Background: Several studies have estimated associations between air pollution and birth outcomes, but few have evaluated potential effects on pregnancy complications.Objective: We investigated whether low-level exposure to air pollution is associated with gestational diabetes and preeclampsia.Methods: High-quality registry information on 81,110 singleton pregnancy outcomes in southern Sweden during 1999–2005 was linked to individual-level exposure estimates with high spatial resolution. Modeled exposure to nitrogen oxides (NOx), expressed as mean concentrations per trimester, and proximity to roads of different traffic densities were used as proxy indicators of exposure to combustion-related air pollution. The data were analyzed by logistic regression, with and without adjusting for potential confounders.Results: The prevalence of gestational diabetes increased with each NOx quartile, with an adjusted odds ratio (OR) of 1.69 (95% CI: 1.41, 2.03) for the highest (> 22.7 µg/m3) compared with the lowest quartile (2.5–8.9 µg/m3) of exposure during the second trimester. The adjusted OR for acquiring preeclampsia after exposure during the third trimester was 1.51 (1.32, 1.73) in the highest quartile of NOx compared with the lowest. Both outcomes were associated with high traffic density, but ORs were significant for gestational diabetes only.Conclusion: NOx exposure during pregnancy was associated with gestational diabetes and preeclampsia in an area with air pollution levels below current air quality guidelines.

We present the results of, to our knowledge, the first Lidar study applied to continuous and simultaneous monitoring of aerial insects, bats and birds. It illustrates how common patterns of flight activity, e.g. insect swarming around twilight, depend on predation risk and other constraints acting on the faunal components. Flight activity was monitored over a rice field in China during one week in July 2016, using a high-resolution Scheimpflug Lidar system. The monitored Lidar transect was about 520 m long and covered approximately 2.5 m3. The observed biomass spectrum was bimodal, and targets were separated into insects and vertebrates in a categorization supported by visual observations. Peak flight activity occurred at dusk and dawn, with a 37 min time difference between the bat and insect peaks. Hence, bats started to feed in declining insect activity after dusk and stopped before the rise in activity before dawn. A similar time difference between insects and birds may have occurred, but it was not obvious, perhaps because birds were relatively scarce. Our observations are consistent with the hypothesis that flight activity of bats is constrained by predation in bright light, and that crepuscular insects exploit this constraint by swarming near to sunset/sunrise to minimize predation from bats.

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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. Expected final online publication date for the Annual Review of Public Health, Volume 42 is April 2021. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

BackgroundPrenatal heavy metals exposure has shown a negative impact on birth weight. However, their influence on different clinical forms of fetal smallness was never assessed.ObjectivesTo 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).MethodIn 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.ResultsMaternal 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.ConclusionFetal 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.

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 H 2 O 2 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 H 2 O 2 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. Nääv et al. Urban PM2.5 Toxic to Trophoblast Cells 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.

Air pollution has been suggested to affect fetal growth, but more data is needed to assess the timing of exposure effects by using ultrasound measures. It is also important to study effects in low exposure areas to assess eventual thresholds of effects. The MAPSS (Maternal Air Pollution in Southern Sweden) cohort consists of linked registry data for around 48,000 pregnancies from an ultrasound database, birth registry and exposure data based on residential addresses. Measures of air pollution exposure were obtained through dispersion modelling with input data from an emissions database (NO) with high resolution (100-500m grids). Air pollution effects were assessed with linear regressions for the following endpoints; biparietal diameter, femur length, abdominal diameter and estimated fetal weight measured in late pregnancy and birth weight and head circumference measured at birth. We estimated negative effects for NO; in the adjusted analyses the decrease of abdominal diameter and femur length were -0.10 (-0.17, -0.03) and -0.13 (-0.17, -0.01)mm, respectively, per 10µg/m increment of NO. We also estimated an effect of NO-exposures on birth weight by reducing birth weight by 9g per 10µg/m increment of NO. We estimated small but statistically significant effects of air pollution on late fetal and birth size and reduced fetal growth late in pregnancy in a geographic area with levels below current WHO air quality guidelines.

BackgroundThe knowledge about air pollution effects on birth weight, prematurity, and small for gestational age (SGA) in low-exposure areas is insufficient.ObjectivesThe aim of this birth cohort study was to investigate whether low-level exposure to air pollution was associated with prematurity and fetal growth and whether there are sex-specific effects.MethodWe combined high-quality registry information on 81,110 births with individually modeled exposure data at residence for nitrogen oxides (NOx) and proximity to roads with differing traffic density. The data were analyzed by logistic and linear regression with and without potential confounders.ResultsWe observed an increased risk for babies being SGA when we compared highest and lowest NOx quartiles, adjusting for maternal age, smoking, sex, and year of birth. After additional adjustment for maternal country of origin and parity (which were highly intercorrelated), the increase was no longer statistically significant. However, in subgroup analyses when we compared highest and lowest NOx quartiles we still observed an increased risk for SGA for girls [odds ratio (OR) = 1.12; 95% confidence interval (CI), 1.01–1.24); we also observed increased risk among mothers who had not changed residency during pregnancy (OR = 1.09; 95% CI, 1.01–1.18). The confounders with the greatest impact on SGA were parity and country of origin. Concerning prematurity, the prevalence was lower in the three higher NOx exposure quartiles compared with the lowest category.ConclusionFor future studies on air pollution effects on birth outcomes, careful control of confounding is crucial.