The Impact of Short-Term Exposure to Air Pollution on the Exhaled Breath of Healthy Adults.
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ABSTRACT:
SUBMITTER: Lammers A
PROVIDER: S-EPMC8038449 | biostudies-literature | 2021 Apr
REPOSITORIES: biostudies-literature
Publications
The Impact of Short-Term Exposure to Air Pollution on the Exhaled Breath of Healthy Adults.
Lammers Ariana A Neerincx Anne H AH Vijverberg Susanne J H SJH Longo Cristina C Janssen Nicole A H NAH Boere A John F AJF Brinkman Paul P Cassee Flemming R FR van der Zee Anke H Maitland AHM
Sensors (Basel, Switzerland) 20210404 7
Environmental factors, such as air pollution, can affect the composition of exhaled breath, and should be well understood before biomarkers in exhaled breath can be used in clinical practice. Our objective was to investigate whether short-term exposures to air pollution can be detected in the exhaled breath profile of healthy adults. In this study, 20 healthy young adults were exposed 2-4 times to the ambient air near a major airport and two highways. Before and after each 5 h exposure, exhaled ...[more]
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Project description:BackgroundDaily changes in ambient concentrations of particulate matter, nitrogen oxides and ozone are associated with increased cardiopulmonary morbidity and mortality, with the lungs and their function being a vulnerable target.MethodsTo evaluate the association between daily changes in air pollution and lung function in healthy adults we obtained annual lung function measurements from a routine worker health surveillance program not designed for research purposes. Forced Vital Capacity (FVC), Forced Expiratory Volume in the first second (FEV1), FEV1/FVC and Peak Expiratory flow (PEF) from a cohort of 2449 employees were associated with daily measurements of PM10, NO2 and ozone at a nearby monitoring station in the North of Belgium. Repeated measures were available for the period 2011-2015.ResultsThe mean (SD) PM10 concentration on the day of the lung function test was 24.9 (15.5) μg/m3. A 10 μg PM10/m3 increase on the day of the clinical examination was associated with a 18.9 ml lower FVC (95% CI: -27.5 to -10.3, p < 0.0001), 12.8 ml lower FEV1 (-19.1 to -6.5; p < 0.0001), and a 51.4 ml/s lower PEF (-75.0 to -27.0; p < 0.0001). The FEV1/FVC-ratio showed no associations. An increase of 10 μgNO2/m3 was associated with a reduction in PEF (-66.1 ml/s (-106.6 to -25.6; p < 0.001)) on the day of the examination.ConclusionsWe found negative associations between daily variations in ambient air pollution and FVC, FEV1 and PEF in healthy adults.
| S-EPMC5471732 | biostudies-literature
Project description:ImportanceThe US Environmental Protection Agency is required to reexamine its National Ambient Air Quality Standards (NAAQS) every 5 years, but evidence of mortality risk is lacking at air pollution levels below the current daily NAAQS in unmonitored areas and for sensitive subgroups.ObjectiveTo estimate the association between short-term exposures to ambient fine particulate matter (PM2.5) and ozone, and at levels below the current daily NAAQS, and mortality in the continental United States.Design, setting, and participantsCase-crossover design and conditional logistic regression to estimate the association between short-term exposures to PM2.5 and ozone (mean of daily exposure on the same day of death and 1 day prior) and mortality in 2-pollutant models. The study included the entire Medicare population from January 1, 2000, to December 31, 2012, residing in 39 182 zip codes.ExposuresDaily PM2.5 and ozone levels in a 1-km × 1-km grid were estimated using published and validated air pollution prediction models based on land use, chemical transport modeling, and satellite remote sensing data. From these gridded exposures, daily exposures were calculated for every zip code in the United States. Warm-season ozone was defined as ozone levels for the months April to September of each year.Main outcomes and measuresAll-cause mortality in the entire Medicare population from 2000 to 2012.ResultsDuring the study period, there were 22 433 862 million case days and 76 143 209 control days. Of all case and control days, 93.6% had PM2.5 levels below 25 μg/m3, during which 95.2% of deaths occurred (21 353 817 of 22 433 862), and 91.1% of days had ozone levels below 60 parts per billion, during which 93.4% of deaths occurred (20 955 387 of 22 433 862). The baseline daily mortality rates were 137.33 and 129.44 (per 1 million persons at risk per day) for the entire year and for the warm season, respectively. Each short-term increase of 10 μg/m3 in PM2.5 (adjusted by ozone) and 10 parts per billion (10-9) in warm-season ozone (adjusted by PM2.5) were statistically significantly associated with a relative increase of 1.05% (95% CI, 0.95%-1.15%) and 0.51% (95% CI, 0.41%-0.61%) in daily mortality rate, respectively. Absolute risk differences in daily mortality rate were 1.42 (95% CI, 1.29-1.56) and 0.66 (95% CI, 0.53-0.78) per 1 million persons at risk per day. There was no evidence of a threshold in the exposure-response relationship.Conclusions and relevanceIn the US Medicare population from 2000 to 2012, short-term exposures to PM2.5 and warm-season ozone were significantly associated with increased risk of mortality. This risk occurred at levels below current national air quality standards, suggesting that these standards may need to be reevaluated.
