Abstract  BACKGROUND: Short-term exposure to elevated air pollution has been associated with higher risk of acute cardiovascular diseases, with systemic oxidative stress induced by air pollution hypothesized as an important underlying mechanism. However, few community-based studies have assessed this association.

METHODS AND RESULTS: Two thousand thirty-five Framingham Offspring Cohort participants living within 50 km of the Harvard Boston Supersite who were not current smokers were included. We assessed circulating biomarkers of oxidative stress including blood myeloperoxidase at the seventh examination (1998-2001) and urinary creatinine-indexed 8-epi-prostaglandin F2α (8-epi-PGF2α) at the seventh and eighth (2005-2008) examinations. We measured fine particulate matter (PM2.5), black carbon, sulfate, nitrogen oxides, and ozone at the Supersite and calculated 1-, 2-, 3-, 5-, and 7-day moving averages of each pollutant. Measured myeloperoxidase and 8-epi-PGF2α were loge transformed. We used linear regression models and linear mixed-effects models with random intercepts for myeloperoxidase and indexed 8-epi-PGF2α, respectively. Models were adjusted for demographic variables, individual- and area-level measures of socioeconomic position, clinical and lifestyle factors, weather, and temporal trend. We found positive associations of PM2.5 and black carbon with myeloperoxidase across multiple moving averages. Additionally, 2- to 7-day moving averages of PM2.5 and sulfate were consistently positively associated with 8-epi-PGF2α. Stronger positive associations of black carbon and sulfate with myeloperoxidase were observed among participants with diabetes than in those without.

CONCLUSIONS: Our community-based investigation supports an association of select markers of ambient air pollution with circulating biomarkers of oxidative stress.

Abstract  TEMPO was selected in 2012 by NASA as the first Earth Venture Instrument, for launch between 2018 and 2021. It will measure atmospheric pollution for greater North America from space using ultraviolet and visible spectroscopy. TEMPO observes from Mexico City, Cuba, and the Bahamas to the Canadian oil sands, and from the Atlantic to the Pacific, hourly and at high spatial resolution (~2.1 km N/S×4.4 km E/W at 36.5°N, 100°W). TEMPO provides a tropospheric measurement suite that includes the key elements of tropospheric air pollution chemistry, as well as contributing to carbon cycle knowledge. Measurements are made hourly from geostationary (GEO) orbit, to capture the high variability present in the diurnal cycle of emissions and chemistry that are unobservable from current low-Earth orbit (LEO) satellites that measure once per day. The small product spatial footprint resolves pollution sources at sub-urban scale. Together, this temporal and spatial resolution improves emission inventories, monitors population exposure, and enables effective emission-control strategies. TEMPO takes advantage of a commercial GEO host spacecraft to provide a modest cost mission that measures the spectra required to retrieve ozone (O3), nitrogen dioxide (NO2), sulfur dioxide (SO2), formaldehyde (H2CO), glyoxal (C2H2O2), bromine monoxide (BrO), IO (iodine monoxide), water vapor, aerosols, cloud parameters, ultraviolet radiation, and foliage properties. TEMPO thus measures the major elements, directly or by proxy, in the tropospheric O3 chemistry cycle. Multi-spectral observations provide sensitivity to O3 in the lowermost troposphere, substantially reducing uncertainty in air quality predictions. TEMPO quantifies and tracks the evolution of aerosol loading. It provides these near-real-time air quality products that will be made publicly available. TEMPO will launch at a prime time to be the North American component of the global geostationary constellation of pollution monitoring together with the European Sentinel-4 (S4) and Korean Geostationary Environment Monitoring Spectrometer (GEMS) instruments.

Abstract  Gaseous and particle emissions from construction engines contribute an important fraction of the total air pollutants released into the atmosphere and are gaining increasing regulatory attention. Robust quantification of nitrogen oxides (NOX) and particulate matter (PM) emissions are necessary to inventory the contribution of construction equipment to atmospheric loadings. Theses emission inventories require emissions factors from construction equipment as a function of equipment type and modes of operation. While the development of portable emissions measurement systems (PEMS) has led to increased studies of construction equipment emissions, emissions data are still much more limited than for on-road vehicles. The goal of this research program was to obtain accurate in-use emissions data from a test fleet of newer construction equipment (model year 2002 or later) using a Code of Federal Requirements (CFR) compliant PEMS system. In-use emission measurements were made from twenty-seven pieces of construction equipment, which included four backhoes, six wheel loaders, four excavators, two scrapers (one with two engines), six bulldozers, and four graders. The engines ranged in model year from 2003 to 2012, in rated horsepower (hp) from 92 to 540 hp, and in hours of operation from 24 to 17,149 h. This is the largest study of off-road equipment emissions using 40 CFR part 1065 compliant PEMS equipment for all regulated gaseous and particulate emissions. Published by Elsevier Ltd.

