Nitrogen Dioxide Exposure Research Articles

Years of life lost from ischaemic and haemorrhagic stroke related to ambient nitrogen dioxide exposure: A multicity study in China

Few multicity studies have been conducted in developing countries to distinguish the acute effects of ambient nitrogen dioxide (NO2) on the years of life lost (YLL) from different subtypes of stroke. We aimed to differentiate the associations between NO2 exposure and YLL from major pathological types of stroke in China, and estimate the relevant economic loss. A time-series study was conducted to explore the associations between short-term NO2 exposure and YLL from ischaemic and haemorrhagic stroke from 2013 to 2017 in 48 Chinese cities. Daily NO2 data and stroke mortality counts for each city were obtained from the National Urban Air Quality Real-time Publishing Platform and Chinese Center for Disease Control and Prevention, respectively. Generalized additive models were applied to estimate the cumulative effects of NO2 in each city, and meta-analysis was used to combine the city-specific estimates. The relevant economic loss was estimated using the method of the value per statistical life year (VSLY). A 10 μg/m3 increase in ambient NO2 concentration on the present day and previous day (lag 0–1) would lead to relatively higher increments in percentage change of YLL from ischaemic stroke (0.82%, 95% CI: 0.46%, 1.19%) than haemorrhagic stroke (0.46%, 95% CI: 0.09%, 0.84%). The association was significantly stronger in the low-education population than high-education population for ischaemic stroke. Furthermore, significantly higher association was found in South China than those in North China for both subtypes of stroke. Economic loss due to excess YLL from ischaemic stroke related to NO2 exposure was higher than that for haemorrhagic stroke. Our study indicated higher association and economic loss of ischaemic than haemorrhagic stroke related to NO2 exposure in China, which informed priorities for type-specific stroke prevention strategies related to NO2 pollution and vulnerable population protection.

Cyclists’ exposure to air pollution and noise in Mexico City

Air pollution and road traffic noise are two important environmental nuisances that could be harmful to the health and well-being of urban populations. In Mexico City, as in many North American cities, there has been an upsurge in bicycle ridership. However, Mexico City is also well known for having high levels of noise and air pollution. The purpose of this study is threefold: 1) evaluate cyclists’ exposure to air pollution (nitrogen dioxide) and road traffic noise; 2) identify local factors that increase or reduce cyclists’ exposure, in paying particular attention to the type of road and bicycle path or lane used; and 3) evaluate the influence of real-time traffic density on cyclists’ exposure. A total of 19 bicycle trips made in central Mexico City neighbourhoods were analyzed, representing nearly 11 hours and 137 km. The results of the Bayesian models show that type of road and bicycle infrastructure taken by the cyclist, and proximity to a main artery all have significant impacts on exposure levels. Finally, the variables introduced to control for the traffic encountered by cyclists had a significant positive effect on noise exposure, and a positive but not significant effect on nitrogen dioxide exposure.

Causal Effects of Air Pollution on Mortality Rate in Massachusetts

Air pollution epidemiology studies have primarily investigated long- and short-term exposures separately, have used multiplicative models, and have been associational studies. Implementing a generalized propensity score adjustment approach with 3.8 billion person-days of follow-up, we simultaneously assessed causal associations of long-term (1-year moving average) and short-term (2-day moving average) exposure to particulate matter with an aerodynamic diameter less than or equal to 2.5 μm (PM2.5), ozone, and nitrogen dioxide with all-cause mortality on an additive scale among Medicare beneficiaries in Massachusetts (2000-2012). We found that long- and short-term PM2.5, ozone, and nitrogen dioxide exposures were all associated with increased mortality risk. Specifically, per 10 million person-days, each 1-μg/m3 increase in long- and short-term PM2.5 exposure was associated with 35.4 (95% confidence interval (CI): 33.4, 37.6) and 3.04 (95% CI: 2.17, 3.94) excess deaths, respectively; each 1-part per billion (ppb) increase in long- and short-term ozone exposure was associated with 2.35 (95% CI: 1.08, 3.61) and 2.41 (95% CI: 1.81, 2.91) excess deaths, respectively; and each 1-ppb increase in long- and short-term nitrogen dioxide exposure was associated with 3.24 (95% CI: 2.75, 3.77) and 5.60 (95% CI: 5.24, 5.98) excess deaths, respectively. Mortality associated with long-term PM2.5 and ozone exposure increased substantially at low levels. The findings suggested that air pollution was causally associated with mortality, even at levels below national standards.

