Asthma is a respiratory disease that can be exacerbated by certain environmental factors. Both formaldehyde (FA) and PM₂.₅, the most common indoor and outdoor air pollutants in mainland China, are closely associated with the onset and development of asthma. To date, however, there is very little report available on whether there is an exacerbating effect of combined exposure to FA and PM₂.₅ at ambient concentrations. In this study, asthmatic mice were exposed to 1 mg/m³ FA, 1 mg/kg PM₂.₅, or a combination of 0.5 mg/m³ FA and 0.5 mg/kg PM₂.₅, respectively. Results demonstrated that both levels of oxidative stress and inflammation were significantly increased, accompanied by an obvious decline in lung function. Further, the initial activation of p38 MAPK and NF-κB that intensified the immune imbalance of asthmatic mice were found to be visibly mitigated following the administration of SB203580, a p38 MAPK inhibitor. Noteworthily, it was found that combined exposure to the two at ambient concentrations could significantly worsen asthma than exposure to each of the two alone at twice the ambient concentration. This suggests that combined exposure to formaldehyde and PM₂.₅ at ambient concentrations may have a synergistic effect, thus causing more severe damage in asthmatic mice. In general, this work has revealed that the combined exposure to FA and PM₂.₅ at ambient concentrations can synergistically aggravate asthma via the p38 MAPK pathway in mice.

Air pollution exposure is a public health emergency, which attributes globally to an estimated seven million deaths on a yearly basis We are all exposed to air pollutants, varying from ambient air pollution hanging over cities to dust inside the home. It is a mixture of airborne particulate matter and gases that can be subdivided into three categories based on particle diameter. The smallest category called PM₀.₁ is the most abundant. A fraction of the particles included in this category might enter the blood stream spreading to other parts of the body. As air pollutants can enter the body via the lungs and gut, growing evidence links its exposure to gastrointestinal and respiratory impairments and diseases, like asthma, rhinitis, respiratory tract infections, Crohn's disease, ulcerative colitis, and abdominal pain. It has become evident that there exists a crosstalk between the respiratory and gastrointestinal tracts, commonly referred to as the gut-lung axis. Via microbial secretions, metabolites, immune mediators and lipid profiles, these two separate organ systems can influence each other. Well-known immunomodulators and gut health stimulators are probiotics, prebiotics, together called synbiotics. They might combat air pollution-induced systemic inflammation and oxidative stress by optimizing the microbiota composition and microbial metabolites, thereby stimulating anti-inflammatory pathways and strengthening mucosal and epithelial barriers. Although clinical studies investigating the role of probiotics, prebiotics, and synbiotics in an air pollution setting are lacking, these interventions show promising health promoting effects by affecting the gastrointestinal- and respiratory tract. This review summarizes the current data on how air pollution can affect the gut-lung axis and might impact gut and lung health. It will further elaborate on the potential role of probiotics, prebiotics and synbiotics on the gut-lung axis, and gut and lung health.

An increasing body of evidence has linked greenspace and various health outcomes in children and adolescents, but the conclusions were inconsistent. For this review, we comprehensively summarized the measurement methods of greenspace, resultant health outcomes, and potential mechanisms from epidemiological studies in children and adolescents (aged ≤19 years). We searched for studies published and indexed in MEDLINE and EMBASE (via Ovid) up to April 11, 2022. There were a total of 9,291 studies identified with 140 articles from 28 countries finally assessed and included in this systematic review. Over 70% of the studies were conducted in highly urbanised countries/regions, but very limited research has been done in low-and middle-income countries and none in Africa. Measures of greenspace varied. Various health outcomes were reported, including protective effects of greenspace exposure on aspects of obesity/overweight, myopia, lung health, circulatory health, cognitive function, and general health in children and adolescents. The associations between greenspace exposure and other health outcomes were inconsistent, especially for respiratory health studies. We pooled odds ratios (OR) using random-effects meta-analysis for health outcomes of asthma (OR = 0.94, 95%CI: 0.84 to 1.06), allergic rhinitis (OR = 0.95; 95% CI: 0.73 to 1.25), and obesity/overweight (OR = 0.91, 95%CI: 0.84 to 0.98) with per 0.1 unit increase in normalized difference in vegetation index (NDVI). These associations have important implications for the assessment and management of urban environment and health in children and adolescents.

