• Energy Research

Air pollution is a grave risk to human health that affects nearly everyone in the world and nearly every organ in the body. Fortunately, it is largely a preventable risk. Reducing pollution at its source can have a rapid and substantial impact on health. Within a few weeks, respiratory and irritation symptoms, such as shortness of breath, cough, phlegm, and sore throat, disappear; school absenteeism, clinic visits, hospitalizations, premature births, cardiovascular illness and death, and all-cause mortality decrease significantly. The interventions are cost-effective. Reducing factors causing air pollution and climate change have strong cobenefits. Although regions with high air pollution have the greatest potential for health benefits, health improvements continue to be associated with pollution decreases even below international standards. The large response to and short time needed for benefits of these interventions emphasize the urgency of improving global air quality and the importance of increasing efforts to reduce pollution at local levels.

Air pollution is a grave risk to human health that affects nearly everyone in the world and nearly every organ in the body. Fortunately, it is largely a preventable risk. Reducing pollution at its source can have a rapid and substantial impact on health. Within a few weeks, respiratory and irritation symptoms, such as shortness of breath, cough, phlegm, and sore throat, disappear; school absenteeism, clinic visits, hospitalizations, premature births, cardiovascular illness and death, and all-cause mortality decrease significantly. The interventions are cost-effective. Reducing factors causing air pollution and climate change have strong cobenefits. Although regions with high air pollution have the greatest potential for health benefits, health improvements continue to be associated with pollution decreases even below international standards. The large response to and short time needed for benefits of these interventions emphasize the urgency of improving global air quality and the importance of increasing efforts to reduce pollution at local levels.

Air pollution is increasingly recognized as a global health emergency with its impacts being wide ranging, more so for low- and middle-income countries where both indoor and outdoor pollution levels are high. In Africa, more than 80% of children live in households which use unclean sources of energy. The effects of both indoor and outdoor pollution on lung health on children who are the most vulnerable to their effects range from acute lower respiratory tract infections to long-term chronic health effects. We reviewed the literature on the effects of air pollution in children in Sub-Saharan Africa from prenatal exposure, infancy and school-going children. Data from Sub-Saharan Africa on quantification of exposures both indoor and outdoor mainly utilizes modelling or self-reporting. Exposures to biomass not only increases the risk of acute respiratory tract infections in young children but also increases the risk of carriage of pathogenic bacteria in the upper respiratory tract. Although there is limited evidence of association between asthma and pollution in African children, airway hyper-responsiveness and lower lung function has been demonstrated in children with higher risk of exposure. Interventions at a policy level to both quantify the exposure levels at a population level are urgently needed to address the possible interventions to limit exposure and improve lung health in children in Sub-Saharan Africa.

Air pollution is increasingly recognized as a global health emergency with its impacts being wide ranging, more so for low- and middle-income countries where both indoor and outdoor pollution levels are high. In Africa, more than 80% of children live in households which use unclean sources of energy. The effects of both indoor and outdoor pollution on lung health on children who are the most vulnerable to their effects range from acute lower respiratory tract infections to long-term chronic health effects. We reviewed the literature on the effects of air pollution in children in Sub-Saharan Africa from prenatal exposure, infancy and school-going children. Data from Sub-Saharan Africa on quantification of exposures both indoor and outdoor mainly utilizes modelling or self-reporting. Exposures to biomass not only increases the risk of acute respiratory tract infections in young children but also increases the risk of carriage of pathogenic bacteria in the upper respiratory tract. Although there is limited evidence of association between asthma and pollution in African children, airway hyper-responsiveness and lower lung function has been demonstrated in children with higher risk of exposure. Interventions at a policy level to both quantify the exposure levels at a population level are urgently needed to address the possible interventions to limit exposure and improve lung health in children in Sub-Saharan Africa.

AbstractPrenatal tobacco exposure (PTE) and prenatal alcohol exposure (PAE) have been associated with an increased risk of delayed neurodevelopment in children as well as differential newborn DNA methylation (DNAm). However, the biological mechanisms connecting PTE and PAE, DNAm, and neurodevelopment are largely unknown. Here we aim to determine whether differential DNAm mediates the association between PTE and PAE and neurodevelopment at 6 (N = 112) and 24 months (N = 184) in children from the South African Drakenstein Child Health Study. PTE and PAE were assessed antenatally using urine cotinine measurements and the ASSIST questionnaire, respectively. Cord blood DNAm was measured using the EPIC and 450 K BeadChips. Neurodevelopment (cognitive, language, motor, adaptive behavior, socioemotional) was measured using the Bayley Scales of Infant and Toddler Development, Third Edition. We constructed methylation risk scores (MRS) for PTE and PAE and conducted causal mediation analysis (CMA) with these MRS as mediators. Next, we conducted a high-dimensional mediation analysis to identify individual CpG sites as potential mediators, followed by a CMA to estimate the average causal mediation effects (ACME) and total effect (TE). PTE and PAE were associated with neurodevelopment at 6 but not at 24 months. PTE MRS reached a prediction accuracy (R2) of 0.23 but did not significantly mediate the association between PTE and neurodevelopment. PAE MRS was not predictive of PAE (R2 = 0.006). For PTE, 31 CpG sites and eight CpG sites were identified as significant mediators (ACME and TEP < 0.05) for the cognitive and motor domains at 6 months, respectively. For PAE, 16 CpG sites and 1 CpG site were significant mediators for the motor and adaptive behavior domains at 6 months, respectively. Several of the associated genes, includingMAD1L1, CAMTA1, andALDH1A2have been implicated in neurodevelopmental delay, suggesting that differential DNAm may partly explain the biological mechanisms underlying the relationship between PTE and PAE and child neurodevelopment.

AbstractPrenatal tobacco exposure (PTE) and prenatal alcohol exposure (PAE) have been associated with an increased risk of delayed neurodevelopment in children as well as differential newborn DNA methylation (DNAm). However, the biological mechanisms connecting PTE and PAE, DNAm, and neurodevelopment are largely unknown. Here we aim to determine whether differential DNAm mediates the association between PTE and PAE and neurodevelopment at 6 (N = 112) and 24 months (N = 184) in children from the South African Drakenstein Child Health Study. PTE and PAE were assessed antenatally using urine cotinine measurements and the ASSIST questionnaire, respectively. Cord blood DNAm was measured using the EPIC and 450 K BeadChips. Neurodevelopment (cognitive, language, motor, adaptive behavior, socioemotional) was measured using the Bayley Scales of Infant and Toddler Development, Third Edition. We constructed methylation risk scores (MRS) for PTE and PAE and conducted causal mediation analysis (CMA) with these MRS as mediators. Next, we conducted a high-dimensional mediation analysis to identify individual CpG sites as potential mediators, followed by a CMA to estimate the average causal mediation effects (ACME) and total effect (TE). PTE and PAE were associated with neurodevelopment at 6 but not at 24 months. PTE MRS reached a prediction accuracy (R2) of 0.23 but did not significantly mediate the association between PTE and neurodevelopment. PAE MRS was not predictive of PAE (R2 = 0.006). For PTE, 31 CpG sites and eight CpG sites were identified as significant mediators (ACME and TEP < 0.05) for the cognitive and motor domains at 6 months, respectively. For PAE, 16 CpG sites and 1 CpG site were significant mediators for the motor and adaptive behavior domains at 6 months, respectively. Several of the associated genes, includingMAD1L1, CAMTA1, andALDH1A2have been implicated in neurodevelopmental delay, suggesting that differential DNAm may partly explain the biological mechanisms underlying the relationship between PTE and PAE and child neurodevelopment.