Abstract  BACKGROUND: Studies have linked ambient air pollution to chronic obstructive pulmonary disease (COPD) healthcare encounters. However, the association between air quality and rescue medication use is unknown.

OBJECTIVES: We assessed the role of air pollution exposure for increased short-acting beta-2-agonist (SABA) use in patients with COPD through use of remote monitoring technology.

METHODS: Participants received a portable electronic inhaler sensor to record the date, time and location for SABA use over a 3-month period. Ambient air pollution data and meteorological data were collected from a centrally located federal monitoring station. Mixed-effects Poisson regression was used to examine the association of daily inhaler use with pollutant levels. Four criteria pollutants (PM2.5, PM10, O3and NO2), two particulate matter species (elemental carbon (EC) and organic carbon), estimated coarse fraction of PM10(PM10-2.5) and four multipollutant air quality measures were each examined separately, adjusting for covariates that passed a false discovery rate (FDR) screening.

RESULTS: We enrolled 35 patients with COPD (94.3% male and mean age: 66.5±8.5) with a mean forced expiratory volume in 1 s (FEV1) % predicted of 44.9+17.2. Participants had a median of 92 observation days (range 52-109). Participants' average SABA inhaler use ranged from 0.4 to 13.1 puffs/day (median 2.8). Controlling for supplemental oxygen use, long-acting anticholinergic use, modified Medical Research Council Dyspnoea Scale and influenza season, an IQR increase in PM10concentration (8.0 µg/m3) was associated with a 6.6% increase in daily puffs (95% CI 3.5% to 9.9%; FDR <0.001). NO2and EC concentration were also significantly associated with inhaler use (3.9% and 2.9% per IQR increase, respectively).

CONCLUSIONS: Exposure to increased ambient air pollution were associated with a significant increase in SABA use for patients with COPD residing in a low-pollution area.

Abstract  BACKGROUND: Evidence for associations between ambient air pollution and preterm birth and stillbirth is inconsistent. Road traffic produces both air pollutants and noise, but few studies have examined these co-exposures together and none to date with all-cause or cause-specific stillbirths.

OBJECTIVES: To analyse the relationship between long-term exposure to air pollution and noise at address level during pregnancy and risk of preterm birth and stillbirth.

METHODS: The study population comprised 581,774 live and still births in the Greater London area, 2006-2010. Outcomes were preterm birth (<37 completed weeks gestation), all-cause stillbirth and cause-specific stillbirth. Exposures during pregnancy to particulate matter with diameter <2.5 μm (PM2.5) and <10 μm (PM10), ozone (O3), primary traffic air pollutants (nitrogen dioxide, nitrogen oxides, PM2.5 from traffic exhaust and traffic non-exhaust), and road traffic noise were estimated based on maternal address at birth.

RESULTS: An interquartile range increase in O3 exposure was associated with elevated risk of preterm birth (OR 1.15 95% CI: 1.11, 1.18, for both Trimester 1 and 2), all-cause stillbirth (Trimester 1 OR 1.17 95% CI: 1.07, 1.27; Trimester 2 OR 1.20 95% CI: 1.09, 1.32) and asphyxia-related stillbirth (Trimester 1 OR 1.22 95% CI: 1.01, 1.49). Odds ratios with the other air pollutant exposures examined were null or <1, except for primary traffic non-exhaust related PM2.5, which was associated with 3% increased odds of preterm birth (Trimester 1) and 7% increased odds stillbirth (Trimester 1 and 2) when adjusted for O3. Elevated risk of preterm birth was associated with increasing road traffic noise, but only after adjustment for certain air pollutant exposures.

DISCUSSION: Our findings suggest that exposure to higher levels of O3 and primary traffic non-exhaust related PM2.5 during pregnancy may increase risk of preterm birth and stillbirth; and a possible relationship between long-term traffic-related noise and risk of preterm birth. These findings extend and strengthen the evidence base for important public health impacts of ambient ozone, particulate matter and noise in early life.

Abstract  The respiratory epithelium provides a physical, functional, and immunologic barrier to protect the host from the potential harming effects of inhaled environmental particles and to guarantee maintenance of a healthy state of the host. When compromised, activation of immune/inflammatory responses against exogenous allergens, microbial substances, and pollutants might occur, rendering individuals prone to develop chronic inflammation as seen in allergic rhinitis, chronic rhinosinusitis, and asthma. The airway epithelium in asthma and upper airway diseases is dysfunctional due to disturbed tight junction formation. By putting the epithelial barrier to the forefront of the pathophysiology of airway inflammation, different approaches to diagnose and target epithelial barrier defects are currently being developed. Using single-cell transcriptomics, novel epithelial cell types are being unraveled that might play a role in chronicity of respiratory diseases. We here review and discuss the current understandings of epithelial barrier defects in type 2-driven chronic inflammation of the upper and lower airways, the estimated contribution of these novel identified epithelial cells to disease, and the current clinical challenges in relation to diagnosis and treatment of allergic rhinitis, chronic rhinosinusitis, and asthma.

