nitrogen-dioxide and Tuberculosis

Tuberculosis (TB) is an infectious disease caused predominantly by Mycobacterium tuberculosis (Mtb). It was responsible for approximately 1.4 million deaths worldwide in 2019. The lack of new drugs to treat drug-resistant strains is a principal factor for the slow rise in TB infections. Our aim is to aid the development of new TB treatments by describing improvements (last decade, 2011-2021) to nitro(NO

Topics: Antitubercular Agents; Drug Development; Heterocyclic Compounds; Humans; Microbial Sensitivity Tests; Mycobacterium tuberculosis; Nitrogen Dioxide; Tuberculosis

A growing number of biological studies suggest that exogenous sulfur dioxide (SO

Topics: Adolescent; Adult; Air Pollutants; Air Pollution; Child; China; Cities; Humans; Male; Middle Aged; Nitrogen Dioxide; Outpatients; Particulate Matter; Sulfur Dioxide; Tuberculosis; Young Adult

Chronic obstructive pulmonary disease (COPD), lung cancer (LC) and tuberculosis (TB) are common chronic lung diseases that generate a large disease burden and significant health care resource use in China. The aim of this study was to quantify spatial patterns and effects of air pollution and meteorological factors on hospitalization of COPD, LC and TB in Beijing. Daily counts of hospitalization for 2010 were obtained from the Beijing Urban Employees Basic Medical Insurance (UEBMI) system. Bayesian hierarchical Poisson regression models were applied to identify spatial patterns of hospitalization for COPD, LC and TB at the district level and explore associations with inhalable particulate matter (aerodynamic diameter <10 μm, PM

Topics: Air Pollutants; Air Pollution; Beijing; Environmental Exposure; Geography; Hospitalization; Humans; Humidity; Lung Diseases; Lung Neoplasms; Meteorological Concepts; Models, Statistical; Nitrogen Dioxide; Particulate Matter; Pulmonary Disease, Chronic Obstructive; Risk Factors; Seasons; Sulfur Dioxide; Temperature; Tuberculosis

Several respirable hazards, including smoking and indoor air pollution from biomass, were suggested to increase the risk of tuberculosis. Few studies have been conducted on ambient air pollution and tuberculosis. We investigated the association between exposure to ambient air pollution and incidence of active tuberculosis.. We conducted a cohort study using 106,678 participants of a community-based screening service in Taiwan, 2005-2012. We estimated individual exposure to air pollution using data from the nearest air quality monitoring station and the road intensity within a 500 m buffer zone. The incidence of tuberculosis was ascertained from the national tuberculosis registry.. After a median follow-up of 6.7 years, 418 cases of tuberculosis occurred. Exposure to fine particulate matter (PM2.5) was associated with increased risk of active tuberculosis (adjusted HR: 1.39/10 μg/m3 (95% CI 0.95 to 2.03)). In addition, traffic-related air pollution including nitrogen dioxide (adjusted HR: 1.33/10 ppb; 95% CI 1.04 to 1.70), nitrogen oxides (adjusted HR: 1.21/10 ppb; 95% CI 1.04 to 1.41) and carbon monoxide (adjusted HR: 1.89/ppm; 95% CI 0.78 to 4.58) was associated with tuberculosis risk. There was a non-significant trend between the length of major roads in the neighbourhood and culture-confirmed tuberculosis (adjusted HR: 1.04/km; 95% CI 0.995 to 1.09).. Our study revealed a possible link between ambient air pollution and risk of active tuberculosis. Since people from developing countries continue to be exposed to high levels of ambient air pollution and to experience high rates of tuberculosis, the impact of worsening air pollution on global tuberculosis control warrants further investigation.

