Increase In NO2 Exposure Research Articles

Short-Term Nitrogen Dioxide Exposure and Emergency Hospital Admissions for Asthma in Children: A Case-Crossover Analysis in England.

There is an increasing body of evidence associating short-term ambient nitrogen dioxide (NO2) exposure with asthma-related hospital admissions in children. However, most studies have relied on temporally resolved exposure information, potentially ignoring the spatial variability of NO2. We aimed to investigate how daily NO2 estimates from a highly resolved spatio-temporal model are associated with the risk of emergency hospital admission for asthma in children in England. We conducted a time-stratified case-crossover study including 111,766 emergency hospital admissions for asthma in children (aged 0-14 years) between 1st January 2011 and 31st December 2015 in England. Daily NO2 levels were predicted at the patients' place of residence using spatio-temporal models by combining land use data and chemical transport model estimates. Conditional logistic regression models were used to obtain the odds ratios (OR) and confidence intervals (CI) after adjusting for temperature, relative humidity, bank holidays, and influenza rates. The effect modifications by age, sex, season, area-level income deprivation, and region were explored in stratified analyses. For each 10 µg/m³ increase in NO2 exposure, we observed an 8% increase in asthma-related emergency admissions using a five-day moving NO2 average (mean lag 0-4) (OR 1.08, 95% CI 1.06-1.10). In the stratified analysis, we found larger effect sizes for male (OR 1.10, 95% CI 1.07-1.12) and during the cold season (OR 1.10, 95% CI 1.08-1.12). The effect estimates varied slightly by age group, area-level income deprivation, and region. Short-term exposure to NO2 was significantly associated with an increased risk of asthma emergency admissions among children in England. Future guidance and policies need to consider reflecting certain proven modifications, such as using season-specific countermeasures for air pollution control, to protect the at-risk population.

The association between air pollution and dementia: results from the Cognitive Function and Ageing Study II and Wales

AbstractBackgroundAir pollution has been recognised as one of the key modifiable risk factors for dementia. In the UK, there is a lack of evidence from population‐based cohort studies including older people from different backgrounds and living environments. Using two multicentre ageing cohorts in England and Wales, the aim of this study is to investigate the potential impact of air pollution on dementia in later life.MethodThis study was based on the Cognitive Function and Ageing Study (CFAS) II (2008‐2011) and Wales (2011‐2013), two longitudinal studies of people aged 65 or above across five centres in England (Cambridgeshire, Newcastle upon Tyne, Nottingham) and Wales (Gwynedd, Neath Port Talbot). A two‐year follow‐up wave was carried out for both studies. Dementia was identified using the Geriatric Mental State and its diagnostic algorithm, Automated Geriatric Examination for Computer Assisted Taxonomy (GMS‐AGEACT). Based on the participants’ postcodes at the baseline, exposure to four air pollutants in 2012, including nitrogen dioxide (NO2), ozone (O3), particulate matter with a diameter ≤10 microns (PM10) and ≤2.5 microns (PM2.5), was estimated using the Community Multiscale Air Quality pollution modelling at a resolution of 20×20 m. Multistate modelling was used to investigate the effects of air pollution exposure on risk of developing dementia over the follow‐up period, incorporating mortality (from national death certification) and adjusting for age, sex, education, study centre and area deprivation.ResultAmong the 11329 participants in CFAS II (N = 7753) and Wales (N = 3576), the median exposure was 17.7 (IQR = 11.6) µg/m3 for NO2, 43.8 (IQR = 11.1) µg/m3 for O3, 15.5 (IQR = 3.1) µg/m3 for PM10 and 10.1 (IQR = 2.8) µg/m3 for PM2.5 and large variation was observed across the five centres. Per unit increase in NO2 exposure was associated with a higher risk of dementia in CFAS II (HR: 1.07; 95%CI: 1.03, 1.12) but not the Welsh cohort (HR: 0.93; 95%CI: 0.86, 1.00) after adjustment. For the other air pollutants, the associations were unclear.ConclusionOur study suggests limited evidence for the impacts of air pollution on dementia. Other environmental factors may influence individual exposure to air pollution and altogether have a complex effect on cognitive health in later life.