Abstract  PURPOSE: Variables in observational studies are commonly subject to measurement error, but the impact of such errors is frequently ignored. As part of the STRengthening Analytical Thinking for Observational Studies Initiative, a task group on measurement error and misclassification seeks to describe the current practice for acknowledging and addressing measurement error.

METHODS: Task group on measurement error and misclassification conducted a literature survey of four types of research studies that are typically impacted by exposure measurement error: (1) dietary intake cohort studies, (2) dietary intake population surveys, (3) physical activity cohort studies, and (4) air pollution cohort studies.

RESULTS: The survey revealed that while researchers were generally aware that measurement error affected their studies, very few adjusted their analysis for the error. Most articles provided incomplete discussion of the potential effects of measurement error on their results. Regression calibration was the most widely used method of adjustment.

CONCLUSIONS: Methods to correct for measurement error are available but require additional data regarding the error structure. There is a great need to incorporate such data collection within study designs and improve the analytical approach. Increased efforts by investigators, editors, and reviewers are needed to improve presentation of research when data are subject to error.

Abstract  This work presents a new high-resolution NO2 dataset derived from the NASA Ozone Monitoring Instrument (OMI) NO2 version 3.0 retrieval that can be used to estimate surface-level concentrations. The standard NASA product uses NO2 vertical profile shape factors from a 1.25 degrees x 1 degrees (similar to 110 km x 110 km) resolution Global Model Initiative (GMI) model simulation to calculate air mass factors, a critical value used to determine observed tropospheric NO2 vertical columns. To better estimate vertical profile shape factors, we use a high-resolution (1.33 km x 1.33 km) Community Multi-scale Air Quality (CMAQ) model simulation constrained by in situ aircraft observations to recalculate tropospheric air mass factors and tropospheric NO2 vertical columns during summertime in the eastern US. In this new product, OMI NO2 tropospheric columns increase by up to 160% in city centers and decrease by 20-50% in the rural areas outside of urban areas when compared to the operational NASA product. Our new product shows much better agreement with the Pandora NO2 and Airborne Compact Atmospheric Mapper (ACAM) NO2 spectrometer measurements acquired during the DISCOVER-AQ Maryland field campaign. Furthermore, the correlation between our satellite product and EPA NO2 monitors in urban areas has improved dramatically: r(2) = 0.60 in the new product vs. r(2) = 0.39 in the operational product, signifying that this new product is a better indicator of surface concentrations than the operational product. Our work emphasizes the need to use both high-resolution and high-fidelity models in order to recalculate satellite data in areas with large spatial heterogeneities in NO x emissions. Although the current work is focused on the eastern US, the methodology developed in this work can be applied to other world regions to produce high-quality region-specific NO2 satellite retrievals.

Abstract  Whether exposure to outdoor air pollution increases the prevalence of rhinoconjunctivitis in children is unclear. Using data from Phase Three of the International Study of Asthma and Allergies in childhood (ISAAC), we investigated associations of rhinoconjunctivitis prevalence in adolescents with model-based estimates of ozone, and satellite-based estimates of fine (diameter < 2.5 μm) particulate matter (PM2.5) and nitrogen dioxide (NO2). Information on rhinoconjunctivitis (defined as self-reported nose symptoms without a cold or flu accompanied by itchy watery eyes in the past 12 months) was available on 505,400 children aged 13-14 years, in 183 centres in 83 countries. Centre-level prevalence estimates were calculated and linked geographically with estimates of long-term average concentrations of NO2, ozone and PM2.5. Multi-level models were fitted adjusting for population density, climate, sex and gross national income. Information on parental smoking, truck traffic and cooking fuel was available for a restricted set of centres (77 in 36 countries). Between centres within countries, the estimated change in rhinoconjunctivitis prevalence per 100 children was 0.171 (95% confidence interval: - 0.013, 0.354) per 10% increase in PM2.5, 0.096 (- 0.003, 0.195) per 10% increase in NO2 and - 0.186 (- 0.390, 0.018) per 1 ppbV increase in ozone. Between countries, rhinoconjunctivitis prevalence was significantly negatively associated with both ozone and PM2.5. In the restricted dataset, the latter association became less negative following adjustment for parental smoking and open fires for cooking. In conclusion, there were no significant within-country associations of rhinoconjunctivitis prevalence with study pollutants. Negative between-country associations with PM2.5 and ozone require further investigation.

