Indoor Endotoxin Exposure and Ambient Air Pollutants Interact on Asthma Outcomes.
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ABSTRACT:
SUBMITTER: Abramson MJ
PROVIDER: S-EPMC6775880 | biostudies-literature | 2019 Sep
REPOSITORIES: biostudies-literature
Publications
Indoor Endotoxin Exposure and Ambient Air Pollutants Interact on Asthma Outcomes.
Abramson Michael J MJ Guo Yuming Y
American journal of respiratory and critical care medicine 20190901 6
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Project description:Rationale: House endotoxin and ambient air pollution are risk factors for asthma; however, the effects of their coexposure on asthma are not well characterized.Objectives: To examine potential synergistic associations of coexposure to house dust endotoxin and ambient air pollutants with asthma outcomes.Methods: We analyzed data of 6,488 participants in the National Health and Nutrition Examination Survey 2005-2006. Dust from bedding and bedroom floor was analyzed for endotoxin content. The Community Multiscale Air Quality Modeling System (CMAQ) and Downscaler Model data were used to determine annual average particulate matter ≤2.5 μm in aerodynamic diameter (PM2.5), ozone (O3), and nitrogen dioxide (NO2) exposures at participants' residential locations. The associations of the coexposures with asthma outcomes were assessed and tested for synergistic interaction.Measurements and Main Results: In adjusted analysis, PM2.5 (CMAQ) (odds ratio [OR], 1.12; 95% confidence interval [CI], 1.07-1.18), O3 (Downscaler Model) (OR, 1.07; 95% CI, 1.02-1.13), and log10 NO2 (CMAQ) (OR, 3.15; 95% CI, 1.33-7.45) were positively associated with emergency room visits for asthma in the past 12 months. Coexposure to elevated concentrations of house dust endotoxin and PM2.5 (CMAQ) was synergistically associated with the outcome, increasing the odds by fivefold (OR, 5.01; 95% CI, 2.54-9.87). A synergistic association was also found for coexposure to higher concentrations of endotoxin and NO2 in children (OR, 3.45; 95% CI, 1.65-7.18).Conclusions: Coexposure to elevated concentrations of residential endotoxin and ambient PM2.5 in all participants and NO2 in children is synergistically associated with increased emergency room visits for asthma. Therefore, decreasing exposure to both endotoxin and air pollution may help reduce asthma morbidity.
| S-EPMC6775869 | biostudies-literature
Project description:BackgroundIt is well established that short-term exposure to ambient air pollutants can exacerbate asthma, the role of early life or long-term exposure is less clear. We assessed the association between severe asthma exacerbations with both birth and annual exposure to outdoor air pollutants with a population-based cohort of asthmatic children in the province of Quebec (Canada).MethodExacerbations of asthma occurring between 1 April 1996 and 31 March 2011 were defined as one hospitalization or emergency room visit with a diagnosis of asthma for children (<13 years old) already diagnosed with asthma. Annual daily average concentrations of ozone (O?) and nitrogen dioxide (NO?) were estimated at the child's residential postal code. Satellite based levels of fine particulate (PM2.5) estimated for a grid of 10 km by 10 km were also assigned to postal codes of residence for the whole province. Hazard ratios (HRs) were estimated from Cox models with a gap time approach for both birth and time-dependant exposure.ResultsOf the 162,752 asthmatic children followed (1,020,280 person-years), 35,229 had at least one asthma exacerbation. The HRs stratified by age groups and adjusted for the year of birth, the ordinal number of exacerbations, sex, as well as material and social deprivation, showed an interquartile range increase in the time-dependant exposure to NO? (4.95 ppb), O? (3.85 ppb), and PM2.5 (1.82 ?g/m³) of 1.095 (95% CI 1.058-1.131), 1.052 (95% CI 1.037-1.066) and 1.025 (95% CI 1.017-1.031), respectively. While a positive association was found to PM2.5, no associations were found between exposure at birth to NO? or O?.ConclusionsOur results support the conclusion, within the limitation of this study, that asthma exacerbations in asthmatic children are mainly associated with time dependent residential exposures less with exposure at birth.