| S-EPMC5783186 | biostudies-literature
Project description:BackgroundMicrocirculation plays an important role in the physiology of cardiovascular health. Air pollution is an independent risk factor for the development and progression of cardiovascular diseases, but the number of studies on the relation between air pollution and the microcirculation is limited.ObjectivesWe examined the relationship between short-term changes in air pollution and microvascular changes.MethodsWe measured retinal microvasculature using fundus image analysis in a panel of 84 healthy adults (52% female), 22-63 years of age, during January-May 2012. Blood vessels were measured as central retinal arteriolar/venular equivalent (CRAE/CRVE), with a median of 2 measurements (range, 1-3). We used monitoring data on particulate air pollution (PM10) and black carbon (BC). Mixed-effect models were used to estimate associations between CRAE/CRVE and exposure to PM10 and BC using various exposure windows.ResultsCRAE and CRVE were associated with PM10 and BC concentrations, averaged over the 24 hr before the retinal examinations. Each 10-µg/m3 increase in PM10 was associated with a 0.93-µm decrease (95% CI: -1.42, -0.45; p = 0.0003) in CRAE and a 0.86-µm decrease (95% CI: -1.42, -0.30; p = 0.004) in CRVE after adjusting for individual characteristics and time varying conditions such as ambient temperature. Each 1-µg/m3 increase in BC was associated with a 1.84-µm decrease (95% CI: -3.18, -0.51; p < 0.001) in CRAE.ConclusionsOur findings suggest that the retinal microvasculature responds to short-term changes in air pollution levels. These results support a mechanistic pathway through which air pollution can act as a trigger of cardiovascular events at least in part through effects on the microvasculature.
| S-EPMC3764070 | biostudies-literature
Project description:Air pollution exposure is now considered a growing concern for global public health. RNA or DNA methylation changes caused by air pollution may be related to the development of cardiovascular disease. To investigate the early biomarkers of air pollution exposure, a panel study of eight college students recorded after a business trip from Qingdao to Shijiazhuang and back to Qingdao was performed in this work. The concentration of PM2.5, PM10, SO2, NO2, and CO in Shijiazhuang was higher than that in Qingdao during the study period. The platelet count was positively correlated with air pollutants of 0-6 day moving averages (βPM2.5 = 88.90; βPM10 = 61.83; βSO2 = 41.13; βNO2 = 57.70; βCO = 62.99, respectively, for an IQR increased). Additionally, internal dose biomarkers 2-OHNa, 1-OHNa, 2-OHFlu, 2,3-OHPhe, and ∑PAHs were also significantly associated with platelet count in participants. Furthermore, PM2.5 and PM10 are positively linked with methylation of one CpG site at platelet mitochondrial gene CO2 (PM2.5 = 0.47; PM10 = 0.25, respectively, for an IQR increase). Both platelet counts and methylation levels returned to their pre-exposure levels after leaving the highly contaminated area. In short, this study investigated the relationship between platelet properties and air pollution exposure, revealing that short-term exposure to air pollution might increase the risk of thrombosis. Our research suggests that platelet count and mitochondrial DNA methylation of mtCO2 site 2 in platelets from healthy adults may be the novel biomarker for acute exposure to air pollution.
