This review highlights the importance of air quality in the African urban development process. We address connections between air pollution and ( a) rapid urbanization, ( b) social problems, ( c) health impacts, ( d) climate change, ( e) policies, and ( f) new innovations. We acknowledge that air pollution levels in Africa can be extremely high and a serious health threat. The toxic content of the pollution could relate to region-specific sources such as low standards for vehicles and fuels, cooking with solid fuels, and burning household waste. We implore the pursuit of interdisciplinary research to create new approaches with relevant stakeholders. Moreover, successful air pollution research must regard conflicts, tensions, and synergies inherent to development processes in African municipalities, regions, and countries. This includes global relationships regarding climate change, trade, urban planning, and transportation. Incorporating aspects of local political situations (e.g., democracy) can also enhance greater political accountability and awareness about air pollution.

A peer-reviewed open access journal published by the National Institute of Environmental Health Sciences

Objective: Epidemiological studies have found air pollution to be a driver of adverse pregnancy outcomes, including gestational diabetes, low term birth weight and preeclampsia. It is unknown what biological mechanisms are involved in this process. A first trimester trophoblast cell line (HTR-8/SVneo) was exposed to various concentrations of PM2.5 (PM2.5) in order to elucidate the effect of urban particulate matter (PM) of size <2.5 μm on placental function. Methods: PM2.5 were collected at a site representative of urban traffic and dispersed in cell media by indirect and direct sonication. The HTR-8 cells were grown under standard conditions. Cellular uptake was studied after 24 and 48 h of exposure by transmission electron microscopy (TEM). The secretion of human chorionic gonadotropin (hCG), progesterone, and Interleukin-6 (IL-6) was measured by ELISA. Changes in membrane integrity and H₂O₂ production were analyzed using the CellTox^TM Green Cytotoxicity and ROSGlo^TM assays. Protease activity was evaluated by MitoTox^TM assay. Mitochondrial function was assessed through high resolution respirometry in an Oroboros O2k-FluoRespirometer, and mitochondrial content was quantified by citrate synthase activity. Results: TEM analysis depicted PM2.5 cellular uptake and localization of the PM2.5 to the mitochondria after 24 h. The cells showed aggregated cytoskeleton and generalized necrotic appearance, such as chromatin condensation, organelle swelling and signs of lost membrane integrity. The mitochondria displayed vacuolization and disruption of cristae morphology. At 48 h exposure, a significant drop in hCG secretion and a significant increase in progesterone secretion and IL-6 production occurred. At 48 h exposure, a five-fold increase in protease activity and a significant alteration of H₂O₂ production was observed. The HTR-8 cells exhibited evidence of increased cytotoxicity with increasing exposure time and dose of PM2.5. No significant difference in mitochondrial respiration or mitochondrial mass could be demonstrated. Conclusion: Following exposure to air pollution, intracellular accumulation of PM may contribute to the placental dysfunction associated with pregnancy outcomes, such as preeclampsia and intrauterine growth restriction, through their direct and indirect effects on trophoblast protein secretion, hormone regulation, inflammatory response, and mitochondrial interference.

Prenatal heavy metals exposure has shown a negative impact on birth weight. However, their influence on different clinical forms of fetal smallness was never assessed. To investigate whether there is a differential association between heavy metals exposure and fetal smallness subclassification into intrauterine growth restriction (IUGR) and small-for-gestational age (SGA). In this prospective case-control study, we included 178 mother–infant pairs; 96 of appropriate for gestational age (AGA) and 82 of small fetuses diagnosed in third trimester. The small ones were further subclassified into IUGR, n = 49 and SGA, n = 33. Cadmium (Cd), mercury (Hg), lead (Pb), arsenic (As) and zinc (Zn) levels were measured in the maternal and cord serum, and in the placentas of the three groups. Maternal serum level of Cd (p<0.001) was higher in the small fetuses compared to AGA. Fetal serum level of Cd (p<0.001) was increased in the small fetuses compared to AGA. Fetal serum level of Hg (p<0.05) showed an increase in SGA compared to both IUGR and AGA. Fetal serum level of Zn was increased in the AGA (p < 0.001) compared to each of the small fetuses groups. Only differences in the levels between the small fetuses’ subgroups were detected in the fetal serum levels of Cd and Hg. Fetal birth weight was negatively correlated with the fetal serum level of Cd (p < 0.001). No differences in the placental heavy metal levels were observed among the groups. Fetal serum levels of Cd showed differential correlation between small fetuses' clinical subclassification, which together with the increased Cd levels in both maternal and fetal serum of the small fetuses reinforce the negative influence of heavy metals on birth weight. These findings provide more opportunities to verify the role of heavy metals exposure in relation to small fetuses’ subclassification.

