples-urban PM2.

Desert dust induces TLR signaling to trigger Th2-dominant lung allergic inflammation via a MyD88-dependent signaling pathway.

Asian sand dust (ASD) is known to exacerbate asthma, although its mechanism is not yet well understood. In this study, when the effects on inflammatory response by LPS present in ASD was investigated by measuring the gene expression of cytokines and chemokines in RAW264.7 cells treated with ASD and/or polymyxin B (PMB), the ASD effects were attenuated by PMB, but not completely.

Spatial correlativity of atmospheric particulate components simultaneously collected in Japan.

The simultaneous sampling of total suspended particles was performed at 14 sites in Japan during July 2008-June 2009. The spatial correlativity of each particulate composition toward Osaka was obtained for nine selected sites to overview the chemical composition and geographical distribution of particulate components across a wide range of areas nationwide. The spatial correlatives of atmospheric particulate components were extended to an even wider range of areas up to 950 km distance (meso-alpha scale region, >200 km) for a far-reaching distance analysis unique in the literature.

PM2.5-rich dust collected from the air in Fukuoka, Kyushu, Japan, can exacerbate murine lung eosinophilia.

PM2.5 can exacerbate asthma. Organic substances adsorbed on PM2.

Aggravation of ovalbumin-induced murine asthma by co-exposure to desert-dust and organic chemicals: an animal model study.

Background: The organic chemicals present in Asian sand dust (ASD) might contribute to the aggravation of lung eosinophila. Therefore, the aggravating effects of the Tar fraction from ASD on ovalbumin (OVA)-induced lung eosinophilia were investigated.

Methods: The Tar fraction was extracted from ASD collected from the atmosphere in Fukuoka, Japan.

Prevalence and Characteristics of Chemical Intolerance: A Japanese Population-Based Study.

Population-based cross-sectional study was performed to estimate the prevalence of chemical intolerance and to examine the characteristics of the sample. A Web-based survey was conducted that included 7,245 adults in Japan. The criteria for chemical intolerance proposed by Skovbjerg yielded a prevalence of 7.

Lung inflammation by fungus, Bjerkandera adusta isolated from Asian sand dust (ASD) aerosol and enhancement of ovalbumin-induced lung eosinophilia by ASD and the fungus in mice.

Background: Bjerkandera adusta (B. adusta) is one of the most important etiological fungi associated with chronic cough. However, precise details of the inflammatory response to exposure are not well understood yet.

Indoor volatile organic compounds and chemical sensitivity reactions.

Studies of unexplained symptoms observed in chemically sensitive subjects have increased the awareness of the relationship between neurological and immunological diseases due to exposure to volatile organic compounds (VOCs). However, there is no direct evidence that links exposure to low doses of VOCs and neurological and immunological dysfunction. We review animal model data to clarify the role of VOCs in neuroimmune interactions and discuss our recent studies that show a relationship between chronic exposure of C3H mice to low levels of formaldehyde and the induction of neural and immune dysfunction.

Effects of two Asian sand dusts transported from the dust source regions of Inner Mongolia and northeast China on murine lung eosinophilia.

The quality and quantity of toxic materials adsorbed onto Asian sand dust (ASD) are different based on dust source regions and passage routes. The aggravating effects of two ASDs (ASD1 and ASD2) transported from the source regions of Inner Mongolia and northeast China on lung eosinophilia were compared to clarify the role of toxic materials in ASD. The ASDs contained different amounts of lipopolysaccharides (LPS) and β-glucan (ASD1ASD2).

Intratracheal administration of fullerene nanoparticles activates splenic CD11b+ cells.

Fullerene nanoparticles ("Fullerenes"), which are now widely used materials in daily life, have been demonstrated to induce elevated pulmonary inflammation in several animal models; however, the effects of fullerenes on the immune system are not fully understood. In the present study, mice received fullerenes intratracheally and were sacrificed at days 1, 6 and 42. Mice that received fullerenes exhibited increased proliferation of splenocytes and increased splenic production of IL-2 and TNF-α.

