The Impact of Short-Term Exposure to Air Pollution on the Exhaled Breath of Healthy Adults.
Ontology highlight
ABSTRACT:
SUBMITTER: Lammers A
PROVIDER: S-EPMC8038449 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
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) ?g/m3. A 10 ?g 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 ?gNO2/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:The 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.To 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.Case-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.Daily 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.All-cause mortality in the entire Medicare population from 2000 to 2012.During 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 ?g/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 ?g/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.In 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: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: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:ImportancePsoriasis is a chronic inflammatory disease with a relapsing-remitting course. Selected environmental factors such as infections, stressful life events, or drugs may trigger disease flares. Whether air pollution could trigger psoriasis flares is still unknown.ObjectiveTo investigate whether short-term exposure to environmental air pollution is associated with psoriasis flares.Design, setting, and participantsThis observational study with both case-crossover and cross-sectional design retrospectively analyzed longitudinal data from September 2013 to January 2020 from patients with chronic plaque psoriasis consecutively attending the outpatient dermatologic clinic of the University Hospital of Verona. For the case-crossover analysis, patients were included who had at least 1 disease flare, defined as Psoriasis Area and Severity Index (PASI) increase of 5 or greater between 2 consecutive assessments in a time frame of 3 to 4 months. For the cross-sectional analysis, patients were included who received any systemic treatment for 6 or more months, with grade 2 or higher consecutive PASI assessment.Main outcomes and measuresWe compared the mean and cumulative (area under the curve) concentrations of several air pollutants (carbon monoxide, nitrogen dioxide, other nitrogen oxides, benzene, coarse particulate matter [PM; 2.5-10.0 μm in diameter, PM10] and fine PM [<2.5 μm in diameter, PM2.5]) in the 60 days preceding the psoriasis flare and the control visits.ResultsA total of 957 patients with plaque psoriasis with 4398 follow-up visits were included in the study. Patients had a mean (SD) age of 61 (15) years and 602 (62.9%) were men. More than 15 000 measurements of air pollutant concentration from the official, open-source bulletin of the Italian Institute for Environmental Protection and Research (ISPRA) were retrieved. Among the overall cohort, 369 (38.6%) patients with psoriasis flare were included in the case-crossover study. We found that concentrations of all pollutants were significantly higher in the 60 days before psoriasis flare (median PASI at the flare 12; IQR, 9-18) compared with the control visit (median PASI 1; IQR, 1-3, P < .001). In the cross-sectional analysis, exposure to mean PM10 over 20 μg/m3 and mean PM2.5 over 15 μg/m3 in the 60 days before assessment were associated with a higher risk of PASI 5 or greater point worsening (adjusted odds ratio [aOR], 1.55; 95% CI, 1.21-1.99; and aOR, 1.25; 95% CI, 1.0-1.57, respectively). Sensitivity analyses that stratified for trimester of evaluation, with various lag of exposure and adjusting for type of treatment, yielded similar results.Conclusions and relevanceThe findings of this case-crossover and cross-sectional study suggest that air pollution may be a trigger factor for psoriasis flare.
| S-EPMC8851365 | biostudies-literature
Project description:Abstract Extensive evidence suggests that ambient air pollution contributes to a higher risk of hospital admissions for cerebrovascular diseases; however, its association with admissions for sequelae of stroke remains unclear. A time‐stratified case‐crossover study was conducted among 31,810 older adults who were admitted to hospital for sequelae of stroke in Guangzhou, China during 2016–2019. For each subject, daily residential exposure to fine particulate matter (PM2.5), inhalable particulate matter (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3) was extracted from a validated grid data set. Conditional logistic regression models were used for exposure‐response analyses. In single‐pollutant models, each interquartile range (IQR) increase of lag 04‐day exposure to CO (IQR: 0.25 mg/m3) and lag 3‐day exposure to O3 (69.6 μg/m3) was significantly associated with a 4.53% (95% confidence interval: 1.67%, 7.47%) and 5.63% (1.92%, 9.48%) increase in odds of hospital admissions for sequelae of stroke, respectively. These associations did not significantly vary across age or sex. With further adjustment for each of the other pollutants in 2‐pollutant models, the association for CO did not change significantly, while the association for O3 disappeared. We estimated that 7.72% of the hospital admissions were attributable to CO exposures. No significant or consistent association was observed for exposure to PM2.5, PM10, SO2, or NO2. In conclusion, short‐term exposure to ambient CO, even at levels below the WHO air quality guideline, was significantly associated with an increased odds of hospital admissions for sequelae of stroke, which may lead to considerable excess hospital admissions. Key Points Short‐term exposure to ambient carbon monoxide (CO) was significantly associated with an increased odds of hospital admissions for sequelae of stroke Ambient CO exposure may contribute to considerable excess hospital admissions for sequelae of stroke Our findings provide useful clues for the public to help prevent hospital admissions for sequelae of stroke by considering the effect of CO exposure
| S-EPMC9696746 | biostudies-literature
Project description:BackgroundShort-term mobile monitoring campaigns to estimate long-term air pollution levels are becoming increasingly common. Still, many campaigns have not conducted temporally-balanced sampling, and few have looked at the implications of such study designs for epidemiologic exposure assessment.ObjectiveWe carried out a simulation study using fixed-site air quality monitors to better understand how different short-term monitoring designs impact the resulting exposure surfaces.MethodsWe used Monte Carlo resampling to simulate three archetypal short-term monitoring sampling designs using oxides of nitrogen (NOx) monitoring data from 69 regulatory sites in California: a year-around Balanced Design that sampled during all seasons of the year, days of the week, and all or various hours of the day; a temporally reduced Rush Hours Design; and a temporally reduced Business Hours Design. We evaluated the performance of each design's land use regression prediction model.ResultsThe Balanced Design consistently yielded the most accurate annual averages; while the reduced Rush Hours and Business Hours Designs generally produced more biased results.SignificanceA temporally-balanced sampling design is crucial for short-term campaigns such as mobile monitoring aiming to assess long-term exposure in epidemiologic cohorts.Impact statementShort-term monitoring campaigns to assess long-term air pollution trends are increasingly common, though they rarely conduct temporally balanced sampling. We show that this approach produces biased annual average exposure estimates that can be improved by collecting temporally-balanced samples.
| S-EPMC9971335 | biostudies-literature
Project description:BACKGROUND: Exposure to traffic-related air pollution is a risk factor for cardiovascular events, probably involving mechanisms of inflammation and coagulation. Little is known about effects of the short exposures encountered while participating in traffic. OBJECTIVES: The objective of the study was to examine effects of exposure of commuters to air pollution on cardiovascular biomarkers. METHODS: Thirty-four healthy adult volunteers commuted for 2 hr by bus, car, or bicycle during the morning rush hour. During the commute, exposure to particle number, particulate matter (PM) ? 2.5 µm in aerodynamic diameter (PM2.5), PM ? 10 µm in diameter (PM10), and soot was measured. We estimated inhaled doses based on heart rate monitoring. Shortly before exposure and 6 hr after exposure, blood samples were taken and analyzed for CC16 (Clara cell protein 16), blood cell count, coagulation markers, and inflammation markers. Between June 2007 and June 2008, 352 pre- and postexposure blood samples were collected on 47 test days. We used mixed models to analyze the associations between exposure and changes in health parameters. RESULTS: We observed no consistent associations between the air pollution exposures and doses and the various biomarkers that we investigated. CONCLUSIONS: Air pollution exposure during commuting was not consistently associated with acute changes in inflammation markers, blood cell counts, or blood coagulation markers.
| S-EPMC3230432 | biostudies-other