| S-EPMC8809460 | biostudies-literature
Project description:We investigated associations between ambient air pollution and microvessel function measured by peripheral arterial tonometry between 2003 and 2008 in the Framingham Heart Study Offspring and Third Generation Cohorts. We measured particulate matter with aerodynamic diameter ≤2.5 µm (PM2.5), black carbon, sulfates, particle number, nitrogen oxides, and ozone by using fixed monitors, and we determined moving averages for 1-7 days preceding vascular testing. We examined associations between these exposures and hyperemic response to ischemia and baseline pulse amplitude, a measure of arterial tone (n = 2,369). Higher short-term exposure to air pollutants, including PM2.5, black carbon, and particle number was associated with higher baseline pulse amplitude. For example, higher 3-day average PM2.5 exposure was associated with 6.3% higher baseline pulse amplitude (95% confidence interval: 2.0, 10.9). However, there were no consistent associations between the air pollution exposures assessed and hyperemic response. Our findings in a community-based sample exposed to relatively low pollution levels suggest that short-term exposure to ambient particulate pollution is not associated with vasodilator response, but that particulate air pollution is associated with baseline pulse amplitude, suggesting potentially adverse alterations in baseline vascular tone or compliance.
| S-EPMC4143083 | biostudies-literature
Project description:Cooking fumes contain aldehydes, alkanoic acids, polycyclic aromatic hydrocarbons, and heterocyclic compounds. The inhalation of cooking fumes entails a risk of deleterious health effects. The aim of this study was to see if the inhalation of cooking fumes alters the expression of inflammatory reactions in the bronchial mucosa and its subsequent systemic inflammatory response in blood biomarkers.Twenty-four healthy volunteers stayed in a model kitchen on two different occasions for 2 or 4 h. On the first occasion, there was only exposure to normal air, and on the second, there was exposure to controlled levels of cooking fumes. On each occasion, samples of blood, exhaled air, and exhaled breath condensate (EBC) were taken three times in 24 h and inflammatory markers were measured from all samples.There was an increase in the concentration of the d-dimer in blood from 0.27 to 0.28 mg ml(-1) on the morning after exposure to cooking fumes compared with the levels the morning before (P-value = 0.004). There was also a trend of an increase in interleukin (IL)-6 in blood, ethane in exhaled air, and IL-1? in EBC after exposure to cooking fumes. In a sub-analysis of 12 subjects, there was also an increase in the levels of ethane--from 2.83 parts per billion (ppb) on the morning before exposure to cooking fumes to 3.53 ppb on the morning after exposure (P = 0.013)--and IL-1?--from 1.04 on the morning before exposure to cooking fumes to 1.39 pg ml(-1) immediately after (P = 0.024).In our experimental setting, we were able to unveil only small changes in the levels of inflammatory markers in exhaled air and in blood after short-term exposure to moderate concentrations of cooking fumes.
| S-EPMC3567812 | biostudies-other
Project description:Ecological studies suggested a link between air pollution and severe COVID-19 outcomes, while studies accounting for individual-level characteristics are limited. In the present study, we aimed to investigate the impact of short-term ambient air pollution exposure on disease severity among a cohort of 569 laboratory confirmed COVID-19 patients admitted to designated hospitals in Zhejiang province, China, from January 17 to March 3, 2020, and elucidate the possible biological processes involved using transcriptomics. Compared with mild cases, severe cases had higher proportion of medical conditions as well as unfavorable results in most of the laboratory tests, and manifested higher air pollution exposure levels. Higher exposure to air pollutants was associated with increased risk of severe COVID-19 with odds ratio (OR) of 1.89 (95% confidence interval (CI): 1.01, 3.53), 2.35 (95% CI: 1.20, 4.61), 2.87 (95% CI: 1.68, 4.91), and 2.01 (95% CI: 1.10, 3.69) for PM2.5, PM10, NO2 and CO, respectively. OR for NO2 remained significant in two-pollutant models after adjusting for other pollutants. Transcriptional analysis showed 884 differentially expressed genes which mainly were enriched in virus clearance related biological processes between patients with high and low NO2 exposure levels, indicating that compromised immune response might be a potential underlying mechanistic pathway. These findings highlight the impact of short-term air pollution exposure, particularly for NO2, on COVID-19 severity, and emphasize the significance in mitigating the COVID-19 burden of commitments to improve air quality.