Weekly prenatal PM2.5 and NO2 exposures in preterm, early term, and full term infants: Decrements in birth weight and critical windows of susceptibility

BackgroundPrevious studies have observed associations between birth weight and prenatal air pollution exposure, but there is not consensus on timing of critical windows of susceptibility. ObjectiveWe estimated the difference in birth weight among preterm, early term and full term births associated with weekly exposure to PM2.5 and NO2 throughout gestation. MethodsWe included all singleton live births in the Lower Peninsula of Michigan (United States) between 2007 and 2012 occurring at or after 32 weeks gestational age (n = 497,897). Weekly ambient PM2.5 and NO2 concentrations were estimated at maternal residences using 1-km gridded data from ensemble-based models. We utilized a distributed lag nonlinear model to estimate the difference in birth weight associated with weekly exposures from the last menstrual period (week 0) through 31 weeks gestation for preterm births; through 36 weeks gestation for early term births; and through 38 weeks gestation for full term births. ResultsIn single-pollutant models, a 5 μg/m3 increase in PM2.5 exposure was associated with a reduction in birth weight among preterm births (−37.1 g [95% confidence interval [CI]: 60.8 g, −13.5 g]); early term births (−13.5 g [95% CI: 26.2 g, −0.67 g]); and full term births (−8.23 g [95% CI: 15.8 g, −0.68 g])]. In single-pollutant models, a 10 ppb increase in NO2 exposure was associated with a −11.7 g (95% CI: 14.46 g, −8.92 g) decrement in birth weight among full term births only. In models co-adjusted for PM2.5 and NO2, PM2.5 exposure was associated with reduced birth weight among preterm births (−36.9 g [95% CI: 61.9 g, −11.8 g]) and NO2 exposure was associated with reduced birth weight among full term births (−11.8 g [95% CI: 14.7 g, −8.94 g]). The largest decrements in birth weight were associated with PM2.5 exposure between approximately 10 and 26 weeks of pregnancy; for NO2 exposure, the largest decrements in birth weight in full term births were associated with exposure between weeks 6–18. ConclusionWe observed the largest and most persistent adverse associations between PM2.5 exposure and birth weight in preterm infants, and between NO2 exposure and birth weight in full term infants. Exposure during the first half of pregnancy had a greater impact on birthweight.

Identifying critical windows of air pollution exposure during preconception and gestational period on birthweight: a prospective cohort study

BackgroundFew studies have assessed air pollution exposure association with birthweight during both preconception and gestational periods.MethodsLeveraging a preconception cohort consisting of 14220 pregnant women and newborn children in Shanghai, China during 2016–2018, we aim to assess associations of NO2 and PM2.5 exposure, derived from high-resolution spatial-temporal models, during preconception and gestational periods with outcomes including term birthweight, birthweight Z-score, small-for-gestational age (SGA) and large-for-gestational age (LGA). Linear and logistic regressions were used to estimate 3-month preconception and trimester-averaged air pollution exposure associations; and distributed lag models (DLM) were used to identify critical exposure windows at the weekly resolution from preconception to delivery. Two-pollutant models and children’s sex-specific associations were explored.ResultsAfter controlling for covariates, one standard deviation (SD) (11.5 μg/m3, equivalent to 6.1 ppb) increase in NO2 exposure during the second and the third trimester was associated with 13% (95% confidence interval: 2 – 26%) and 14% (95% CI: 1 – 29%) increase in SGA, respectively; and one SD (9.6 μg/m3) increase in PM2.5 exposure during the third trimester was associated with 15% (95% CI: 1 – 31%) increase in SGA. No association have been found for outcomes of birthweight, birthweight Z-score and LGA. DLM found that gestational weeks 22–32 were a critical window, when NO2 exposure had strongest associations with SGA. The associations of air pollution exposure tended to be stronger in female newborns than in male newborns. However, no significant associations of air pollution exposure during preconception period on birthweight outcomes were found.ConclusionConsistent with previous studies, we found that air pollution exposure during mid-to-late pregnancy was associated with adverse birthweight outcomes.

Effects of Air Pollution Exposure during Preconception and Pregnancy on Gestational Diabetes Mellitus.

This study aimed to investigate the association between air pollution and gestational diabetes mellitus (GDM) in small- and medium-sized cities, identify sensitive periods and major pollutants, and explore the effects of air pollution on different populations. A total of 9820 women who delivered in Handan Maternal and Child Health Hospital in the Hebei Province from February 2018 to July 2020 were included in the study. Logistic regression and principal component logistic regression models were used to assess the effects of air pollution exposure during preconception and pregnancy on GDM risk and the differences in the effects across populations. The results suggested that each 20 μg/m3 increase in PM2.5 and PM10 exposure during preconception and pregnancy significantly increased the risk of GDM, and a 10 μg/m3 increase in NO2 exposure during pregnancy was also associated with the risk of GDM. In a subgroup analysis, pregnant women aged 30-35 years, nulliparous women, and those with less than a bachelor's education were the most sensitive groups. This study provides evidence for an association between air pollution and the prevalence of GDM, with PM2.5, PM10, and NO2 as risk factors for GDM.

