Oxidant Air Pollution Research Articles

Application of an integrated device for ultra-low temperature desulfurization and denitration in large rotary kiln

To tackle the problem of excessive nitrogen oxide emissions during the denitration process of the lime rotary kiln at Beitai Iron Mine, it was proposed to integrate ultra-low temperature SCR denitration catalysts and a moving-burden bed reactor into a radial combined desulfurization and denitration device to achieve ultra-low temperature denitration in a low-sulfur state. The self-built integrated device features two desulphurization beds and one denitration bed, through which the flue gas passes successively in a radial flow manner. Industrial test results indicate that the denitration efficiency reached an average of 96.07% at temperatures ranging from 70 to 130°C during a 14-day test period, indicating a good denitration effect. The ultra-low temperature SCR denitration device has been put into use, effectively reducing nitrogen oxide emissions and air pollution, while also promoting the optimization and upgrading of the energy structure. The research results can provide a reference for the environmental management of mining and processing enterprises.

Early-Life Exposure to Air Pollution and Childhood Asthma Cumulative Incidence in the ECHO CREW Consortium

Exposure to outdoor air pollution contributes to childhood asthma development, but many studies lack the geographic, racial and ethnic, and socioeconomic diversity to evaluate susceptibility by individual-level and community-level contextual factors. To examine early life exposure to fine particulate matter (PM2.5) and nitrogen oxide (NO2) air pollution and asthma risk by early and middle childhood, and whether individual and community-level characteristics modify associations between air pollution exposure and asthma. This cohort study included children enrolled in cohorts participating in the Children's Respiratory and Environmental Workgroup consortium. The birth cohorts were located throughout the US, recruited between 1987 and 2007, and followed up through age 11 years. The survival analysis was adjusted for mother's education, parental asthma, smoking during pregnancy, child's race and ethnicity, sex, neighborhood characteristics, and cohort. Statistical analysis was performed from February 2022 to December 2023. Early-life exposures to PM2.5 and NO2 according to participants' birth address. Caregiver report of physician-diagnosed asthma through early (age 4 years) and middle (age 11 years) childhood. Among 5279 children included, 1659 (31.4%) were Black, 835 (15.8%) were Hispanic, 2555 (48.4%) where White, and 229 (4.3%) were other race or ethnicity; 2721 (51.5%) were male and 2596 (49.2%) were female; 1305 children (24.7%) had asthma by 11 years of age and 954 (18.1%) had asthma by 4 years of age. Mean values of pollutants over the first 3 years of life were associated with asthma incidence. A 1 IQR increase in NO2 (6.1 μg/m3) was associated with increased asthma incidence among children younger than 5 years (HR, 1.25 [95% CI, 1.03-1.52]) and children younger than 11 years (HR, 1.22 [95% CI, 1.04-1.44]). A 1 IQR increase in PM2.5 (3.4 μg/m3) was associated with increased asthma incidence among children younger than 5 years (HR, 1.31 [95% CI, 1.04-1.66]) and children younger than 11 years (OR, 1.23 [95% CI, 1.01-1.50]). Associations of PM2.5 or NO2 with asthma were increased when mothers had less than a high school diploma, among Black children, in communities with fewer child opportunities, and in census tracts with higher percentage Black population and population density; for example, there was a significantly higher association between PM2.5 and asthma incidence by younger than 5 years of age in Black children (HR, 1.60 [95% CI, 1.15-2.22]) compared with White children (HR, 1.17 [95% CI, 0.90-1.52]). In this cohort study, early life air pollution was associated with increased asthma incidence by early and middle childhood, with higher risk among minoritized families living in urban communities characterized by fewer opportunities and resources and multiple environmental coexposures. Reducing asthma risk in the US requires air pollution regulation and reduction combined with greater environmental, educational, and health equity at the community level.