| S-EPMC9550293 | biostudies-literature
Project description:OBJECTIVE: To examine the short-term effect of ambient air pollution on daily acute respiratory emergency room visits among adults.METHODS: A time-series study (June 2017-February 2019) was carried out among adults (≥18 years) visiting a multi-specialty hospital in Delhi. We evaluated the association between the daily levels of particulate matter (PM) <2.5 μm in diameter (PM2.5) and PM <10 μm in diameter (PM10), ozone (O₃), nitrogen dioxide (NO₂), carbon monoxide (CO) and sulphur dioxide and daily count of emergency room (ER) visits for acute respiratory symptoms. Generalised additive model (GAM) was used with the Poisson link function to analyse the associations for 0-1 to 0-7 lag days.RESULTS: A total of 69,400 ER visits were recorded, of which 2,669 were by adults due to acute respiratory symptoms. At 0-7 lag days, an increment of 1 standard deviation in NO₂ and PM2.5 concentration was associated with a percentage increase in acute respiratory ER visits of respectively 53.0% (95% CI 30.84-78.97) and 19.5% (95% CI 4.53-36.65). During 0-7 lag days, a positive trend was observed at higher concentrations of CO (>1.86-3.28 mg/m³), while a negative significant association was observed at low concentrations of CO (<1.171 mg/m³).CONCLUSION: Short-term exposure to ambient NO2 and PM2.5 was associated with acute respiratory emergency visits of adults at lag 0-7 days.
| S-EPMC10519391 | biostudies-literature
Project description:ImportanceMounting ecological evidence shows an association between short-term air pollution exposure and COVID-19, yet no study has examined this association on an individual level.ObjectiveTo estimate the association between short-term exposure to ambient air pollution and SARS-CoV-2 infection among Swedish young adults.Design, setting, and participantsThis time-stratified case-crossover study linked the prospective BAMSE (Children, Allergy Milieu, Stockholm, Epidemiology [in Swedish]) birth cohort to the Swedish national infectious disease registry to identify cases with positive results for SARS-CoV-2 polymerase chain reaction (PCR) testing from May 5, 2020, to March 31, 2021. Case day was defined as the date of the PCR test, whereas the dates with the same day of the week within the same calendar month and year were selected as control days. Data analysis was conducted from September 1 to December 31, 2021.ExposuresDaily air pollutant levels (particulate matter with diameter ≤2.5 μm [PM2.5], particulate matter with diameter ≤10 μm [PM10], black carbon [BC], and nitrogen oxides [NOx]) at residential addresses were estimated using dispersion models with high spatiotemporal resolution.Main outcomes and measuresConfirmed SARS-CoV-2 infection among participants within the BAMSE cohort. Distributed-lag models combined with conditional logistic regression models were used to estimate the association.ResultsA total of 425 cases were identified, of whom 229 (53.9%) were women, and the median age was 25.6 (IQR, 24.9-26.3) years. The median exposure level for PM2.5 was 4.4 [IQR, 2.6-6.8] μg/m3 on case days; for PM10, 7.7 [IQR, 4.6-11.3] μg/m3 on case days; for BC, 0.3 [IQR, 0.2-0.5] μg/m3 on case days; and for NOx, 8.2 [5.6-14.1] μg/m3 on case days. Median exposure levels on control days were 3.8 [IQR, 2.4-5.9] μg/m3 for PM2.5, 6.6 [IQR, 4.5-10.4] μg/m3 for PM10, 0.2 [IQR, 0.2-0.4] μg/m3 for BC, and 7.7 [IQR, 5.3-12.8] μg/m3 for NOx. Each IQR increase in short-term exposure to PM2.5 on lag 2 was associated with a relative increase in positive results of SARS-CoV-2 PCR testing of 6.8% (95% CI, 2.1%-11.8%); exposure to PM10 on lag 2, 6.9% (95% CI, 2.0%-12.1%); and exposure to BC on lag 1, 5.8% (95% CI, 0.3%-11.6%). These findings were not associated with NOx, nor were they modified by sex, smoking, or having asthma, overweight, or self-reported COVID-19 respiratory symptoms.Conclusions and relevanceThe findings of this case-crossover study of Swedish young adults suggest that short-term exposure to particulate matter and BC was associated with increased risk of positive PRC test results for SARS-CoV-2, supporting the broad public health benefits of reducing ambient air pollution levels.
| S-EPMC9021914 | biostudies-literature
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.
| S-EPMC8478827 | biostudies-literature