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Introduction: Ambient air pollution is a known risk factor for adverse birth outcomes, but the role of ultrafine particles (UFPs) is not well understood. Aircraft-origin UFPs adversely affect air quality over large residential areas downwind of airports, but their reproductive health burden remains uninvestigated., Objectives: This analysis evaluated whether UFPs from jet aircraft emissions are associated with increased rates of preterm birth (PTB) among pregnant mothers living downwind of Los Angeles International Airport (LAX)., Methods: This population-based study used birth records, provided by the California Department of Public Health, to ascertain birth outcomes and a novel, validated geospatial UFP dispersion model approach to estimate in utero exposures. All mothers who gave birth from 2008 to 2016 while living within 15 km of LAX were included in this analysis ( N = 174,186 ; including 15,134 PTBs)., Results: In utero exposure to aircraft-origin UFPs was positively associated with PTB. The odds ratio (OR) per interquartile range (IQR) increase [9,200 particles per cubic centimeter (cc)] relative UFP exposure was 1.04 [95% confidence interval (CI): 1.02, 1.06]. When comparing the fourth quartile of UFP exposure to the first quartile, the OR for PTB was 1.14 (95% CI: 1.08, 1.20), adjusting for maternal demographic characteristics, exposure to traffic-related air pollution, and airport-related noise., Conclusion: Our results suggest that emissions from aircraft play an etiologic role in PTBs, independent of noise and traffic-related air pollution exposures. These findings are of public health concern because UFP exposures downwind of airfields are common and may affect large, densely populated residential areas. https://doi.org/10.1289/EHP5732.

With emerging evidence that diesel exhaust exposure poses distinct risks to human health, the need for fine-scale models of diesel exhaust pollutants is growing. We modeled the spatial distribution of several nitrated polycyclic aromatic hydrocarbons (NPAHs) to identify fine-scale gradients in diesel exhaust pollution in two Seattle, WA neighborhoods. Our modeling approach fused land-use regression, meteorological dispersion modeling, and pollutant monitoring from both fixed and mobile platforms. We applied these modeling techniques to concentrations of 1-nitropyrene (1-NP), a highly specific diesel exhaust marker, at the neighborhood scale. We developed models of two additional nitroarenes present in secondary organic aerosol: 2-nitropyrene and 2-nitrofluoranthene. Summer predictors of 1-NP, including distance to railroad, truck emissions, and mobile black carbon measurements, showed a greater specificity to diesel sources than predictors of other NPAHs. Winter sampling results did not yield stable models, likely due to regional mixing of pollutants in turbulent weather conditions. The model of summer 1-NP had an R(2) of 0.87 and cross-validated R(2) of 0.73. The synthesis of high-density sampling and hybrid modeling was successful in predicting diesel exhaust pollution at a very fine scale and identifying clear gradients in NPAH concentrations within urban neighborhoods.

Rationale: More than 25 million American children breathe polluted air on diesel school buses. Emission reduction policies exist, but the health impacts to individual children have not been evaluated., Methods: Using a natural experiment, we characterized the exposures and health of 275 school bus riders before, during, and after the adoption of clean technologies and fuels between 2005 and 2009. Air pollution was measured during 597 trips on 188 school buses. Repeated measures of exhaled nitric oxide (FeNO), lung function (FEV1, FVC), and absenteeism were also collected monthly (1,768 visits). Mixed-effects models longitudinally related the adoption of diesel oxidation catalysts (DOCs), closed crankcase ventilation systems (CCVs), ultralow-sulfur diesel (ULSD), or biodiesel with exposures and health., Measurements and Main Results: Fine and ultrafine particle concentrations were 10-50% lower on buses using ULSD, DOCs, and/or CCVs. ULSD adoption was also associated with reduced FeNO (-16% [95% confidence interval (CI), -21 to -10%]), greater changes in FVC and FEV1 (0.02 [95% CI, 0.003 to 0.05] and 0.01 [95% CI, -0.006 to 0.03] L/yr, respectively), and lower absenteeism (-8% [95% CI, -16.0 to -0.7%]), with stronger associations among patients with asthma. DOCs, and to a lesser extent CCVs, also were associated with improved FeNO, FVC growth, and absenteeism, but these findings were primarily restricted to patients with persistent asthma and were often sensitive to control for ULSD. No health benefits were noted for biodiesel. Extrapolating to the U.S. population, changed fuel/technologies likely reduced absenteeism by more than 14 million/yr., Conclusions: National and local diesel policies appear to have reduced children's exposures and improved health.