Air pollution and oxidative stress in adults suffering from airway diseases. Insights from the Gene Environment Interactions in Respiratory Diseases (GEIRD) multi-case control study

Air pollution is a leading risk factor for global mortality and morbidity. Oxidative stress is a key mechanism underlying air-pollution-mediated health effects, especially in the pathogenesis/exacerbation of airway impairments. However, evidence lacks on subgroups at higher risk of developing more severe outcomes in response to air pollution. This multi-centre study aims to evaluate the association between air pollution and oxidative stress in healthy adults and in patients affected by airway diseases from the Italian GEIRD (Gene Environment Interactions in Respiratory Diseases) multi-case control study. Overall, 1841 adults (49 % females, 20–83 years) were included from four Italian centres: Pavia, Sassari, Turin, and Verona. Following a 2-stage screening process, we identified 1273 cases of asthma, chronic bronchitis, rhinitis, or COPD and 568 controls. Systemic oxidative stress was quantified by urinary 8-isoprostane and 8-OH-dG. Individual residential exposures to NO2, PM10, PM2.5, and O3 were derived using an innovative five-stage machine-learning-based approach. Linear mixed regression models tested the association between oxidative stress biomarkers and air pollution tertiles, adjusting by age, sex, BMI, smoking, education and season, with recruiting centres as random intercept. Only cases exhibited higher levels of log-transformed 8-isoprostane and 8-OH-dG in association with NO2 (β: 0.30 95 % CI: 0.08–0.52 and 0.20 95 % CI: 0.03–0.37), PM10 (0.34 95 % CI: 0.12–0.55 and 0.21 95 % CI: 0.05–0.37) and PM2.5 (0.27 95 % CI: 0.09–0.49 and 0.18 95 % CI: 0.02–0.34) as compared to the first tertile of exposure. No significant associations were observed for summer O3. Our findings suggest that exposure to air pollution may increase systemic oxidative stress levels in people suffering from airway diseases. This introduces a potential novel approach available for future epidemiological studies and Public Health for effective prevention strategies oriented at the quantification of early biological effects in susceptible people, whose additional risk level might be currently underrated. Air-pollution-mediated exacerbations, driven by oxidative stress, still deserve our attention.

Oxidative Stress and Air Pollution: Its Impact on Chronic Respiratory Diseases

Redox regulation participates in the control of various aspects of metabolism. Reactive oxygen and nitrogen species participate in many reactions under physiological conditions. When these species overcome the antioxidant defense system, a distressed status emerges, increasing biomolecular damage and leading to functional alterations. Air pollution is one of the exogenous sources of reactive oxygen and nitrogen species. Ambient airborne particulate matter (PM) is important because of its complex composition, which includes transition metals and organic compounds. Once in contact with the lungs' epithelium, PM components initiate the synthesis of inflammatory mediators, macrophage activation, modulation of gene expression, and the activation of transcription factors, which are all related to the physiopathology of chronic respiratory diseases, including cancer. Even though the pathophysiological pathways that give rise to the development of distress and biological damage are not fully understood, scientific evidence indicates that redox-dependent signaling pathways are involved. This article presents an overview of the redox interaction of air pollution inside the human body and the courses related to chronic respiratory diseases.

Using biochar to control nitric oxide air pollution

This study deals with the ability of Rice Husk Biochar (RHB) to adsorb and reduce the concentration of 90 ppm Nitric Oxide (NO) gas which passed through it with a 1.2 liter/min flow rate within 8 minutes. The characteristics of biochar before and after adsorption were studied by SEM, EDAX, and FTIR analyses. To study the effect of different factors on adsorption the effect of manufacturing temperatures of biochar was studied by using two degrees 450 °C and 500 °C. It has also been measured the effect of biochar particles size using two types of size, coarse (C) and fine (F). The effect of the shape of the measurement system on the adsorption was also measured using two types of systems A and B. In general, the RHB450C A gives the best adsorption capacity for NO (95.7 mg/g) followed by RHB450F A (41.9 mg/g) followed by RHB500C A (24.8 mg/g). Both Langmuir and Freundlich isothermal models were applied to mathematical modelling of NO adsorption, and based on the coefficient of determination (r2) Langmuir’s model provided a perfect fit to the experimental data. It was also found that the pseudo-first-order model is suitable for studying adsorption kinetics.

Transcriptomics Underlying Pulmonary Ozone Pathogenesis Regulated by Inflammatory Mediators in Mice.

