BACKGROUND: Indoor air pollution (IAP) from environmental tobacco smoke (ETS) and biomass fuel smoke (BMS) poses respiratory health risks, with children and women bearing the major burden. OBJECTIVES: We used a systematic review and meta-analysis to investigate the relation between childhood tuberculosis (TB) and exposure to ETS and BMS. METHODS: We searched three databases for epidemiological studies that investigated the association of childhood TB with exposure to ETS and BMS. We calculated pooled estimates and heterogeneity for studies eligible for inclusion in the meta-analysis and stratified studies on ETS by outcome. RESULTS: Five case-control and three cross-sectional studies were eligible for inclusion in the meta-analysis and quality assessment. Pooled effect estimates showed that exposure to ETS is associated with tuberculous infection and TB disease (OR 1.9, 95%CI 1.4–2.9) among exposed compared to non-exposed children. TB disease in ETS studies produced a pooled OR of 2.8 (95%CI 0.9–4.8), which was higher than the OR for tuberculous infection (OR 1.9, 95%CI 0.9–2.9) for children exposed to ETS compared to non-exposed children. Studies on BMS exposure were too few and too small to permit a conclusion. CONCLUSION: Exposure to ETS increases the risk of childhood TB disease or tuberculous infection.

Crude measures of exposure to indicate indoor air pollution have been associated with the increased risk for acquiring tuberculosis. Our study aimed to determine an association between childhood pulmonary tuberculosis (PTB) and exposure to indoor air pollution (IAP), based on crude exposure predictors and directly sampled and modelled pollutant concentrations. In this case control study, children diagnosed with PTB were compared to children without PTB. Questionnaires about children’s health; and house characteristics and activities (including household air pollution) and secondhand smoke (SHS) exposure were administered to caregivers of participants. A subset of the participants’ homes was sampled for measurements of PM10 over a 24-h period (n = 105), and NO2 over a period of 2 to 3 weeks (n = 82). IAP concentrations of PM10 and NO2 were estimated in the remaining homes using predictive models. Logistic regression was used to look for association between IAP concentrations, crude measures of IAP, and PTB. Of the 234 participants, 107 were cases and 127 were controls. Pollutants concentrations (μg/m3) for were PM10 median: 48 (range: 6.6–241) and NO2 median: 16.7 (range: 4.5–55). Day-to-day variability within- household was large. In multivariate models adjusted for age, sex, socioeconomic status, TB contact and HIV status, the crude exposure measures of pollution viz. cooking fuel type (clean or dirty fuel) and SHS showed positive non-significant associations with PTB. Presence of dampness in the household was a significant risk factor for childhood TB acquisition with aOR of 2.4 (95% CI: 1.1–5.0). The crude exposure predictors of indoor air pollution are less influenced by day-to-day variability. No risk was observed between pollutant concentrations and PTB in children for PM10 and NO2. Our study suggests increased risk of childhood tuberculosis disease when children are exposed to SHS, dirty cooking fuel, and dampness in their homes. Yet, HIV status, age and TB contact are the most important risk factors of childhood PTB in this population.

Background: Despite the recognition of the importance of indoor microbial exposures on children’s health, the role of different microbial agents in development and aggravation of respiratory symptoms and diseases is only poorly understood. This study aimed to assess whether exposure to microbial aerosols within the indoor environment are associated with respiratory symptoms among children under-5 years of age.Methods: A systematic literature search was conducted on PubMed, Web of Science, GreenFILE, ScienceDirect, EMBASE and Cochrane library through February 2020. Studies that investigated the exposure–response relationship between components of the indoor microbial communities and respiratory symptoms among under-five children were eligible for inclusion. A random-effect meta-analysis was applied to estimate pooled relative risk (RR) and 95% confidence interval (CI) for study specific high versus low microbial exposures. The potential effect of individual studies on the overall estimate was evaluated using leave-one-out analysis, while heterogeneity was evaluated byI²statistics using RevMan 5.3.Results: Fifteen studies were eligible for inclusion in a meta-analysis. The pooled risk estimate suggested that increased microbial exposure was associated with an increased risk of respiratory symptoms [pooled relative risk (RR): 1.24 (1.09, 1.41),P = 0.001]. The association was strongest with exposure to a combination ofAspergillus,Penicillium, Cladosporium and Alternariaspecies [pooled RR: 1.73 (1.30, 2.31),P = 0.0002]. Stratified analysis revealed an increased risk of wheeze [pooled RR: 1.20 (1.05, 1.37),P = 0.007 and allergic rhinitis [RR: 1.18 (0.94, 1.98),P = 0.16] from any microbial exposure.Conclusions: Microbial exposures are, in general, associated with risk of respiratory symptoms. Future studies are needed to study the indoor microbiome more comprehensively, and to investigate the mechanism of these associations.

The high incidence cancer rates are due to factors such as behavior, occupational exposures, genetics, environmental pollution and infections. The aim of this study was to identify risk factors associated with lung cancer among patients seen in the public health facilities in KwaZulu-Natal, South Africa. In this case-control study, 75 cases and 159 controls were interviewed using a structured close-ended questionnaire. Logistic regression showed a positive association between lung cancer and tobacco smoking (OR = 2.86, 95% CI: 1.21–6.77) and exposure to passive smoke (OR = 3.28, 95% CI: 1.48–7.30). When adjusted for other covariates, tobacco smoking and passive smoke were still positively associated with increased risk of lung cancer. Alcohol consumption (aORs ranging from 2.79 to 3.35) and history of lung disease (aORs ranging from 9.91 to 12.1) were statistically significantly associated with lung cancer. Our study suggests that tobacco smoke exposure is the major cause of lung cancer, and increased exposure to occupational and environmental carcinogenic substances, alcohol consumption and history of lung disease increase the risk of lung cancer. Based on our findings, policy development and planning of prevention strategies incorporating smoking legislations, occupational health and safety are essential in South Africa.