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The Influence of Short-Term Weather Parameters and Air Pollution on Adolescent Airway Inflammation.

ABSTRACT: Fraction of exhaled Nitric Oxide (FeNO) is a marker of airway inflammation. We examined the main effects and interactions of relative humidity (RH) and air pollution on adolescents' FeNO. Two thousand and forty-two participants from the 15-year follow-up of the German GINIplus and LISA birth cohorts were included. Daily meteorological (maximum [Tmax], minimum [Tmin] and mean [Tmean] temperatures and RH) and air pollution [Ozone (O₃), nitrogen dioxide (NO₂) and particulate matter < 2.5 µm (PM_2.5)] were assessed. Linear models were fitted with Ln(FeNO) as the outcome. Increases in FeNO indicate an increase in lung inflammation. Increased FeNO was associated with an increase in temperature, PM_2.5, O₃ and NO₂. A 5% increase in RH was associated with a decrease in FeNO. Interactions between RH and high (p = 0.007) and medium (p = 0.050) NO₂ were associated with increases in FeNO; while interactions between RH and high (p = 0.042) and medium (p = 0.040) O₃ were associated with decreases in FeNO. Adverse effects were present for male participants, participants with low SES, participants with chronic respiratory disease, and participants from Wesel. Short-term weather and air pollution have an effect on lung inflammation in German adolescents. Future research should focus on further assessing the short-term effect of multiple exposures on lung inflammation in adolescents.

SUBMITTER: Areal AT

PROVIDER: S-EPMC10572171 | biostudies-literature | 2023 Sep

REPOSITORIES: biostudies-literature

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The Influence of Short-Term Weather Parameters and Air Pollution on Adolescent Airway Inflammation.

Areal Ashtyn Tracey AT Singh Nidhi N Zhao Qi Q Berdel Dietrich D Koletzko Sibylle S von Berg Andrea A Gappa Monika M Heinrich Joachim J Standl Marie M Abramson Michael J MJ Schikowski Tamara T

International journal of environmental research and public health 20230925 19

Fraction of exhaled Nitric Oxide (FeNO) is a marker of airway inflammation. We examined the main effects and interactions of relative humidity (RH) and air pollution on adolescents' FeNO. Two thousand and forty-two participants from the 15-year follow-up of the German GINIplus and LISA birth cohorts were included. Daily meteorological (maximum [Tmax], minimum [Tmin] and mean [Tmean] temperatures and RH) and air pollution [Ozone (O<sub>3</sub>), nitrogen dioxide (NO<sub>2</sub>) and particulate m ...[more]

PMID: 37835097

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Project description:BackgroundAir pollution is a large environmental health hazard whose exposure and health effects are unequally distributed among individuals. This is, at least in part, due to gene-environment interactions, but few studies exist. Thus, the current study aimed to explore genetic susceptibility to airway inflammation from short-term air pollution exposure through mechanisms of gene-environment interaction involving the SFTPA, GST and NOS genes.MethodsFive thousand seven hundred two adults were included. The outcome measure was fraction of exhaled nitric oxide (FeNO), at 50 and 270 ml/s. Exposures were ozone (O3), particulate matter < 10 µm (PM10), and nitrogen dioxide (NO2) 3, 24, or 120-h prior to FeNO measurement. In the SFTPA, GST and NOS genes, 24 single nucleotide polymorphisms (SNPs) were analyzed for interaction effects. The data were analyzed using quantile regression in both single-and multipollutant models.ResultsSignificant interactions between SNPs and air pollution were found for six SNPs (p < 0.05): rs4253527 (SFTPA1) with O3 and NOx, rs2266637 (GSTT1) with NO2, rs4795051 (NOS2) with PM10, NO2 and NOx, rs4796017 (NOS2) with PM10, rs2248814 (NOS2) with PM10 and rs7830 (NOS3) with NO2. The marginal effects on FeNO for three of these SNPs were significant (per increase of 10 µg/m3):rs4253527 (SFTPA1) with O3 (β: 0.155, 95%CI: 0.013-0.297), rs4795051 (NOS2) with PM10 (β: 0.073, 95%CI: 0.00-0.147 (single pollutant), β: 0.081, 95%CI: 0.004-0.159 (multipollutant)) and NO2 (β: -0.084, 95%CI: -0.147; -0.020 (3 h), β: -0.188, 95%CI: -0.359; -0.018 (120 h)) and rs4796017 (NOS2) with PM10 (β: 0.396, 95%CI: 0.003-0.790).ConclusionsIncreased inflammatory response from air pollution exposure was observed among subjects with polymorphisms in SFTPA1, GSTT1, and NOS genes, where O3 interacted with SFTPA1 and PM10 and NO2/NOx with the GSTT1 and NOS genes. This provides a basis for the further exploration of biological mechanisms as well as the identification of individuals susceptible to the effects of outdoor air pollution.