Ozone (O3) is the predominant oxidant air pollutant associated with airway inflammation, lung dysfunction, and the worsening of preexisting respiratory diseases. We previously demonstrated the injurious roles of pulmonary immune receptors, tumor necrosis factor receptor (TNFR), and toll-like receptor 4, as well as a transcription factor NF-κB, in response to O3 in mice. In the current study, we profiled time-dependent and TNFR- and NF-κB-regulated lung transcriptome changes by subacute O3 to illuminate the underlying molecular events and downstream targets. Mice lacking Tnfr1/Tnfr2 (Tnfr-/-) or Nfkb1 (Nfkb1-/-) were exposed to air or O3. Lung RNAs were prepared for cDNA microarray analyses, and downstream and upstream mechanisms were predicted by pathway analyses of the enriched genes. O3 significantly altered the genes involved in inflammation and redox (24 h), cholesterol biosynthesis and vaso-occlusion (48 h), and cell cycle and DNA repair (48–72 h). Transforming growth factor-β1 was a predicted upstream regulator. Lack of Tnfr suppressed the immune cell proliferation and lipid-related processes and heightened epithelial cell integrity, and Nfkb1 deficiency markedly suppressed lung cell cycle progress during O3 exposure. Common differentially regulated genes by TNFR and NF-κB1 (e.g., Casp8, Il6, and Edn1) were predicted to protect the lungs from cell death, connective tissue injury, and inflammation. Il6-deficient mice were susceptible to O3-induced protein hyperpermeability, indicating its defensive role, while Tnf-deficient mice were resistant to overall lung injury caused by O3. The results elucidated transcriptome dynamics and provided new insights into the molecular mechanisms regulated by TNFR and NF-κB1 in pulmonary subacute O3 pathogenesis.

Influence of Dose Metrics on Associations between Exposure to Black Carbon and Exhaled Nitric Oxide in Children with Asthma

BACKGROUND AND AIM: Few studies examined the associations between fractional exhaled nitric oxide (FeNO) and traffic-related air pollution (TRAP) from individual dosimetry models. Our study aimed to assess the associations between FeNO and black carbon (BC, as a surrogate of TRAP) from four dose metrics. Besides, we aimed to examine if more refined dose metrics would impact the health risk estimates. METHODS: We recruited 35 children with asthma living in environmental justice communities. Daily FeNO measurements were followed for up to 30 days for each child. Four dose metrics were calculated based on measurements from a central-site and personal monitors, with and without estimates of inhalation rates based on a self-reported time-activity questionnaire. Linear mixed effect models were used to test the associations of BC at different lag periods and FeNO. RESULTS:Exposure to BC was positively associated with FeNO within the first 24 hours of exposure. A log-transformed interquartile range increase in inhaled dose from metrics that used central-site estimates (Model A, C) increased 7% (95% CI: 1% - 14%) and 6% (95% CI: 0% - 13%) in FeNO at lag 0-6 hours in the adjusted model 4. The strength of association persisted at lag 7-12 hours and then decreased and became insignificant at longer lag periods. Similarly, the inhaled dose from personal monitored estimates (Model B, D) was positively associated with FeNO within the first 24 hours. Using personal BC measurements or dynamic inhalation rate did not improve prediction of changes in FeNO. CONCLUSIONS:Our findings revealed that inhaled BC dose significantly increases FeNO level within the first 24 hours of exposure. Our results provide evidence that personal exposure to BC was associated with airway inflammation among children with asthma. Our results also add to the limited number of studies that compared the effect estimates among alternative dose metrics within a single study. KEYWORDS: traffic-related, air pollution, Short-term exposure, asthma, Children's environmental health

Atmospheric mercury in the Latrobe Valley, Australia: Case study June 2013

Gaseous elemental mercury observations were conducted at Churchill, Victoria, in Australia from April to July, 2013, using a Tekran 2537 analyzer. A strong diurnal variation with daytime average values of 1.2–1.3 ng m–3 and nighttime average values of 1.6–1.8 ng m–3 was observed. These values are significantly higher than the Southern Hemisphere average of 0.85–1.05 ng m–3. Churchill is in the Latrobe Valley, approximately 150 km East of Melbourne, where approximately 80% of Victoria’s electricity is generated from low-rank brown coal from four major power stations: Loy Yang A, Loy Yang B, Hazelwood, and Yallourn. These aging generators do not have any sulfur, nitrogen oxide, or mercury air pollution controls. Mercury emitted in the 2015–2016 year in the Latrobe Valley is estimated to have had an externalized health cost of $AUD88 million. Air pollution mercury simulations were conducted using the Weather Research and Forecast model with Chemistry at 3 × 3 km resolution. Electrical power generation emissions were added using mercury emissions created from the National Energy Market’s 5-min energy distribution data. The strong diurnal cycle in the observed mercury was well simulated (R2 = .49 and P value = 0.00) when soil mercury emissions arising from several years of wet and dry deposition in a radius around the power generators was included in the model, as has been observed around aging lignite coal power generators elsewhere. These results indicate that long-term air and soil sampling in power generation regions, even after the closure of coal fired power stations, will have important implications to understanding the airborne mercury emissions sources.