| S-EPMC4997457 | biostudies-literature
Project description:BackgroundAlthough it is well established that air pollutants can exacerbate asthma, the link with new asthma onset in children is less clear.ObjectiveWe assessed the association between the onset of childhood asthma with both time of birth and time-varying exposures to outdoor air pollutants.MethodAn open cohort of children born in the province of Québec, Canada, was created using linked medical-administrative databases. New cases of asthma were defined as one hospital discharge with a diagnosis of asthma or two physician claims for asthma within a 2 year period. Annual ozone (O3) levels were estimated at the child's residence for all births 1999-2010, and nitrogen dioxide (NO2) levels during 1996-2006 were estimated for births on the Montreal Island. Satellite based concentrations of fine particles (PM2.5) were estimated at a 10 km × 10 km resolution and assigned to residential postal codes throughout the province (1996-2011). Hazard ratios (HRs) were assessed with Cox models for the exposure at the birth address and for the time-dependent exposure. We performed an indirect adjustment for secondhand smoke (SHS).ResultsWe followed 1,183,865 children (7,752,083 person-years), of whom 162,752 became asthmatic. After controlling for sex and material and social deprivation, HRs for an interquartile range increase in exposure at the birth address to NO2 (5.45 ppb), O3 (3.22 ppb), and PM2.5 (6.50 ?g/m3) were 1.04 (95% CI: 1.02, 1.05), 1.11 (95% CI: 1.10, 1.12), and 1.31 (95% CI: 1.28, 1.33), respectively. Effects of O3 and PM2.5 estimated with time-varying Cox models were similar to those estimated using exposure at birth, whereas the effect of NO2 was slightly stronger (HR = 1.07; 95% CI: 1.05, 1.09).ConclusionsAsthma onset in children appears to be associated with residential exposure to PM2.5, O3 and NO2.CitationTétreault LF, Doucet M, Gamache P, Fournier M, Brand A, Kosatsky T, Smargiassi A. 2016. Childhood exposure to ambient air pollutants and the onset of asthma: an administrative cohort study in Québec. Environ Health Perspect 124:1276-1282;?http://dx.doi.org/10.1289/ehp.1509838.
| S-EPMC4977042 | biostudies-literature
Project description:RationaleCertain outdoor air pollutants cause asthma exacerbations in children. To advance understanding of these relationships, further characterization of the dose-response and pollutant lag effects are needed, as are investigations of pollutant species beyond the commonly measured criteria pollutants.ObjectivesInvestigate short-term associations between ambient air pollutant concentrations and emergency department visits for pediatric asthma.MethodsDaily counts of emergency department visits for asthma or wheeze among children aged 5 to 17 years were collected from 41 Metropolitan Atlanta hospitals during 1993-2004 (n = 91,386 visits). Ambient concentrations of gaseous pollutants and speciated particulate matter were available from stationary monitors during this time period. Rate ratios for the warm season (May to October) and cold season (November to April) were estimated using Poisson generalized linear models in the framework of a case-crossover analysis.Measurements and main resultsBoth ozone and primary pollutants from traffic sources were associated with emergency department visits for asthma or wheeze; evidence for independent effects of ozone and primary pollutants from traffic sources were observed in multipollutant models. These associations tended to be of the highest magnitude for concentrations on the day of the emergency department visit and were present at relatively low ambient concentrations.ConclusionsEven at relatively low ambient concentrations, ozone and primary pollutants from traffic sources independently contributed to the burden of emergency department visits for pediatric asthma.
| S-EPMC2921597 | biostudies-literature
Project description:Background:Environmental contributions to pediatric asthma morbidity have been studied extensively in urban settings; exposures characteristic of agricultural and rural communities have received less attention despite a comparable burden of morbidity. Methods:We obtained repeated urine samples (n = 139) from 16 school-age children with asthma in the Yakima Valley of Washington State between July and October 2012. Biomarkers of organophosphate (OP) pesticide exposure (dialkyl phosphates [DAPs]) and asthma exacerbation (leukotriene E4 [LTE4]) were analyzed in samples. Corresponding 24-hour average particulate matter <2.5 ?g (PM2.5) and maximum 8-hour ozone concentration data for the study period were available from local monitoring stations. We evaluated the independent and multi-pollutant associations between LTE4 and exposure to ambient air pollutants and DAPs using generalized estimating equations. For multi-domain and multi-pollutant models, we created categorized pollution combination levels and estimated the relative health impact of exposure to pollutant mixtures. Results:In single-pollutant models, an interquartile range increase in exposures to DAPs was associated with increase in LTE4 levels (?: 4.1 [0.6-7.6] pg/mg). PM2.5 and ozone were also associated with increase in LTE4, though confidence intervals contained the null value. Increase in LTE4 levels was consistently associated with increase in median-dichotomized multi-pollutant combination exposures; the highest effect estimates were observed with joint highest (vs. the lowest) category of the three-pollutant exposure (PM2.5, ozone, and OP; ?: 53.5, 95% confidence interval = 24.2, 82.8 pg/mg). Conclusion:Concurrent short-term exposure to criteria air pollutants and OPs in an agricultural community was associated with an increase in a marker of asthma morbidity.
