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\"Air traffic management (ATM) comprises a highly complex socio-technical system that keeps air traffic flowing safely and efficiently, worldwide, every minute of the year. Over the last few decades, several ambitious ATM performance improvement programmes have been undertaken. Such programmes have mostly delivered local technological solutions, whilst corresponding ATM performance improvements have fallen short of stakeholder expectations. In hindsight, this can be substantially explained from a complexity science perspective: ATM is simply too complex to address through classical approaches such as system engineering and human factors. In order to change this, complexity science has to be embraced as ATM's 'best friend'. The applicability of complexity science paradigms to the analysis and modelling of future operations is driven by the need to accommodate long-term air traffic growth within an already-saturated ATM infrastructure\"--Provided by publisher.

IntroductionElevated particulate matter (PM) concentrations of anthropogenic and/or desert dust origin are associated with increased morbidity among children with asthma.ObjectiveThe Mitigating the Health Effects of Desert Dust Storms Using Exposure-Reduction Approaches randomised controlled trial assessed the impact of exposure reduction recommendations, including indoor air filtration, on childhood asthma control during high desert dust storms (DDS) season in Cyprus and Greece.Design, participants, interventions and settingPrimary school children with asthma were randomised into three parallel groups: (a) no intervention (controls); (b) outdoor intervention (early alerts notifications, recommendations to stay indoors and limit outdoor physical activity during DDS) and (c) combined intervention (same as (b) combined with indoor air purification with high efficiency particulate air filters in children’s homes and school classrooms. Asthma symptom control was assessed using the childhood Asthma Control Test (c-ACT), spirometry (forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC)) and fractional exhaled nitric oxide (FeNO).ResultsIn total, 182 children with asthma (age; mean=9.5, SD=1.63) were evaluated during 2019 and 2021. After three follow-up months, the combined intervention group demonstrated a significant improvement in c-ACT in comparison to controls (β=2.63, 95% CI 0.72 to 4.54, p=0.007), which was more profound among atopic children (β=3.56, 95% CI 0.04 to 7.07, p=0.047). Similarly, FEV1% predicted (β=4.26, 95% CI 0.54 to 7.99, p=0.025), the need for any asthma medication and unscheduled clinician visits, but not FVC% and FeNO, were significantly improved in the combined intervention compared with controls.ConclusionRecommendations to reduce exposure and use of indoor air filtration in areas with high PM pollution may improve symptom control and lung function in children with asthma.Trial registration number NCT03503812.

Exposure to traffic-related air pollution (TRAP) has been associated with increased risks of respiratory diseases, but the biological mechanisms are not yet fully elucidated. Our aim was to evaluate the respiratory responses and explore potential biological mechanisms of TRAP exposure in a randomized crossover trial. We conducted a randomized crossover trial in 56 healthy adults. Each participant was exposed to high- and low-TRAP exposure sessions by walking in a park and down a road with high traffic volume for 4 h in random order. Respiratory symptoms and lung function, including forced expiratory volume in the first second ( ), forced vital capacity (FVC), the ratio of to FVC, and maximal mid-expiratory flow (MMEF), were measured before and after each exposure session. Markers of 8-isoprostane, tumor necrosis ( ), and ezrin in exhaled breath condensate (EBC), and surfactant proteins D (SP-D) in serum were also measured. We used linear mixed-effects models to estimate the associations, adjusted for age, sex, body mass index, meteorological condition, and batch (only for biomarkers). Liquid chromatography-mass spectrometry was used to profile the EBC metabolome. Untargeted metabolome-wide association study (MWAS) analysis and pathway enrichment analysis using mummichog were performed to identify critical metabolomic features and pathways associated with TRAP exposure. Participants had two to three times higher exposure to traffic-related air pollutants except for fine particulate matter while walking along the road compared with in the park. Compared with the low-TRAP exposure at the park, high-TRAP exposure at the road was associated with a higher score of respiratory symptoms [2.615 (95% CI: 0.605, 4.626), ] and relatively lower lung function indicators [ (95% CI: , ), ] for and (95% CI: , ; ) for MMEF]. Exposure to TRAP was significantly associated with changes in some, but not all, biomarkers, particularly with a (95% CI: 0.297, 0.691; ) increase for serum SP-D and a (95% CI: , ; ) decrease for EBC ezrin. Untargeted MWAS analysis revealed that elevated TRAP exposure was significantly associated with perturbations in 23 and 32 metabolic pathways under positive- and negative-ion modes, respectively. These pathways were most related to inflammatory response, oxidative stress, and energy use metabolism. This study suggests that TRAP exposure might lead to lung function impairment and respiratory symptoms. Possible underlying mechanisms include lung epithelial injury, inflammation, oxidative stress, and energy metabolism disorders. https://doi.org/10.1289/EHP11139.

