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Numerous epidemiological studies have reported that ozone (O₃) and temperature are independently associated with health outcomes, but modification of the effects of O₃ on health outcomes by temperature, and vice versa, has not been fully described. This study aimed to investigate effect modification by temperature on the association between O₃ and emergency ambulance dispatches (EADs) in Japan. Data on daily air pollutants, ambient temperature, and EADs were obtained from eight Japanese cities from 2007 to 2015. A distributed lag non-linear model combined with Poisson regression was performed with temperature as a confounding factor and effect modifier to estimate the effects of O₃ on EADs at low (<25th percentile), moderate (25th-75th percentile), and high (>75th percentile) temperature for each city. The estimates obtained from each city were pooled by random-effects meta-analysis. When temperature was entered as a confounder, the estimated effects of O₃ on EADs for all acute, cardiovascular, and respiratory illnesses were largest at lag 0 (current-day lag). Therefore, this lag was used to further estimate the effects of O₃ on EADs in each temperature category. The estimated effects of O₃ on EADs for all acute, cardiovascular, and respiratory illnesses in all eight Japanese cities increased with increasing temperature. Specifically, a 10 ppb increase in O₃ was associated with 0.80 % (95 % CI: 0.25 to 1.35), 0.19 % (95 % CI: -0.85 to 1.25), and 1.14 % (95 % CI: -0.01 to 2.31) increases in the risk of EADs for all acute, cardiovascular, and respiratory illnesses, respectively, when city-specific daily temperature exceeded the 75th percentile. Our findings suggest that the association between O₃ and EADs for all acute, cardiovascular, and respiratory illnesses is the highest during high temperature. Finding of this study can be used to develop potential mitigation measures against O₃ exposure in high temperature environment to reduce its associated adverse health eff

[Background:] Microplastics (MPs) are small particles of plastic (≤ 5mm in diameter). In recent years, oral exposure to MPs in living organisms has been a cause of concern. Leaky gut syndrome (LGS), associated with a high-fat diet (HFD) in mice, can increase the entry of foreign substances into the body through the intestinal mucosa. [Objectives:] We aimed to evaluate the pathophysiology of intestinal outcomes associated with consuming a high-fat diet and simultaneous intake of MPs, focusing on endocrine and metabolic systems. [Methods:] C57BL6/J mice were fed a normal diet (ND) or HFD with or without polystyrene MP for 4 wk to investigate differences in glucose tolerance, intestinal permeability, gut microbiota, as well as metabolites in serum, feces, and liver. [Results:] In comparison with HFD mice, mice fed the HFD with MPs had higher blood glucose, serum lipid concentrations, and nonalcoholic fatty liver disease (NAFLD) activity scores. Permeability and goblet cell count of the small intestine (SI) in HFD-fed mice were higher and lower, respectively, than in ND-fed mice. There was no obvious difference in the number of inflammatory cells in the SI lamina propria between mice fed the ND and mice fed the ND with MP, but there were more inflammatory cells and fewer anti-inflammatory cells in mice fed the HFD with MPs in comparison with mice fed the HFD without MPs. The expression of genes related to inflammation, long-chain fatty acid transporter, and Na⁺/glucose cotransporter was significantly higher in mice fed the HFD with MPs than in mice fed the HFD without MPs. Furthermore, the genus Desulfovibrio was significantly more abundant in the intestines of mice fed the HFD with MPs in comparison with mice fed the HFD without MPs. Muc2 gene expression was decreased when palmitic acid and microplastics were added to the murine intestinal epithelial cell line MODE-K cells, and Muc2 gene expression was increased when IL-22 was added. [Discussion:] Our findings suggest

