Sensing of pathogens by specialized receptors is the hallmark of the innate immunity. Innate immune response also mounts a defense response against various allergens and pollutants including particulate matter present in the atmosphere. Air pollution has been included as the top threat to global health declared by WHO which aims to cover more than three billion people against health emergencies from 2019 to 2023. Particulate matter (PM), one of the major components of air pollution, is a significant risk factor for many human diseases and its adverse effects include morbidity and premature deaths throughout the world. Several clinical and epidemiological studies have identified a key link between the PM existence and the prevalence of respiratory and inflammatory disorders. However, the underlying molecular mechanism is not well understood. Here, we investigated the influence of air pollutant, PM 10 (particles with aerodynamic diameter less than 10 μm) during RNA virus infections using Highly Pathogenic Avian Influenza (HPAI) – H5N1 virus. We thus characterized the transcriptomic profile of lung epithelial cell line, A549 treated with PM 10 prior to H5N1infection, which is known to cause severe lung damage and respiratory disease. We found that PM 10 enhances vulnerability (by cellular damage) and regulates virus infectivity to enhance overall pathogenic burden in the lung cells. Additionally, the transcriptomic profile highlights the connection of host factors related to various metabolic pathways and immune responses which were dysregulated during virus infection. Collectively, our findings suggest a strong link between the prevalence of respiratory illness and its association with the air quality.
In the nearly saturated human respiratory tract, the presence of water-soluble substances in the inhaled aerosols can cause change in the size distribution of the particles. This consequently alters the lung deposition profiles of the inhaled airborne particles. Similarly, the presence of high concentration of hygroscopic aerosols also affects the water vapor and temperature profiles in the respiratory tract. A model is presented to analyze these effects in human respiratory system. The model solves simultaneously the heat and mass transfer equations to determine the size evolution of respirable particles and gas-phase properties within human respiratory tract. First, the model predictions for nonhygroscopic aerosols are compared with experimental results. The model results are compared with experimental results of sodium chloride particles. The model reproduces the major features of the experimental data. The water vapor profile is significantly modified only when a high concentration of particles is present. The model is used to study the effect of equilibrium assumptions on particle deposition. Simulations show that an infinite dilution solution assumption to calculate the saturation equilibrium over droplet could induce errors in estimating particle growth. This error is significant in the case of particles of size greater than 1 mum and at number concentrations higher than 10(5)/cm(3).
Wastewater contains a variety of microorganisms, and unit operations in the plants could release these biological components into the air environment. These airborne biological particles could have adverse health effects on plant workers and the downwind population. This study provides a first report on the concentration and characterization of the airborne biological particles in six wastewater treatment plants in Mumbai, India. The study indicates that 49% and 27% of the samples exceed, respectively, the exposure limit for airborne endotoxin and bacteria in occupational settings. Endotoxin was identified as the single most important component of the particulate matter responsible for induction of proinflammatory indicator (tumor necrosis factor-α) in in vitro assay. Identification of several clinically important bacterial species in the samples suggests that the workers at the treatment plant are exposed to opportunistic and infectious bacteria. Principal component analysis was used to identify the groups among the bacterial species which serves as the signature for transport study. Analysis also shows that the component related to spore-forming bacteria is present in all samples.
In the nearly saturated human respiratory tract, the presence of water-soluble substances in inhaled aerosols can cause change in the size distribution of particles. This consequently alters the lung deposition profiles of the inhaled airborne particles. The magnitude of particle deposition in the lung is affected by the soluble component present in the particle. This is estimated by a numerical model. The model solves the condensation growth equation to determine the size evolution of respirable particles within the human respiratory tract. The water uptake by the particles in the respiratory tract results in change of size and density of the particles, and these changes are incorporated for estimating the particle deposition efficiency. The model results are compared with experimental results of sodium chloride particles. The model reproduces the major features of the experimental data. The simulations indicate that the particle can grow up to two times or more of its original size due to water uptake, depending on the quantity of the soluble matter it carries and thus can have significant effect on particle deposition efficiency. The study investigated the effect of soluble compounds in estimating total and regional lung dose of ambient particulate matter measured in Mumbai, India. The particle mass size distribution and composition considered for the ambient particulate matter, the variation in the total mass dose due to the growth was modest. But, the regional lung dose was significantly affected by the hygroscopic growth.