Role of antenatal anxiety in the relationship between maternal exposure to nitrogen dioxide and small for gestational age: A birth cohort study

BackgroundBoth Nitrogen dioxide (NO2) exposure and antenatal anxiety have individually been associated with small for gestational age (SGA). Little is known, however, about whether there is effect modification of antenatal anxiety on NO2-related SGA. MethodsThe prospective birth cohort study included 1823 mother-newborn pairs in Guangzhou, China, from January 2017 to April 2020. Exposure to NO2 during the pre-conceptional and prenatal periods was estimated using an inverse distance weighted method. Antenatal anxiety was assessed by Trait Anxiety Inventory. SGA was determined by the Chinese gestational age- and sex-specific birthweight standards. Cox proportional hazards regression models was used to estimate hazard ratios (HRs) and 95 % confidence intervals (CIs) for SGA as per 10 μg/m3 increase in NO2. Modifying effects of trait anxiety on NO2-related SGA were identified by stratified analyses, and three-dimensional response surface plots and two-dimensional heat maps. ResultsEach 10 μg/m3 increase in NO2 exposure during the third trimester was significantly associated with SGA risk among overall participants (HR = 1.221, 95 % CI: 1.014–1.471) and primipara (HR = 1.271, 95 % CI: 1.023–1.579). We found significant effect modification of anxiety level for NO2-related SGA in the third trimester (Pinteraction < 0.05). Pregnant women with higher levels of trait anxiety were more likely to deliver SGA newborns, particularly for those with high trait anxiety (HR = 1.781, 95 % CI: 1.007–2.945). Primiparous women were more susceptible. ConclusionsThis study provides evidence that antenatal trait anxiety may modify the effects of maternal NO2 exposure on SGA risk. The third trimester could be a critical window of susceptibility.

Air pollution exposure and social responsiveness in childhood: The cincinnati combined childhood cohorts.

Autism Spectrum Disorder (ASD) affects about 1 in 44 children and environmental exposures may contribute to disease onset. Air pollution has been associated with adverse neurobehavioral outcomes, yet little research has examined its association with autistic-like behaviors. Therefore, our objective was to examine the association between exposure to air pollution, including NO2 and PM2.5, during pregnancy and the first year of life to ASD-like behaviors during childhood. Participants (n=435) enrolled in the Cincinnati Childhood Allergy and Air Pollution Study and the Health Outcomes and Measures of the Environment Study were included in the analysis. Daily exposures to NO2 and PM2.5 at the residential addresses of participants were estimated using validated spatiotemporal models and averaged to obtain prenatal and first year exposure estimates. ASD-like behaviors were assessed via the Social Responsiveness Scale (SRS) questionnaire at age 12. Linear regression models adjusting for confounders were applied to estimate the association between pollutants and SRS scores. After adjusting for covariates, the association between NO2 and PM2.5 and SRS scores remained positive but were no longer statistically significant. Prenatal and first year exposure to NO2 were associated with total SRS T-scores with an estimated 0.4 point increase (95% CI: -0.7, 1.6) per 5.2ppb increase in NO2 exposure and 0.7 point (95% CI: -0.3, 1.6) per 4.2ppb increase in NO2 exposure, respectively. For PM2.5, a 2.6μg/m3 increase in prenatal exposure was associated with a 0.1 point increase (95% CI: -1.1, 1.4) in SRS Total T-scores and a 1.3μg/m3 increase first year of life was associated with a 1 point increase (95% CI: -0.2, 2.3). In summary, exposure to NO2 and PM2.5 during pregnancy and the first year of life were not significantly associated with higher autistic-like behaviors measured with SRS scores after adjustment of covariates. Additional research is warranted given prior studies suggesting air pollution contributes to ASD.

The Role of Neighborhood Air Pollution Exposure on Somatic Non-Small Cell Lung Cancer Mutations in the Los Angeles Basin (2013-2018).