We measured the spatial pattern of particle number (PN) concentrations downwind from the Los Angeles International Airport (LAX) with an instrumented vehicle that enabled us to cover larger areas than allowed by traditional stationary measurements. LAX emissions adversely impacted air quality much farther than reported in previous airport studies. We measured at least a 2-fold increase in PN concentrations over unimpacted baseline PN concentrations during most hours of the day in an area of about 60 km(2) that extended to 16 km (10 miles) downwind and a 4- to 5-fold increase to 8-10 km (5-6 miles) downwind. Locations of maximum PN concentrations were aligned to eastern, downwind jet trajectories during prevailing westerly winds and to 8 km downwind concentrations exceeded 75 000 particles/cm(3), more than the average freeway PN concentration in Los Angeles. During infrequent northerly winds, the impact area remained large but shifted to south of the airport. The freeway length that would cause an impact equivalent to that measured in this study (i.e., PN concentration increases weighted by the area impacted) was estimated to be 280-790 km. The total freeway length in Los Angeles is 1500 km. These results suggest that airport emissions are a major source of PN in Los Angeles that are of the same general magnitude as the entire urban freeway network. They also indicate that the air quality impact areas of major airports may have been seriously underestimated.

Background: Fine particulate air pollution (PM2.5) is a global health concern, as exposure to PM2.5 has consistently been found to be associated with increased cardiovascular morbidity and mortality. Although adult exposure to traffic related PM2.5, which is largely derived from diesel exhaust (DE), has been associated with increased cardiac hypertrophy, there are limited investigations into the potential effect of in utero and early life exposure on adult susceptibility to heart disease. In this study, we investigate the effect of in utero and early life exposure to DE on adult susceptibility to heart failure., Methods: Female C57BL/6 J mice were exposed to either filtered air (FA) or DE for 3 weeks (≈ 300 μg/m3 PM2.5 for 6 hours/day, 5 days/week) and then introduced to male breeders for timed matings. Female mice were exposed to either FA or DE throughout pregnancy and until offspring were 3 weeks of age. Offspring were then transferred to either FA or DE for an additional 8 weeks of exposure. At 12 weeks of age, male offspring underwent a baseline echocardiographic assessment, followed by a sham or transverse aortic constriction (TAC) surgery to induce pressure overload. Following sacrifice three weeks post surgery, ventricles were processed for histology to assess myocardial fibrosis and individual cardiomyocyte hypertrophy. mRNA from lung tissue was isolated to measure expression of inflammatory cytokines IL6 and TNFα., Results: We observed that mice exposed to DE during in utero and early life development have significantly increased susceptibility to cardiac hypertrophy, systolic failure, myocardial fibrosis, and pulmonary congestion following TAC surgery compared to FA control, or adult DE exposed mice. In utero and early life DE exposure also strongly modified the inflammatory cytokine response in the adult lung., Conclusions: We conclude that exposure to diesel exhaust air pollution during in utero and early life development in mice increases adult susceptibility to heart failure. The results of this study may imply that the effects of air pollution on cardiovascular disease in human populations may be strongly mediated through a 'fetal origins' of adult disease pathway. Further investigations on this potential pathway of disease are warranted.

Context: Inhalation of fine particulate matter (PM₂.₅) is associated with acute pulmonary inflammation and impairments in cardiovascular function. In many regions, PM₂.₅ is largely derived from diesel exhaust (DE), and these pathophysiological effects may be due in part to oxidative stress resulting from DE inhalation. The antioxidant glutathione (GSH) is important in limiting oxidative stress-induced vascular dysfunction. The rate-limiting enzyme in GSH synthesis is glutamate cysteine ligase and polymorphisms in its catalytic and modifier subunits (GCLC and GCLM) have been shown to influence vascular function and risk of myocardial infarction in humans., Objective: We hypothesized that compromised de novo synthesis of GSH in Gclm⁻/⁺ mice would result in increased sensitivity to DE-induced lung inflammation and vascular effects., Materials and Methods: WT and Gclm⁻/⁺ mice were exposed to DE via inhalation (300 μg/m³) for 6 h. Neutrophil influx into the lungs, plasma GSH redox potential, vascular reactivity of aortic rings and aortic nitric oxide (NO•) were measured., Results: DE inhalation resulted in mild bronchoalveolar neutrophil influx in both genotypes. DE-induced effects on plasma GSH oxidation and acetylcholine (ACh)-relaxation of aortic rings were only observed in Gclm⁻/⁺ mice. Contrary to our hypothesis, DE exposure enhanced ACh-induced relaxation of aortic rings in Gclm⁻/⁺ mice., Discussion and Conclusion: THESE data support the hypothesis that genetic determinants of antioxidant capacity influence the biological effects of acute inhalation of DE. However, the acute effects of DE on the vasculature may be dependent on the location and types of vessels involved. Polymorphisms in GSH synthesis genes are common in humans and further investigations into these potential gene-environment interactions are warranted.

