Epidemiologic Evidence of and Potential Mechanisms by Which Second-Hand Smoke Causes Predisposition to Latent and Active Tuberculosis

Bai, Xiyuan; Aerts, Shanae; Verma, Deepshikha; Ordway, Diane; Chan, Edward D.

doi:10.4110/in.2018.18.e22

Cited by 15 publications

(17 citation statements)

References 154 publications

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“…Patra et al [22] reviewed 12 studies and reported an almost 2-fold increased risk of active PTB from second-hand exposure and an increased risk of latent TB infection (pooled RR 1.67, 95% CI 1.12–2.48). This finding was confirmed in a review by Bai et al (2018) who reported that the susceptibility for latent and active TB among those exposed to second-hand smoke may be singly or in combination due to suppressed anti-TB immunity and enhanced activity of immunosuppressive N2 neutrophils [23]. Second-hand smoke is a growing concern in regions where PTB poses a significant health risk.…”

Section: Discussionsupporting

confidence: 55%

Environmental Silica Dust Exposure and Pulmonary Tuberculosis in Johannesburg, South Africa

Kootbodien

Iyaloo

Wilson

et al. 2019

IJERPH

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Background: Occupational crystalline silica dust exposure is associated with an elevated risk of pulmonary tuberculosis (PTB). However, there is less evidence for an association with environmental silica dust exposure. Methods: A cross-sectional study of 310 participants was conducted in an exposed community living within 2 km of gold mine tailings and an unexposed population residing more than 10 km from the nearest gold mine tailing. Chest radiographs (n = 178) were read for PTB, past or current, by three readers. Results: Past or current PTB was radiologically identified in 14.4% (95%CI 9.2–21.8) in the exposed and 7.5% (95%CI 2.8–18.7) in the unexposed groups. Multivariate logistic regression models suggested that PTB prevalence was independently associated with exposure to second-hand smoke (OR = 8.13, 95%CI 1.16–57.22), a lower body mass index (OR = 0.88, 95%CI 0.80–0.98), previous diagnosis and treatment of PTB (OR = 8.98, 95%CI 1.98–40.34), and exposure to dust in the workplace from sand, construction, and/or mining industries (OR = 10.2, 95%CI 2.10–50.11). Conclusion: We found no association between PTB and environmental exposure to gold mine tailing dust. However, workplace silica dust exposure is a significant risk factor for PTB in South Africa, and PTB patients of working age should be screened for silica exposure.

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Section: Discussionsupporting

confidence: 55%

Environmental Silica Dust Exposure and Pulmonary Tuberculosis in Johannesburg, South Africa

Kootbodien

Iyaloo

Wilson

et al. 2019

IJERPH

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“…Their next study showed that passive smokers also had an increased risk of developing latent and active tuberculosis. This susceptibility may be due to the increased exposure to the tubercle bacilli from the increased cough seen in smokers, along with suppressed anti-tuberculosis immunity, enhanced activity of immunosuppressive N2 neutrophils or Tregs, or a combination of these factors 21 . Gleeson et al report on human alveolar macrophages in smokers to be attenuated significantly, with consequent impairment of the glycolytic response to M. tuberculosis infection, which is crucial in the early host immune response to the pathogen 22 .…”

Section: Discussionmentioning

confidence: 99%

The Role of Cigarette Smoking and Alcohol Consumption in Pulmonary Tuberculosis Development and Recurrence