Abstract  Although outdoor air pollution and particulate matter in outdoor air have been consistently linked with increased lung cancer risk, the evidence for associations at other cancer sites is limited. Bladder cancer shares several risk factors with lung cancer and some positive associations of ambient air pollution and bladder cancer risk have been observed. This study examined associations of ambient air pollution and bladder cancer risk in the large-scale Spanish Bladder Cancer Study. Estimates of ambient fine particulate matter (PM2.5 ) and nitrogen dioxide (NO2 ) concentrations were assigned to the geocoded participant residence of 938 incident bladder cancer cases and 973 hospital controls based on European multicity land-use regression models. Adjusted odds ratios (ORs) and 95% confidence intervals (CI) for associations of ambient air pollution and bladder cancer risk were estimated using unconditional logistic regression models. Overall, there was no clear association between either ambient PM2.5 (OR per 5.9 μg/m3  = 1.06, 95% CI 0.71-1.60) or NO2 (OR per 14.2 μg/m3  = 0.97, 95% CI 0.84-1.13) concentrations and incident bladder cancer risk. There was no clear evidence for effect modification according to age group, sex, region, education, cigarette smoking status, or pack-years. Results were also similar among more residentially stable participants and in two-pollutant models. Overall, there was no clear evidence for associations of ambient PM2.5 and NO2 concentrations and incident bladder cancer risk. Further research in other large-scale population studies is needed with detailed information on measured or modeled estimates of ambient air pollution concentrations and individual level risk factors.

Abstract  BACKGROUND: Air pollution has many adverse health effects, but the combined or synergistic effects of multiple ambient air pollutants on anti-nuclear antibodies (ANA, a serologic marker of systemic autoimmune rheumatic disease, SARDs) have never been assessed.

OBJECTIVE: To flexibly model ANA and individual and joint associations of long-term exposures to nitrogen dioxide (NO2), ozone (O3), and fine particles matter (PM2.5) using a Bayesian Kernel machine regression (BKMR) approach and to compare the results to those from individual logistic regressions.

METHODS: Serum ANA positivity was determined for randomly selected CARTaGENE general population subjects in Quebec, Canada. CARTaGENE is a public research platform created for investigating the associations of environmental, genomic, and lifestyle factors on chronic diseases. Ambient NO2, O3, and PM2.5 estimates, derived from ground-measurement and chemical-transport-model simulated concentrations, were assigned to subjects based on residential postal codes at the time of blood collection. Our models adjusted for age, sex, French Canadian origin, smoking, and family income.

RESULTS: Concentrations of NO2, O3, and PM2.5 were closely correlated in space. In the 5485 CARTaGENE subjects studied, we did not see clear associations between NO2, PM2.5 or O3 and ANA positivity, with either the BKMR or logistic models.

CONCLUSIONS: BKMR did not uncover associations between ANA positivity and individual levels or combined exposures of NO2, O3, and PM2.5; neither did simpler logistic models. Additional studies (in younger populations, in distinct race/ethnicity groups, and/or in jurisdictions with high air pollution levels) would be helpful to reinforce current findings.

Abstract  Strain a/j mice were exposed by inhalation for 6 hours/day, 5 days/week, for six months to carbon disulfide, 1,2-dibromoethane, ethylene oxide, naphthalene, nitrogen dioxide, or vinyl chloride. Significant increases in pulmonary adenoma formation were observed following exposure to 300 ppm carbon disulfide; 20 and 50 ppm 1,2-dibromoethane; 70 and 200 ppm ethylene oxide; 10 ppm no 2; and 50, 200, and 500 ppm vinyl chloride compared with control animals. Exposure of mice to 30 ppm naphthalene did not elicit a significant adenoma response. The results provide further information for the validation of this in vivo model as a tool for predicting oncogenic potential following chemical exposure.

Abstract  Background: Despite recent studies linking air pollution to neurodegenerative illness, evidence relating air pollution and Parkinson's disease (PD) remains scarce. We conducted a population-based cohort study in Ontario, Canada, to determine the association between air pollution and incident PD.

Methods: Using health administrative databases, we identified all adults aged 55-85 years, free of PD, and who lived in Ontario on 1 April 2001 (∼2.2 million). Individuals were followed up until 31 March 2013. We derived long-term average exposures to fine particulate matter (particles ≤2.5 µm in diameter, or PM2.5), nitrogen dioxide (NO2) and ozone from satellite-based estimates, land-use regression models and optimal interpolation methods, respectively. Using 2-year lags in exposures, we linked these estimates to individuals' annual postal codes from 1994 (7 years before cohort inception). We applied spatial random-effects Cox proportional hazards models, adjusting for individual- and area-level characteristics. We also performed sensitivity analyses, such as considering longer lags in exposures and stratifying by selected characteristics.

