Particulate matter (PM) released from the processes of livestock production has a negative impact on the health of animals and workers. Herein, the concentration, major chemical components, morphology and microbiological compositions of particulate matter 2.5 (PM2.5, particles with aerodynamic diameter less than 2.5 μm) in a broiler breeding house were investigated. The results showed that the PM2.5 distribution in the chicken house was affected by the illumination, draught fans, chicken frame structure and activity of the chickens in the broiler breeding house. Component analysis showed that organic carbon (OC) accounted for the largest proportion, and followed by element carbon (EC), SO42−, NO3−, NH4+, Na+, K+ and Ca2+. Ultrastructural observations revealed that the shape of PM2.5 had a round, rectangular, chain-like and irregular shape. The concentration of endotoxin was approximately 0.3 EU/m3. Microbiological analysis showed that at the genus level, the pathogenic bacteria included Staphylococcus, Corynebacterium, Enterococcus, Parabacteroides, Escherichia and Megamonas. The abundant harmful fungi were Aspergillus, Scopulariopsis, Wallemia, and Fusarium. Through redundancy analysis (RDA) analysis, we determined that OC, EC, Na+, K+, and NH4+ had strong correlations with Brachybacterium, Brevibacterium, Corynebacterium, Escherichia, Scopulariopsis and Microascus. SO42− was closely related to Scopulariopsis and Salinicoccus. Salinicoccus was also strongly correlated with NO3−. Our results indicated that feed, faeces, and outside soot are contributed to the increase in PM2.5 concentration in the chicken house, while the sources of the dominant bacterial and fungi might be feed, faeces, suspended outside soil and cereal crops.

Interactions between the intestine and the liver, the so-called ‘gut-liver axis’, play a crucial role in the onset of hepatic steatosis and non-alcoholic fatty liver disease. However, not much is known about the impact of environmental pollutants on the gut-liver axis and consequent hepatic steatosis. Bisphenol A (BPA), a widely used plasticiser, is an important environmental contaminant that affects gut microbiota. We hypothesised that BPA induces hepatic steatosis by promoting gut microbiota dysbiosis and activating the gut-liver axis. In this study, male CD-1 mice were fed with diet containing BPA (50 μg/kg body weight/day) for 24 weeks. Dietary exposure to BPA increased lipid contents and fat accumulation in the liver. Analysis of 16 S rRNA gene sequencing revealed that the diversity of gut microbiota reduced and the composition of gut microbiota was altered in the BPA-fed mice. Further, the abundance of Proteobacteria, a marker of dysbacteria, increased, whereas the abundance of Akkermansia, a gut microbe associated with increased gut barrier function and reduced inflammation, markedly decreased. Expression levels of intestinal tight junction proteins (zona occludens-1 and occludin) also decreased drastically, leading to increased intestinal permeability and elevated levels of endotoxins. Furthermore, BPA up-regulated the expression of Toll-like receptor 4 (TLR4) and phosphorylation of nuclear factor-kappa B (NF-κB) in the liver and increased the production of inflammatory cytokines, including interleukin-1β, interleukin-18, tumour necrosis factor-α, and interleukin-6. Take together, our work indicated that dietary intake of BPA induced hepatic steatosis, and this was closely related to dysbiosis of gut microbiota, elevated endotoxin levels, and increased liver inflammation through the TLR4/NF-κB pathway.

Sustained cultivation of Bacillus thuringiensis (Bt) transgenic crops requires stable transgene expression under variable abiotic conditions. We studied the interactions of Bt toxin production and chronic ozone exposure in Bt cry1Ac-transgenic oilseed rape and found that the insect resistance trait is robust under ozone elevations. Bt Cry1Ac concentrations were higher in the leaves of Bt oilseed rape grown under elevated ozone compared to control treatment, measured either per leaf fresh weight or per total soluble protein of leaves. The mean relative growth rate of a Bt target herbivore, Plutella xylostella L. larvae was negative on Bt plants in all ozone treatments. On the non-transgenic plants, larval feeding damage was reduced under elevated ozone. Our results indicate the need for monitoring fluctuations in Bt toxin concentrations to reveal the potential of ozone exposure for altering dosing of Bt proteins to target and non-target herbivores in field environments experiencing increasing ozone pollution. Elevated atmospheric ozone can induce fluctuations in insecticidal protein concentrations in transgenic plants.