Lampalo

Jukić

Bingulac-Popović

et al. 2019

ACC

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During a two-year period (2001-2003), 464 patients were treated for tuberculosis at Jordanovac Department for Lung Diseases in Croatia. Besides pulmonary tuberculosis in 97.7% of patients, patients were also treated for tuberculous pleurisy (0.9%), tuberculous laryngitis (0.6%), tuberculous meningitis (0.2%), tuberculous pericarditis (0.2%) and urogenital tuberculosis (0.4%). Out of the total number of patients, 57.3% declared themselves to be active smokers (men were predominant and made up to 80.8%) and 20.9% to be active alcohol consumers. Both risk factors, i.e. smoking and alcohol consumption, were present in 15.1% of all patients. The most common comorbidities were diabetes mellitus (30.4%), cardiac diseases (11.2%) and chronic obstructive pulmonary disease (8.0%). Lung carcinoma was the most common malignant disease (n=51), with Mycobacterium tuberculosis isolated in 33% of them. Seventy-two of 464 (15.5%) patients had recurrences of tuberculosis. Of these, 30.5% had one of the risk factors (20.8% were smokers and 9.7% consumed alcohol), while 32.5% of patients had both risk factors. In conclusion, cigarette smoking was proved to be the most significant risk factor for development of pulmonary tuberculosis and its recurrence.

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“…CS exposure weakens the pulmonary immune system [ 5 ], compromising the protective activity of macrophages, resulting in decreased production of proinflammatory cytokines [ 4 ] and recruitment of T cells [ 6 , 7 ]. In the case of Mycobacterium tuberculosis ( Mtb ), smoking-associated immune dysfunction promotes bacterial survival in macrophages [ 8 , 9 ]. Additionally, CS exposure prevents granuloma formation [ 1 , 3 , 6 ], leading to accelerated disease severity and progression [ 5 , 10 ].…”

Section: Introductionmentioning

confidence: 99%

Effects of Cigarette Smoke Condensate on Growth and Biofilm Formation by Mycobacterium tuberculosis

Cholo

Rasehlo

Venter

et al. 2020

BioMed Research International

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Background and Objectives. Cigarette smoke (CS) is a major risk factor contributing to the burden of tuberculosis. Little is known, however, about the effects of CS exposure on growth and persistence of Mycobacterium tuberculosis (Mtb) organisms. This issue has been addressed in the current study, which is focused on the effects of cigarette smoke condensate (CSC) on the growth and viability of Mtb planktonic and biofilm-forming cultures. Materials and Methods. The planktonic and biofilm-forming cultures were prepared in Middlebrook 7H9 and Sauton broth media, respectively, using Mtb strain, H37Rv. The effects of CSC at concentrations of 0.05-3.12 mg/L on growth, biofilm formation and structure were evaluated using microplate Alamar Blue assay, spectrophotometric procedure and scanning electron microscopy (SEM), respectively. Involvement of reactive oxygen species in CSC-mediated biofilm formation was investigated by including catalase in biofilm-forming cultures. Results. CSC did not affect the growth of planktonic bacteria, but rather led to a statistically significant increase in biofilm formation at concentrations of 0.4-3.12 mg/L, as well as in the viability of biofilm-forming bacteria at CSC concentrations of 0.2-1.56 mg/L. SEM confirmed an agglomerated biofilm matrix and irregular bacterial morphology in CSC-treated biofilms. Inclusion of catalase caused significant attenuation of CSC-mediated augmentation of biofilm formation by Mtb, implying involvement of oxidative stress. These findings demonstrate that exposure of Mtb to CSC resulted in increased biofilm formation that appeared to be mediated, at least in part, by oxidative stress, while no effect on planktonic cultures was observed. Conclusion. Smoking-related augmentation of biofilm formation by Mtb may contribute to persistence of the pathogen, predisposing to disease reactivation and counteracting the efficacy of antimicrobial chemotherapy.

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Epidemiologic Evidence of and Potential Mechanisms by Which Second-Hand Smoke Causes Predisposition to Latent and Active Tuberculosis

Cited by 15 publications

References 154 publications

Environmental Silica Dust Exposure and Pulmonary Tuberculosis in Johannesburg, South Africa

Environmental Silica Dust Exposure and Pulmonary Tuberculosis in Johannesburg, South Africa

The Role of Cigarette Smoking and Alcohol Consumption in Pulmonary Tuberculosis Development and Recurrence

Effects of Cigarette Smoke Condensate on Growth and Biofilm Formation by Mycobacterium tuberculosis

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