Results: During the study period, we identified 38 745 newly diagnosed cases of PD. Each interquartile increment (3.8 µg/m3) of PM2.5 was associated with a 4% increase in incident PD (95% confidence interval, 1.01-1.08) after adjusting for various covariates. We also found positive associations for NO2 and ozone [hazard ratios (HRs) ranged from 1.03 to 1.04]. The associations for all exposures were unaltered with various sensitivity analyses except for considering longer lags, which somewhat attenuated the estimates, particularly for NO2 and ozone.

Conclusions: Exposure to air pollution, especially PM2.5, was found to be related to incident PD.

Abstract  Urban ozone (O3) pollution is influenced by the transport of wildfire smoke but observed impacts are highly variable. We investigate O3 impacts from smoke in 18 western US cities during July-September, 2013-2017, with ground-based monitoring data from Air Quality System sites, using satellite-based Hazard Mapping System (HMS) Fire and Smoke Product to identify overhead smoke. We present four key findings. First, O3 and PM2.5 (particulate matter < 2.5 µm in diameter) are elevated at nearly all sites on days influenced by smoke, with the greatest mean enhancement occurring during multi-day smoke events; nitrogen oxides (NOx) are not consistently elevated across all sites. Second, PM2.5 and O3 exhibit a nonlinear relationship such that O3 increases with PM2.5 at low to moderate 24-h PM2.5, peaks around 30-50 μg m-3, and declines at higher PM2.5. Third, the rate of increase of morning O3 is higher and NO/NO2 ratios are lower on smoke-influenced days, which could result from additional atmospheric oxidants in smoke. Fourth, while the HMS product is a useful tool for identifying smoke, O3 and PM2.5 are elevated on days before and after HMS-identified smoke events implying that a significant fraction of smoke events is not detected.

Abstract  The TROPOspheric Monitoring Instrument (TROPOMI) is used to derive top-down NOX emissions for two large power plants and three megacities in North America. We first re-process the vertical column NO2 with an improved air mass factor to correct for a known systematic low bias in the operational retrieval near urban centers. For the two power plants, top-down NOX emissions agree to within 10% of the emissions reported by the power plants. We then derive top-down NOX emissions rates for New York City, Chicago, and Toronto, and compare them to projected bottom-up emissions inventories. In this analysis of 2018 NOX emissions, we find a +22% overestimate for New York City, a −21% underestimate in Toronto, and good agreement in Chicago in the projected bottom-up inventories when compared to the top-down emissions. Top-down NOX emissions also capture intraseasonal variability, such as the weekday versus weekend effect (emissions are +45% larger on weekdays versus weekends in Chicago). Finally, we demonstrate the enhanced capabilities of TROPOMI, which allow us to derive a NOX emissions rate for Chicago using a single overpass on July 7, 2018. The large signal-to-noise ratio of TROPOMI is well-suited for estimating NOX emissions from relatively small sources and for sub-seasonal timeframes.

Abstract  Background Air pollution has been suggested as a risk factor for chronic obstructive pulmonary disease (COPD), but evidence is sparse and inconsistent. Objectives We examined the association between long-term exposure to low-level air pollution and COPD incidence. Methods Within the ‘Effects of Low-Level Air Pollution: A Study in Europe’ (ELAPSE) study, we pooled data from three cohorts, from Denmark and Sweden, with information on COPD hospital discharge diagnoses. Hybrid land use regression models were used to estimate annual mean concentrations of particulate matter with a diameter < 2.5 µm (PM2.5), nitrogen dioxide (NO2), and black carbon (BC) in 2010 at participants’ baseline residential addresses, which were analysed in relation to COPD incidence using Cox proportional hazards models. Results Of 98,058 participants, 4,928 developed COPD during 16.6 years mean follow-up. The adjusted hazard ratios (HRs) and 95% confidence intervals for associations with COPD incidence were 1.17 (1.06, 1.29) per 5 µg/m3 for PM2.5, 1.11 (1.06, 1.16) per 10 µg/m3 for NO2, and 1.11 (1.06, 1.15) per 0.5 10−5m−1 for BC. Associations persisted in subset participants with PM2.5 or NO2 levels below current EU and US limit values and WHO guidelines, with no evidence for a threshold. HRs for NO2 and BC remained unchanged in two-pollutant models with PM2.5, whereas the HR for PM2.5 was attenuated to unity with NO2 or BC. Conclusions Long-term exposure to low-level air pollution is associated with the development of COPD, even below current EU and US limit values and possibly WHO guidelines. Traffic-related pollutants NO2 and BC may be the most relevant.