Depending on their concentrations, sizes, and types, particulate matters of biological origins (bioPM) significantly affect human health. However, for different air environments, they are not well characterized and can vary considerably. As an example, we investigated the bioPM differences at an urban (Beijing) site and a rural (Wangdu) site in the North China Plain (NCP) using an online monitoring instrument, an ultraviolet aerodynamic particle sizer (UV-APS), the limulus amebocyte lysate (LAL) assay, and a high-throughput sequencing method. Generally, lower concentrations of viable bioPM (hourly mean: 1.3 × 10³ ± 1.6 × 10³ m⁻³) and endotoxin (0.66 ± 0.16 EU/m³) in Beijing were observed compared to viable bioPM (0.79 × 10⁵ ± 1.4 × 10⁵ m⁻³) and endotoxin (15.1 ± 23.96 EU/m³) at the Wangdu site. The percentage of viable bioPM number concentration in the total PM was 3.1% in Beijing and 6.4% in Wangdu. Approximately 80% of viable bioPM was found to be in the range from 1 to 2.5 μm. Nevertheless, the size distribution patterns for viable bioPM at the Beijing and Wangdu sites differed and were affected by PM pollution, leading to distinct lung deposition profiles. Moreover, the distinct diurnal variations in viable bioPM on clean days were dimmed by the PM pollution at both sites. Distinct bacterial community structures were found in the air from the Beijing and Wangdu sites. The bacterial community in urban Beijing was dominated by genus Lactococcus (49.5%) and Pseudomonas (15.1%), while the rural Wangdu site was dominated by Enterococcus (65%) and Paenibacillus (10%). Human-derived genera, including Myroides, Streptococcus, Propionibacterium, Dietzia, Helcococcus, and Facklamia, were higher in Beijing, suggesting bacterial emission from humans in the urban air environment. Our results show that different air harbors different biological species, and people residing in different environments thus could have very different biological particle exposure.

That an alteration of the intestinal permeability is associated with gut barrier function has been increasingly evident, which plays an important role in human and animal health. Bisphenol A (BPA), an industrial compound used worldwide, has recently been classified as an environmental pollutant. One of our earlier studies has demonstrated that BPA disrupts the intestinal barrier function by inducing apoptosis and inhibiting cell proliferation in the human colonic epithelial cells line. In this study, we investigated the effects of dietary BPA uptake on the colonic barrier function in mice, as well as the intestinal permeability. Dietary BPA uptake was observed to destroy the morphology of the colonic epithelium and increase the pathology score. The levels of endotoxin, diamine peroxidase, D-lactate, and zonulin were found to have been significantly elevated in both plasma and colonic mucosa. A decline in the number of intestinal goblet cells and in mucin 2 gene expression was observed in the mice belonging to the BPA group. The results of immunohistochemistry revealed that the expression of tight junction proteins (ZO-1, occludin, and claudin-1) in colonic epithelium of BPA mice decreased significantly, and their gene abundance was also inhibited. Moreover, dietary BPA uptake was also found to have significantly reduced colonic microbial diversity and altered microbial structural composition. The functional profiles of colonic bacterial community exhibited adverse effects of dietary BPA intake on the endocrine and digestive systems, as well as the transport and catabolism functions. Collectively, our study highlighted that dietary BPA increased the colonic permeability, and this effect was closely related to the disruption of intestinal chemistry and physical and biological barrier functions.