The presence of urban greenspace may lead to reduced personal exposure to air pollution via several mechanisms, for example, increased dispersion of airborne particulates; however, there is a lack of real-time evidence across different urban contexts. Study participants were 79 adolescents with asthma who lived in Delhi, India and were recruited to the Delhi Air Pollution and Health Effects (DAPHNE) study. Participants were monitored continuously for exposure to PM₂.₅ (particulate matter with an aerodynamic diameter of less than 2.5 μm) for 48 h. We isolated normal day-to-day walking journeys (n = 199) from the personal monitoring dataset and assessed the relationship between greenspace and personal PM₂.₅ using different spatial scales of the mean Normalised Difference Vegetation Index (NDVI), mean tree cover (TC), and proportion of surrounding green land use (GLU) and parks or forests (PF). The journeys had a mean duration of 12.7 (range 5, 53) min and mean PM₂.₅ personal exposure of 133.9 (standard deviation = 114.8) μg/m³. The within-trip analysis showed weak inverse associations between greenspace markers and PM₂.₅ concentrations only in the spring/summer/monsoon season, with statistically significant associations for TC at the 25 and 50 m buffers in adjusted models. Between-trip analysis also indicated inverse associations for NDVI and TC, but suggested positive associations for GLU and PF in the spring/summer/monsoon season; no overall patterns of association were evident in the autumn/winter season. Associations between greenspace and personal PM₂.₅ during walking trips in Delhi varied across metrics, spatial scales, and season, but were most consistent for TC. These mixed findings may partly relate to journeys being dominated by walking along roads and small effects on PM₂.₅ of small pockets of greenspace. Larger areas of greenspace may, however, give rise to observable spatial effects on PM₂.₅, which vary by season.

Allergic diseases have been one of the leading causes of chronic disorders in the United States. Animal studies have suggested that exposures to perchlorate, nitrate, and thiocyanate could induce allergic inflammation. However, the associations have not been examined among general populations. Here, we investigated data of 7030 participants aged ≥6 years from the National Health and Nutritional Examination Survey (NHANES) 2005–2006. Urinary levels of perchlorate, nitrate, and thiocyanate were measured by ion chromatography combined with electrospray tandem mass spectrometry. Information on allergic symptoms (hay fever, allergy, rash, sneeze, wheeze, eczema, and current asthma) was collected by questionnaire. Allergic sensitization was defined by a concentration ≥150 kU/L for total immunoglobulin E (IgE) levels. The associations were estimated using multivariate-adjusted logistic regression models. A positive association was observed for urinary nitrate and eczema (p < 0.001 for the trend). Compared with quartile 1 (lowest quartile), the odds ratios of eczema with 95% confidence intervals [ORs (95% CIs)] from quartiles 2 to 4 were 1.72 (95% CI, 1.41, 2.09), 1.94 (1.53, 2.47) and 2.10 (1.49, 2.97) for urinary nitrate. In addition, urinary thiocyanate was positively related to sneeze (ORQ₄ ᵥₛ. Q₁: 1.25, 95% CI: 1.01, 1.55; p = 0.015 for the trend). However, urinary perchlorate was not correlated with any allergic-related outcome. Additionally, the associations were different among subgroups in a four-level polytomous model. Thus, our results suggested that exposures to nitrate and thiocyanate may be associated with allergic symptoms. Further investigations are warranted to concentrate on the practical strategies to monitor exposure levels and the latent mechanisms of the relationship between exposure and allergy.