Effect of maternal HIV infection, BMI and NOx air pollution exposure on birth outcomes in South African pregnant women genotyped for the p53 Pro72Arg (rs1042522).

Tumour suppressor protein, p53, plays a role in modulating innate immune responses, DNA repair, cell cycle arrest, senescence and apoptosis. Maternal nitrogen oxide (NOx) air pollution exposure, body mass index (BMI), human immunodeficiency virus (HIV) infection and p53 Pro72Arg (rs1042522) affect foetal growth. We investigated whether the aforementioned factors influence birth outcomes in a South African population. Pregnant women (n=300; HIV -ve=194 and HIV +ve=106) were genotyped for the p53 rs1042522 using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), and further stratified based on HIV status, infants' birthweight (BW; NBW: normal BW [>2,500g] and LBW: low BW [<2,500g]) and gestational age (GA; NGA: normal GA [>37weeks] and PTB: preterm birth [≤37weeks]). A land use regression model was developed to characterize maternal NOx exposure. Pearson's correlation and multivariate regression analysis statistical tests were used to determine the effect of rs1042522 genotyped pregnant women's BMI and NOx exposure on maternal blood pressure and haemoglobin and iron levels, and infants' anthropometric measurements and Appearance Pulse Grimace Activity and Respiration (APGAR) scores. The prevalence of LBW and PTB was 14.7% and 18.7%, respectively. The LBW group had a higher frequency of the variant Arg-allele versus NBW group (47.7% vs. 31.4%, p=.0046, OR=2.0, 95% CI=1.26-3.17). No association was observed between NGA and PTB groups. A significant association between BMI and systolic blood pressure (r=.50, p=.00; B=0.76, p=.002) and birth length (r=-.28, p=.01; B=-0.107, p=.011), and NOx and birth length (r=-.26, p=.08; B=-0.191, p=.046) and birthweight (B=-8.87, p=.048) was observed in HIV-infected mothers with the variant Pro/Arg+Arg/Arg genotypes. Mothers from the LBW group with the variant genotypes displayed an association between NOx and diastolic blood pressure (r=.58, p=.04), blood iron levels (r=-.60, p=.04; B=-0.204, p=.004), APGAR scores at 1min (r=-.86, p=.00; B=-0.101, p=.003) and 5min (r=-.75, p=.01) and birth length (r=-.61, p=.04), and BMI and diastolic blood pressure (r=.72, p=.01). In the PTB group, maternal variant genotypes and NOx were associated with blood haemoglobin levels (B=-0.132, p=.045) and APGAR scores at 1min (B=-0.161, p=.045) and 5min (B=-0.147, p=.043). Maternal rs1042522 Arg-allele, HIV infection, BMI and NOx exposure collectively play a role in lowering blood iron levels, gestational hypertension and LBW outcomes.

Early life exposure to air pollution and incidence of childhood asthma, allergic rhinitis and eczema.

RationaleThere is growing evidence that air pollution may contribute to the development of childhood asthma and other allergic diseases. In this follow-up of the Toronto Child Health Evaluation Questionnaire (T-CHEQ) study, we examined associations between early life exposures to air pollution and incidence of asthma, allergic rhinitis and eczema from birth through adolescence.Methods1286 T-CHEQ participants were followed from birth until outcome (March 31, 2016) or loss to follow-up, with a mean of 17 years of follow-up. Concentrations of nitrogen dioxide (NO2), ozone (O3) and particulate matter with a 50% cut-off aerodynamic diameter of 2.5 µm (PM2.5) from January 1, 1999 to December 31, 2012 were assigned to participants based on their postal codes at birth using ground observations, chemical/meteorological models, remote sensing and land-use regression models. Study outcomes included incidence of physician-diagnosed asthma, allergic rhinitis and eczema. Cox proportional hazard regression models were used to estimate hazard ratios per interquartile range of exposures and outcomes, adjusting for potential confounders.ResultsHazard ratios of 1.17 (95% CI 1.05–1.31) for asthma and 1.07 (95% CI 0.99–1.15) for eczema were observed for total oxidants (O3 and NO2) at birth. No significant increase in risk was found for PM2.5.ConclusionsExposures to oxidant air pollutants (O3 and NO2) but not PM2.5 were associated with an increased risk of incident asthma and eczema in children. This suggests that improving air quality may contribute to the prevention of asthma and other allergic disease in childhood and adolescence.