| S-EPMC6571181 | biostudies-literature
Project description:Air quality modeling could potentially improve exposure estimates for use in epidemiological studies. We investigated this application of air quality modeling by estimating location-specific (point) and spatially-aggregated (county level) exposure concentrations of particulate matter with an aerodynamic diameter less than or equal to 2.5 μm (PM(2.5)) and ozone (O(3)) for the eastern U.S. in 2002 using the Community Multi-scale Air Quality (CMAQ) modeling system and a traditional approach using ambient monitors. The monitoring approach produced estimates for 370 and 454 counties for PM(2.5) and O(3), respectively. Modeled estimates included 1861 counties, covering 50% more population. The population uncovered by monitors differed from those near monitors (e.g., urbanicity, race, education, age, unemployment, income, modeled pollutant levels). CMAQ overestimated O(3) (annual normalized mean bias=4.30%), while modeled PM(2.5) had an annual normalized mean bias of -2.09%, although bias varied seasonally, from 32% in November to -27% in July. Epidemiology may benefit from air quality modeling, with improved spatial and temporal resolution and the ability to study populations far from monitors that may differ from those near monitors. However, model performance varied by measure of performance, season, and location. Thus, the appropriateness of using such modeled exposures in health studies depends on the pollutant and metric of concern, acceptable level of uncertainty, population of interest, study design, and other factors.
| S-EPMC3543158 | biostudies-literature
Project description:BackgroundImpaired in utero fetal growth trajectory may have long term health consequences of the newborns and increase risk of adulthood metabolic diseases. Prenatal exposure to air pollution has been linked to fetal development restriction; however, the impact of exposure to ambient air pollutants on the entire course of intrauterine fetal development has not been comprehensively investigated.MethodsDuring 2015-2018, two cohorts of mother-infant dyads (N = 678 and 227) were recruited in Shanghai China, from which three categories of data were systematically collected: (1) daily exposure to six air pollutants during pregnancy, (2) fetal biometry in the 2nd (gestational week 24, [GW24]) and 3rd trimester (GW36), and (3) neonatal outcomes at birth. We investigated the impact of prenatal exposure to air pollutant mixture on the trajectory of fetal development during the course of gestation, adjusting for a broad set of potential confounds.ResultsPrenatal exposure to PM2.5, PM10, SO2 and O3 significantly reduced fetal biometry at GW24, where SO2 had the most potent effect. For every 10 μg/m3 increment increase of daily SO2 exposure during the 1st trimester shortened femur length by 2.20 mm (p = 6.7E-21) translating to 5.3% reduction from the average of the study cohort. Prenatal air pollution exposure also decreased fetal biometry at GW36 with attenuated effect size. Comparing to the lowest exposed quartile, fetus in the highest exposed quartile had 6.3% (p = 3.5E-5) and 2.1% (p = 2.4E-3) lower estimated intrauterine weight in GW24 and GW36, respectively; however, no difference in birth weight was observed, indicating a rapid catch-up growth in the 3rd trimester.ConclusionsTo our knowledge, for the first time, we demonstrated the impact of prenatal exposure to ambient air pollutants on the course of intrauterine fetal development. The altered growth trajectory and rapid catch-up growth in associated with high prenatal exposure may lead to long-term predisposition for adulthood metabolic disorders.