Epidemiology suggests ambient temperature is the triggers and potential activator of asthma. The role of high and low temperatures on airway inflammation of asthma, and the underlying molecular mechanism are not yet understood. A mouse model of asthma was adopted in our experiment. The BALB/c mice were exposed at different temperature for 4 h (2 h in the morning and 2 h in the afternoon) on weekday. The exposure temperatures were 10 °C, 24 °C and 40 °C. Ovalbumin (OVA) was used to sensitize the mice on days 14, 18, 22, 26, and 30, followed by an aerosol challenge for 30 min from day 32–38. After the final OVA challenge, lung function, serum protein and pulmonary inflammation were assessed. Comparing the OVA with the saline group at 24 °C, we saw a significant increase in: serum Total-IgE (p < 0.05); OVA-sIgE (p < 0.01); IL-4 (p < 0.05); IL-1β (p < 0.01); IL-6 (p < 0.01); TNF-α (p < 0.01); and the ratio of IL-4/IFN-γ (p < 0.01). At the same time, there was a significant decrease in IFN-γ (p < 0.01). As the temperature increase, there is a U shape for immune proteins and pro-inflammatory factors with a peak value at 24 °C, exception for IFN-γ (inverted U-shape). After the high and low temperature exposure, the Ri and Re increased significantly, while Cldyn decreased significantly compared with the 24 °C group. Histopathological analysis of the OVA groups showed airway remodeling, airway wall thickening and deforming, and subepithelial fibrosis. More obvious changes were found in the high and low temperature exposure groups. The immunohistochemistry suggested that TRPs changed with temperatures. High and low temperatures can aggravate airway inflammation in a mouse model of asthma. TRPs play an important role in temperature aggravation of allergic asthma. The results suggest that asthmatics should avoid exposure to high and low temperatures for too long time.

The proportion of asthma patients with mild to moderate exacerbations is far greater than the number who experience episodes that are severe enough to require emergency room visits or hospital admission. However the routinely collected data from hospitals is absent in the past.To evaluate associations between short-term exposures to air pollutants and hospital outpatient visits for asthma in China.We obtained data for 143,057 asthma outpatient visits from the largest hospitals in 17 Chinese cities, between Jan 01 2013 and Dec 31 2015. We used daily concentrations of air pollutants measured by the China National Environmental Monitoring Centre. We used a time-stratified case-crossover design, and fitted conditional logistic regression models to determine the associations.Particulate matter ≤10μm in diameter (PM10) and nitrogen dioxide (NO2) were associated with increased risks of hospital outpatient visits for asthma on the same day, while the effects were delayed for particulate matter ≤2.5μm in diameter (PM2.5) and sulphur dioxide (SO2). For the cumulative effect model at lag05 days, 10 μg/m3 increase in air pollutants concentrations were correlated with hospital outpatient visits for asthma with odds ratios (ORs) and 95% confidence intervals 1.004 (1.000-1.008) for PM2.5, 1.005 (1.002-1.008) for PM10, 1.030 (1.021-1.040) for NO2, and 1.015 (1.008-1.021) for SO2. Almost one in nine (10.9%; 7.7, 13.9%) hospital outpatient visits for asthma were attributable to NO2.Short-term exposures to PM2.5, PM10, NO2 and SO2 were associated with hospital outpatient visits for asthma in China.

