NO2 Exposure Research Articles

Ambient air pollution, genetic risk and telomere length in UK biobank.

Telomere length (TL) is a biomarker of genomic aging. The evidence on the association between TL and air pollution was inconsistent. Besides, the modification effect of genetic susceptibility on the air pollution-TL association remains unknown. We aimed to evaluate the association of ambient air pollution with TL and further assess the modification effect of genetic susceptibility. 433,535 participants with complete data of TL and air pollutants in UK Biobank were included. Annual average exposure of NO2, NOx, PM10 and PM2.5 was estimated byapplying land use regression models. Genetic risk score (GRS) was constructed using reported telomere-related SNPs. Leukocyte TL was measured by quantitative polymerase chain reaction (qPCR). Multivariable linear regression models were employed to conduct associational analyses. Categorical exposure models and RCS models both indicated U-shaped (for NO2 and NOx) and L-shaped (for PM10 and PM2.5) correlations between air pollution and TL. In comparison to the lowest quartile, the 2nd and 3rd quartile of NO2 (q2: -1.3% [-2.1%, -0.4%]; q3: -1.2% [-2.0%, -0.3%], NOx (q2: -1.3% [-2.1%, -0.5%]; q3: -1.4% [-2.2%, -0.5%]), PM2.5 (q2: -0.8% [-1.7%, 0.0%]; q3: -1.3% [-2.2%, -0.5%]), and the third quartile of PM10 (q3: -1.1% [-1.9%, -0.2%]) were inversely associated with TL. The highest quartile of NO2 was positively correlated with TL (q4: 1.0% [0.0%, 2.0%]), whereas the negative correlation between the highest quartile of other pollutants and TL was also attenuated and no longer significant. In the genetic analyses, synergistic interactions were observed between the 4th quartile of three air pollutants (NO2, NOx, and PM2.5) and genetic risk. Our study for the first time revealed a non-linear trend for the association between air pollution and telomere length. The genetic analyses suggested synergistic interactions between air pollution and genetic risk on theair pollution-TL association. These findings may shed new light on air pollution's health effects, offer suggestions for identifying at-risk individuals, and provide hints regarding further investigation into gene-environment interactions.

Does air pollution exposure affect semen quality? Evidence from a systematic review and meta-analysis of 93,996 Chinese men.

Air pollution may impair male fertility, but it remains controversial whether air pollution affects semen quality until now. We undertake a meta-analysis to explore potential impacts of six pollutants exposure during the entire window (0-90 days prior to ejaculation) and critical windows (0-9, 10-14, and 70-90 days prior to ejaculation) on semen quality. Seven databases were retrieved for original studies on the effects of six pollutants exposure for 90 days prior to ejaculation on semen quality. The search process does not limit the language and search date. We only included original studies that reported regression coefficients (β) with 95% confidence intervals (CIs). The β and 95% CIs were pooled using the DerSimonian-Laird random effect models. PM2.5 exposure was related with decreased total sperm number (10-14 lag days) and total motility (10-14, 70-90, and 0-90 lag days). PM10 exposure was related with reduced total sperm number (70-90 and 0-90 lag days) and total motility (0-90 lag days). NO2 exposure was related with reduced total sperm number (70-90 and 0-90 lag days). SO2 exposure was related with declined total motility (0-9, 10-14, 0-90 lag days) and total sperm number (0-90 lag days). Air pollution affects semen quality making it necessary to limit exposure to air pollution for Chinese men. When implementing protective measures, it is necessary to consider the key period of sperm development.