| S-EPMC7363555 | biostudies-literature
Project description:BackgroundBecause ambient air pollution exposure occurs as mixtures, consideration of joint effects of multiple pollutants may advance our understanding of the health effects of air pollution.MethodsWe assessed the joint effect of air pollutants on pediatric asthma emergency department visits in Atlanta during 1998-2004. We selected combinations of pollutants that were representative of oxidant gases and secondary, traffic, power plant, and criteria pollutants, constructed using combinations of criteria pollutants and fine particulate matter (PM2.5) components. Joint effects were assessed using multipollutant Poisson generalized linear models controlling for time trends, meteorology, and daily nonasthma upper respiratory emergency department visit counts. Rate ratios (RRs) were calculated for the combined effect of an interquartile range increment in each pollutant's concentration.ResultsIncreases in all of the selected pollutant combinations were associated with increases in warm-season pediatric asthma emergency department visits (eg, joint-effect RR = 1.13 [95% confidence interval = 1.06-1.21] for criteria pollutants, including ozone, carbon monoxide, nitrogen dioxide, sulfur dioxide, and PM2.5). Cold-season joint effects from models without nonlinear effects were generally weaker than warm-season effects. Joint-effect estimates from multipollutant models were often smaller than estimates based on single-pollutant models, due to control for confounding. Compared with models without interactions, joint-effect estimates from models including first-order pollutant interactions were largely similar. There was evidence of nonlinear cold-season effects.ConclusionsOur analyses illustrate how consideration of joint effects can add to our understanding of health effects of multipollutant exposures and also illustrate some of the complexities involved in calculating and interpreting joint effects of multiple pollutants.
| S-EPMC4724194 | biostudies-literature
Project description:BackgroundBiomass burning has been shown to be a major source of poor indoor air quality (IAQ) in developing and higher income countries across the world. Specifically, wood burning for cooking and heating contributes to high indoor concentrations of fine (particles with aerodynamic diameters<2.5μm; PM2.5) and coarse (particles with aerodynamic diameters <10μm and >2.5μm; PMc) particulate matter. Endotoxin, predominantly found within the coarse fraction of airborne particulate matter, is associated with proinflammatory effects and adverse outcomes among susceptible populations. The aim of this study was to assess the efficacy of air filter interventions in reducing indoor PM2.5, PMc, and PMc-associated endotoxin concentrations in homes using a wood stove for primary heating.ResultsHomes (n=48) were randomized to receive in-room air filtration units with either a high efficiency filter (i.e. active) or a lower efficiency fiberglass filter (i.e., placebo). The active filter intervention showed a 66% reduction in indoor PM2.5 concentrations (95% CI: 42.2% to 79.7% reduction) relative to the placebo intervention. Both the active and the placebo filters were effective in substantially reducing indoor concentrations of PMc (63.3% and 40.6% average reduction for active and placebo filters, respectively) and PMc-associated endotoxin concentrations (91.8% and 80.4% average reductions, respectively).ConclusionsThese findings support the use of high efficiency air filtration units for reducing indoor PM2.5 in homes using a wood stove for primary heating. We also discovered that using lower efficiency, lower cost filter alternatives can be effective for reducing PMc and airborne endotoxin in homes burning biomass fuel.
| S-EPMC6394836 | biostudies-literature
Project description:This investigation determined the effects of air pollution on childhood asthma hospitalization in regions with differing air pollution levels in Taiwan over a long time period. Data of childhood hospital admissions for asthma in patients aged 0?18 years and air quality in eight regions for the period 2001?2012 in Taiwan were collected. Poisson generalized linear regression analysis was employed to identify the relative risks of hospitalization due to asthma in children associated with exposure to varying levels of air pollutants with a change in the interquartile range after adjusting for temperature and relative humidity. Particulate matter ?2.5 ?m (PM2.5), particulate matter ?10 ?m (PM10), ozone (O?), sulfur dioxide (SO?), and nitrogen dioxide (NO?), were positively associated with childhood asthma hospitalization, while O? was negatively associated with childhood asthma hospitalization. SO? was identified as the most significant risk factor. The relative risks for asthma hospitalization associated with air pollutants were higher among children aged 0?5 years than aged 6?18 years and were higher among males than females. The effects of air pollution on childhood asthma were greater in the higher-level air pollution regions, while no association was observed in the lower-level air pollution regions. These findings may prove important for policymakers involved in implementing policies to reduce air pollution.
| S-EPMC6351918 | biostudies-literature