Project description:Background Air pollution and severe weather conditions can adversely affect cardiovascular disease emergencies. Nevertheless, it remains unclear whether air pollutants and low ambient temperature can trigger the occurrence of acute aortic dissection (AAD) in cold regions. Methods We applied a retrospective analysis to assess the short-term effects of air pollution and ambient temperature on the occurrence of AAD in Harbin, China. A total of 564 AAD patients were enrolled from a major hospital in Harbin between January 1, 2017, and February 5, 2021. Weather condition data and air pollutant concentrations, including fine particulate matter smaller than 10 μm (PM10) and 2.5 μm in diameter (PM2.5), nitrogen dioxide (NO2), sulfur dioxide (SO2), carbon monoxide (CO), and ozone (O3), were collected every day. Conditional logistic regressions and correlation analysis were applied to analyze the relationship of environmental and atmospheric parameters with AAD occurrence at lags of 0 to 7 days. Specifically, we appraised the air quality index, CO, NO2, SO2, O3, PM10, PM2.5, temperature, dew point temperature, atmospheric pressure, and cloud amount. Results A total of 1,496 days at risk were assessed, of which 564 patients developed AAD. Specifically, AAD did not occur on 1,043 (69.72%) days, while 1 or more cases occurred on 453 (30.28%) days. Several pollution and weather predictors for AAD were confirmed by multilevel modeling. The air quality index (p = 0.0012), cloud amount (p = 0.0001), and concentrations of PM2.5 (p = 0.0004), PM10 (p = 0.0013), NO2 (p = 0.0007) and O3 (p = 0.0001) predicted AAD as early as 7 days before the incident (lag of 7 days) in the study period. However, only concentrations of the air pollutants NO2 (p = 0.0468) and O3 (p = 0.011) predicted the occurrence of AAD after the COVID-19 outbreak. Similar predictive effects were observed for temperature, dew point temperature, and atmospheric pressure (all p < 0.05) on all days. Conclusion The risk of AAD is closely related to air pollution and weather characteristics in Harbin. While causation was not determined, the impact of air pollutants on the risk of AAD was reduced after the COVID-19 outbreak.

Project description:BackgroundThe association between long-term exposure to air pollution and local inflammation in the lung has rarely been investigated in the general population of elderly subjects before. We investigated this association in a population-based cohort of elderly women from Germany.MethodsIn a follow-up examination of the SALIA cohort study in 2008/2009, 402 women aged 68 to 79 years from the Ruhr Area and Borken (Germany) were clinically examined. Inflammatory markers were determined in exhaled breath condensate (EBC) and in induced sputum (IS). We used traffic indicators and measured air pollutants at single monitoring stations in the study area to assess individual traffic exposure and long-term air pollution background exposure. Additionally long-term residential exposure to air pollution was estimated using land-use regression (LUR) models. We applied multiple logistic and linear regression analyses adjusted for age, indoor mould, smoking, passive smoking and socio-economic status and additionally conducted sensitivity analyses.ResultsInflammatory markers showed a high variability between the individuals and were higher with higher exposure to air pollution. NO derivatives, leukotriene (LT) B4 and tumour necrosis factor-? (TNF-?) showed the strongest associations. An increase of 9.42 ?g/m3 (interquartile range) in LUR modelled NO2 was associated with measureable LTB4 level (level with values above the detection limit) in EBC (odds ratio: 1.38, 95% CI: 1.02 -1.86) as well as with LTB4 in IS (%-change: 19%, 95% CI: 7% - 32%). The results remained consistent after exclusion of subpopulations with risk factors for inflammation (smoking, respiratory diseases, mould infestation) and after extension of models with additional adjustment for season of examination, mass of IS and urban/rural living as sensitivity analyses.ConclusionsIn this analysis of the SALIA study we found that long-term exposure to air pollutants from traffic and industrial sources was associated with an increase of several inflammatory markers in EBC and in IS. We conclude that long-term exposure to air pollution might lead to changes in the inflammatory marker profile in the lower airways in an elderly female population.

Project description:BackgroundShort-term exposures to air pollution and temperature have been reported to be associated with inflammation and oxidative stress. However, mechanistic understanding of the affected metabolic pathways is still lacking and literature on the short-term exposure of air-pollution on the metabolome is limited.ObjectivesWe aimed to determine changes in the plasma metabolome and associated metabolic pathways related to short-term exposure to outdoor air pollution and temperature.MethodsWe performed mass-spectrometry based untargeted metabolomic profiling of plasma samples from a large and well-characterized cohort of men (Normative Aging Study) to identify metabolic pathways associated with short-term exposure to PM2.5, NO2, O3, and temperature (one, seven-, and thirty-day average of address-specific predicted estimates). We used multivariable linear mixed-effect regression and independent component analysis (ICA) while simultaneously adjusting for all exposures and correcting for multiple testing.ResultsOverall, 456 white men provided 648 blood samples, in which 1158 metabolites were quantified, between 2000 and 2016. Average age and body mass index were 75.0 years and 27.7 kg/m2, respectively. Only 3% were current smokers. In the adjusted models, NO2, and temperature showed statistically significant associations with several metabolites (19 metabolites for NO2 and 5 metabolites for temperature). We identified six metabolic pathways (sphingolipid, butanoate, pyrimidine, glycolysis/gluconeogenesis, propanoate, and pyruvate metabolisms) perturbed with short-term exposure to air pollution and temperature. These pathways were involved in inflammation and oxidative stress, immunity, and nucleic acid damage and repair.ConclusionsThis is the first study to report an untargeted metabolomic signature of temperature exposure, the largest to report an untargeted metabolomic signature of air pollution, and the first to use ICA. We identified several significant plasma metabolites and metabolic pathways associated with short-term exposure to air pollution and temperature; using an untargeted approach. Those pathways were involved in inflammation and oxidative stress, immunity, and nucleic acid damage and repair. These results need to be confirmed by future research.

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The Influence of Short-Term Weather Parameters and Air Pollution on Adolescent Airway Inflammation.

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The Influence of Short-Term Weather Parameters and Air Pollution on Adolescent Airway Inflammation.

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