Exposure to traffic-related air pollution is associated with risk of cardiovascular disease and mortality. We examined whether exposure to diesel exhaust increased blood pressure (BP) in human subjects. We analyzed data from 45 nonsmoking subjects, 18 to 49 years of age in double-blinded, crossover exposure studies, randomized to order. Each subject was exposed to diesel exhaust, maintained at 200 μg/m(3) of fine particulate matter, and filtered air for 120 minutes on days separated by ≥2 weeks. We measured BP pre-exposure, at 30-minute intervals during exposure, and 3, 5, 7, and 24 hours from exposure initiation and analyzed changes from pre-exposure values. Compared with filtered air, systolic BP increased at all of the points measured during and after diesel exhaust exposure; the mean effect peaked between 30 and 60 minutes after exposure initiation (3.8 mm Hg [95% CI: -0.4 to 8.0 mm Hg] and 5.1 mm Hg [95% CI: 0.7-9.5 mm Hg], respectively). Sex and metabolic syndrome did not modify this effect. Combining readings between 30 and 90 minutes, diesel exhaust exposure resulted in a 4.4-mm Hg increase in systolic BP, adjusted for participant characteristics and exposure perception (95% CI: 1.1-7.7 mm Hg; P=0.0009). There was no significant effect on heart rate or diastolic pressure. Diesel exhaust inhalation was associated with a rapid, measurable increase in systolic but not diastolic BP in young nonsmokers, independent of perception of exposure. This controlled trial in humans confirms findings from observational studies. The effect may be important on a population basis given the worldwide prevalence of exposure to traffic-related air pollution.

There is considerable debate regarding inhaled diesel exhaust particulate (DEP) causing impairments in vascular reactivity. Although there is evidence that inhaled particles can translocate from the lung into the systemic circulation, it has been suggested that inflammatory factors produced in the lung following macrophage particle engulfment also pass into the circulation. To investigate these differing hypotheses, we used in vitro systems to model each exposure. By using a direct exposure system and a macrophage-endothelial cell co-culture model, we compared the effects of direct DEP exposure and exposure to inflammatory factors produced by DEP-treated macrophages, on endothelial cell mRNA levels for eNOS, iNOS, endothelin-1, and endothelin-converting-enzyme-1. As markers of oxidative stress, we measured the effects of DEP treatment on glutathione (GSH) synthesis genes and on total GSH. In addition, we analyzed the effect of DEP treatment on monocyte chemo-attractant protein-1. Direct DEP exposure increased endothelial GCLC and GCLM as well as total GSH in addition to increased eNOS, iNOS, and Mcp1 mRNA. Alternatively, inflammatory factors released from DEP-exposed macrophages markedly up-regulated endothelial iNOS and Mcp1 while modestly down-regulating eNOS. These data support both direct exposure to DEP and the release of inflammatory cytokines as explanations for DEP-induced impairments in vascular reactivity., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Context: Inhalation of ambient fine particulate matter (PM₂.₅) is associated with adverse respiratory and cardiovascular effects. A major fraction of PM₂.₅ in urban settings is diesel exhaust particulate (DEP), and DEP-induced lung inflammation is likely a critical event mediating many of its adverse health effects. Oxidative stress has been proposed to be an important factor in PM₂.₅-induced lung inflammation, and the balance between pro- and antioxidants is an important regulator of this inflammation. An important intracellular antioxidant is the tripeptide thiol glutathione (GSH). Glutamate cysteine ligase (GCL) carries out the first step in GSH synthesis. In humans, relatively common genetic polymorphisms in both the catalytic (Gclc) and modifier (Gclm) subunits of GCL have been associated with increased risk for lung and cardiovascular diseases., Objective: This study was aimed to determine the effects of Gclm expression on lung inflammation following DEP exposure in mice., Materials and Methods: We exposed Gclm wild type, heterozygous, and null mice to DEP via intranasal instillation and assessed lung inflammation as determined by neutrophils and inflammatory cytokines in lung lavage, inflammatory cytokine mRNA levels in lung tissue, as well as total lung GSH, Gclc, and Gclm protein levels., Results: The Gclm heterozygosity was associated with a significant increase in DEP-induced lung inflammation when compared to that of wild type mice., Discussion and Conclusion: This finding indicates that GSH synthesis can mediate DEP-induced lung inflammation and suggests that polymorphisms in Gclm may be an important factor in determining adverse health outcomes in humans following inhalation of PM₂.₅.

Hourly averaged particle size distributions measured at a centrally located urban site in Seattle were analyzed through the application of bilinear positive matrix factorization (PMF) and Unmix to study underlying size distributions and their daily patterns. A total of 1051 samples each with 16 size intervals from 20 to 400 nm were obtained from a differential mobility particle sizer operating between December 2000 and February 2001. Both PMF and Unmix identify four similar underlying factors in the size distributions. Factor 1 is an accumulation mode particle size spectrum that shows a regular nocturnal pattern, and factor 2 is a larger particle distribution. Factor 3 is assigned as a traffic-related particle distribution, based on its correlations with accompanying gas-phase measurements, and has a regular weekday-high rush-hour pattern. Factor 4 is a traffic-related particle size distribution that has a regular rush-hour pattern on weekdays as well as weekends. Conditional probability functions (CPF) were computed using wind profiles and factor contributions. The results of CPF analysis suggest that these factors are correlated with surrounding particle sources of wood burning, secondary aerosol, diesel emissions, and motor vehicle emissions.