Abstract  The interrelationships among long-term ambient air pollution exposure, emotional distress and cognitive decline in older adulthood remain unclear. Long-term exposure may impact cognitive performance and subsequently impact emotional health. Conversely, exposure may initially be associated with emotional distress followed by declines in cognitive performance. Here we tested the inter-relationship between global cognitive ability, emotional distress, and exposure to PM2.5 (particulate matter with aerodynamic diameter <2.5 μm) and NO2 (nitrogen dioxide) in 6118 older women (aged 70.6 ± 3.8 years) from the Women’s Health Initiative Memory Study. Annual exposure to PM2.5 (interquartile range [IQR] = 3.37 μg/m3) and NO2 (IQR = 9.00 ppb) was estimated at the participant’s residence using regionalized national universal kriging models and averaged over the 3-year period before the baseline assessment. Using structural equation mediation models, a latent factor capturing emotional distress was constructed using item-level data from the 6-item Center for Epidemiological Studies Depression Scale and the Short Form Health Survey Emotional Well-Being scale at baseline and one-year follow-up. Trajectories of global cognitive performance, assessed by the Modified-Mini Mental State Examination (3MS) annually up to 12 years, were estimated. All effects reported were adjusted for important confounders. Increases in PM2.5 (β = -0.144 per IQR; 95% CI = −0.261; −0.028) and NO2 (β = −0.157 per IQR; 95% CI = −0.291; −0.022) were associated with lower initial 3MS performance. Lower 3MS performance was associated with increased emotional distress (β = −0.008; 95% CI = −0.015; −0.002) over the subsequent year. Significant indirect effect of both exposures on increases in emotional distress mediated by exposure effects on worse global cognitive performance were present. No statistically significant indirect associations were found between exposures and 3MS trajectories putatively mediated by baseline emotional distress. Our study findings support cognitive aging processes as a mediator of the association between PM2.5 and NO2 exposure and emotional distress in later-life.

Abstract  Air pollution epidemiological studies often use outdoor concentrations from central-site monitors as exposure surrogates, which can induce measurement error. The goal of this study was to improve exposure assessments of ambient fine particulate matter (PM2.5), elemental carbon (EC), nitrogen oxides (NOx), and carbon monoxide (CO) for a repeated measurements study with 15 individuals with coronary artery disease in central North Carolina called the Coronary Artery Disease and Environmental Exposure (CADEE) Study. We developed a fine-scale exposure modeling approach to determine five tiers of individual-level exposure metrics for PM2.5, EC, NOx, CO using outdoor concentrations, on-road vehicle emissions, weather, home building characteristics, time-locations, and time-activities. We linked an urban-scale air quality model, residential air exchange rate model, building infiltration model, global positioning system (GPS)-based microenvironment model, and accelerometer-based inhaled ventilation model to determine residential outdoor concentrations (Cout_home, Tier 1), residential indoor concentrations (Cin_home, Tier 2), personal outdoor concentrations (Cout_personal, Tier 3), exposures (E, Tier 4), and inhaled doses (D, Tier 5). We applied the fine-scale exposure model to determine daily 24-h average PM2.5, EC, NOx, CO exposure metrics (Tiers 1-5) for 720 participant-days across the 25 months of CADEE. Daily modeled metrics showed considerable temporal and home-to-home variability of Cout_home and Cin_home (Tiers 1-2) and person-to-person variability of Cout_personal, E, and D (Tiers 3-5). Our study demonstrates the ability to apply an urban-scale air quality model with an individual-level exposure model to determine multiple tiers of exposure metrics for an epidemiological study, in support of improving health risk assessments.

Abstract  Background: Adverse birth outcomes are more frequent among mothers with inflammatory bowel diseases (IBDs) than non-IBD mothers. In recent studies, air pollution, such as high concentrations of nitrogen dioxide (NO2), is reckoned as a risk factor for preterm birth in the general population. In this study, we investigated whether IBD mothers are at higher risk of preterm birth when exposed to NO2 compared to non-IBD mothers.Methods: We used information from the Norwegian Mother, Father and Child Cohort Study (MoBa). The pregnancy cohort was linked to the Norwegian Medical Birth Registry and air-pollution exposure data available from a subset of the study cohort. The relevant outcome in this study was preterm birth. A total of 16,170 non-IBD and 92 IBD mothers were included in the study.Results: The mean exposure of NO2 during the pregnancy was similar for IBD and non-IBD mothers, 13.7 (6.9) μg/m3 and 13.6 (4.2) μg/m3, respectively.IBD mothers with higher exposure of NO2 in the second and third trimester were at significant risk of preterm birth compared to non-IBD mothers [OR = 1.28 (CI 95%: 1.04-1.59) and OR = 1.23 (95% CI: 1.06-1.43), respectively]. The mean NO2 exposure was significantly higher in IBD mothers with preterm birth than in IBD mothers who delivered at term, at 19.58 (1.57) μg/m3 and 12.89 (6.37) μg/m3, respectively.Conclusions: NO2 exposure influenced the risk of preterm birth in IBD mothers. Higher risk of preterm birth in IBD was associated with higher exposure of NO2, suggesting vulnerability of preterm birth in IBD when exposed to NO2.