Room-temperature reduction of NO2 in a Li-NO2 battery: a proof of concept

Although considerable effort has been devoted to purifying nitrogen oxides (NOx), it is still challenging to effectively reduce NOx at room temperature and ambient pressure without catalysts. In this study, as a proof-of-concept, we have for the first time demonstrated the room-temperature reduction of nitrogen dioxide (NO2) using a rechargeable lithium-nitrogen dioxide (Li-NO2) battery. The battery shows a capacity of 884 mAh g−1 at 50 mA g−1 (an actual energy density of 666 Wh kg−1) and a promising electrochemical Faraday efficiency (FE) of 67%. The unique properties of Li-NO2 rechargeable batteries not only provide a way to reduce and recycle NO2 but also highlight the potential of oxidative air pollutants as energy sources for next-generation electrochemical energy storage (EES) systems.

Air pollution-associated changes in biomarkers of diabetes risk.

Ambient particulate matter (PM) and nitrogen oxide (NOx) air pollution may be diabetogenic. To examine longitudinal associations of short- and longer-term mean PM ≤10 μm (PM10), PM ≤2.5 μm (PM2.5), and NOx concentrations with five biomarkers of diabetes risk. We studied a stratified, random minority oversample of nondiabetic Women's Health Initiative clinical trials participants with biomarkers and geocoded participant address-specific mean air pollution concentrations available at repeated visits (years = 1993-2004; n = 3,915; mean age = 62.7 years; 84% white). We log-transformed the biomarkers, then used multi-level, mixed-effects, longitudinal models weighted for sampling design/attrition and adjusted for sociodemographic, clinical, and meteorological covariates to estimate their associations with air pollutants. Biomarkers exhibited null to suggestively negative associations with short- and longer-term PM10 and NOx concentrations, e.g., -3.1% (-6.1%, 0.1%), lower homeostatic model assessment of insulin resistance per 10 μg/m3 increase in 12-month PM10. A statistically significant interaction by impaired fasting glucose (IFG) at baseline in this analysis indicated potentially adverse effects only among women with versus without IFG, i.e., 1.4% (-3.5%, 6.5%) versus -4.6% (-7.9%, -1.1%), P interaction < 0.05. In contrast, longer-term PM2.5 concentrations were largely but not statistically significantly associated with higher biomarkers. Low-level short-term PM10 and NOx concentrations may have negligible adverse effects on biomarkers of diabetes risk. Although longer-term mean PM2.5 concentrations showed primarily null associations with these biomarkers, results suggestively indicated that PM2.5 exposure over the range of concentrations experienced in the United States may adversely affect biomarkers of diabetes risk at the population level, as may longer-term mean PM10 concentrations among women with IFG.

SAT-262 Differential Metabolic, Thermal, and Pulmonary Responses to Early Life Ozone Exposure in Male and Female Rats