Limited previous work has identified a relationship between exposure to ambient air pollution and aggressive somatic lung tumor mutations. More work is needed to confirm this relationship, especially using spatially resolved air pollution. We aimed to quantify the association between different air pollution metrics and aggressive tumor biology. Among patients treated at City of Hope Comprehensive Cancer Center in Duarte, CA (2013–2018), three non-small cell lung cancer somatic tumor mutations, TP53, KRAS, and KRAS G12C/V, were documented. PM2.5 exposure was assessed using state-of-the art ensemble models five and ten years before lung cancer diagnosis. We also explored the role of NO2 using inverse-distance-weighting approaches. We fitted logistic regression models to estimate odds ratio (OR) and their 95% confidence intervals (CIs). Among 435 participants (median age: 67, female: 51%), an IQR increase in NO2 exposure (3.5 μg/m3) five years before cancer diagnosis was associated with an increased risk in TP53 mutation (OR, 95% CI: 1.30, 0.99–1.71). We found an association between highly-exposed participants to PM2.5 (>12 μg/m3) five and ten years before cancer diagnosis and TP53 mutation (OR, 95% CI: 1.61, 0.95–2.73; 1.57, 0.93–2.64, respectively). Future studies are needed to confirm this association and better understand how air pollution impacts somatic profiles and the molecular mechanisms through which they operate.

Interaction effect of prenatal and postnatal exposure to ambient air pollution and temperature on childhood asthma.

Although mounting evidence has associated air pollution and environmental temperature with children's health problems, it is unclear whether there is an interaction between these factors on childhood asthma. To explore the effects of temperature-pollution interactions during pre- and post-natal periods on asthma among pre-schoolers. A retrospective cohort study of 39,782 pre-schoolers was performed during 2010-2012, in seven cities in China. Exposure to three temperature indicators (TI) and three critical ambient air pollutants, including particulate matter with aerodynamic diameter≤10μm (PM10), sulfur dioxide (SO2) and nitrogen dioxide (NO2) as proxies of industrial and vehicular air pollution, was estimated by an inverse distance weighted (IDW) method. Two-level logistical regression analysis was used to examine the association between both pre- and post-natal exposure and childhood asthma in terms of odds ratio (OR) and 95% confidence interval (CI). Asthma prevalence in pre-schoolers at age of 3-6years (6.9%) was significantly associated with traffic-related air pollutant (NO2) exposure, with ORs (95% CI) of 1.17 (1.06, 1.28), 1.19 (1.05-1.34) and 1.16 (1.03-1.31) for an IQR increase in NO2 exposure during lifetime, pregnancy, and entire postnatal period respectively. Furthermore, childhood asthma was positively associated with exposure to increased temperature during lifetime, pregnancy, and entire postnatal period with ORs (95% CI)=1.89 (1.66, 2.16), 1.47 (1.34, 1.61), and 1.15 (1.11, 1.18) respectively, while was negatively associated with decreased temperatures. Childhood asthma was positively related with exposure to extreme heat days (EHD) during postnatal period particularly in first year of life respectively with ORs (95% CI)=1.23 (1.04, 1.46) and 1.26 (1.07, 1.47), but was not related with extreme cold days (ECD) exposure. A combination of high air pollutant levels and high temperatures significantly increased the risk of asthma during both pre- and post-natal periods. Strikingly, we found a significantly positive interaction of temperature and PM10 or SO2 on asthma risk among boys and younger children. Prenatal and postnatal exposure to ambient air pollution and high temperatures are independently and jointly associated with asthma risk in early childhood.

Identifying Sensitive Windows of Exposure to NO2 and Fetal Growth Trajectories in a Spanish Birth Cohort.

Background:We previously identified associations between trimester-specific NO2 exposures and reduced fetal growth in the Spanish INfancia y Medio Ambiente (INMA) project. Here, we use temporally refined exposure estimates to explore the impact of narrow (weekly) windows of exposure on fetal growth.Methods:We included 1,685 women from INMA with serial ultrasounds at 12, 20, and 34 gestational weeks. We measured biparietal diameter (BPD), femur length, and abdominal circumference (AC) and from them calculated estimated fetal weight (EFW). We calculated z-scores describing trajectories of each parameter during early (0–12 weeks), mid (12–20 weeks), and late (20–34 weeks) pregnancy, based on longitudinal growth curves from mixed-effects models. We estimated weekly NO2 exposures at each woman’s residence using land-use regression models. We applied distributed lag nonlinear models to identify sensitive windows of exposure. We present effect estimates as the percentage change in fetal growth per 10 μg/m3 increase in NO2 exposure, and we calculated cumulative effect estimates by aggregating estimates across adjacent lags.Results:We identified weeks 5–12 as a sensitive window for NO2 exposure on late EFW (cumulative β = −3.0%; 95% CI = −4.1%, −1.9%). We identified weeks 6–19 as a sensitive window for late growth in BPD (cumulative β = −2.0%; 95% CI = −2.7%, −1.4%) and weeks 8–13 for AC (cumulative β = −0.68%; 95% CI = −0.97%, −0.40%). We found suggestive evidence that third trimester NO2 exposure is associated with increased AC, BPD, and EFW growth in late pregnancy.Conclusions:Our findings are consistent with the hypothesis that NO2 exposure is associated with alterations in growth of EFW, BPD, and AC dependent on the specific timing of exposure during gestation.