Health Risks of Nitrogen Dioxide Exposure Among Primary School Children in Ogan Ilir, South Sumatra, Indonesia: Effect on Lung Function

Nitrogen dioxide (NO2) is one of the most dangerous air pollutants as regards human health. Increased traffic volumes on the east-lane roadside of South Sumatra have led to increased NO2 concentrations. In terms of age and NO2, children are the greatest risk group. The aim of this research was to estimate health risks of NO2 and analyze the correlation between exposure and lung capacity. This was an analytical study, with a cross-sectional design and risk analysis. The study group consisted of 100 children of primary school age. The results showed that the noncancer hazard index (HI)for NO2 exposure based on real-time data was 1.138. In the study population, as shown by the noncancer HI, 22% of students in OganIlir were classified as not at risk (HI < 1), whereas 78% were classified as at risk (HI ≥ 1). According to the results of simple linear regression, FEV1 (Pearson’s test: 0.0001) and FVC (Pearson’s test: 0.0001) showed a significant correlation with noncancer NO2 risk. The results of simulations suggested that a value of 0.176 mg/m3 can be used as a quality standard recommendation (health advisory) for NO2 exposure in roadside schools, especially schools abutting inter-provincial roads in South Sumatra

Obesity may enhance the adverse effects of NO2 exposure in urban schools on asthma symptoms in children

Sparse data address the effects of nitrogen dioxide (NO2) exposure in inner-city schools on obese students with asthma. We sought to evaluate relationships between classroom NO2 exposure and asthma symptoms and morbidity by body mass index (BMI) category. The School Inner-City Asthma Study enrolled students aged 4 to 13 years with asthma from 37 inner-city schools. Students had baseline determination of BMI percentile. Asthma symptoms, morbidity, pulmonary inflammation, and lung function were monitored throughout the subsequent academic year. Classroom NO2 data, linked to enrolled students, were collected twice per year. We determined the relationship between classroom NO2 levels and asthma outcomes by BMI stratification. A total of 271 predominantly black (35%) or Hispanic students (35%) were included in analyses. Fifty percent were normal weight (5-84th BMI percentile), 15% overweight (≥85-94th BMI percentile), and 35% obese (≥95th BMI percentile). For each 10-parts per billion increase in NO2, obese students had a significant increase in the odds of having an asthma symptom day (odds ratio [OR], 1.86; 95% CI, 1.15-3.02) and in days caregiver changed plans (OR, 4.24; 95% CI, 2.33-7.70), which was significantly different than normal weight students who exhibited no relationship between NO2 exposure and symptom days (OR, 0.90; 95% CI, 0.57-1.42; pairwise interaction P= .03) and change in caregiver plans (OR, 1.37; 95% CI, 0.67-2.82; pairwise interaction P= .02). Relationships between NO2 levels and lung function and fractional exhaled nitric oxide did not differ by BMI category. If we applied a conservative Holm-Bonferroni correction for 16 comparisons (obese vs normal weight and overweight vs normal weight for 8 outcomes), these findings would not meet statistical significance (all P> .003). Obese BMI status appears to increase susceptibility to classroom NO2 exposure effects on asthma symptoms in inner-city children. Environmental interventions targeting indoor school NO2 levels may improve asthma health for obese children. Although our findings would not remain statistically significant after adjustment for multiple comparisons, the large effect sizes warrant future study of the interaction of obesity and pollution in pediatric asthma.