The essential role that early life events (i.e., intrauterine growth restriction) and environmental exposures (i.e., air pollution) play in development of childhood asthma and obesity are only partly understood. Notably, asthmatic children who develop obesity through adolescence have poorer disease outcomes. In our previous studies we showed that exposure of Long-Evans rats to the oxidant air pollutant, ozone (O3), during implantation [gestational days (GD) 5 and 6; 0.8 ppm x 4h] resulted in growth restriction at GD21. The aims of this study were to determine whether gestational ± repeated peri-adolescent O3-exposure (0.4-0.8 ppm x 4h; once/week at 5, 6, and 7 weeks-of-age) would alter offspring metabolism, body, or lung growth, and acute thermal or pulmonary responses to O3. Using 2-way ANOVA with Dunnett’s post hoc correction, responses in males (M) and females (F) were evaluated separately; all O3-exposed groups were compared to controls [air-exposed dams + PN-Air-(x3)] of the corresponding sex. By postnatal (PN) day 45, results showed that in males, dam O3-exposure was associated with augmented body “height” (skull base-to-tail head) and increases in serum triglyceride, and cholesterol levels; but not body weight, weight adjusted by height (gm/cm), or corrected lung (fixed) volume (mL/cm height x100%). PN-O3x3 exposures were associated with increased HOMA-IR ratios and further increases in cholesterol. In females, dam O3-exposure was associated with lower lung volumes and increased serum cholesterol; while PN-O3x3 exposure was associated with reduced weight/height (gm/cm). For both sexes, the degree of acute hypothermia was altered in association with both dam- and especially PN-O3 exposures; whereas lung injury (e.g., increased protein leakage) and inflammation (e.g., neutrophils) in lung lavage fluid, were increased chiefly by PN-O3 exposure. Particularly in males, lesser inflammatory responses were observed in O3+O3x3 rats (e.g., reduced KC-GRO and IL-6 cytokine levels) compared to Air+O3x3 rats. Conversely, lavage fluid TNFα concentrations were increased only in the O3+O3x3 males. Taken together, data suggest that O3 exposure during gestation played a greater role in predisposing offspring to dyslipidemia, whereas peri-adolescent exposure dominated the acute hypothermia and inflammatory responses. Importantly, males exposed to both gestational and postnatal O3 appeared to (A) develop greater dyslipidemia (a precursor of metabolic syndrome) and (B) altered lung innate inflammatory responses − potentially influencing TH-1 to TH-2 balance (a precursor to allergic asthma) later in life. (This abstract does not reflect USEPA policy).

Resonance light scattering aptasensor for urinary 8-hydroxy-2'-deoxyguanosine based on magnetic nanoparticles: a preliminary study of oxidative stress association with air pollution.

An aptamer based method is described for the determination of 8-hydroxy-2'-deoxyguanosine (8-OHdG) using resonance light scattering (RLS). Magnetic nanoparticles (MNPs) were employed as RLS probes. The probe DNA was placed on the surface of MNPs, which produces a rather low RLS signal. If, however, probe DNA hybridizes with the aptamer against 8-OHdG, a sandwich structure will be formed. This results in a significant enhancement of RLS intensity. The aptamer was used as the recognition element to capture 8-OHdG. 8-OHdG has a stronger affinity for the aptamer than probe DNA, and the conformation of the aptamer therefore switches from a double-stranded to a G-quadruplex structure. As a result, MNPs labeled with probe DNA are released, and RLS intensity decreases. The method allows 8-OHdG to be detected with a linear response in the 32 pM - 12.0nM concentration range and an 11 pM limit of detection (at 3.29SB/m, according to the recent recommendation of IUPAC). The MNPs can be reused 5 times by applying an external magnetic field for collection. The method was successfully applied to analyze human urine samples for its content of 8-OHdG. It was also found that the levels of 8-OHdG noticeably increased with the increase of the Air Quality Index. Conceivably, the method is a viable tool to investigate the relationship between 8-OHdG levels and the effect of air pollution. Graphical abstract A reusable sensing strategy was constructed to detect urinary 8-OHdG based on "turn-off" resonance light scattering. The LOD was as low as 11 pM. This study showed some preliminary data for the association between oxidative stress and air pollution.

Acute inhalation of ozone induces DNA methylation of apelin in lungs of Long-Evans rats

Apelin has cardiopulmonary protective properties that promote vasodilation and maintenance of the endothelial barrier. While reductions in apelin have been identified as a contributor to various lung diseases, including pulmonary edema, its role in the effect of air pollutants has not been examined. Thus, in the current study, we sought to investigate if apelin is a downstream target of inhaled ozone and if such change in expression is related to altered DNA methylation in the lung. Male, Long-Evans rats were exposed to filtered air or 1.0 ppm ozone for 4 h. Ventilation changes were assessed using whole-body plethysmography immediately following exposure, and markers of pulmonary edema and inflammation were assessed in the bronchoaveolar lavage (BAL) fluid. The enzymatic regulators of DNA methylation were measured in the lung, along with methylation and hydroxymethylation of the apelin promoter. Data showed that ozone exposure was associated with increased enhanced pause and protein leakage in the BAL fluid. Ozone exposure reduced DNA cytosine-5-methyltransferase (DNMT) activity and Dnmt3a/b gene expression. Exposure-induced upregulation of proliferating cell nuclear antigen, indicative of DNA damage, repair, and maintenance methylation. Increased methylation and reduced hydroxymethylation were measured on the apelin promoter. These epigenetic modifications accompanied ozone-induced reduction of apelin expression and development of pulmonary edema. In conclusion, epigenetic regulation, specifically increased methylation of the apelin promoter downstream of DNA damage, may lead to reductions in protective signaling of the apelinergic system, contributing to the pulmonary edema observed following the exposure to oxidant air pollution.