Dysregulation of immune responses in an allergic mouse model following low-level toluene exposure.

To investigate the effect of low-level toluene inhalation on immune regulation in an allergic mouse model, C3H/HeN mice were exposed to 0, 5, 50, or 500ppm of toluene for 6h/day, 5 days/week for 3 or 6 weeks. For allergic mouse model, half of the mice in each group were immunized with ovalbumin (OVA). Allergic mice exposed to toluene for 3 weeks did not exhibit any changes in their plasma, lung or spleen samples.

Thymocytes are activated by toluene inhalation through the transcription factors NF-κB, STAT5 and NF-AT.

Toluene has been extensively examined for effects on the central nervous system. To investigate the influence of low-level inhalation of toluene on the naive immune cells, male C3H/HeN mice were exposed to filtered air (control) and 50 ppm of toluene for 3 weeks. Low-level exposure resulted in (1) increased proliferation of thymocytes, (2) IL-2 production induced in thymocytes and (3) activation of the transcription factors NF-κB, STAT5 and NF-AT in thymocytes.

Different sensitivity in expression of transcription factor mRNAs in congenic mice following exposure to low-level toluene.

To investigate the relationship between sensitivity to toluene exposure and genetic background, male congenic mice, C57BL/10 (H-2(b)) and B10.BR/Sg (H-2(k)) were exposed to 0, 5, and 50 ppm toluene for 6 h per day, 5 days per week for 6 weeks. Groups of mice were injected with ovalbumin (OVA) intraperitoneally before starting exposure schedule and these mice were then challenged with aerosolized OVA as a booster.

Modification of the relationship between urinary 8-OHdG and hippuric acid concentration by GSTM1, GSTT1, and ALDH2 genotypes.

Urinary hippuric acid (HA) has been widely used as a biological marker of occupational exposure to toluene, although it is no longer valid for low levels of toluene exposure. Toluene exposure is known to induce oxidative DNA damage and the metabolism is affected by genetic polymorphisms of some metabolizing enzymes. Therefore, genetic polymorphisms of these metabolizing enzymes must be considered in the evaluation of oxidative stress caused by toluene exposure.

Strain differences influence N-methyl-D-aspartate receptor subunit gene expression in the olfactory bulb of an allergic mouse model following toluene exposure.

Objective: Genetic variation is a causative factor in differing sensitivities to environmental chemicals. The present study explored whether differences in mouse strains influence N-methyl-D-aspartate (NMDA) receptor expression in the olfactory bulb after low-level toluene exposure.

Methods: Ten-week-old male C3H/HeN (H-2(k)), BALB/c (H-2(d)) and C57BL/10 (H-2(b)) mice were exposed to 0, 5, 50 or 500 ppm of toluene for 6 h per day, 5 days per week for 6 weeks.

Up-regulation of neurotrophin-related gene expression in mouse hippocampus following low-level toluene exposure.

To investigate the role of strain differences in sensitivity to low-level toluene exposure on neurotrophins and their receptor levels in the mouse hippocampus, 8-week-old male C3H/HeN, BALB/c and C57BL/10 mice were exposed to 0, 5, 50, or 500 ppm toluene for 6h per day, 5 days per week for 6 weeks in an inhalation chamber. We examined the expressions of neurotrophin-related genes and receptors in the mouse hippocampus using real-time reverse transcription polymerase chain reaction (RT-PCR). The expression of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), tyrosine kinase (Trk) A, and TrkB mRNAs in the C3H/HeN mice hippocampus was significantly higher in the mice exposed to 500 ppm toluene.

Children's immunology, what can we learn from animal studies (2): Modulation of systemic Th1/Th2 immune response in infant mice after prenatal exposure to low-level toluene and toll-like receptor (TLR) 2 ligand.

It has been reported that the newborn immune system differs quantitatively and functionally from that of adults. Development of the immune system has important implications for childhood diseases. The immaturity of the immune system in the prenatal or suckling stage may contribute to susceptibility to environmental toxic chemical exposure.