Prenatal air pollution exposure and growth and cardio-metabolic risk in preschoolers

ObjectivesWe investigated the association between outdoor air pollutants exposure in the first trimester of pregnancy, and growth and cardio-metabolic risk at four years of age, and evaluated the mediating role of birth weight. MethodsWe included mother-child pairs (N = 1,724) from the Spanish INMA birth cohort established in 2003–2008. First trimester of pregnancy nitrogen dioxide (NO2) and fine particles (PM2.5) exposure levels were estimated. Height, weight, waist circumference, blood pressure, and lipids were measured at four years of age. Body mass index (BMI) trajectories from birth to four years were identified. ResultsIncreased PM2.5 exposure in the first trimester of pregnancy was associated with decreased z-scores of weight (zWeight) and BMI (zBMI) (zWeight change per interquartile range increase in PM2.5 exposure = −0.12; 95% CI: −0.23, −0.01; zBMI change = −0.12; 95% CI: −0.23, −0.01). Higher NO2 and PM2.5 exposure was associated to a reduced risk of being in a trajectory with accelerated BMI gain, compared to children with the average trajectory. Birth weight partially mediated the association between PM2.5 and zWeight and zBMI. PM2.5 and NO2 were not associated with the other cardio-metabolic risk factors. ConclusionsThis comprehensive study of many growth and cardio-metabolic risk related outcomes suggests that air pollution exposure during pregnancy may be associated with delays in physical growth in the early years after birth. These findings imply that pregnancy exposure to air pollutants has a lasting effect on growth after birth and require follow-up at later child ages.

Nitrogen dioxide exposures from biomass cookstoves in the Peruvian Andes.

Household air pollution from biomass cookstoves is a major contributor to global morbidity and mortality, yet little is known about exposures to nitrogen dioxide (NO2 ). To characterize NO2 kitchen area concentrations and personal exposures among women with biomass cookstoves in the Peruvian Andes. We measured kitchen area NO2 concentrations at high-temporal resolution in 100 homes in the Peruvian Andes. We assessed personal exposure to NO2 in a subsample of 22 women using passive samplers. Among 97 participants, the geometric mean (GM) highest hourly average NO2 concentration was 723ppb (geometric standard deviation (GSD) 2.6) and the GM 24-hour average concentration was 96ppb (GSD 2.6), 4.4 and 2.9 times greater than WHO indoor hourly (163ppb) and annual (33ppb) guidelines, respectively. Compared to the direct-reading instruments, we found similar kitchen area concentrations with 48-hour passive sampler measurements (GM 108ppb, GSD 3.8). Twenty-seven percent of women had 48-hour mean personal exposures above WHO annual guidelines (GM 18ppb, GSD 2.3). In univariate analyses, we found that roof, wall, and floor type, as well as higher SES, was associated with lower 24-hour kitchen area NO2 concentrations. Kitchen area concentrations and personal exposures to NO2 from biomass cookstoves in the Peruvian Andes far exceed WHO guidelines. More research is warranted to understand the role of this understudied household air pollutant on morbidity and mortality and to inform cleaner-cooking interventions for public health.

Association between short-term exposure to ambient air pollutants and the risk of tuberculosis outpatient visits: A time-series study in Hefei, China

BackgroundThe current evidence has presented mixed results between air pollutants exposure and the progression of tuberculosis (TB). The purpose of this study was to explore the association between short-term exposure to air pollutants and the risk of TB outpatient visits in Hefei, China. MethodsTime-series analysis was used to assess the effect of short-term exposure to ambient air pollutants on the risk of TB outpatient visits. A Poisson generalized linear regression model combined with a distributed lag non-linear model (DLNM) was applied to explore the association. The effects of different gender (male, female), age (≤65 years old, >65 years old) and season (cold season, warm season) on the risk of TB were investigated by stratified analysis. Sensitivity analyses were conducted to test the robustness of our findings. ResultsA total of 22,749 active TB cases were identified from November 1, 2013 to December 31, 2018 in Hefei. The overall exposure-response curve showed that the concentration of particulate matter with aerodynamic diameter less than 2.5 μm (PM2.5) and nitrogen dioxide (NO2) exposure were positively correlated with the risk of TB outpatient visits, while ozone (O3) and sulfur dioxide (SO2) exposure were negatively correlated with the risk of TB outpatient visits. The maximum lag-specific and cumulative relative risk (RR) of TB outpatient visits were 1.057 [95%CI: 1.002–1.115, lag 3 day] and 1.559 (95%CI: 1.057–2.300, lag 13 days) for each 10 μg/m³ increase in PM2.5; 1.026 (95% CI: 1.008–1.044, lag 0 day) and 1.559 (95%CI: 1.057–2.300, lag 07 days) for each 10 μg/m³ increase in NO2; 0.866 (95% CI: 0.801–0.935, lag 5 day) and 0.852 (95%CI: 1.01–1.11, lag 0–14 days) for each 10 μg/m³ increase in SO2 in the single-pollutant model. There was only a negative association between O3 exposure and the cumulative risk of TB outpatient visits (RR = 0.960, 95%CI: 0.936–0.984, lag 07 days). Stratified analyses showed that the effects of SO2 and O3 exposure were different between warm and cold seasons. The effect of NO2 exposure remained statistically significant in male, younger, and cold season subgroups. Besides, elderly people are more susceptible to PM2.5 exposure. ConclusionThis study suggests that exposure to PM2.5, NO2, SO2, and O3 are associated with the risk of TB outpatient visits. Seasonal variation may have a greater impact on the risk of TB outpatient visits compared with gender and age.