Air pollution, residential greenness and metabolic dysfunction during early pregnancy in the INfancia y Medio Ambiente (INMA) Cohort

BACKGROUND AND AIM: Despite being studied extensively, the role of air pollution in gestational diabetes remains unclear, and there is limited evidence of the beneficial impact of residential greenness on metabolic dysfunction during pregnancy. Our objective was to examine associations of both air pollution and residential greenness on glucose intolerance and abnormal serum lipids among pregnant women. METHODS: We used data from more than 2,200 mothers from Gipuzkoa, Sabadell and Valencia who were enrolled in the Spanish INfancia y Medio Ambiente (INMA) Project from 2003—2008. We obtained spatiotemporally resolved estimates of fine particulate matter (PM₂.₅) and nitrogen dioxide (NO₂) exposures in early pregnancy and estimated residential greenness using satellite-based Normal Difference Vegetation Index (NDVI) within 100-, 300- and 500-meter buffers surrounding the mother’s residence. We applied mixed models with random effect for cohort to separately evaluate associations between each of the three exposures of interest (PM₂.₅, NO₂, or NDVI) and a) glucose intolerance (defined as either impaired glucose tolerance (IGT) or gestational diabetes mellitus (GDM)) and b) abnormal lipid levels. RESULTS:No associations were observed between a 5 µg/m³ increase in first trimester PM₂.₅ exposure and glucose intolerance (OR = 1.0, 95% CI: 0.9, 1.2), high cholesterol (OR = 1.0, 95% CI: 0.9, 1.2), or high triglycerides (OR= 1.0, 95% CI: 0.9, 1.2). Null associations were also observed for a 10 µg/m³ increase in NO₂ exposure. We also observed no association between NDVI and any of the metabolic outcomes and results were similar irrespective of buffer size. CONCLUSIONS:Given the lack of evidence in our study, other investigations are needed to assess effects of air pollution and residential greenness on metabolic dysfunction during pregnancy. KEYWORDS: Particulate matter, oxides of nitrogen, green space, pregnancy outcomes

Nitrogen dioxide exposure during pregnancy and risk of spontaneous abortion: a case-control study in China

Background Evidence on the relationship between prenatal exposure to NO2 and CO and spontaneous abortion (SAB) is insufficient. We investigated whether there is an association between maternal exposure to nitrogen dioxide (NO2) and carbon monoxide (CO) before and during pregnancy and SAB. Methods We conducted a case-control study using medical records of 2445 pregnant women who admitted for abortion prior to 20 weeks of gestational age from January 2014 to December 2019 at a tertiary-care hospital in Shanghai, China. Of the 2445 participants, 1075 were SAB cases and 1370 were healthy controls (underwent elective abortions). Maternal exposure to NO2 and CO before and during pregnancy was estimated using daily air pollution concentration data. Multivariable logistic regression models were constructed to quantify the relationships between maternal exposure to NO2 or CO and the risk of SAB while controlling for potential confounders. Results NO2 exposure levels during pregnancy were significantly higher in SAB cases than in healthy controls (42.26 vs. 40.67, p < .01). NO2 exposure during pregnancy was positively associated with the risk of SAB. An interquartile range (16 μg/m3) increase in NO2 exposure was associated with 68% increase in the odds of SAB (OR = 1.68, 95% CI, 1.28, 2.21). Analyses of associations by quartile of NO2 exposure showed that elevated NO2 exposure during pregnancy was associated with increased odds of SAB in linear dose–response manners. Compared with the lowest quartile of NO2 exposure, the odds of SAB in the fourth quartile of NO2 exposure increased 61% (OR = 1.61, 95% CI, 1.03–2.53). No associations of CO exposure with SAB risk were observed. Conclusions Our study suggested that exposure to NO2 during early pregnancy was associated with increased risk of SAB. Further studies are needed to confirm our results and explore the potential biological mechanism underlying these associations.