Bacterial endotoxins are a component of particulate matter (PM) with anticipated health implications, yet we know little about how host reception of endotoxin through toll-like receptor 4 (TLR4) is affected by its association with other PM components. Subsequently, we investigated the relationship between endotoxin concentration (recombinant Factor C (rFC) assay) and host recognition (HEK Blue-TLR4 NF-kB reporter cell line based assay) in various compositions of urban PM, including road traffic, industrial and urban green land use classes. While the assays did not correlate strongly between each other, the TLR4 reporter cell line was found to be better correlated to the IL-8 response of PM. Furthermore, the ability of the quantified endotoxin (rFC assay) to stimulate the TLR4/MD-2 complex was significantly affected by the urban land use class, where traffic locations were found to be significantly higher in bioactive endotoxin than the industrial and green locations. We subsequently turned our attention to PM composition and characterized the samples based on transition metal content (through ICP-MS). The effect of nickel and cobalt – previously reported to activate the hTLR4/MD-2 complex – was found to be negligible in comparison to that of iron. Here, the addition of iron as a factor significantly improved the regression model between the two endotoxin assays, explaining 77% of the variation of the TLR4 stimulation and excluding the significant effect of land use class. Moreover, the effect of iron proved to be more than a correlation, since dosing LPS with Fe²⁺ led to an increase up to 64% in TLR4 stimulation, while Fe²⁺ without LPS was unable to stimulate a response. This study shows that endotoxin quantification assays (such as the rFC assay) may not always correspond to human biological recognition of endotoxin in urban PM, while its toxicity can be synergistically influenced by the associated PM composition.

Jumping on the bed is a favorite behavior of children; however, no study has investigated the increased air pollutants resulting from jumping on the bed. Therefore, we aimed to investigate the elevated concentrations of particulate matter (PM) and bioaerosols from jumping on the bed and making the bed. Simulation of jumping on the bed and making the bed was performed at sixty schoolchildren's houses in Taiwan. PM10, PM2.5, PM1 (PM with aerodynamic diameter less than 10, 2.5, and 1 μm, respectively) and airborne bacteria, fungi and endotoxin concentrations were simultaneously measured over simulation and background periods. Our results show the increase of PM10, PM2.5, PM1, airborne bacteria and fungi through the behavior of jumping on the bed (by 414 μg m-3, 353 μg m-3, 349 μg m-3, 6569 CFU m-3 and 978 CFU m-3, respectively). When making the bed, the PM10, PM2.5, PM1, airborne bacteria and fungi also significantly increased by 4.69 μg m-3, 4.09 μg m-3, 4.15 μg m-3, 8569 CFU m-3, and 779 CFU m-3, respectively. Airborne endotoxin concentrations significantly increased by 21.76 EU m-3 following jumping on the bed and making the bed. Moreover, when jumping on the bed, higher PM2.5 and PM1 concentrations in houses with furry pets rather than no furry pets, and less airborne fungi in apartments than in townhouses were found. For making the bed, lower airborne fungi was found in houses using essential oils rather than no essential oils using. The airborne endotoxin concentrations were positively associated with furry pets and smokers in the homes and negatively correlated to the home with window opening with a statistical significance during the periods of jumping on the bed and making the bed. In conclusion, significant increases of PM and bioaerosols during jumping on the bed and making the bed may need to be concerned.