Application of land use regression to assess exposure and identify potential sources in PM2.5, BC, NO2 concentrations

BackgroundUnderstanding spatial variation of air pollution is critical for public health assessments. Land Use Regression (LUR) models have been used increasingly for modeling small-scale spatial variation in air pollution concentrations. However, they have limited application in China due to the lack of spatially resolved data. ObjectiveBased on purpose-designed monitoring networks, this study developed LUR models to predict fine particulate matter (PM2.5), black carbon (BC) and nitrogen dioxide (NO2) exposure and to identify their potential outdoor-origin sources within an urban/rural region, using Taizhou, China as a case study. MethodTwo one-week integrated samples were collected at 30 PM2.5 (BC) sites and 45 NO2 sites in each two distinct seasons. Samples of 1/3 of the sites were collected simultaneously. Annual adjusted average was calculated and regressed against pre-selected GIS-derived predictor variables in a multivariate regression model. ResultsLUR explained 65% of the spatial variability in PM2.5, 78% in BC and 73% in NO2. Mean (±Standard Deviation) of predicted PM2.5, BC and NO2 exposure levels were 48.3 (±6.3) μg/m3, 7.5 (±1.4) μg/m3 and 27.3 (±8.2) μg/m3, respectively. Weak spatial corrections (Pearson r = 0.05–0.25) among three pollutants were observed, indicating the presence of different sources. Regression results showed that PM2.5, BC and NO2 levels were positively associated with traffic variables. The former two also increased with farm land use; and higher NO2 levels were associated with larger industrial land use. The three pollutants were correlated with sources at a scale of ≤5 km and even smaller scales (100–700m) were found for BC and NO2. ConclusionWe concluded that based on a purpose-designed monitoring network, LUR model can be applied to predict PM2.5, NO2 and BC concentrations in urban/rural settings of China. Our findings highlighted important contributors to within-city heterogeneity in outdoor-generated exposure, and indicated traffic, industry and agriculture may significantly contribute to PM2.5, NO2 and BC concentrations.

Association Between Ambient Air Pollution and Elevated Risk of Tuberculosis Development.

BackgroundBroad-scale evidence has shown the significant association between ambient air pollutants and the development of tuberculosis (TB). However, the impact of air quality on the risk of TB in Taiwan is still poorly understood.ObjectiveTo develop a probabilistic integrated population-level risk assessment approach for evaluating the contribution of ambient air pollution exposure to the risk of TB development among different regions of Taiwan.Materials and methodsA Bayesian-based probabilistic risk assessment model was implemented to link exposure concentrations of various air pollutants quantified in a probabilistic manner with the population-based exposure-response models developed by using an epidemiological investigation.ResultsThe increment of the risk of TB occurred in a region with a higher level of air pollution, indicating a strong relationship between ambient air pollution exposures and TB incidences. Carbon monoxide (CO) exposure showed the highest population attributable fraction (PAF), followed by nitrogen oxides (NOX) and nitrogen dioxide (NO2) exposures. In a region with higher ambient air pollution, it is most likely (80% risk probability) that the contributions of CO exposure to development of TB were 1.6–12.2% (range of median PAFs), whereas NOX and NO2 exposures contributed 1.2–9.8% to developing TB.ConclusionOur findings provide strong empirical support for the hypothesis and observations from the literature that poor air quality is highly likely to link aetiologically to the risk of TB. Therefore, substantial reductions in CO, NOX, and NO2 exposures are predicted to have health benefits to susceptible and latently infected individuals that provide complementary mitigation efforts in reducing the burden of TB. Considering that people continue to be exposed to both TB bacilli and ambient air pollutants, our approach can be applied for different countries/regions to identify which air pollutants contribute to a higher risk of TB in order to develop potential mitigation programs.