Genetic and environmental factors both contribute to the development of Autism Spectrum Disorder (ASD) and Attention-Deficit/Hyperactivity Disorder (ADHD). One suggested environmental risk factor for ASD and ADHD is air pollution, but knowledge of its effects, especially in low-exposure areas, are limited. Here, we investigate risks for ASD and ADHD associated with prenatal exposure to air pollution in an area with air pollution levels generally well below World Health Organization (WHO) air quality guidelines. We used an epidemiological database (MAPSS) consisting of virtually all (99%) children born between 1999 and 2009 (48,571 births) in the study area, in southern Sweden. MAPSS consists of data on modelled nitrogen oxide (NOx) levels derived from a Gaussian dispersion model; maternal residency during pregnancy; perinatal factors collected from a regional birth registry; and socio-economic factors extracted from Statistics Sweden. All ASD and ADHD diagnoses in our data were undertaken at the Malmö and Lund Departments of Child and Adolescent Psychiatry, using standardized diagnostic instruments. We used logistic regression analyses to obtain estimates of the risk of developing ASD and ADHD associated with different air pollution levels, with adjustments for potential perinatal and socio-economic confounders. In this longitudinal cohort study, we found associations between air pollution exposure during the prenatal period and and the risk of developing ASD. For example, an adjusted Odds Ratio (OR) of 1.40 and its 95% Confidence Interval (CI) (95% CI: 1.02-1.93) were found when comparing the fourth with the first quartile of NOx exposure. We did not find similar associations on the risk of developing ADHD. This study contributes to the growing evidence of a link between prenatal exposure to air pollution and autism spectrum disorders, suggesting that prenatal exposure even below current WHO air quality guidelines may increase the risk of autism spectrum disorders.

Ambient air pollution is considered a major environmental health threat to pregnant women. Our previous work has shown an association between exposure to airborne particulate matter (PM) and an increased risk of developing pre-eclamspia. It is now recognized that many pregnancy complications are due to underlying placental dysfunction, and this tissue plays a pivotal role in pre-eclamspia. Recent studies have shown that PM can enter the circulation and reach the human placenta but the effects of PM on human placental function are still largely unknown. In this work we investigated the effects of airborne PM on trophoblast cells. Human, first trimester trophoblast cells (HTR-8/SV) were exposed to urban pollution particles (Malmö PM2.5; Prague PM10) for up to seven days in vitro and were analysed for uptake, levels of hCGβ and IL-6 secretion and proteomic analysis. HTR-8/SVneo cells rapidly endocytose PM within 30 min of exposure and particles accumulate in the cell in perinuclear vesicles. High doses of Prague and Malmö PM (500–5000 ng/ml) significantly decreased hCGβ secretion and increased IL-6 secretion after 48 h exposure. Exposure to PM (50 ng/ml) for 48h or seven days led to reduced cellular growth and altered protein expression. The differentially expressed proteins are involved in networks that regulate cellular processes such as inflammation, endoplasmic reticulum stress, cellular survival and molecular transport pathways. Our studies suggest that trophoblast cells exposed to low levels of urban PM respond with reduced growth, oxidative stress, inflammation and endoplasmic reticulum stress after taking up the particles by endocytosis. Many of the dysfunctional cellular processes ascribed to the differentially expressed proteins in this study, are similar to those described in PE, suggesting that low levels of urban PM may disrupt cellular processes in trophoblast cells. Many of the differentially expressed proteins identified in this study are involved in inflammation and may be potential biomarkers for PE.