Airborne particulate matter (PM) has become a serious health issue causing pulmonary diseases such as asthma. Due to the side effects and non-specificity of conventional drugs, there is a need to develop natural-product-based alternative treatments. Sargassum horneri is a brown alga shown to have anti-oxidant, anti-inflammatory, and anti-allergic effects. Thus, we sought to determine whether ethanol extract of Sargassum horneri (SHE) mitigates the effect of PM exposure on asthma development. To establish a mouse model of asthma, BALB/c mice were sensitized with ovalbumin (OVA, 10 μg) and challenged with PM (5 mg/m³) for 7 days consecutively. SHE (200, 400 mg/kg), Prednisone (5 mg/kg), or PBS was daily administrated orally before PM exposure. SHE mitigated PM exacerbated dendritic cell activation. More importantly, SHE restrained Th2 polarization by attenuating transcription factors GATA3 and STAT5, which further mitigated the expression of Th2 cytokines interleukin (IL)-4, IL-5, and IL-13 in the lung homogenates of PM-exacerbated asthmatic mice. SHE further attenuated PM-exacerbated eosinophil infiltration in the lung, trachea, and BALF. In addition, SHE markedly mitigated the activation of mast cells and the IgE level in serum. Concomitantly, SHE further restrained the Th17 cell response in PM-exposed allergic mice through attenuating expression of transcription factors RORγT, STAT3 and expression of relevant effector cytokines IL-17a. This resulted in mitigated neutrophil infiltration in the lung. Taken together, SHE significantly suppressed PM-exacerbated hypersecretion of mucus in asthmatic mice. These results suggest that SHE has therapeutic potential for treating PM-exacerbated allergic asthma through concomitantly inhibiting Th2/Th17 responses.

Evidence of health effects following early life exposure to short-to-medium duration of high pollution levels is extremely limited.We aimed to evaluate the associations between: 1. intrauterine exposure to fine particulate matter (PM2.5) from coal mine fire emissions and the frequencies of general practitioner attendances and dispensations of prescribed asthma inhalers, steroid skin creams, and antibiotics during the first year of life; 2. infant exposure and those outcomes during the year following the fire.All participants were recruited from the Latrobe Valley of Victoria, Australia. Participants’ 24-h average and hourly peak mine fire-specific PM2.5 exposures from 09/02/2014 to 31/03/2014 were estimated using chemical transport modelling. Outcome data were obtained from the Australian Medicare Benefits Schedule and Pharmaceutical Benefits Scheme from each child’s birth to 31/12/2016. We used negative binomial and logistic regression models to independently assess risks of the outcomes associated with every 10 and 100 μg m−3 increase in average or peak PM2.5 exposure, respectively, while adjusting for potential confounders.We included 286 of 311 children whose parents consented to be linked, comprising 77 with no exposure, 88 with intrauterine exposure and 121 with exposure in infancy. 10- and 100- μg m−3 increases in average and peak PM2.5 exposure during infancy were associated with greater incidence of antibiotics being dispensed during the year following the fire: the adjusted incidence rate ratios were 1.24 (95% CI 1.02, 1.50, p = 0.036) and 1.14 (1.00, 1.31, p = 0.048) respectively. No other significant associations were observed.Exposure to coal mine fire emissions during infancy was associated with increased dispensing of antibiotics. This could reflect increased childhood infections or increased prescriptions of antibiotics in the year following the fire.

Exposure to fine atmospheric Particulate Matter (PM) is one of the major environmental causes involved in the development of inflammatory lung diseases, such as chronic obstructive pulmonary disease (COPD) or asthma. When PM is penetrating in the pulmonary system, alveolar macrophages represent the first line of defense, in particular by triggering a pro-inflammatory response, and also by their ability to recruit infiltrating macrophages from the bone marrow. The aim of this in vitro study was to evaluate the gene expression and cytokine production involved in the toxicological and inflammatory responses of infiltrating macrophages, as well as the Extracellular Vesicles (EVs) production, after their exposure to PM. The ability of these EVs to convey information related to PM exposure from exposed macrophages to pulmonary epithelial cells was also evaluated.Infiltrating macrophages respond to fine particles exposure in a conventional manner, as their exposure to PM induced the expression of Xenobiotic Metabolizing Enzymes (XMEs) such as CYP1A1 and CYP1B1, the enzymes involved in oxidative stress SOD2, NQO1 and HMOX as well as pro-inflammatory cytokines in a dose-dependent manner. Exposure to PM also induced a greater release of EVs in a dose-dependent manner. In addition, the produced EVs were able to induce a pro-inflammatory phenotype on pulmonary epithelial cells, with the induction of the release of IL6 and TNFα proinflammatory cytokines. These results suggest that infiltrating macrophages participate in the pro-inflammatory response induced by PM exposure and that EVs could be involved in this mechanism.