Association between air pollution and risk of vascular dementia: A multipollutant analysis in Taiwan

Evidence regarding the association of specific air pollutants with vascular dementia (VaD) risk is limited. In this nested case–control study, we enrolled 831 adults aged >65 years with VaD (International Classification of Diseases, Ninth Revision, Clinical Modification code 290.4x) newly diagnosed during 2005–2013; 3324 controls were age-, sex-, and VaD diagnosis year–matched with the study patients. Both patients with VaD and controls were selected from among a cohort of one million beneficiaries of Taiwan’s National Health Insurance program, all of whom were registered in 2005. Exposure to the mean daily air pollutant concentration, derived from 76 fixed air quality monitoring stations, in 3, 5, and 7 years before VaD diagnosis was assessed using the spatial analysis method (i.e., ordinary kriging) on ArcGIS. A logistic regression model was used to calculate covariate-adjusted odds ratios (ORs) of VaD in relation to specific air pollutants. After potential confounders and other air pollutants were controlled for, high concentrations of coarse particulate matter (10 µm or less in diameter) and carbon monoxide (CO) were sporadically associated with higher OR of VaD. The most prominent association was observed for nitrogen dioxide (NO2) exposure within 5 and 7 years before diagnosis. Compared with the <25th percentile of NO2 exposure, the 25th–50th, 50th–75th, and >75th percentiles of NO2 exposure significantly increased ORs (95% confidence intervals): 1.62 (1.28–2.23), 1.61 (1.11–2.33), and 2.22 (1.35–3.65) within 5 years before diagnosis, respectively, and 1.59 (1.20–2.11), 1.65 (1.15–2.37), and 2.05 (1.28–3.28) within 7 years before diagnosis, respectively. We found that higher NO2 exposure in the past was significantly associated with an elevated risk of VaD. Although less consistent, higher exposure to CO was also associated with a higher risk of VaD. Most NO2 in cities originates from motor vehicle exhaust; other sources of NO2 are petrol and metal refining, electricity generation from coal-fired power stations, other manufacturing industries, and food processing. Future studies should investigate associations of VaD with specific sources of NO2.

Burden of disease due to nitrogen dioxide exposure in Germany

Abstract Background Numerous studies identified adverse effects of air pollution on health. According to the recent Global Burden of Disease Study about 2.9 million people died prematurely due to the effects of ambient particulate matter (PM) pollution in 2016, which resulted in about 70 million years of life lost (YLL). In addition to PM, a growing body of evidence shows convincing associations between nitrogen dioxide (NO2) with several health outcomes. The case study provides a health risk assessment for NO2 in Germany. Methods A systematic review was performed to select health outcomes with strong evidence for an association with NO2 and to derive an updated exposure-response function (ERF). The exposure assessment was performed on a 1x1 km2 grid by combining measured and modelled data (annual means of NO2 background concentration) with population density. Exposure data and the ERF were combined by the population attributable fraction formula. The main analysis was performed using a counterfactual of 10 µg/m3. Results Only for cardiovascular mortality the evidence for the association with long-term NO2-exposure was rated as “strong”. Thus, the main analysis merely included this outcome. For the year 2014, 5,966 (95% CI: 2,031-9,893) attributable deaths and 49,726 (95% CI: 16,929-82,456) YLL were estimated. Looking at time trends a decrease of disease burden was observed compared to the year 2007 where 7,832 (95% CI: 2,669-12,973) attributable deaths and 69.244 (95% CI: 23.601-114.690) YLL due to NO2 were calculated. Conclusions Our results show a considerable burden due to NO2 in Germany. Compared to previous estimates for PM (ca. 41,100 attributable deaths in 2014) the burden due to NO2 is much lower. However, due to methodological constraints we could not incorporate higher concentrations from traffic hotspots. This, and the fact that we only considered one health outcome in our main analysis, suggests that our results might be an underestimation.

