Air Pollution And Tb: Is There A Link?

Tuberculosis (TB) is a respiratory infectious disease caused by Mycobacterium tuberculosis, which spreads when infected people expel bacteria into the air, for example, by coughing. It is one of the leading causes of mortality and morbidity worldwide. While indoor air pollution is a well-known risk factor for TB, the link between outdoor air pollution and TB development is less understood. Studies have found a positive correlation between exposure to air pollutants and the risk of developing TB, with specific pollutants such as PM2.5, PM10, SO2, NO2, CO, and O3 increasing the number of TB cases. The impact of outdoor air pollution on TB development is an area of ongoing research, especially in highly populated and polluted regions.

Indoor air pollution is a well-known risk factor for tuberculosis

Tuberculosis (TB) is a respiratory infectious disease caused by Mycobacterium tuberculosis, which spreads when infected individuals expel bacteria into the air, for example, by coughing. It is one of the top 10 causes of death worldwide, with approximately 10 million new cases and 1.4 million deaths from the disease in 2019.

Several studies have found a positive correlation between exposure to air pollutants and the risk of TB. For example, a study in the Beijing-Tianjin-Hebei region of China found a total of 653,373 cases of PTB, with a positive correlation between PTB cases and exposure to air pollutants PM2.5, O3, and NO2. Another study in Wulumuqi, China, found that exposure to air pollutants PM2.5, SO2, NO2, and CO increased the risk of TB after a delay of 3 months. A similar study in Hefei, China, also found a positive correlation between short-term exposure to ambient air pollutants and the risk of tuberculosis outpatient visits.

The underlying mechanisms for the increase in TB risk with ambient air pollution exposure are likely multifactorial. Animal studies have shown that long-term exposure to diesel exhaust can reduce macrophage functions, resulting in an indirect increase in the mycobacterial load. In addition, exposure to PM2.5 can impair the immune function of anti-mycobacterial T cells and decrease the release of pro-inflammatory cytokines, further increasing the risk of TB.

Outdoor air pollution and tuberculosis development

Tuberculosis (TB) is a respiratory infectious disease caused by Mycobacterium tuberculosis, which spreads when infected people expel bacteria into the air, for example, by coughing. It typically affects the lungs but can also affect other sites. It is one of the leading causes of mortality and morbidity worldwide. In 2019, there were approximately 10 million new cases of TB globally, and 1.4 million people died from the disease.

Indoor air pollution is a well-known risk factor for TB development, with firewood, charcoal, and wood-burning kilns being common sources of indoor air pollution. The association between indoor air pollution and TB was suggested as early as 1911. However, the impact of outdoor air pollution on TB development has not been fully examined until recently.

Several studies have now investigated the link between outdoor air pollution and TB development. One study in the Seoul metropolitan area of South Korea found that annual SO2 levels are associated with an increased risk of TB in males. Another study in Wulumuqi, China, found that a single pollutant model of PM2.5, PM10, SO2, NO2, CO, and O3 increased the risk of TB. The same study also found that a two-factor model of PM10 + NO2 increased the risk of TB.

Additionally, a study in the Beijing-Tianjin-Hebei region of China investigated the impact of three main air pollutants: PM2.5, O3, and NO2. The results showed a total of 653,373 cases of PTB (pulmonary tuberculosis) in the region from January 2005 to December 2017. Another study in Jinan, China, explored the effects of short- and long-term residential concentrations of ambient air pollutants on the risk of drug-resistant TB.

The underlying mechanisms for the increased risk of TB development with outdoor air pollution exposure are multifactorial. Animal studies have shown that long-term exposure to diesel exhaust can reduce macrophage functions, resulting in an indirect increase in the mycobacterial load. In addition, exposure to outdoor air pollution particles has been found to weaken the body's immunity against TB.

In summary, outdoor air pollution is a contributing factor to the development of TB, with various studies providing empirical support for this link. The impact of outdoor air pollution on TB development is particularly relevant in highly populated urban areas, where industrialization, vehicular traffic, and other sources of pollution increase the risk of exposure. Further research is needed to fully understand the complex relationship between outdoor air pollution and TB development and to inform the development of effective prevention and control strategies.

Air pollution impairs the human respiratory system

Tuberculosis (TB) is an infectious disease caused by the bacillus Mycobacterium tuberculosis. It typically affects the lungs but can also affect other sites. It is one of the leading causes of mortality and morbidity worldwide. Indoor air pollution is a well-known risk factor for TB development, and the association between the two was suggested as early as 1911.

Several studies have found a link between air pollution and the incidence of TB. For example, a study in the Beijing-Tianjin-Hebei region of China, an area with high levels of air pollution, identified 653,373 cases of PTB (pulmonary tuberculosis). Another study in Wulumuqi, China, found that a single pollutant model of PM2.5, PM10, SO2, NO2, CO, and O3 increased the number of TB cases by 0.09%, 0.08%, 0.58%, 0.42%, 6.9%, and 0.57%, respectively. A similar study in South Korea found that annual SO2 levels are associated with an increased risk of TB in males.

The impact of outdoor air pollution on the development of TB has not been fully examined, but epidemiological research shows that tuberculosis is more prevalent in people exposed to air pollution, especially indoor air pollution. For instance, in homes where firewood or charcoal is used for cooking, the risk of developing TB is five times greater than in other areas. Urbanization and industrialization contribute to air pollution and are linked to an increased risk of TB.

