Indoor air pollution (IAP) and environmental tobacco smoke (ETS) are associated with lower respiratory tract illness (LRTI) or wheezing in children. However, the effect of the timing of these exposures, specifically antenatal versus postnatal, and of alternate fuel sources such as the increasingly used volatile organic compounds have not been well studied. We longitudinally investigated the effect of antenatal or postnatal IAP and ETS on LRTI or wheezing prevalence and severity in African infants.
Mother and infant pairs enrolled over a 3-year period in a birth cohort study in two centres in Paarl, South Africa, were followed for the first year of life for LRTI or wheezing illness. We measured exposure to IAP (particulate matter, nitrogen dioxide, sulphur dioxide, carbon monoxide, and volatile organic compounds benzene and toluene) using devices placed in homes, antenatally and postnatally. We measured ETS longitudinally by maternal self-report and by urine cotinine measures. Study staff trained in recognition of LRTI or wheeze documented all episodes, which were categorised according to WHO case definition criteria. We used multivariate logistic and Poisson regressions to explore associations.
Antenatal exposures were the predominant risk factors associated with LRTI or wheezing illness. Toluene was a novel exposure associated with severe LRTI. Urgent and effective interventions focusing on antenatal environmental factors are required, including smoking cessation programmes targeting women of childbearing age pre-conception and pregnant women.
Bill & Melinda Gates Foundation, Discovery Foundation, South African Thoracic Society AstraZeneca Respiratory Fellowship, Medical Research Council South Africa, National Research Foundation South Africa, and CIDRI Clinical Fellowship.
Lower respiratory tract illness (LRTI), principally pneumonia, remains the leading cause of under-5 mortality in low-income and middle-income countries (LMICs), with a very high burden of disease in LMIC settings including Africa.1 Wheezing illness is common in young children and asthma is the most common non-communicable disease in African children.2 Indoor air pollution (IAP) and environmental tobacco smoke (ETS) exposure have been strongly associated with the development of childhood respiratory illness, but little data are available on the effect of the timing of exposures on child respiratory health.3, 4
Antenatally, in-utero tobacco smoke exposure has been shown to affect lung growth and predispose to development of LRTI or wheezing disorders.5 Potential mechanisms include the toxic effects of the numerous chemicals found in tobacco smoke on the developing respiratory system,6 suppression of fetal breathing or direct genotoxicity,7 the effects of nicotine on lung collagen deposition,6 and impaired immune function from imbalances in T-helper-1 and T-helper-2 cell responses.8 Although its role is less clear, antenatal IAP exposure is postulated to affect lung development through an interplay of maternal and placenta-fetal factors including oxidative stress resulting in placental insufficiency with decreased transport of oxygen and nutrients to the developing fetus.9 Postnatal IAP or ETS exposure might disrupt pulmonary defences leading to epithelial inflammation and affect microbial colonisation and systemic inflammation, particularly if the alveolar capillary membrane is breached.3 Most studies have focused on the association of postnatal IAP exposure on child respiratory health;10 separating the effects of antenatal versus postnatal exposure is difficult, with few studies able to delineate this.9, 11
In this African birth cohort study, in which exposures were objectively and longitudinally measured antenatally and postnatally, LRTI or wheezing was common and associated with antenatal rather than postnatal exposure to ETS or to IAP. Antenatal exposure to toluene, a volatile organic compound, was identified as a novel exposure associated with LRTI, h