Combined effects of multiple prenatal exposure to pollutants on birth weight: The Mothers and Children's Environmental Health (MOCEH) study

BackgroundIncreasing evidence shows that prenatal environmental exposures is a risk factor for restricted intrauterine growth. However, only a few studies have examined the effects of multiple environmental exposures on fetal growth. ObjectiveTo investigate the effects of prenatal exposure on multiple environmental pollutants (heavy metals, bisphenol, phthalates, and air pollutants) on birth weight. MethodsThe Mothers and Children's Environmental Health study is a prospective birth cohort comprising a total of 719 mother-child pairs, including 466 pairs undergoing early pregnancy exposure and 542 pairs of late pregnancy exposure. The concentrations of three heavy metals (mercury, lead, and cadmium) in the maternal blood samples were measured. The concentrations of three phthalate metabolites [mono(2-ethyl-5-hydroxyhexyl) phthalate, mono(2-ethyl-5-oxohexyl) phthalate, and mono-n-butyl phthalate] and bisphenol A in maternal urine samples were measured. Daily exposure to ambient particulate matter (PM10) and nitrogen dioxide (NO2) exposure was estimated based on residence and averaged by gestational age. To assess the combined effect of multiple pollutants, principal components analysis (PCA) and supervised principal components analysis (SCPA) were conducted. ResultsBased on PCA, the components representing PM10 and NO2 exposure during early pregnancy were significantly associated with birth weight of −32.68 g (95% CI: -64.45 g to −0.91 g) per unit increase of the corresponding component. In SCPA model, the components representing NO2 exposure during early pregnancy and the combined exposure to mercury and lead during late pregnancy were negatively associated with birth weight of −46.63 g (95% CI: -90.65 g to −2.62 g) and −55.32 g (95% CI: -99.01 g to −11.64 g), respectively, per unit increase of the corresponding component. ConclusionBased on our multi-pollutant model, PM10 and NO2 exposure in early pregnancy and the combined effect of Pb and Hg in late pregnancy were associated with reduced birth weight. Our results suggest that exposure to various pollutants during pregnancy has a significant cumulative effect on birth weight, even if each pollutant is at a level below the concentration required for direct effect.

Synergistic Association of House Endotoxin Exposure and Ambient Air Pollution with Asthma Outcomes.

Rationale: House endotoxin and ambient air pollution are risk factors for asthma; however, the effects of their coexposure on asthma are not well characterized.Objectives: To examine potential synergistic associations of coexposure to house dust endotoxin and ambient air pollutants with asthma outcomes.Methods: We analyzed data of 6,488 participants in the National Health and Nutrition Examination Survey 2005-2006. Dust from bedding and bedroom floor was analyzed for endotoxin content. The Community Multiscale Air Quality Modeling System (CMAQ) and Downscaler Model data were used to determine annual average particulate matter ≤2.5 μm in aerodynamic diameter (PM2.5), ozone (O3), and nitrogen dioxide (NO2) exposures at participants' residential locations. The associations of the coexposures with asthma outcomes were assessed and tested for synergistic interaction.Measurements and Main Results: In adjusted analysis, PM2.5 (CMAQ) (odds ratio [OR], 1.12; 95% confidence interval [CI], 1.07-1.18), O3 (Downscaler Model) (OR, 1.07; 95% CI, 1.02-1.13), and log10 NO2 (CMAQ) (OR, 3.15; 95% CI, 1.33-7.45) were positively associated with emergency room visits for asthma in the past 12 months. Coexposure to elevated concentrations of house dust endotoxin and PM2.5 (CMAQ) was synergistically associated with the outcome, increasing the odds by fivefold (OR, 5.01; 95% CI, 2.54-9.87). A synergistic association was also found for coexposure to higher concentrations of endotoxin and NO2 in children (OR, 3.45; 95% CI, 1.65-7.18).Conclusions: Coexposure to elevated concentrations of residential endotoxin and ambient PM2.5 in all participants and NO2 in children is synergistically associated with increased emergency room visits for asthma. Therefore, decreasing exposure to both endotoxin and air pollution may help reduce asthma morbidity.