Background Childhood exposure to air pollution contributes to cardiovascular disease in adulthood. Immune and oxidative stress disturbances might mediate the effects of air pollution on the cardiovascular system, but the underlying mechanisms are poorly understood in adolescents. Therefore, we aimed to identify immune biomarkers linking air pollution exposure and blood pressure levels in adolescents. Methods We randomly recruited 100 adolescents (mean age, 16 years) from Fresno, California. Using central-site data, spatial-temporal modeling, and distance weighting exposures to the participant’s home, we estimated average pollutant levels [particulate matter (PM), polyaromatic hydrocarbons (PAH), ozone (O 3 ), carbon monoxide (CO) and nitrogen oxides (NO x )]. We collected blood samples and vital signs on health visits. Using proteomic platforms, we quantitated markers of inflammation, oxidative stress, coagulation, and endothelial function. Immune cellular characterization was performed via mass cytometry (CyTOF). We investigated associations between pollutant levels, cytokines, immune cell types, and blood pressure (BP) using partial least squares (PLS) and linear regression, while adjusting for important confounders. Results Using PLS, biomarkers explaining most of the variance in air pollution exposure included markers of oxidative stress (GDF-15 and myeloperoxidase), acute inflammation (C-reactive protein), hemostasis (ADAMTS, D-dimer) and immune cell types such as monocytes. Most of these biomarkers were independently associated with the air pollution levels in fully adjusted regression models. In CyTOF analyses, monocytes were enriched in participants with the highest versus the lowest PM 2.5 exposure. In both PLS and linear regression, diastolic BP was independently associated with PM 2.5 , NO, NO 2 , CO and PAH 456 pollution levels ( P  ≤ 0.009). Moreover, monocyte levels were independently related to both air pollution and diastolic BP levels ( P  ≤ 0.010). In in vitro cell assays, plasma of participants with high PM 2.5 exposure induced endothelial dysfunction as evaluated by eNOS and ICAM-1 expression and tube formation. Conclusions For the first time in adolescents, we found that ambient air pollution levels were associated with oxidative stress, acute inflammation, altered hemostasis, endothelial dysfunction, monocyte enrichment and diastolic blood pressure. Our findings provide new insights on pollution-related immunological and cardiovascular disturbances and advocate preventative measures of air pollution exposure.

Globally, nearly 3 billion people rely on solid fuels for cooking and heating, the vast majority residing in low- and middle-income countries (LMICs). The resulting household air pollution (HAP) is a leading environmental risk factor, accounting for an estimated 1.6 million premature deaths annually. Previous interventions of cleaner stoves have often failed to reduce exposure to levels that produce meaningful health improvements. There have been no multicountry field trials with liquefied petroleum gas (LPG) stoves, likely the cleanest scalable intervention. This paper describes the design and methods of an ongoing randomized controlled trial (RCT) of LPG stove and fuel distribution in 3,200 households in 4 LMICs (India, Guatemala, Peru, and Rwanda). We are enrolling 800 pregnant women at each of the 4 international research centers from households using biomass fuels. We are randomly assigning households to receive LPG stoves, an 18-month supply of free LPG, and behavioral reinforcements to the control arm. The mother is being followed along with her child until the child is 1 year old. Older adult women (40 to of age) living in the same households are also enrolled and followed during the same period. Primary health outcomes are low birth weight, severe pneumonia incidence, stunting in the child, and high blood pressure (BP) in the older adult woman. Secondary health outcomes are also being assessed. We are assessing stove and fuel use, conducting repeated personal and kitchen exposure assessments of fine particulate matter with aerodynamic diameter ( ), carbon monoxide (CO), and black carbon (BC), and collecting dried blood spots (DBS) and urinary samples for biomarker analysis. Enrollment and data collection began in May 2018 and will continue through August 2021. The trial is registered with ClinicalTrials.gov (NCT02944682). This study will provide evidence to inform national and global policies on scaling up LPG stove use among vulnerable populations. https://doi.org/10.1289/EHP6407.