Topics: Adult; Air Pollutants; Air Pollution; Carbon Monoxide; Cohort Studies; Environmental Exposure; Female; Humans; Incidence; Male; Middle Aged; Nitrogen Dioxide; Nitrogen Oxides; Particulate Matter; Risk; Taiwan; Tuberculosis; Vehicle Emissions

Background. The relationship between air pollution and exacerbation of respiratory diseases is well established. Nevertheless, its association with hemoptysis has been poorly investigated. This paper describes the relationship of air pollutants with severe hemoptysis. Methods. All consecutive subjects with severe hemoptysis during a 5-year period were included. The relationship between the contamination measurements and the frequency of embolizations was analyzed using Poisson regressions. In these regressions, the dependent variable was the monthly number of embolizations in a given month and the independent variable was either the concentration of an air contaminant during the same month, the concentration of the air contaminant during the previous month, or the difference between the two. Results. A higher total number of embolizations per month were observed over the months with increases in the concentration of NO. The number of embolizations was 2.0 in the 33 months with no increases in the concentration of NO, 2.1 in the 12 months with small increases, 2.2 in the 5 months with moderate increases, 2.5 in the 4 months with large increases, and 4.0 in the 5 months with very large increases. Conclusion. There is association between hemoptysis and increases in the concentration of atmospheric NO in Badalona (Spain).

Topics: Adult; Aged; Air Pollution; Bronchial Arteries; Bronchiectasis; Carbon Monoxide; Embolization, Therapeutic; Environmental Exposure; Female; Hemoptysis; Humans; Male; Middle Aged; Neoplasms; Nitric Oxide; Nitrogen Dioxide; Ozone; Particulate Matter; Pulmonary Disease, Chronic Obstructive; Regression Analysis; Retrospective Studies; Seasons; Severity of Illness Index; Spain; Sulfur Dioxide; Tuberculosis

To test the toxicity of reactive nitrogen intermediates (RNI), including authentic nitric oxide (NO), nitrogen dioxide (NO2), and peroxynitrite anion (ONOO-), a potent oxidant derived from NO and superoxide anion, on various mycobacterial strains including M. tuberculosis.. Relatively avirulent mycobacteria including M. smegmatis and BCG, as well as the pathogenic M. Bovis Ravenel and M. tuberculosis Erdman and the clinical isolate M160 (also known as the C strain) were tested for their susceptibility to the toxic effects of NO, NO2, and ONOO-, Deaerated, NO-saturated solutions as well as an anaerobic in vitro system in which mycobacteria can be exposed to desired concentrations of authentic NO or NO2, were employed in these studies. An in vitro ONOO- killing assay was used to examine the adverse effects of this NO-derived oxidant on the various strains of mycobacteria.. Both NO and NO2 exhibit antimycobacterial activity, with the former being more potent. Results obtained using ONOO- killing assay revealed that while avirulent mycobacteria including BCG and M. smegmatis are susceptible to this NO-derived oxidant, the virulent Erdman strain of M. tuberculosis and M. bovis, as well as the clinical tuberculous isolate M160, are remarkably resistant.. These results suggest that the interactions between RNI and various species of mycobacteria could be highly specific. And since activated macrophages produce peroxynitrite, the significance of the ONOO- resistance of M. tuberculosis strains in relation to intracellular survival deserves further investigation.

Topics: Adult; Anions; Drug Resistance, Microbial; Humans; Mycobacterium; Mycobacterium bovis; Mycobacterium smegmatis; Mycobacterium tuberculosis; Nitric Oxide; Nitrites; Nitrogen Dioxide; Tuberculosis

The present study concerns the effect of hydrocortisone (HC) on the effector functions of Bacillus Calmette Guerin-purified protein derivative (BCG-PPD)-activated macrophages. Such activated macrophages release greater amounts of H2O2 and NO2-, inhibit the intracellular proliferation of T. gondii and kill L. monocytogenes more efficiently than resident macrophages. This activation was not fully expressed by macrophages from BCG-activated mice that had received a subcutaneous injection of HC 2 days before intraperitoneal injection of PPD, since the inhibition of the intracellular proliferation of T. gondii, the release of NO2- and the rate of intracellular killing of L. monocytogenes were lower than in macrophages from BCG-PPD-activated mice. However, treatment with HC did not impair the release of H2O2 by BCG-PPD-activated macrophages. The results show that the treatment of infected mice with HC inhibits their ability to develop adequate intracellular microbicidal mechanisms.

Topics: Animals; Hydrocortisone; Hydrogen Peroxide; Listeria monocytogenes; Macrophage Activation; Macrophages; Male; Mice; Mice, Inbred CBA; Mycobacterium bovis; Nitrogen Dioxide; Toxoplasma; Tuberculosis; Tumor Necrosis Factor-alpha