Association of short-term nitrogen dioxide exposure with hospitalization for urolithiasis in Xinxiang, China: a time series study

Urolithiasis accounts for the highest incidence of all urologic-associated hospitalizations. However, few studies have explored the effect of nitrogen dioxide (NO2) on hospitalizations for urolithiasis. We included 5956 patients with urolithiasis, collected daily meteorological and air pollution data between 2016 and 2021, and analyzed the associations between air pollutants and hospitalization, length of the hospital stay, and hospitalization costs attributable to urolithiasis. NO2 exposure was associated with an increased risk of hospitalization for urinary tract stones. For each 10-μg/m3 increase and 1-day lag of NO2, the maximum daily effect on the risk of hospitalization for urolithiasis was 1.020 (95% confidence interval [CI]: 1.001–1.039), and the cumulative effect peaked on lag day 4 (relative risk [RR]: 1.061; 95% CI: 1.003–1.122). Attribution scores and quantitative analysis revealed that the mean number of hospital days and mean hospital costs were 16 days and 21,164.39 RMB, respectively. Up to 5.75% of all urolithiasis hospitalizations were estimated to be attributable to NO2, and the cost of NO2-related urolithiasis hospitalizations reached approximately 3,430,000 RMB. Stratified analysis showed that NO2 had a more sensitive impact on urolithiasis hospitalizations in women and in those aged ≥65 years. Notably, men and those younger than 65 years of age (exclude people aged 65) incurred more costs for urolithiasis hospitalizations. In the population level, the association between NO2 and risk of urolithiasis hospitalization was more pronounced during the warm season. NO2 can increase hospitalizations for urolithiasis for Xinxiang City residents, and there is a cumulative lag effect. Focusing on air pollution may have practical significance in terms of the prevention and control of urolithiasis.

Effect of Meteorological Factors and Air Pollutants on Daily Hospital Admissions for Ischemic Heart Disease in Lanzhou, China

Introduction: Meteorological factors and air pollutants are believed to be associated with cardiovascular disease. Ischemic heart disease (IHD) is a major public health issue worldwide. Few studies have investigated the associations among meteorological factors, air pollutants, and IHD daily hospital admissions in Lanzhou, China. Methods: We conducted a distributed lag nonlinear model on the basis of 5-year data, aiming at disentangling the impact of meteorological factors and air pollutants on IHD hospital admissions. All IHD daily hospital admissions recorded from January 1, 2015, and December 31, 2019, were obtained from three hospitals in Lanzhou, China. Daily air pollutant concentrations and meteorological data were synchronously collected from Gansu Meteorological Administration and Lanzhou Environmental Protection Administration. Stratified analyses were performed by sex and two age groups. Results: A total of 23,555 IHD hospital admissions were recorded, of which 10,477 admissions were for coronary artery disease (CAD) and 13,078 admissions were for acute coronary syndrome. Our results showed that there was a nonlinear (J-shaped) relationship between temperature and IHD hospital admissions. The number of IHD hospital admissions was positively correlated with NO2, O3, humidity, and pressure, indicating an increased risk of hospital admissions for IHD under NO2, O3, humidity, and pressure exposure. Meanwhile, both extremely low (−12°C) and high (30°C) temperatures reduced IHD hospital admissions, but the harmful effect increased with the lag time in Lanzhou, China, while the cold effect was more pronounced and long-lasting than the heat effect. Subgroup analysis demonstrated that the risk on CAD hospital admissions increased significantly in females and <65 years of age at −12°C. Conclusion: Our findings added to the growing evidence regarding the potential impact of meteorological factors and air pollutants on policymaking from the perspective of hospital management efficiency.

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.

Role of potassium loading in ZnO-based gas sensors under NO2 exposure – Operando diffuse reflectance infrared Fourier transform spectroscopic study

Unloaded, 0.08 and 0.9 at% potassium (K)-loaded ZnO gas sensors were investigated using operando diffuse reflectance infrared Fourier transform (DRIFT) spectroscopy combined with simultaneous direct current (DC) sensor resistance measurements. At 250 °C in humidified (10%) synthetic air, during NO2 exposure, K-loaded ZnO exhibits a resistance decrease, which is contrary to the usual response of unloaded ZnO. Using DRIFTS, it was observed that for K-loaded ZnO, under NO2 exposure, free nitrates (such as KNO3) are formed and surface oxygen is removed, which explains the observed decrease in resistance. Moreover, the presence of K-related carbonates was confirmed through X-ray photoelectron spectroscopy. In addition, decomposition of monodentate carbonates was observed during the formation of free nitrates. To the best of our knowledge, this is the first time the peculiar sensor response of K-loaded ZnO to NO2 is reported and explained.