Interactions between ambient air pollution and obesity on lung function in children: The Seven Northeastern Chinese Cities (SNEC) Study

Children are vulnerable to air pollution-induced lung function deficits, and the prevalence of obesity has been increasing in children. To evaluate the joint effects of long-term PM1 (particulate matter with an aerodynamic diameter ≤ 1.0 μm) exposure and obesity on children's lung function, a cross-sectional sample of 6740 children (aged 7–14 years) was enrolled across seven northeastern Chinese cities from 2012 to 2013. Weight and lung function, including forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), peak expiratory flow (PEF), and maximal mid-expiratory flow (MMEF), were measured according to standardized protocols. Average PM1, PM2.5, PM10 and nitrogen dioxide (NO2) exposure levels were estimated using a spatiotemporal model, and sulphur dioxide (SO2) and ozone (O3) exposure were estimated using data from municipal air monitoring stations. Two-level logistic regression and general linear models were used to analyze the joint effects of body mass index (BMI) and air pollutants. The results showed that long-term air pollution exposure was associated with lung function impairment and there were significant interactions with BMI. Associations were stronger among obese and overweight than normal weight participants (the adjusted odds ratios (95% confidence intervals) for PM1 and lung function impairments in three increasing BMI categories were 1.50 (1.07–2.11) to 2.55 (1.59–4.07) for FVC < 85% predicted, 1.44 (1.03–2.01) to 2.51 (1.53–4.11) for FEV1 < 85% predicted, 1.34 (0.97–1.84) to 2.04 (1.24–3.35) for PEF < 75% predicted, and 1.34 (1.01–1.78) to 1.93 (1.26–2.95) for MMEF < 75% predicted). Consistent results were detected in linear regression models for PM1, PM2.5 and SO2 on FVC and FEV1 impairments (PInteraction < 0.05). These modification effects were stronger among females and older participants. These results can provide policy makers with more comprehensive information for to develop strategies for preventing air pollution induced children's lung function deficits among children.

A retrospective cohort study of long-term nitrogen dioxide exposure and incident hypertension

Objective: To investigate the effect of long-term exposure of nitrogen dioxide on the incidence of hypertension. Methods: From March to December 2009, 37 386 eligible residents from four cities in northern China (Tianjin, Shenyang, Taiyuan, and Rizhao) were enrolled in a follow-up study by using the random cluster sampling method. Demographic characteristics, lifestyle, history of diseases, and self-report situation of hypertension were collected by using questionnaire. Based on the average annual concentration of NO2 during the period from the cohort to the onset of hypertension as an estimate of exposure, the effect of NO2 exposure on hypertension was analyzed by employing Cox proportional hazards model. The interactions between NO2 exposure and different characteristics (age, sex, body mass index, smoking, alcohol consumption, education, economy, exercise, and fruit intake) were also examined. Results: The baseline age of residents was (43.74±13.78) years, and the body mass index (BMI) was (22.56±2.92) kg/m(2). During an average follow-up time of 11.40 years, 2 619 (7.0%) new cases of hypertension were reported. The overall mean environmental pollution levels during the study period for the entire cohort was (40.74±17.07) μg/m(3). After adjusting for age, sex, BMI, family history of hypertension, socio-economic information, and lifestyle, the hazard ratio (HR) of incident hypertension with a 10 μg/m(3) increase of NO2 was 1.21 (95%CI: 1.18-1.25). Compared with residents aged 60 years and over (HR=1.19, 95%CI: 1.14-1.26), former and current smoking (HR=1.20, 95%CI: 1.14-1.25), and high-frequency fruit consumption (HR=1.17, 95%CI: 1.13-1.21), residents younger than 60 years (HR=1.28, 95%CI: 1.25-1.32), non-smoker (HR=1.23, 95%CI: 1.19-1.27), and low-frequency fruit consumption (HR=1.27, 95%CI: 1.20-1.35) had stronger interaction effect with NO2 (all P values for interaction<0.05). Conclusion: NO2 exposure may lead to the onset of hypertension, which has a stronger effect on people younger than 60 years old, without smoking history and with low-frequency fruit consumption.

CC16 Levels into Adult Life Are Associated with Nitrogen Dioxide Exposure at Birth.