Neonatal rat age, sex and strain modify acute antioxidant response to ozone

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death in the US and its impact continues to increase in women. Oxidant insults during critical periods of early life appear to increase risk of COPD through-out the life course. To better understand susceptibility to early life exposure to oxidant air pollutants we used Fisher (F344), Sprague-Dawley (SD) and Wistar (WIS) male and female neonatal rat pups to assess: (A) if strain (i.e. genetics), sex, or stage of early life development affected baseline lung antioxidant or redox enzyme levels and (B) if these same factors modulated antioxidant responsiveness to acute ozone exposure (1 ppm × 2 h) on post-natal day (PND) 14, 21, or 28. In air-exposed pups from PND14-28, some parameters were unchanged (e.g. uric acid), some decreased (e.g. superoxide dismutase), while others increased (e.g. glutathione recycling enzymes) especially post-weaning. Lung total glutathione levels decreased in F344 and SD pups, but were relatively unchanged in WIS pups. Post-ozone exposure, data suggest that: (1) the youngest (PND14) pups were the most adversely affected; (2) neonatal SD and WIS pups, especially females, were more prone to ozone effects than males of the same age and (3) F344 neonates (females and males) were less susceptible to oxidative lung insult, not unlike F344 adults. Differences in antioxidant levels and responsiveness between sexes and strains and at different periods of development may provide a basis for assessing later life health outcomes – with implications for humans with analogous genetic or dietary-based lung antioxidant deficits.

Abstract P070: Glucose, Insulin, Insulin Resistance and Exposure to Ambient Air Pollution

Background: Numerous studies suggest that long-term exposure to ambient particulate matter (PM) and nitrogen oxide (NOx) air pollution may be diabetogenic, but little is known about the effects of shorter-term exposures on markers of diabetes risk. Therefore, our objective was to determine whether short- and long-term ambient PM and NOx exposures are associated with glucose, insulin, and insulin resistance measures. Methods: We studied a stratified, random minority oversample of non-diabetic Women’s Health Initiative (WHI) clinical trials participants for whom estimates of fasting glucose, fasting insulin, insulin resistance, and geocoded address-specific daily mean concentrations of PM &lt; 10 μm (PM 10 ), PM &lt; 2.5 μm (PM 2.5 ), and NOx were available at screening and up to three follow-up visits between 1993-2004 (total n=4,019; mean age: 62.2 yr; 24% black; 12% Hispanic; 51% white). We measured insulin resistance using the homeostatic model assessment [HOMA], triglyceride to high-density lipoprotein cholesterol ratio, and the triglyceride-glucose index. We log-transformed the glucose, insulin, and insulin resistance measures, then used multi-level, mixed, longitudinal models weighted for sampling design / attrition and adjusted for sociodemographic, clinical, and meteorological covariates to estimate their associations with 2- and 365-day mean PM 10 and NOx and 365-day mean PM 2.5 concentrations. Results: Measures of glucose homeostasis decreased with short-term exposure to ambient PM 10 . For example, we found a -0.2% (95% confidence interval: -0.4%, 0.1%), -0.9% (-1.7%, -0.1%), and -1.1% (-2.0%, -0.3%) change in glucose, insulin, and HOMA per 10 μg/m 3 increase in the 2-day mean PM 10 concentration. In contrast, we found generally null results per 10 μg/m 3 increase in 365-day mean PM 10 concentration. Measures of glucose homeostasis similarly did not appear to be associated with short- and long-term increases in mean NOx or PM 2.5 concentrations. Conclusion: The findings suggest that responses to ambient exposure to PM 10 in women may be adaptive (i.e. capable of re-establishing normal glucose homeostasis and improving insulin sensitivity) over the short-term. Endoplasmic reticulum stress-response mechanisms involving decreases in protein misfolding may help explain this observed phenomena. Contrary to previous studies, results also suggest that sustained exposure to ambient PM and NOx has nominal influence on glucose homeostasis.