Early life exposure to air pollution and psychotic-like experiences, emotional symptoms, and conduct problems in middle childhood

BackgroundAir pollution has been linked to a variety of childhood mental health problems, but results are inconsistent across studies and the effect of exposure timing is unclear. We examined the associations between air pollution exposure at two time-points in early development and psychotic-like experiences (PLEs), and emotional and conduct symptoms, assessed in middle childhood (mean age 11.5 years).MethodsParticipants were 19,932 children selected from the NSW Child Development Study (NSW-CDS) with available linked multi-agency data from birth, and self-reported psychotic-like experiences (PLEs) and psychopathology at age 11–12 years (middle childhood). We used binomial logistic regression to examine associations between exposure to nitrogen dioxide (NO2) and particulate matter less than 2.5 μm (PM2.5) at two time-points (birth and middle childhood) and middle childhood PLEs, and emotional and conduct symptoms, with consideration of socioeconomic status and other potential confounding factors in adjusted models.ResultsIn fully adjusted models, NO2 exposure in middle childhood was associated with concurrent PLEs (OR = 1.10, 95% CI = 1.02–1.20). Similar associations with PLEs were found for middle childhood exposure to PM2.5 (OR = 1.05, 95% CI = 1.01–1.09). Neither NO2 nor PM2.5 exposure was associated with emotional symptoms or conduct problems in this study.ConclusionsThis study highlights the need for a better understanding of potential mechanisms of action of NO2 in the brain during childhood.

Ambient Nitrogen Dioxide and Hospitalizations of Full-Spectrum Respiratory Diseases: A National Case-Crossover Study.

Few multicity studies have examined the acute effects of nitrogen dioxide (NO2) on respiratory disease (RD), especially its specific causes. This study aimed to investigate the associations between short-term exposure to NO2 and hospitalization of full-spectrum RDs in China. Hospitalization of 10 major categories and 40 cause-specific RDs were obtained from 20 provinces over the study period of 2013-2020. A time-stratified case-crossover study was conducted at the individual level to explore the associations between NO2 and RDs. NO2 was significantly associated with increased hospitalization of eight major RDs (acute upper respiratory infections, influenza and pneumonia, acute lower respiratory infections, upper respiratory tract diseases, chronic lower respiratory diseases, respiratory interstitium diseases, pleura diseases, and other respiratory diseases) and 18 specific causes of RDs, with the largest associations observed on lag 0-1 day. The effect estimates ranged from 0.75 to 4.09% per 10 μg/m3 of NO2 exposure. The associations remained robust after controlling for copollutants. The concentration-response curves were mostly positive and linear. This nationwide study provides comprehensive information on the acute effects of NO2 on respiratory morbidity across the full spectrum, highlighting the need for caution with regard to this important traffic-related air pollutant in current pollution control programs.

Exposure to ambient air pollutants is associated with an increased incidence of hyperuricemia: A longitudinal cohort study among Chinese government employees