Prenatal Ambient Air Pollutants and Maternal Depressive Symptoms at 12 months Postpartum

Background: Depression is the leading cause of mental health-related morbidity, particularly among women. Ambient air pollutants are modifiable exposures that have increasingly been associated with depression and pregnancy is a period that may increase maternal susceptibility to environmental exposures. We examined whether exposures to prenatal ambient air pollutants are associated with maternal depressive symptoms at 12 months postpartum. Methods: Women participating in the MADRES cohort—an ongoing cohort of predominantly low income, Hispanic women in Los Angeles—were followed from pregnancy through 12 months postpartum with a series of visits and phone calls. At the 12-month study visit, women were orally administered the Center for Epidemiologic Studies-Depression (CES-D) scale as part of a questionnaire on home exposures, social stressors, sociodemographics, and health history. Residential address histories were recorded from one year prior to conception through 12 months postpartum and average ambient pollutant estimates of NO2, PM10, PM2.5 and O3 were spatially interpolated at participants’ residential locations. Logistic regression models were fitted to evaluate associations between trimester-specific and 9-month average levels across pregnancy of ambient air pollutants and probable depression (score of ≥16 on the CES-D) at 12 months postpartum, adjusting for maternal age and recruitment site (N=101). Results: We found that second trimester ambient NO2 levels were associated with a two-fold increased odds of probable depression at 12 months (OR=2.03 per SD increase in NO2 exposure, 95% CI: 1.24, 3.33). Similar results were found for 9-month prenatal average NO2 (OR=1.88, 95% CI: 1.07, 3.32). Prenatal ambient PM10, PM2.5, and O3 levels were not significantly associated with depressive symptoms at 12 months postpartum. Conclusions: Prenatal ambient NO2 levels were associated with increased maternal depressive symptoms at 12 months postpartum. These results underscore the need to better understand the contribution of modifiable environmental risk factors during critical susceptible exposure periods.

Air pollution and IgE sensitization in 4 European birth cohorts—the MeDALL project

Whether long-term exposure air to pollution has effects on allergic sensitization is controversial. Our aim was to investigate associations of air pollution exposure at birth and at the time of later biosampling with IgE sensitization against common food and inhalant allergens, or specific allergen molecules, in children aged up to 16 years. A total of 6163 children from 4 European birth cohorts participating in the Mechanisms of the Development of ALLergy [MeDALL] consortium were included in this meta-analysis of the following studies: Children, Allergy, Milieu, Stockholm, Epidemiology (BAMSE) (Sweden), Influences of Lifestyle-Related Factors on the Human Immune System and Development of Allergies in Childhood (LISA)/German Infant Study on the Influence of Nutrition Intervention PLUS Environmental and Genetic Influences on Allergy Development (GINIplus) (Germany), and Prevention and Incidence of Asthma and Mite Allergy (PIAMA) (The Netherlands). The following indicators were modeled by land use regression: individual residential outdoor levels of particulate matter with aerodynamic diameters less than 2.5 μm, less than 10 μm, and between 2.5 and 10 μm; PM2.5 absorbance (a measurement of the blackness of PM2.5 filters); and nitrogen oxides levels. Blood samples drawn at ages 4 to 6 (n= 5989), 8 to 10 (n= 6603), and 15 to 16 (n= 5825) years were analyzed for IgE sensitization to allergen extracts by ImmunoCAP. Additionally, IgE against 132 allergen molecules was measured by using the MedALL microarray chip (n= 1021). Air pollution was not consistently associated with IgE sensitization to any common allergen extract up to age 16 years. However, allergen-specific analyses suggested increased risks of sensitization to birch (odds ratio [OR]= 1.12 [95% CI= 1.01-1.25] per 10-μg/m3 increase in NO2 exposure). In a subpopulation with microarray data, IgE to the major timothy grass allergen Phleum pratense 1 (Phl p 1) and the cat allergen Felis domesticus 1 (Fel d 1) greater than 3.5 Immuno Solid-phase Allergen Chip standardized units for detection of IgE antibodies were related to PM2.5 exposure at birth (OR= 3.33 [95% CI= 1.40-7.94] and OR= 4.98 [95% CI= 1.59-15.60], respectively, per 5-μg/m3 increase in exposure). Air pollution exposure does not seem to increase the overall risk of allergic sensitization; however, sensitization to birch as well as grass pollen Phl p 1 and cat Fel d 1 allergen molecules may be related to specific pollutants.