The air quality in Upper Northern Thailand (UNT) deteriorates during seasonal vegetation fire events, causing adverse effects especially on respiratory health outcomes. This study aimed to quantitatively estimate respiratory morbidity from vegetation fire smoke exposure, and to assess the impact of a burning ban enforced in 2016 on morbidity burden in UNT. We computed daily population exposure to fire-originated PM₁₀ and estimated its health burden during a 5-year period from 2014 to 2018 using daily fire-originated PM₁₀ concentration and the concentration–response function for short-term exposure to PM10 from vegetation fire smoke and respiratory morbidity. In subgroups classified as children and older adults, the health burden of respiratory morbidity was estimated using specific effect coefficients from previous studies conducted in UNT. Finally, we compared the health burden of respiratory morbidity before and after burning ban enforcement. Approximately 130, 000 hospital visits for respiratory diseases were estimated to be attributable to fire-originated PM₁₀ in UNT from 2014 to 2018. This estimation accounted for 1.3% of total hospital visits for respiratory diseases during the 5-year period, and 20% of those during burning events. Age-specific estimates revealed a larger impact of PM₁₀ in the older adult group. The number of hospital visits for respiratory diseases attributable to fire-originated PM₁₀ decreased from 1.8% to 0.5% after the burning ban policy was implemented in the area. Our findings suggest that PM₁₀ released from vegetation fires is a health burden in UNT. The prohibition of the burning using regulatory measure had a positive impact on respiratory morbidity in this area.

Only a few studies have investigated the association between long-term exposure to air pollution and alterations of serum lipids and blood sugar level in developing countries. The present longitudinal study examined associations between long-term air pollution exposure and serum lipids [total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C)] and fasting glucose (FG) in workers of the Electricity Generating Authority of Thailand (EGAT) in the Bangkok metropolitan region (BMR) of Thailand. We performed secondary analyses using the data obtained from 1, 839 participants (mean age, 58.3 years as of 2002) of the EGAT1 cohort study (2002–2012). The average concentration of each air pollutants (PM₁₀, O₃, NO₂, SO₂, and CO) at the sub-district level in BMR from 2002 to 2012 were estimated using the ordinary kriging method. Exposure periods were averaged to 3 months prior to laboratory testing. Linear mixed effects models were used to estimate associations between air pollution and serum lipids and blood sugar. After controlling for potential confounders, an interquartile range increment of PM₁₀, SO₂, and CO was associated with elevated LDL-C [6.6% (95%CI: 4.3, 9.0), 11.1% (7.2, 15.2), and 1.9% (1.1, 2.7), respectively] and FG [2.8% (1.5, 4.2), 6.8% (4.5, 9.1), and 1.1% (0.6, 1.5), respectively]. In addition, PM10, SO2, and CO were inversely associated with HDL-C [-1.8% (−3.7, 0.1), −3.3% (−6.2, −0.3), and −1.1 (−1.7, −0.5), respectively]. O₃ was negatively associated with TC, LDL-C, TG, and FG. These findings suggest inhalation of air pollutants may increase the risk of impaired metabolism of glucose and lipids.

Epidemiological and experimental studies have shown that di-(2-ethylhexyl) phthalate (DEHP), a plasticizer, can aggravate allergic diseases. DEHP promotes adaptive immune responses, although its effect on the innate immune system remains largely unknown. The present study investigated the effects of DEHP on group 2 innate lymphoid cells (ILC2) that produce Th2 cytokines in response to epithelial cell-derived cytokines, such as interleukin (IL)-33. ILC2 (lineage-negative, CD45.2⁺, Sca1⁺, KLRG1⁺) were isolated from the lungs of C57BL/6 J mice. Co-exposure to DEHP and IL-33 significantly increased IL-5 release from ILC2, whose level was higher than that of the vehicle and IL-33 alone. The effects of DEHP in the presence of IL-33 showed an inverted-U dose-response. The present is the first report showing that DEHP exacerbates allergy through the innate immune system.