High quality personal exposure data is fundamental to understanding the health implications of household energy interventions, interpreting analyses across assigned study arms, and characterizing exposure-response relationships for household air pollution. This paper describes the exposure data collection for the Household Air Pollution Intervention Network (HAPIN), a multicountry randomized controlled trial of liquefied petroleum gas stoves and fuel among 3,200 households in India, Rwanda, Guatemala, and Peru. The primary objectives of the exposure assessment are to estimate the exposure contrast achieved following a clean fuel intervention and to provide data for analyses of exposure-response relationships across a range of personal exposures. Exposure measurements are being conducted over the 3-y time frame of the field study. We are measuring fine particulate matter [PM  in aerodynamic diameter ( )] with the Enhanced Children's MicroPEM™ (RTI International), carbon monoxide (CO) with the USB-EL-CO (Lascar Electronics), and black carbon with the OT21 transmissometer (Magee Scientific) in pregnant women, adult women, and children of age, primarily via multiple 24-h personal assessments (three, six, and three measurements, respectively) over the course of the 18-month follow-up period using lightweight monitors. For children we are using an indirect measurement approach, combining data from area monitors and locator devices worn by the child. For a subsample (up to 10%) of the study population, we are doubling the frequency of measurements in order to estimate the accuracy of subject-specific typical exposure estimates. In addition, we are conducting ambient air monitoring to help characterize potential contributions of exposure from background concentration. Stove use monitors (Geocene) are being used to assess compliance with the intervention, given that stove stacking (use of traditional stoves in addition to the intervention gas stove) may occur. The tools and approaches being used for HAPIN to estimate personal exposures build on previous efforts and take advantage of new technologies. In addition to providing key personal exposure data for this study, we hope the application and learnings from our exposure assessment will help inform future efforts to characterize exposure to household air pollution and for other contexts. https://doi.org/10.1289/EHP6422.

Background Combustion-generated fine particulate matter (PM2.5) is associated with cardiovascular morbidity. Both traffic-related air pollution and residential wood combustion may be important, but few studies have compared their impacts. Objectives To assess and compare effects of traffic-related and woodsmoke PM2.5 on endothelial function and systemic inflammation (C reactive protein, interleukin-6 and band cells) among healthy adults in Vancouver, British Columbia, Canada, using high efficiency particulate air (HEPA) filtration to introduce indoor PM2.5 exposure gradients. Methods We recruited 83 healthy adults from 44 homes in traffic-impacted or woodsmoke-impacted areas to participate in this randomised, single-blind cross-over intervention study. PM2.5 concentrations were measured during two consecutive 7-day periods, one with filtration and the other with ‘placebo filtration’. Endothelial function and biomarkers of systematic inflammation were measured at the end of each 7-day period. Results HEPA filtration was associated with a 40% decrease in indoor PM2.5 concentrations. There was no relationship between PM2.5 exposure and endothelial function. There was evidence of an association between indoor PM2.5 and C reactive protein among those in traffic-impacted locations (42.1% increase in C reactive protein per IQR increase in indoor PM2.5, 95% CI 1.2% to 99.5%), but not among those in woodsmoke-impacted locations. There were no associations with interleukin-6 or band cells. Conclusions Evidence of an association between C reactive protein and indoor PM2.5 among healthy adults in traffic-impacted areas is consistent with the hypothesis that traffic-related particles, even at relatively low concentrations, play an important role in the cardiovascular effects of the urban PM mixture. Trial registration number http://www.clinicaltrials.gov (NCT01570062).