BackgroundIt is widely recognized that ambient air pollution can induce various detrimental health outcomes. However, evidence linking ambient air pollutants and hyperuricemia incidence is scarce. ObjectivesTo assess the association between long-term air pollution exposure and the risk of hyperuricemia. MethodsIn this study, a total of 5854 government employees without hyperuricemia were recruited and followed up from January 2018 to June 2021 in Hunan Province, China. Hyperuricemia was defined as serum uric acid (SUA) level of >420 μmol/L for men and >360 μmol/L for women or use of SUA-lowering medication or diagnosed as hyperuricemia during follow-up. Data from local air quality monitoring stations were used to calculate individual exposure levels of PM10, PM2.5, SO2 and NO2 by inverse distance weightingn (IDW) method. Cox proportional hazard model was applied to evaluate the causal relationships between air pollutant exposures and the risk of hyperuricemia occurrence after adjustment for potential confounders and meanwhile, restricted cubic spline was used to explore the dose-response relationships. ResultsThe results indicated that exposures to PM10 (hazard ratio, HR = 1.042, 95% conficence interal, 95% CI: 1.028, 1.057), PM2.5 (HR = 1.204, 95% CI: 1.141, 1.271) and NO2 (HR = 1.178, 95% CI: 1.125,1.233) were associated with an increased HR of hyperuricemia. In addition, a nonlinear dose-response relationship was found between PM10 exposure level and the HR of hyperuricemia (p for nonlinearity = 0.158) with a potential threshold of 50.11 μg/m3. Subgroup analysis demonstrated that participants usually waking up at night and using natural ventilation were more vulnerable to the exposures of PM10, PM2.5, NO2, and SO2. ConclusionLong-term exposures to ambient PM10, PM2.5 and NO2 are associated with an increased incidence of hyperuricemia among Chinese government employees.

Can traffic-related air pollution trigger myocardial infarction within a few hours of exposure? Identifying hourly hazard periods

IntroductionTraffic-related air pollution can trigger myocardial infarction (MI). However, the hourly hazard period of exposure to nitrogen dioxide (NO2), a common traffic tracer, for incident MI has not been fully evaluated. Thus, the current hourly US national air quality standard (100 ppb) is based on limited hourly-level effect estimates, which may not adequately protect cardiovascular health. ObjectivesWe characterized the hourly hazard period of NO2 exposure for MI in New York state (NYS), USA, from 2000 to 2015. MethodsFor nine cities in NYS, we obtained data on MI hospitalizations from the NYS Department of Health Statewide Planning and Research Cooperative System and hourly NO2 concentrations from the US Environmental Protection Agency’s Air Quality System database. We used city-wide exposures and a case-crossover study design with distributed lag non-linear terms to assess the relationship between hourly NO2 concentrations over 24 h and MI, adjusting for hourly temperature and relative humidity. ResultsThe mean NO2 concentration was 23.2 ppb (standard deviation: 12.6 ppb). In the six hours preceding MI, we found linearly increased risk with increasing NO2 concentrations. At lag hour 0, a 10 ppb increase in NO2 was associated with 0.2 % increased risk of MI (Rate Ratio [RR]: 1.002; 95 % Confidence Interval [CI]: 1.000, 1.004). We estimated a cumulative RR of 1.015 (95 % CI: 1.008, 1.021) for all 24 lag hours per 10 ppb increase in NO2. Lag hours 2–3 had consistently elevated risk ratios in sensitivity analyses. ConclusionsWe found robust associations between hourly NO2 exposure and MI risk at concentrations far lower than current hourly NO2 national standards. Risk of MI was most elevated in the six hours after exposure, consistent with prior studies and experimental work evaluating physiologic responses after acute traffic exposure. Our findings suggest that current hourly standards may be insufficient to protect cardiovascular health.

Green and facile production of UTSA-16 (Zn) in aqueous media with improved CO2 adsorption performance