Abstract  BACKGROUND: The Child-Mother binomial is potentially susceptible to the toxic effects of pollutants because some chemicals interfere with placental transfer of nutrients, thus affecting fetal development, and create an increased the risk of low birth weight, prematurity and intrauterine growth restriction.

OBJECTIVE: To evaluate the impact of prenatal exposure to nitrogen oxides (NOx) on birth weight in a cohort of Mexican newborns.

METHODOLOGY: We included 745 mother-child pair participants of the POSGRAD cohort study. Information on socio-demographic characteristics, obstetric history, health history and environmental exposure during pregnancy were readily available and the newborns' anthropometric measurements were obtained at delivery. Prenatal NOx exposure assessment was evaluated using a Land-Use Regression predictive models considering local monitoring from 60 sites on the State of Morelos. The association between prenatal exposure to NOx and birth weight was estimated using a multivariate linear regression models.

RESULTS: The average birth weight was 3217 ± 439 g and the mean of NOx concentration was 21 ppb (Interquartile range, IQR = 6.95 ppb). After adjusting for maternal age and other confounders, a significant birthweight reduction was observed for each IQR of NOx increase (ß = -39.61 g, 95% CI: -77.00; -2.21; p = 0.04).

CONCLUSIONS: Our results provides evidence that prenatal NOx exposure has a negative effect on birth weight, which may influence the growth and future development of the newborn.

Abstract  Epidemiological studies have reported significant associations of outdoor NO2 with daily mortality. These studies used ambient NO2 concentrations as a proxy of personal exposure of outdoor-originated NO2 (PEO NO2), which may lead to biased health effect estimates. This study was aiming to explore whether modified outdoor NO2 exposure can reduce this error. We performed a Monte Carlo simulation to estimate the outdoor-originated NO2 concentration in residential buildings in 271 Chinese cities from 2013 to 2015, and then PEO NO2 was obtained according to time-activity-location patterns of people. We adopted a typical time-series analysis to compare the mortality associations between PEO and outdoor NO2. The averaged concentrations of PEO and outdoor NO2 were 16.5 mu g/m(3) and 31.6 mu g/m(3), respectively. PEO NO2 showed a better model fitting and larger effect for its daily mortality association. A 10 mu g/m(3) increase in two-day moving average concentration of PEO and outdoor NO2 was associated with a 2.08% (1.70%, 2.45%) and 1.03% (0.83%, 1.22%) increase in total mortality, respectively. Our study revealed that personal exposure to NO2 modified from outdoor NO2 concentrations may better reflect the health effects of air pollutants, and such evidence might be useful for future policy making and air pollution regulations.

Abstract  BACKGROUND: Inter-mortality displacement (IMD) between cause-specific mortalities has not been introduced in air pollution epidemiology. Investigation into IMD would provide insights on the actual health burden of air pollution and interpretation of associations. We aimed to investigate IMD regarding short-term effect of air pollution on mortality.

METHODS: We illustrated manifestations and interpretations of lag-mortality associations. If IMD exists, a net increase of one cause-specific death can be offset by a net decrease of other cause-specific deaths. We conducted a time-series analysis to estimate associations of ambient particulate matter smaller than 10 µm (PM10), ozone (O3), sulphur dioxide (SO2), nitrogen dioxide (NO2) and carbon monoxide (CO) with mortality, considering lags up to the previous 45 days, for seven major cities of South Korea from 2006 to 2013. Attributable mortality cases were identified.

RESULTS: For O3, respiratory mortality [11 929 cases, 95% empirical confidence interval (eCI), 5358, 17 688 cases] was counterbalanced by cardiovascular mortality (-11 272 cases, 95% eCI: -22 444, -629 cases). All-cause mortality was 37 148 cases (95% eCI: 4448, 68 782 cases). For PM10, respiratory deaths were 9167 cases (95% eCI: 563, 16 521 cases), and cardiovascular deaths were 6929 cases (95% eCI: -11 793, 24 138 cases). Estimates for SO2 were comparable to those for PM10. All-cause mortality attributable to NO2 was explained by short-term mortality displacement. No associations with mortality were found for CO.

CONCLUSIONS: IMD may exist in the relationship between air pollution and mortality. The actual relationship between air pollution and cause-specific mortality may be masked by IMD.