Short-term health effects of ambient PM₂.₅ have been established with numerous studies, but evidence in Asian countries is limited. This study aimed to investigate the short-term effects of PM₂.₅ on acute health outcomes, particularly all-cause, cardiovascular, respiratory, cerebrovascular and neuropsychological outcomes. We utilized daily emergency ambulance dispatches (EAD) data from eight Japanese cities (2007–2011). Statistical analyses included two stages: (1) City-level generalized linear model with Poisson distribution; (2) Random-effects meta-analysis in pooling city-specific effect estimates. Lag patterns were explored using (1) unconstrained-distributed lags (lag 0 to lag 7) and (2) average lags (lag: 0–1, 0–3, 0–5, 0–7). In all-cause EAD, significant increases were observed in both shorter lag (lag 0: 1.24% (95% CI: 0.92, 1.56)) and average lag 0–1 (0.64% (95% CI: 0.23, 1.06)). Increases of 1.88% and 1.48% in respiratory and neuropsychological EAD outcomes, respectively, were observed at lag 0 per 10 µg/m3 increase in PM₂.₅. While respiratory outcomes demonstrated significant average effects, no significant effect was observed for cardiovascular outcomes. Meanwhile, an inverse association was observed in cerebrovascular outcomes. In this study, we observed that effects of PM₂.₅ on all-cause, respiratory and neuropsychological EAD were acute, with average effects not exceeding 3 days prior to EAD onset.

Epidemiologic studies have revealed that Asian sand dust particles (ASDs) can affect respiratory and immune health represented by asthma. Factors responsible for the exacerbation of asthma remain unclear. The fungus Bjerkandera adusta (B.ad) and polycyclic aromatic hydrocarbons such as benzo[a]pyrene (BaP) have been identified in ASDs collected from the atmosphere when an ASD event occurred. We investigated the effects of B.ad and BaP related to ASDs on respiratory and immune systems. Bone marrow‐derived antigen‐presenting cells (APCs) and splenocytes from atopic prone NC/Nga mice and human airway epithelial cells were exposed to the B.ad or to BaP in the presence and absence of heated‐ASDs (H‐ASDs). B.ad and BaP in both the presence and absence of H‐ASDs increased the expression of cell surface molecules on APCs. H‐ASDs alone slightly activated APCs. The expressions induced by B.ad were higher than those induced by BaP in the presence and absence of H‐ASDs. There were no remarkable effects on the activation of splenocytes or the proinflammatory responses in airway epithelial cells. These results suggest that B.ad rather than BaP contributes to the exacerbation of asthma regardless of the presence or absence of sand particles, particularly by the activation of the immune system via APCs.

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 PM2.5 was investigated. TLR2-, TLR4-, MyD88-deficient and WT BALB/c mice were intratracheally challenged with PM2.5 +/− ovalbumin (OVA) four times at 2-week intervals. PM2.5 increased neutrophil numbers and KC in bronchoalveolar lavage fluid and caused slight peribronchiolar inflammation in WT mice. However, these changes were attenuated, but not completely suppressed in gene-deficient mice, especially in MyD88−/− mice. In WT mice, PM2.5 + OVA exacerbated OVA-related lung eosinophilia. This exacerbation includes increase of IL-5, IL-13, eotaxin and MCP-3; infiltration of eosinophils into the airway submucosa; proliferation of goblet cells in the airway epithelium; and the production of antigen-specific IgE and IgG1 in serum. All these effects were stronger in TLR2−/− mice than in TLR4−/− mice. In MyD88−/− mice, this pro-inflammatory mediator-inducing ability was considerably weak and lung pathology was negligible. These results suggest that urban PM2.5 may exacerbate allergic inflammation in the murine lung via a TLR2/TLR4/MyD88-signaling pathway. PM2.5-bound trace microbial elements, such as lipopolysaccharide may be a strong candidate for exacerbation of murine lung eosinophilia.

Environmental changes are thought to be the main factor in the rapid increase and worsening of allergic diseases. While there have been significant changes in many environmental factors, including in environments such as residential, health and sanitation, food, and water/soil/atmospheric environments, the root of each of these changes is likely an increase in chemical substances. In fact, various environmental pollutants, such as air pollutants and chemical substances, have been shown to worsen various allergies in experimental studies. For example, diesel exhaust particles (DEPs), which are an agglomeration of particles and a wide array of chemical substances, aggravate asthma, primarily due to the principle organic chemical components of DEPs. In addition, environmental chemicals such as phthalate esters, which are commonly used as plasticizers in plastic products, also aggravate atopic dermatitis. It has also become evident that extremely small nanomaterials and Asian sand dust particles can enhance allergic inflammation. While the underlying mechanisms that cause such aggravation are becoming clearer at the cellular and molecular levels, methods to easily and quickly evaluate (screen) the ever-increasing amount of environmental pollutants for exacerbating effects on allergies are also under development. To eliminate and control allergic diseases, medical measures are necessary, but it is also essential to tackle this issue by ameliorating environmental changes.