UTSA-16 (Zn) is the most promising adsorbent for CO2 capture because of its excellent CO2 capture performance and low material cost. An eco-friendly synthesis method for UTSA-16 (Zn) was investigated by changing the ratio of water to ethanol in solution (60:40 to 100:0) under microwave irradiation with different washing conditions: 1. diethyl ether and methanol washing (DEMW), 2. diethyl ether and water washing (DEWW), and 3. water washing (WW). Synthesis at an optimal ratio of water to ethanol (100:0) presented the best CO2 adsorption capacity of 5.08 mmol/g and CO2/N2 selectivity of 120. The integrity of the samples was investigated in terms of the particle morphology, crystallinity, porosity, and thermal stability using scanning electron microscopy, X-ray diffraction, Brunauer–Emmett–Teller analysis, and thermogravimetric analysis. The stability of pelletized UTSA-16 (Zn) synthesized in a water-only solution was examined by exposing samples to humid air and acidic gases (NO2 and SO2); the pellets exhibited excellent stability to humid air and NO2 exposure. Additionally, the pellets exhibited excellent recyclability during the temperature swing adsorption–desorption process.

Incident risk and burden of cardiovascular diseases attributable to long-term NO2 exposure in Chinese adults

BackgroundA number of studies suggested a nexus between long-term exposure to nitrogen dioxide (NO2) and the incidence of cardiovascular disease (CVD), while population-based cohort evidence in low- and middle-income countries was extensively sparse. MethodsWe carried out an 8-year longitudinal study (2010–2018) in a nationwide dynamic cohort of 36,948 Chinese adult participants, who were free of CVD at baseline. Annual average estimates of NO2 exposure were predicted using a well-validated spatiotemporal model and assigned to study participants based on their residential counties. Considering death as a competing risk event, Fine-Gray competing risk models with time-varying exposures at an annual scale were used to quantify incident risks of overall CVD, hypertension, and stroke associated with a 10-μg/m3 rise in NO2 exposure. Using the meta-analysis approach, we performed a pooled analysis of hazard ratio (HR) drawn from this and prior multinational cohort studies for the assessment of attributable burden. NO2-attributable overall CVD incidents in China were evaluated by city and province for years 2010 and 2018, referring to a counterfactual exposure level of 10 μg/m3 (2021 World Health Organization [WHO] air quality guidelines). A decomposition method was used to decompose net change in NO2-attributable CVD incidents during 2010 and 2018 into 3 primary contributions of driving factors (i.e., changes in NO2 exposure, population size, and incidence rate). ResultsA total of 4428 overall CVD events (hypertension 2448, stroke 1044) occurred during a median follow-up period of 6.1 years. Annual mean NO2 concentration from 2010 to 2018 was 20.0 μg/m3 (range: 6.9–57.4 μg/m3). An increase of 10-µg/m3 in NO2 was associated with an HR of 1.558 (95% confidence interval [CI]: 1.477, 1.642) for overall CVD, 1.521 (95% CI: 1.419, 1.631) for hypertension, and 1.664 (95% CI: 1.485, 1.865) for stroke. Longitudinal associations of NO2 exposure with incident CVD were nearly linear over the exposure range, suggesting no discernible thresholds. Subgroup analyses indicated significantly higher NO2-associated risks of incident CVD among urban residents and overweight/obese individuals. According to pooled HR of NO2-CVD association (1.108, 95% CI: [1.007, 1.219]) from 10 multinational cohort studies, we estimated totally 1.44 million incident CVD cases attributable to NO2 exposure in 2018, representing a substantial decrease of 0.41 million compared to the estimate in 2010 (1.85 million) in mainland of China. Nationally, from 2010 to 2018, the attributable incident cases greatly dropped by 22.4%, which was dominantly driven by declined NO2 concentration (−47.1%) that had offset far from the rise of CVD incidence rate (+19.6%) and population growth (+5.1%). ConclusionsThis study provided nationwide cohort evidence for elevated risks of CVD incidence associated with long-term ambient NO2 exposure among Chinese adults, particularly in urban areas and among overweight/obese individuals. Our findings highlighted that reducing NO2 exposure below 2021 WHO guideline could help prevent a substantial portion of incident CVD cases in China.

Pre-admission ambient air pollution and blood soot particles predict hospitalisation outcomes in COVID-19 patients.