Rationale: Lung function and growth are adversely associated with nitrogen dioxide (NO2) exposure. Lower levels of circulating club cell secretory protein (CC16) in childhood are also associated with subsequent decreased lung function. NO2 exposure may induce epithelial damage in lungs and alter club cell proliferation and morphology.Objectives: To determine if increased ambient NO2 levels at participants' home addresses in early life were associated with decreased levels of CC16 from age 6 to 32 years.Methods: Participants were enrolled at birth in the Tucson Children's Respiratory Study and had circulating CC16 measured at least once between age 6 and 32. Linear mixed models were used to determine the association between estimated ambient NO2 exposure at participants' home address at birth or age 6 with CC16 levels from age 6 to 32.Measurements and Main Results: NO2 exposures at birth or age 6 were available for 777 children with one or more CC16 measurement. We found a negative association between NO2 exposure and CC16 levels, with a 4.7% (95% confidence interval, -8.6 to -0.7) decrease in CC16 levels from age 6 to 32 per interquartile range increase in NO2 exposure (6.0 ppb) at the participants' birth address. We observed modification by race (p interaction = 0.04), with stronger associations among participants with at least one black parent (-29.6% [95% confidence interval, -42.9% to -13.2%] per interquartile range). NO2 at participant's age 6 address was not significantly associated with CC16 levels (-1.9%; 95% confidence interval, -6.3 to 2.6).Conclusions: Higher exposure to NO2 at birth is associated with persistently low levels of CC16 from 6 to 32 years.

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.

Exposure to Particles and Nitrogen Dioxide Among Workers in the Stockholm Underground Train System

ObjectivesExposure to fine particles in urban air has been associated with a number of negative health effects. High levels of fine particles have been detected at underground stations in big cities. We investigated the exposure conditions in four occupational groups in the Stockholm underground train system to identify high-exposed groups and study variations in exposure.MethodsPM1 and PM2.5 were measured during three full work shifts on 44 underground workers. Fluctuations in exposure were monitored by a real-time particle monitoring instrument, pDR, DataRAM. Qualitative analysis of particle content was performed using inductively coupled plasma mass spectrometry. Nitrogen dioxide was measured using passive monitors.ResultsFor all underground workers, the geometric mean (GM) of PM1 was 18 μg/m3 and of PM2.5 was 37 μg/m3. The particle exposure was highest for cleaners/platform workers, and the GM of PM1 was 31.6 μg/m3 [geometric standard deviation (GSD), 1.6] and of PM2.5 was 76.5 μg/m3 (GSD, 1.3); the particle exposure was lowest for ticket sellers, and the GM of PM1 was 4.9 μg/m3 (GSD, 2.1) and of PM2.5 was 9.3 μg/m3 (GSD, 1.5). The PM1 and PM2.5 levels were five times higher in the underground system than at the street level, and the particles in the underground had high iron content. The train driver's nitrogen dioxide exposure level was 64.1 μg/m3 (GSD, 1.5).ConclusionsCleaners and other platform workers were statistically significantly more exposed to particles than train drivers or ticket sellers. Particle concentrations (PM2.5) in the Stockholm underground system were within the same range as in the New York underground system but were much lower than in several older underground systems around the world.

Is breast cancer a result of epigenetic responses to traffic-related air pollution? A review of the latest evidence.

Environmental toxicants can exert adverse health effects via epigenetic regulation. We conducted a review of studies assessing traffic-related air pollution (TRAP) exposure and breast cancer (BC) risk, and the evidence for epigenetic mediation. 14 epidemiological studies demonstrated associations between TRAP exposure and BC risk, in which a total of 26 comparisons were assessed. 11 of these comparisons reported a positive association; whereas 15 comparisons were negative. Five publications linked TRAP exposure to epigenetic alterations in genes that may be related to BC risk. One animal study provided evidence of TRAP-treatment inducing breast tumorigenesis. Associations between TRAP components polycyclic aromatic hydrocarbons (PAH) and nitrogen dioxide (NO2) and BC risk were more consistent. While evidence for epigenetic regulation remains limited, polycyclic aromatic hydrocarbons (PAH) and nitrogen dioxide (NO2) exposures may alter methylation of breast tumorigenic genes (e.g., EPHB2, LONP1). Future epigenomic studies with environmental measures are needed to interrogate the relationship between TRAP and BC risk.