BackgroundPersonal monitoring can estimate individuals’ exposures to environmental pollutants; however, accuracy depends on consistent monitor wearing, which is under evaluated.ObjectiveTo study the association between device wearing and personal air pollution exposure.MethodsUsing personal device accelerometry data collected in the context of a randomized cooking intervention in Ghana with three study arms (control, improved biomass, and liquified petroleum gas (LPG) arms; N = 1414), we account for device wearing to infer parameters of PM2.5 and CO exposure.ResultsDevice wearing was positively associated with exposure in the control and improved biomass arms, but weakly in the LPG arm. Inferred community-level air pollution was similar across study arms (~45 μg/m3). The estimated direct contribution of individuals’ cooking to PM2.5 exposure was 64 μg/m3 for the control arm, 74 μg/m3 for improved biomass, and 6 μg/m3 for LPG. Arm-specific average PM2.5 exposure at near-maximum wearing was significantly lower in the LPG arm as compared to the improved biomass and control arms. Analysis of personal CO exposure mirrored PM2.5 results.ConclusionsPersonal monitor wearing was positively associated with average air pollution exposure, emphasizing the importance of high device wearing during monitoring periods and directly assessing device wearing for each deployment.SignificanceWe demonstrate that personal monitor wearing data can be used to refine exposure estimates and infer unobserved parameters related to the timing and source of environmental exposures.Impact statementsIn a cookstove trial among pregnant women, time-resolved personal air pollution device wearing data were used to refine exposure estimates and infer unobserved exposure parameters, including community-level air pollution, the direct contribution of cooking to personal exposure, and the effect of clean cooking interventions on personal exposure. For example, in the control arm, while average 48 h personal PM2.5 exposure was 77 μg/m3, average predicted exposure at near-maximum daytime device wearing was 108 μg/m3 and 48 μg/m3 at zero daytime device wearing. Wearing-corrected average 48 h personal PM2.5 exposures were 50% lower in the LPG arm than the control and improved biomass and inferred direct cooking contributions to personal PM2.5 from LPG were 90% lower than the other arms. Our recommendation is that studies assessing personal exposures should examine the direct association between device wearing and estimated mean personal exposure.

In the global COVID-19 epidemic, humans are faced with a new challenge. The concept of quarantine as a preventive measure has changed human activities in all aspects of life. This challenge has led to changes in the environment as well. The air quality index is one of the immediate concrete parameters. In this study, the actual potential of quarantine effects on the air quality index and related variables in Tehran, the capital of Iran, is assessed, where, first, the data on the pollutant reference concentration for all measuring stations in Tehran, from February 19 to April 19, from 2017 to 2020, are monitored and evaluated. This study investigated the hourly concentrations of six particulate matters (PM), including PM2.5, PM10, and air contaminants such as nitrogen dioxide (NO 2 ), sulfur dioxide (SO2), ozone (O3), and carbon monoxide (CO). Changes in pollution rate during the study period can be due to reduced urban traffic, small industrial activities, and dust mites of urban and industrial origins. Although pollution has declined in most regions during the COVID-19 quarantine period, the PM2.5 rate has not decreased significantly, which might be of natural origins such as dust. Next, the air quality index for the stations is calculated, and then, the interpolation is made by evaluating the root mean square (RMS) of different models. The local and global Moran index indicates that the changes and the air quality index in the study area are clustered and have a high spatial autocorrelation. The results indicate that although the bad air quality is reduced due to quarantine, major changes are needed in urban management to provide favorable conditions. Contaminants can play a role in transmitting COVID-19 as a carrier of the virus. It is suggested that due to the rise in COVID-19 and temperature in Iran, in future studies, the effect of increased temperature on COVID-19 can be assessed.

BackgroundMaternal exposure to fine particulate matter (PM2.5) was associated with pregnancy complications. However, we still lack comprehensive evidence regarding which specific chemical components of PM2.5 are more harmful for maternal and foetal health.ObjectiveWe focused on exposure over the first trimester (0–13 weeks of gestation), which includes the early placentation period, and investigated whether PM2.5 and its components were associated with placenta-mediated pregnancy complications (combined outcome of small for gestational age, preeclampsia, placental abruption, and stillbirth).MethodsFrom 2013 to 2015, we obtained information, from the Japan Perinatal Registry Network database, on 83,454 women who delivered singleton infants within 23 Tokyo wards (≈627 km2). Using daily filter sampling of PM2.5 at one monitoring location, we analysed carbon and ion components, and assigned the first trimester average of the respective pollutant concentrations to each woman.ResultsThe ORs of placenta-mediated pregnancy complications were 1.14 (95% CI = 1.08–1.22) per 0.51 μg/m3 (interquartile range) increase of organic carbon and 1.11 (1.03–1.18) per 0.06 μg/m3 increase of sodium. Organic carbon was also associated with four individual complications. There was no association between ozone and outcome.SignificanceThere were specific components of PM2.5 that have adverse effects on maternal and foetal health.