Air pollution exposure is one of the major risk factors for aggravation of respiratory diseases. We investigated whether exposure to air pollution and accumulated black carbon (BC) particles in blood were associated with coronavirus disease 2019 (COVID-19) disease severity, including the risk for intensive care unit (ICU) admission and duration of hospitalisation. From May 2020 until March 2021, 328 hospitalised COVID-19 patients (29% at intensive care) were recruited from two hospitals in Belgium. Daily exposure levels (from 2016 to 2019) for particulate matter with aerodynamic diameter <2.5 µm and <10 µm (PM2.5 and PM10, respectively), nitrogen dioxide (NO2) and BC were modelled using a high-resolution spatiotemporal model. Blood BC particles (internal exposure to nano-sized particles) were quantified using pulsed laser illumination. Primary clinical parameters and outcomes included duration of hospitalisation and risk of ICU admission. Independent of potential confounders, an interquartile range (IQR) increase in exposure in the week before admission was associated with increased duration of hospitalisation (PM2.5 +4.13 (95% CI 0.74-7.53) days, PM10 +4.04 (95% CI 1.24-6.83) days and NO2 +4.54 (95% CI 1.53-7.54) days); similar effects were observed for long-term NO2 and BC exposure on hospitalisation duration. These effect sizes for an IQR increase in air pollution on hospitalisation duration were equivalent to the effect of a 10-year increase in age on hospitalisation duration. Furthermore, for an IQR higher blood BC load, the OR for ICU admission was 1.33 (95% CI 1.07-1.65). In hospitalised COVID-19 patients, higher pre-admission ambient air pollution and blood BC levels predicted adverse outcomes. Our findings imply that air pollution exposure influences COVID-19 severity and therefore the burden on medical care systems during the COVID-19 pandemic.

Causal links between long-term exposure to NO2 and the risk of cardiovascular hospitalization

Objective: To determine the causal association between long-term Nitrogen dioxide (NO2) exposure and the risk of cardiovascular hospitalization. Methods: Based on a sub-cohort of a community-based prospective cohort study, a total of 36 271 participants were recruited from 35 communities randomly selected in Guangzhou in 2015. The annual average exposure of NO2, demographic characteristics, lifestyle factors, and information on the causes of hospitalization was collected. We applied marginal structural Cox models to investigate the effect of NO2 on cardiovascular hospitalization. Demographic and behavioral factors also stratified results. Results: The mean age of participants in the present study was (50.9±17.8) years, and the cardiovascular admission rate was 8.7%, with 203 822 person-years of follow-up. The annual mean NO2 concentration was 48.7 μg/m3 during 2015-2020. For each 10 μg/m3 increase in NO2 concentrations, the HRs (95%CIs) of total cardiovascular hospitalization, cardiovascular hospitalization, and cerebrovascular hospitalization were 1.33 (1.16-1.52), 1.36 (1.16-1.60) and 1.25 (1.00-1.55), respectively. Participants who were never married/married, with secondary education, high exercise frequency, or non-smokers/current smokers may be more susceptible than their counterparts. Conclusion: Long-term exposure to NO2 significantly increased hospitalization risk for cardiovascular disease.

Assessment of children's personal and land use regression model-estimated exposure to NO2 in Springfield, Massachusetts