Associations between urinary biomarkers of oxidative stress and air pollutants observed in a randomized crossover exposure to steel mill emissions.

The effects of industrial air pollution on human health have not been as thoroughly investigated as those of urban air pollution which originates mostly from automotive transport. To better assess the health impacts of point sources of industrial air pollution, a randomized crossover exposure study was conducted. Sixty one young and healthy volunteers were randomly assigned to spend five consecutive eight-hour days near a steel mill or at a location five kilometres away. After a nine or sixteen-day washout period, volunteers spent another five consecutive days at the second site. Meteorological conditions and air pollutants were monitored at both exposure sites. On each exposure day, the first morning urine was collected along with a second urine sample obtained immediately before leaving the exposure site at the end of the day. Urinary levels of biomarkers of oxidative stress 8-hydroxy-2'-deoxyguanosine (8-OHdG, a biomarker of oxidative DNA damage), malondialdehyde (MDA, a biomarker of lipid peroxidation), 8-isoprostane (8-IsoP, a bioactive metabolite resulting from the peroxidation of arachidonic acid) and Vascular Endothelial Growth Factor (VEGF, involved in response to oxidative stress) were measured. According to mixed-effects linear regression models, intra-individual variations in 8-OHdG urinary levels were significantly associated with exposure site, but surprisingly, lower levels were observed at the steel mill site. Delayed, temporally-defined associations with specific air pollutants were observed for 8-OHdG, 8-IsoP and VEGF. However, these associations were subtle, presented complex patterns and their biological consequences remain unclear.

Smoking and Cerebral Oxidative Stress andAir Pollution: A Dreadful Equation withParticulate Matter Involved and One More Powerful Reason Not to Smoke Anything!

Smoking has serious health effects. Cigarettes, including tobacco, marijuana, and electronic nicotine delivery systems are very effective ways to inhale harmful amounts of fine and ultrafine particulate matter. Does size matter? Yes, indeed! The smaller the particle you inhale, the higher the ability to produce reactive oxygen species and to readily access the brain. In this issue of the Journal of Alzheimer's Disease, Durazzo provides evidence of an association between active cigarette tobacco smoking in cognitively-normal elders and increased cerebral oxidative stress, while in actively smoking Alzheimer's disease (AD) patients, the association was also seen with smaller left and total hippocampal volumes. This paper has highly relevant results of interest across the US and the world because millions of people are active smokers and they have other genetic and environmental risk factors that could play a key role in the development/worsening of brain oxidative stress and neurodegeneration. Smoking basically anything producing aerosols with particulate matter in the fine and ultrafine size range is detrimental to your brain. Marijuana and e-cigarette use has grown steadily among adolescents and young adults. Smoking-related cerebral oxidative stress is a potential mechanism promoting AD pathology and increased risk for AD. Current knowledge also relates fine and ultrafine particles exposures influencing neurodevelopmental processes in utero. The results from Durazzo et al. should be put in a broader context, a context that includes evaluating the oxidative stress of nano-aerosols associated with cigarette emissions and their synergistic effects with air pollution exposures. AD is expected to increase in the US threefold by the year 2050, and some of these future AD patients are smoking and vaping right now. Understanding the impact of everyday exposures to long-term harmful consequences for brain health is imperative.

Application of glutathione to antagonize H2O2-induced oxidative stress in rat tracheal epithelial cells

With increasing industrialization, numerous air pollutants are generated. This research aimed to investigate the effects of inhalation of oxidative pollutants. H2O2 was used to simulate oxidative air pollutants, and glutathione, a reducing agent that is widely distributed in organisms, was used as an antagonist, to protect cells from oxidative stress. H2O2 was diluted using two gradients (0.05 mM, 0.20 mM, 0.80 mM, 3.20 mM and 0.05 mM, 0.10 mM, 0.15 mM, 0.20 mM) and GSH was dissolved at 20 μM. MTT, MDA, ROS, GSH, and TSLP were used as biomarkers to evaluate oxidative stress and possible resulting molecular events. A dose–response relationship was observed between H2O2 concentrations and the above-mentioned biomarkers. Glutathione significantly reduced levels of oxidative stress.