Abstract  BACKGROUND: Cardiovascular malformations account for nearly one-third of all congenital anomalies, making these the most common type of birth defects. Little is known regarding the influence of ambient ultrafine particles (<0.1 μm) (UFPs) on their occurrence.

OBJECTIVE: This population-based study examined the association between prenatal exposure to UFPs and congenital heart defects (CHDs).

METHODS: A total of 158,743 singleton live births occurring in the City of Toronto, Canada between April 1st 2006 and March 31st 2012 were identified from a birth registry. Associations between exposure to ambient UFPs between the 2nd and 8th week post conception when the foetal heart begins to form and CHDs identified at birth were estimated using random-effects logistic regression models, adjusting for personal- and neighbourhood-level covariates. We also investigated multi-pollutant models accounting for co-exposures to PM2.5, NO2 and O3.

RESULTS: A total of 1468 CHDs were identified. In fully adjusted models, UFP exposures during weeks 2 to 8 of pregnancy were not associated with overall CHDs (Odds Ratio (OR) per interquartile (IQR) increase = 1.02, 95% CI: 0.96-1.08). When investigating subtypes of CHDs, UFP exposures were associated with ventricular septal defects (Odds Ratio (OR) per interquartile (IQR) increase = 1.13, 95% CI: 1.03-1.33), but not with atrial septal defect (Odds Ratio (OR) per interquartile (IQR) increase = 0.89, 95% CI: 0.74-1.06).

CONCLUSION: This is the first study to evaluate the association between prenatal exposure to UFPs and the risk of CHDs. UFP exposures during a critical period of embryogenesis were associated with an increased risk of ventricular septal defect.

Abstract  BACKGROUND: High-income nations have the highest rates of inflammatory bowel disease (IBD). The incidence of pediatric-onset IBD is increasing faster than IBD diagnosed in older individuals. Previous epidemiological studies have shown that air pollution might be a risk factor for development of earlier-onset IBD, but results remain mixed.

OBJECTIVES: The objective of this study was to evaluate the associations between maternal and early-life exposures to nitrogen dioxide (NO2), fine particulate matter (PM2.5), ozone (O3,) and oxidant capacity (Ox) and risk of pediatric-onset IBD diagnosis.

METHODS: We conducted a retrospective cohort study using linked population-based health administrative data. Singleton livebirths in Ontario, Canada between April 1st, 1991 and March 31st, 2014 were included. We investigated the association between weekly exposures during pregnancy and annual exposures from birth until the age of 18 years, and IBD diagnosed <18 years of age using Cox proportional hazards models. We reported hazard ratios (HR) and 95% confidence intervals (CI) for an associated increase in the interquartile range (IQR) of each pollutant. Models were mutually adjusted for exposures in both prenatal and postnatal periods, as well as for sex, rurality of residence at birth, maternal IBD, and neighborhood income.

RESULTS: 2,218,789 newborns were included in this study, of whom 2491 developed IBD during follow-up. Increased associations with pediatric-onset IBD were noted for childhood exposure to Ox (HR 1.08, 95% CI 1.01-1.16). IBD development was also associated with Ox during the second trimester (HR 1.21, 95% CI 1.03-1.42), but not the overall pregnancy period (HR 1.12, 95% CI 0.79-1.59). There were no associations of IBD with exposure to NO2, PM2.5, or O3.

DISCUSSION: Exposure to Ox during childhood was associated with IBD < 18 years. This suggests that air pollution may impact the developing child physiology in such a way that leads to early onset of IBD.

Abstract  Asthma affects millions of people globally and is especially concerning in populations living with poor air quality. This study examines the association of ambient outdoor air pollutants on asthma-related emergency department (ED) visits in children and adults throughout the Pittsburgh region. A time-stratified case-crossover design is used to analyze the lagged effects of fine particulate matter (PM2.5) and gaseous pollutants, e.g., ozone (O3), sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide (CO) on asthma-related ED visits (n = 6682). Single-, double-, and multi-pollutant models are adjusted for temperature and analyzed using conditional logistic regression. In children, all models show an association between O3 and increased ED visits at lag day 1 (OR: 1.12, 95% CI, 1.03-1.22, p < 0.05) for the double-pollutant model (OR: 1.10, 95% CI: 1.01-1.20, p < 0.01). In adults, the single-pollutant model shows associations between CO and increased ED visits at lag day 5 (OR: 1.13, 95% CI, 1.00-1.28, p < 0.05) and average lag days 0-5 (OR: 1.22, 95% CI: 1.00-1.49, p < 0.05), and for NO2 at lag day 5 (OR: 1.04, 95% CI: 1.00-1.07, p < 0.05). These results show an association between air pollution and asthma morbidity in the Pittsburgh region and underscore the need for mitigation efforts to improve public health outcomes.