Ambient nitrogen dioxide (NO2) is derived from tailpipe vehicle emission and is linked with various of health outcomes. Personal exposure monitoring is crucial for accurate assessment of the associated disease risks. This study aimed to evaluate the utility of a wearable air pollutant sampler in determining the personal NO2 exposure of school children for comparison with a model-based personal exposure assessment. We employed cost-effective, wearable passive samplers to directly measure personal exposure of 25 children (aged 12–13 years) in Springfield, MA to NO2 over a five-day period in winter 2018. NO2 levels were additionally measured at 40 outdoor sites in the same region using stationary passive samplers. A land use regression (LUR) model was developed based on the ambient NO2 measures, with a good prediction performance (R2 = 0.72) using road lengths, distance to highway, and institutional land area as predictor variables. Time-weighted averages (TWA), which incorporated the time-activity patterns of participants and LUR-derived estimates in children's primary microenvironments (homes, the school and commute paths), were calculated as an indirect measure of personal NO2 exposure. Results indicated that the conventional residence-based exposure estimate approach, often used in epidemiological studies, differed from the direct personal exposure and could overestimate the personal exposure by up to 109 %. TWA improved personal NO2 exposure estimates by accounting for the time activity patterns of individuals, a difference of 5.4 % ± 34.2 % was found for exposures compared to wristband measurements. Nevertheless, the personal wristband measurements exhibited a large variability due to the potential contributions from indoor and in-vehicle NO2 sources. The findings suggest that exposure to NO2 can be highly personalized based on individual activities and contact with pollutants in specific microenvironments, reaffirming the importance of measuring personal exposure.

Effect of NO2 exposure on airway inflammation and oxidative stress in asthmatic mice

Nitrogen dioxide (NO2) is a widespread air pollutant. Epidemiological evidence indicates that NO2 is associated with an increase of incidence rate and mortality of asthma, but its mechanism is still unclear. In this study, we exposed mice to NO2 (5 ppm, 4 h per day for 30 days) intermittently to investigate the development and potential toxicological mechanisms of allergic asthma. We randomly assigned 60 male Balb/c mice to four groups: saline control, ovalbumin (OVA) sensitization, NO2 alone, and OVA+NO2 groups. The involved mechanisms were found from the perspective of airway inflammation and oxidative stress. The results showed that NO2 exposure could aggravate lung inflammation in asthmatic mice, and airway remodeling was characterized by significant thickening of the airway wall and infiltration of inflammatory cells. Moreover, NO2 would aggravate the airway hyperresponsiveness (AHR), which is characterized by significantly elevated inspiratory resistance (Ri) and expiratory resistance (Re), as well as decreased dynamic lung compliance (Cldyn). In addition, NO2 exposure promoted pro-inflammatory cytokines (IL-6 and TNF-α) and serum immunoglobulin (IgE) production. The imbalance of Th1/Th2 cell differentiation (IL-4 increased, IFN-γ reduced, IL-4/IFN-γ significantly increased) played a key role in the inflammatory response of asthma under NO2 exposure. In a nutshell, NO2 exposure could promote allergic airway inflammation and increase asthma susceptibility. The levels of ROS and MDA among asthmatic mice exposed to NO2 increased significantly, while GSH levels sharply decreased. These findings may provide better toxicological evidence for the mechanisms of allergic asthma risk due to NO2 exposure.

Ambient NO2 hinders neutrophil extracellular trap formation in rats: Assessment of the role of neutrophil autophagy

NO2 has been known to impair immunity and exacerbate susceptibility to infectious diseases. However, scant notice has been taken of the effect of NO2 on neutrophils. Neutrophil extracellular traps (NETs) formation is necessary for NETosis development by neutrophils as an immune system against pathogens. By analyzing the morphology and signature components of NETs, we focused for the first time on finding that 10 ppm of NO2 exposure for 15 consecutive days can hinder the formation of NETs. Next, we used NO2 in vivo derivatives to probe the mechanism for NETs formation in vitro. Our findings showed that NO2 suppression of respiratory burst levels and mitogen-activated protein kinase (MAPK)/Phosphoinositide 3-kinase (PI3K)-protein kinase B (AKT) signaling was related to NO2 reduction in NETs formation. Inhibition of phorbol myristate acetate (PMA)-induced NETs formation by NO2 hindered autophagy, as evidenced by increased mTOR protein expression, decreased LC3 protein expression, and reduced autophagic vesicles. By activating mTOR-mediated autophagy, rapamycin (Rapa) reduced the inhibition of PMA-induced NETs by NO2. This study will provide valuable insights into the mechanisms of immunotoxicity of NO2, new insights into the etiology of diseases linked to NETs formation, and a theoretical basis for protection against such illnesses.