The underlying mechanisms for the increased risk of TB development with air pollution exposure are multifactorial. Animal studies have shown that long-term exposure to diesel exhaust can reduce macrophage functions, resulting in an indirect increase in the mycobacterial load. In addition, exposure to air pollution particles has been found to weaken the body's immunity against TB.

In conclusion, air pollution, particularly indoor air pollution, is a risk factor for the development of TB. The impact of outdoor air pollution on TB development requires further investigation, but evidence suggests that it may also play a role. Preventing overexposure to air pollutants and developing mitigation strategies are essential to reducing the TB burden and improving respiratory health outcomes.

Air pollution and drug-resistant tuberculosis

Tuberculosis (TB) is a respiratory infectious disease caused by Mycobacterium tuberculosis, which spreads when infected people expel bacteria into the air, for example, by coughing. It typically affects the lungs (pulmonary TB) but can also affect other sites (extrapulmonary TB). It is one of the leading causes of mortality and morbidity worldwide.

Indoor air pollution is a well-known risk factor for TB development, and the association between indoor air pollution and TB was suggested as early as 1911. However, the possible link between outdoor air pollution and TB development has not been fully examined until recently.

Several studies have found a positive association between air pollution and TB incidence. For example, a study in the Beijing-Tianjin-Hebei region of China, a highly polluted region, found a total of 653,373 cases of PTB. Another study in Wulumuqi, China, found that a single pollutant model showed that all air pollutants (PM2.5, PM10, SO2, NO2, CO, and O3) would increase the risk of TB. The number of TB cases increased by 0.09%, 0.08%, 0.58%, 0.42%, 6.9%, and 0.57%, respectively, for every increase of 1 μg/m3 (or 1 mg/m3) in the concentration of these pollutants.

Additionally, air pollution has been linked to an increased risk of drug-resistant tuberculosis (DR-TB). A study in Jinan, China, found that high exposure to PM2.5, PM10, and CO was significantly associated with increased incidence of multi-drug resistance (MDR) in both single- and multi-pollutant regression models. The positive association between PM2.5 and MDR was most pronounced at 540 days of exposure, while for O3, it was observed at 180 days of exposure, and for PM10 and CO, it was observed from 90 to 540 days of exposure.

In summary, there is growing evidence that air pollution, including both indoor and outdoor pollution, contributes to the incidence of TB and DR-TB. Further research is needed to fully understand the mechanisms underlying these associations and to develop effective control strategies to reduce the burden of TB worldwide.

Air pollution and tuberculosis prevalence in urban slums

Tuberculosis (TB) is a respiratory infectious disease caused by Mycobacterium tuberculosis, which spreads when people who are sick with TB expel bacteria into the air, for example, by coughing. It typically affects the lungs but can also affect other sites. It is one of the leading causes of mortality and morbidity worldwide. According to a World Health Organization (WHO) report, about 10.4 million people suffered from TB in 2016, including 6.3 million new cases. WHO estimated that about a quarter of the world’s population was infected with Mycobacterium tuberculosis, making these people potentially at risk of developing TB. The heaviest burden falls on people living in urban slums, where the risk of developing TB is five times as great as in other areas. Slum populations are often impoverished and live in crowded conditions, so there’s potential for the transmission of the bacteria that cause TB.

Indoor air pollution is a well-known risk factor for TB development. The association between indoor air pollution and TB was suggested as early as 1911. The possible link between outdoor air pollution and TB development has not been examined fully, although there is a growing body of evidence suggesting an association between air pollution exposure and TB incidence. In a study in the Beijing–Tianjin–Hebei region, a cultural center in China with a high population density, it was found that exposure to PM2.5 and NO2 was significantly associated with an increased risk of PTB, while exposure to O3 was associated with a decreased risk of PTB. Another study in Wulumuqi, China, found that all air pollutants (PM2.5, PM10, SO2, NO2, CO, and O3) in this study would have an increased risk of tuberculosis. A 10 μg/m3 increase in the NO2 concentration was associated with an increased risk of PTB for a lag period of between 0 months and 2 months.

In subsequent NIH-funded studies, Stephan Schwander assessed particles collected from the air in Mexico City, which is plagued by urban outdoor air pollution. He also collected lung and blood immune cells from Mexico City residents. That study showed that inhaling urban air pollution particles weakens the body’s immunity against tuberculosis. Two additional studies by Schwander’s group provide further details about the particles’ effects on immune cell functions and demonstrate that both the sizes of the particles and the season in which they are collected can modify their biological effects. Schwander says that people living in slums might face a perfect storm of factors—including air pollution—that compound their TB risk. He wants to study TB transmission in a slum in Kampala, Uganda, building on a pilot study he conducted in ten homes there in 2017. He hopes his research might pave the way for new tuberculosis prevention strategies, such as improved regulation of pollution sources, more thoughtful urban development, or rigorous health monitoring of at-risk people.

In a study in the Seoul metropolitan area, South Korea, it was found that the annual SO2 level is associated with an increased risk of TB in males. Another study indicated that in vitro exposure to SO2 decreased production or release of tumor necrosis factor-α (TNF-α) and interleukin-1. TNF-α is crucial for host defenses against M. tuberculosis because it plays a central role in the containment of tuberculous bacilli through granuloma formation. Thus, the association between SO2 exposure and the development of active TB in our study may have been mediated by the negative effect of SO2 on reactive oxygen intermediate and TNF-α.

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