Nitrogen dioxide and asthma emergency department visits in California, USA during cold season (November to February) of 2005 to 2015: A time-stratified case-crossover analysis

Nitrogen dioxide (NO2) is responsible for aggravating respiratory diseases, particularly asthma. The aim of this study is to investigate the association between NO2 exposure and asthma emergency department (ED) visits during the cold season (November–February) in five populated locations (Sacramento, San Francisco, Fresno, Los Angeles, and San Diego) of California from 2005 to 2015 (1320 Days). Conditional logistic regression models were used to obtain the odds ratio (OR) and 95% confidence interval (CI) associated with a 5 ppb increase in NO2 concentration for the 19,735 ED visits identified. An increase in NO2 exposure increased the odds of having asthma ED visits for the studied population. The potential effect modification by sex (female and male), race (White, Black, Hispanic, and Asian), and age (2–5, 6–18, 19–40, 41–64, and ≥65) was explored. A 5 ppb increase in the concentration of NO2 during lag 0–30 was associated with a 56% increase in the odds of having an asthma ED visit (OR = 1.560, CI: 1.428–1.703). Sex was not found to be a modifier. Asthma ED visits among all the races/ethnicities (except Asians) were associated with NO2 exposure. Whites had the highest OR 75% (OR = 1.750, CI: 1.417–2.160) at lag 0–30 in response to NO2 exposure. The association between NO2 exposure and asthma ED visits was positive among all age groups except for 19 to 40 years old; the OR was higher among 2 to 18 year old (at lag 0–30: age group 2–5 (OR = 1.699, CI: 1.399–2.062), and age group 6–18 (OR = 1.568, CI 1.348–1.825)). For stratification by location, San Diego and Fresno were found to have the highest OR, compared to the other studied locations.

Numerical investigations of reactive pollutant dispersion and personal exposure in 3D urban-like models

With satisfactory validation by experimental data, we perform computational fluid dynamic(CFD) simulations with the standard k-ε model to investigate how NO–NO2–O3 photochemistry and turbulent mixing influence reactive pollutant dispersion and vehicular NOx exposure in 21-row(neighborhood-scale~1 km) three-dimensional(3D) medium-dense urban models with an approaching wind parallel(perpendicular) to the main(secondary) streets. Personal intake fraction P_iF and its spatially-averaged values for the entire building (i.e. building intake fraction <P_iF>B) are adopted for reactive/passive exposure analysis with/without NOx-O3-photochemistry.Some meaningful findings are proposed: 1) There are flow adjustment processes coupling turbulent mixing and chemical reactions through urban areas (i.e. secondary Street 1 to 20). NO–NO2–O3 photochemistry induces O3 depletion and NO conversion into NO2 producing significant increase in NO2 exposure and slight decrease in NO exposure compared with passive dispersion. 2) With span-wise NOx sources, Street 10 in the fully-developed region experiences weaker wind and subsequently greater <P_iF>B(0.207 ppm) than Street 3(0.135 ppm) in the upstream flow-adjustment region. <P_iF>B descends exponentially from the target building toward downstream, and Street 10 experiences quicker decay rates. 3) With stream-wise NOx sources along the main street, <P_iF>B first ascends, then reaches equilibrium values (e.g.0.046–0.049 ppm). 4) If background O3 concentration [O3] rises from 20 ppbv to 40 and 100 ppbv, more NO is oxidized by O3 to generate NO2. As [O3] = 20 ppbv, if NO–NO2 emission ratio decreases from 10 to 5, NO2 exposure is partly offset but NO exposure change little. Present methodologies are confirmed effective to investigate impacts of more complicated meteorological conditions and chemical mechanisms on exposure in urban districts.

Combined effects of traffic air pollution and home environmental factors on preterm birth in China

BackgroundAlthough mounting evidence have linked traffic-related air pollution (TRAP) with increased risk of preterm birth (PTB), whether it can interact with indoor environmental factors remains unknown, and its window(s) susceptibility at the stage of gestation is unclear. ObjectiveTo explore PTB risk for prenatal exposure to traffic-related air pollution and home environmental factors during pregnancy, so as to identify critical window(s) in the combined effect of traffic air pollution and main home environmental factor(s) on PTB development. MethodsA retrospective cohort study of 3,509 preschool children was performed in Changsha, China during 2011–2012. The PTB prevalence was reported by the parents based on a questionnaire. We estimated each mother's exposure to traffic-related air pollutant NO2 in different windows of gestation, including conception month, three trimesters, birth month, and whole gestation. Maternal exposure to home environmental factors was considered by renovation (new furniture/redecoration) in pregnancy, and mold/damp stains and window condensation during perinatal period. Associations of PTB with both ambient NO2 and home environmental factors, and their interactions on PTB were evaluated by logistic regression models using odds ratio (OR) with 95% confidence interval (CI). ResultsTraffic air pollutant NO2 exposure in utero was significantly associated with PTB, with adjusted odds ratio (OR) (95% CI) of 1.41 (1.00–1.98) for an IQR increase in NO2 exposure during whole pregnancy, particularly in the conception month and 1st trimester. We further found a positive relationship between perinatal exposure to mold/damp stains in the homes and PTB, OR (95% CI) = 1.73 (1.04–2.90). Especially, we detected a significant interaction between outdoor NO2 and indoor mold/damp stains on PTB risk. Male and female foetus were respectively more susceptible to perinatal mold/dampness at home and outdoor NO2 exposure in early gestation. ConclusionOur finding indicates that both outdoor traffic air pollutant and indoor mold/dampness play key roles in PTB development, and their interaction effect in early pregnancy significantly increases PTB risk.