Effects of ambient fine particulates, nitrogen dioxide, and ozone on maturation of functional brain networks across early adolescence

BackgroundAir pollution is linked to neurodevelopmental delays, but its association with longitudinal changes in brain network development has yet to be investigated. We aimed to characterize the effect of PM2.5, O3, and NO2 exposure at ages 9–10 years on changes in functional connectivity (FC) over a 2-year follow-up period, with a focus on the salience (SN), frontoparietal (FPN), and default-mode (DMN) brain networks as well as the amygdala and hippocampus given their importance in emotional and cognitive functioning. MethodsA sample of children (N = 9,497; with 1–2 scans each for a total of 13,824 scans; 45.6% with two brain scans) from the Adolescent Brain Cognitive Development (ABCD) Study® were included. Annual averages of pollutant concentrations were assigned to the child’s primary residential address using an ensemble-based exposure modeling approach. Resting-state functional MRI was collected on 3T MRI scanners. First, developmental linear mixed-effect models were performed to characterize typical FC development within our sample. Next, single- and multi-pollutant linear mixed-effect models were constructed to examine the association between exposure and intra-network, inter-network, and subcortical-to-network FC change over time, adjusting for sex, race/ethnicity, income, parental education, handedness, scanner type, and motion. ResultsDevelopmental profiles of FC over the 2-year follow-up included intra-network integration within the DMN and FPN as well as inter-network integration between the SN-FPN; along with intra-network segregation in the SN as well as subcortical-to-network segregation more broadly. Higher PM2.5 exposure resulted in greater inter-network and subcortical-to-network FC over time. In contrast, higher O3 concentrations resulted in greater intra-network, but less subcortical-to-network FC over time. Lastly, higher NO2 exposure led to less inter-network and subcortical-to-network FC over the 2-year follow-up period. ConclusionTaken together, PM2.5, O3, and NO2 exposure in childhood relate to distinct changes in patterns of network maturation over time. This is the first study to show outdoor ambient air pollution during childhood is linked to longitudinal changes in brain network connectivity development.

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.

Лечебная эффективность Н-холинолитика N,N-диэтил-5,5-дифенил-2-пентиниламина на моделях некардиогенного отека легких

The existing non-cardiogenic pulmonary edema (NCPE) treatment methods are not sufficiently effective. N,N-Diethyl-5,5-diphenyl-2-pentynylamine hydrochloride (DDPA), the N-cholinolitic drug, is of interest as a potential remedy for treatment of toxic pulmonary edema (TPE). The study was aimed to determine therapeutic efficacy of the drug in animal TPE models. TPE in white rats was induced through intraperitoneal thiourea injection or nitrogen dioxide inhalation. Treatment of animals involved inhalation of the DDPA aqueous solution. The efficacy was estimated based on the animals’ survival rate and lung gravimetry data. The results were assessed based on descriptive statistics using the Student's t-test. In the model of thiourea-induced NCPE, the drug administered after the toxic exposure increased the animals’ survival rate and significantly decreased lung hydration levels (149% vs. 262.5% in non-treated animals). In the model of nitrogen dioxideinduced NCPE, the drug significantly increased the rats’ survival rate within the period between 0 and 5 h, however, the differences became non-significant within 24 h. The treated animals had 15–20% lower respiratory rate and pulmonary coefficients than non-treated animals 5 h after the NO2 exposure. The use of DDPA improved the survival rate and overall health in both TPE models, however, the thiourea-based model showed better treatment outcomes compared to the NO2–based model. Such differences can be explained by the deeper and more disruptive nature of the lung tissue injury caused by nitrogen dioxide compared to that caused by thiourea. Thus, the use of DDPA in individuals with injuries induced by pulmonotoxic chemicals may be promising at the prehospital stage.