Multiple chemical sensitivity (MCS) is a disorder characterized by nonspecific and recurrent symptoms from various organ systems associated with exposure to low levels of chemicals. Patients with MCS process odors differently than controls do. Previously, we suggested that this odor processing was associated with increased regional cerebral blood flow (rCBF) in the prefrontal area during olfactory stimulation using near-infrared spectroscopic (NIRS) imaging. The aim of this study was to investigate the association of odor thresholds and changes in rCBF during olfactory stimulation at odor threshold levels in patients with MCS. We investigated changes in the prefrontal area using NIRS imaging and a T&T olfactometer during olfactory stimulation with two different odorants (sweet and fecal) at three concentrations (zero, odor recognition threshold, and normal perceived odor level) in 10 patients with MCS and six controls. The T&T olfactometer threshold test and subjective assessment of irritating and hedonic odors were also performed. The results indicated that the scores for both unpleasant and pungent odors were significantly higher for those for sweet odors at the normal perceived level in patients with MCS than in controls. The brain responses at the recognition threshold (fecal odor) and normal perceived levels (sweet and fecal odors) were stronger in patients with MCS than in controls. However, significant differences in the odor detection and recognition thresholds and odor intensity score between the two groups were not observed. These brain responses may involve cognitive and memory processing systems during past exposure to chemicals. Further research regarding the cognitive features of sensory perception and memory due to past exposure to chemicals and their associations with MCS symptoms is needed.

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.

The effects of environmental pollutants on airway clearance have not been well elucidated. This study examined mucociliary transport using different sized-fluorescent particles on polarized human airway epithelial cells which were maintained in an air-liquid interface (ALI) culture system. The effects of hydrogen peroxide (H2O2) exposure on mucociliary transport were also investigated. The movement of fluorescent particles with diameters of 10-14 and 2.5-4.5 µm was observed by fluorescent microscopy as an index of the mucociliary transport. The mixture of the particles with two different sizes was propelled concentrically on the apical surface by the interaction of ciliary activity and mucus in the control condition, whereas H2O2 exposure for 24 h significantly inhibited the movement of the particles. The particle sizes did not affect their movement after the control or H2O2 exposure. These results suggest that particle tracking on polarized human airway epithelial cells is a useful experimental tool for the evaluation of the effect of environmental pollutants on mucociliary transport. In addition, reactive oxygen species may impair mucociliary transport, leading to the airway damage and exacerbation of respiratory diseases.

Although the adverse health effects of nanoparticles have been proposed and are being clarified, their aggravating effects on pre-existing pathological conditions have not been fully investigated. In this review, we provide insights into the immunotoxicity of both airborne and engineered nanoparticles as an exacerbating factor on hypersusceptible subjects, especially those with immune-mediated pulmonary inflammation, using our in vivo experimental model. First, we exhibit the effects of nanoparticles on pulmonary inflammation induced by bacterial endotoxin (lipopolysaccharide: LPS) as a disease model in innate immunity, and demonstrate that nanoparticles instilled through both an intratracheal tube and an inhalation system can exacerbate the lung inflammation. Second, we introduce the effects of nanoparticles on allergic pulmonary inflammation as a disease model in adaptive immunity, and show that repetitive pulmonary exposure to nanoparticles has aggravating effects on allergic inflammation, including adjuvant effects on Th2-milieu. Third, we show that very small nanoparticle exposure exacerbates emphysematous pulmonary inflammation, which is concomitant with enhanced lung expression of proinflammatory molecules (including those that are innate immunity related). Taken together, nanoparticle exposure may synergistically facilitate pathological pulmonary inflammation via both innate and adaptive immunological impairment.