Effects of personal nitrogen dioxide exposure on airway inflammation and lung function

BackgroundFew epidemiological studies have evaluated the respiratory effects of personal exposure to nitrogen dioxide (NO2), a major traffic-related air pollutant. The biological pathway for these effects remains unknown. ObjectivesTo evaluate the short-term effects of personal NO2 exposure on lung function, fractional exhaled nitric oxide (FeNO) and DNA methylation of genes involved. MethodsWe conducted a longitudinal panel study among 40 college students with four repeated measurements in Shanghai from May to October in 2016. We measured DNA methylation of the key encoding genes of inducible nitric oxide synthase (NOS2A) and arginase (ARG2). We applied linear mixed-effect models to assess the effects of NO2 on respiratory outcomes. ResultsPersonal exposure to NO2 was 27.39 ± 23.20 ppb on average. In response to a 10-ppb increase in NO2 exposure, NOS2A methylation (%5 mC) decreased 0.19 at lag 0 d, ARG2 methylation (%5 mC) increased 0.21 and FeNO levels increased 2.82% at lag 1 d; and at lag 2 d the percentage of forced vital capacity, forced expiratory volume in 1 s and peak expiratory flow in predicted values decreased 0.12, 0.37 and 0.67, respectively. The model performance was better compared with those estimated using fixed-site measurements. These effects were robust to the adjustment for co-pollutants and weather conditions. ConclusionsOur study suggests that short-term personal exposure to NO2 is associated with NOS2A hypomethylation, ARG2 hypermethylation, respiratory inflammation and lung function impairment. The use of personal measurements may better predict the respiratory effects of NO2.

Supplemental Folate and the Relationship Between Traffic-Related Air Pollution and Livebirth Among Women Undergoing Assisted Reproduction.

Traffic-related air pollution has been linked to higher risks of infertility and miscarriage. We evaluated whether folate intake modified the relationship between air pollution and livebirth among women using assisted reproductive technology (ART). Our study included 304 women (513 cycles) presenting to a fertility center in Boston, Massachusetts (2005-2015). Diet and supplements were assessed by food frequency questionnaire. Spatiotemporal models estimated residence-based daily nitrogen dioxide (NO2), ozone, fine particulate, and black carbon concentrations in the 3 months before ART. We used generalized linear mixed models with interaction terms to evaluate whether the associations between air pollutants and livebirth were modified by folate intake, adjusting for age, body mass index, race, smoking, education, infertility diagnosis, and ART cycle year. Supplemental folate intake significantly modified the association of NO2 exposure and livebirth (P = 0.01). Among women with supplemental folate intakes of <800 μg/day, the odds of livebirth were 24% (95% confidence interval: 2, 42) lower for every 20-parts-per-billion increase in NO2 exposure. There was no association among women with intakes of ≥800 μg/day. There was no effect modification of folate on the associations between other air pollutants and livebirth. High supplemental folate intake might protect against the adverse reproductive consequences of traffic-related air pollution.

Carbon monoxide (CO) and nitric dioxide (NO2) exposure during fetal life: impact on neonatal and placental weight, a prospective study

Objective: This prospective study aims to analyze how CO and NO2 exposure during pregnancy affects birth and placental weight as well as umbilical arterial pH.Study design: The population in study includes 3614 women born in Italy, living in Lombardia Region, consecutively admitted to the Clinica Mangiagalli for an elective cesarean section from January 2004 to December 2006. Outdoor air quality data was provided by the Department of the Regional Environmental Protection Agency and obtained by a network of fixed monitoring stations distributed in eight geographical areas across the region.Results: A positive association was found between birth weight and the concentration of CO to whom women were exposed during the last 10 d of pregnancy (mean change g + 28, 95% CI +1 to +55, p .04). Conversely, placental weight was not influenced by exposure to CO while a statistically significant weight reduction was related to an increase in NO2 exposure during the last trimester of pregnancy.Conclusion: Fetal weight was positively associated with an increased exposure to CO during the last 10 d of pregnancy. NO2 exposure was associated to a placental weight reduction. These findings underline the existence of a complex biological role of such pollutants, especially of CO, in cell oxygenation at a placental level.