Particulate mass size distributions were measured during cooking and non-cooking periods in three Indian urban household kitchens with Liquefied Petroleum Gas as fuel. Based on the measured mass size distributions, fraction of particulate deposition in the respiratory system were calculated for a healthy Indian female using a deterministic lung deposition model. Respiratory physiological data of Indian women were collected from the published data. These physiological parameters were incorporated in the model to determine the particulate deposition in the respiratory system. The cooking generated very high concentration of particles 4 to 5 times more than the non-cooking background periods. Particulate size distributions in both cooking and non-cooking periods showed bimodal characteristics. Cooking process generated particles predominantly in accumulation mode (0.1-0.3 µm) whereas during non-cooking periods particulates are found in coarse mode (1.0-2.0 µm). Also, during frying process, the particulates were found to have a predominant coarser/droplet mode 0.7-1.0 µm. The highest deposition was observed in pulmonary region during cooking periods. The study shows that the daily particulate dose to the urban Indian women from domestic cooking is comparable with the dose resulting from outdoor particulate exposure.
25Sensing of pathogens by specialized receptors is the hallmark of the innate immune response. 26Innate immune response also mounts a defense response against various allergens and pollutants 27 including particulate matter present in the atmosphere. Air pollution has been included as the top 28 threat to global health declared by WHO which aims to cover more than three billion people against 29 health emergencies from 2019-2023. Particulate matter (PM), one of the major components of air 30 pollution, is a significant risk factor for many human diseases and its adverse effects include 31 morbidity and premature deaths throughout the world. Several clinical and epidemiological studies 32 have identified a key link between the PM composition and the prevalence of respiratory and 33 inflammatory disorders. However, the underlying molecular mechanism is not well understood. 34Here, we investigated the influence of air pollutant, PM10 during RNA virus infections using highly 35 pathogenic avian influenza (HPAI). We thus characterized the transcriptomic profile of lung 36 epithelial cell line, A549 treated with PM10 prior to infection with (HPAI) H5N1 influenza virus, 37 which is known to severely affect the lung and cause respiratory damage. We found that PM10 38 regulates virus infectivity and enhances overall pathogenic burden in the lung cells. Additionally, 39 the transcriptomic profile highlights the connection of host factors related to various metabolic 40 pathways and immune responses which were dysregulated during virus infection. Overall our 41 findings suggest a strong link between the prevalence of respiratory illness and the air quality. 42 43 44 45 Keywords: Particulate Matter (PM10), Virus Infection, Infectious Disease, Innate Immunity and 46 Metabolic Pathways-Related Genes. 47India and associated health concerns in term of occurrence of disease [14][15][16][17][18][19]. Although, most of 65 the studies were based on the epidemiological data and cross-sectional studies, there were few 66 studies about involvement of PM in respiratory diseases [20][21][22], asthma [23], cancer [24-27], 67 tuberculosis [28, 29] . It has been known that PM can induce innate immunity and can change the 68 level of cytokines, upon its exposure to the airways of humans [30][31][32][33]. PM were readily associated 69 with respiratory infections such as chronic obstructive pulmonary disease (COPD) [34][35][36][37] and it 70 is also reported to be associated with the respiratory syncytial virus (RSV) and influenza virus 71infections. [38][39][40][41]. Yet these studies are limited to epidemiological, cross -sectional studies [22, 72 42-44]. 73Here, we isolated and characterized PM10 from a heavily industrialized city Bengaluru, India and 74 checked its effect on RNA virus infection. We observed and concluded that PM10 hijacks the innate 75 immune system upon viral infection and significantly enhanced the viral replication of the RNA 76 viruses like new-castle disease virus (NDV), influenza virus -H1N1 (PR8) and H5N1. By 77...
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