Exposure to Particulate Matter (PM) could function as an adjuvant depending on the city of origin in mice allergic asthma models. Therefore, our aim was to determine whether inhalation of fine particles (PM2.5) from Mexico City could act as an adjuvant inducing allergic sensitization and/or worsening the asthmatic response in guinea pig, as a suitable model of human asthma. Experimental groups were Non-Sensitized (NS group), sensitized with Ovalbumin (OVA) plus Aluminum hydroxide (Al(OH)3) as adjuvant (S + Adj group), and sensitized (OVA) without adjuvant (S group). All the animals were exposed to Filtered Air (FA) or concentrated PM2.5 (5 h/daily/3 days), employing an aerosol concentrator system, PM2.5 composition was characterized. Lung function was evaluated by barometric plethysmography (Penh index). Inflammatory cells present in bronchoalveolar lavage were counted as well as OVA-specific IgG1 and IgE were determined by ELISA assay. Our results showed in sensitized animals without Al(OH)3, that the PM2.5 exposure (609 ± 12.73 μg/m3) acted as an adjuvant, triggering OVA-specific IgG1 and IgE concentration. Penh index increased ∼9-fold after OVA challenge in adjuvant-sensitized animals as well as in S + PM2.5 group (∼6-fold), meanwhile NS + FA and S + FA lacked response. S + Adj + PM2.5 group showed an increase significantly of eosinophils and neutrophils in bronchoalveolar lavage. PM2.5 composition was made up of inorganic elements and Polycyclic Aromatic Hydrocarbons, as well as endotoxins and β-glucan, all these components could act as adjuvant. Our study demonstrated that acute inhalation of PM2.5 acted as an adjuvant, similar to the aluminum hydroxide effect, triggering allergic asthma in a guinea pig model. Furthermore, in sensitized animals with aluminum hydroxide an enhancing influence of PM2.5 exposure was observed as specific-hyperresponsiveness to OVA challenge (quickly response) and eosinophilic and neutrophilic airway inflammation. Fine particles from Mexico City is a complex mix, which play a significant role as adjuvant in allergic asthma.

In vitro tests using human adenocarcinomic alveolar epithelial cell line A549 and small mouse monocyte-macrophage cell line J774A.1 were conducted to test toxicity of six PM (particulate matter) samples from Beijing. The properties of the samples differ significantly. The production of inflammatory cytokine (TNF-α for J774A.1) and chemokine (IL-8 for A549) and the level of intracellular reactive oxygen species (ROS) were used as endpoints. There was a positive correlation between water soluble organic carbon and DTT-based redox activity. Both cell types produced increased levels of inflammatory mediators and had higher level of intracelllar ROS, indicating the presence of PM-induced inflammatory response and oxidative stress, which were dose-dependent and significantly different among the samples. The releases of IL-8 from A549 and TNF-α from J774A.1 were significantly correlated to PM size, Zeta potential, endotoxin, major metals, and polycyclic aromatic hydrocarbons. No correlation between ROS and these properties was identified.

Microbiota associated with airborne particulate matter (PM) is an important indicator of indoor pollution as they can be pathogenic and cause serious health threats to the exposed occupants. Present study aimed to investigate the level of culturable microbes associated with PM and their toxicological characterization in urban and rural houses of Pune city. Highest concentration of bacterial aerosols observed to be associated with PM₁₀ size fraction in urban site (2136 ± 285 CFU/m³) whereas maximum fungal concentration has been measured in rural houses (1521 ± 302 CFU/m³). Predominantly found bacterial species were Bacillus sp., S. aureus, and Pseudomonas aeruginosa and fungal species were Aspergillus sp., Cladosporium sp., and Penicillium sp. in both urban and rural residential premises. Concentration of endotoxin measured using the kinetic Limulus Amebocyte Lysate assay exhibited that the level of endotoxin in both urban and rural sites are associated with household characteristics and the activities performed in indoor as well as outdoor. Cell free DTT assay confirmed the ability of these airborne microbes to induce the production of reactive oxygen species (ROS) varying along with the types of microorganisms. On exposure of A549 cells to airborne microbes, a significant decrease in cell viability was observed in terms of both necrosis and apoptosis pathway. Elevated production of nitric oxide (NO) and proinflammatory cytokines in epithelial cells and macrophages clearly suggest the inflammatory nature of these airborne microbes. Results derived from the present study demonstrated that the indoor air of urban and rural houses of Pune is contaminated in terms of microbial load. Therefore, attention should be paid to control the factors favoring the microbial growth in order to safeguard the health of exposed inhabitants.