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Synergistic Association of House Endotoxin Exposure and Ambient Air Pollution with Asthma Outcomes.

ABSTRACT: 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 (PM_2.5), 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, PM_2.5 (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 PM_2.5 (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 PM_2.5 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.

SUBMITTER: Mendy A

PROVIDER: S-EPMC6775869 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundRecent studies suggest that household endotoxin and allergens can modify the impact of air pollutants on development of asthma; however, epidemiological evidence is limited and conflicting.ObjectivesTo investigate whether pet ownership modified the association between ambient air pollution and asthma in children.MethodsWe conducted a population-based cross-sectional study, the Seven Northeast Cities Study in China and recruited a total of 59,754 children from 94 schools during 2012-2013. Long-term air pollutant concentrations, including airborne particulate matter with a diameter of 1 μm or less (PM1 ), PM2.5 , PM10 , and nitrogen dioxide (NO2 ) from 2009 to 2012 were estimated using a random forest model. We collected information of respiratory health in children using the Epidemiologic Standardization Project Questionnaire of the American Thoracic Society (ATS-DLD-78-A). Regression models were used to evaluate associations between pet ownership and air pollution on asthma after adjusting for potential covariates.ResultsExposure to increasing levels of air pollutants was associated with higher prevalence of asthma, but associations were significantly attenuated in children who owned pets. For example, compared to children without pets, those who owned pets did not have an increased risk of symptoms of asthma (odds ratio, 1.01, 95% confidence interval: 0.78, 1.30), wheeze (0.96, 95% confidence interval [CI]: 0.76, 1.21), and cough (1.01, 95% CI: 0.87, 1.18) for each 10 µg/m3 increase in PM1 (P-int < 0.05). Similar trends were observed for other air pollutants. Dog and bird ownership decreased the associations of asthma and cough with air pollutant exposure. The main findings were consistent with a series of sensitivity analyses.ConclusionCurrent pet ownership may reduce the adverse impact of long-term air pollution on childhood asthma. Longitudinal studies are needed to confirm this finding which could have important implications for public health.

Project description:Importance:Air pollutants interact with estrogen nuclear receptors, but their effect on thyroid signaling is less clear. Thyroid function is of particular importance for pregnant women because of the thyroid's role in fetal brain development. Objective:To determine the short-term association of exposure to air pollution in the first trimester with thyroid function throughout pregnancy. Design, Setting, and Participants:In this cohort study, 9931 pregnant women from 4 European cohorts (the Amsterdam Born Children and Their Development Study, the Generation R Study, Infancia y Medio Ambiente, and Rhea) and 1 US cohort (Project Viva) with data on air pollution exposure and thyroid function during pregnancy were included. The recruitment period for the Amsterdam Born Children and Their Development Study was January 2003 to March 2004; for Generation R, April 2002 to January 2006; for Infancia y Medio Ambiente, November 2003 to January 2008; for Rhea, February 2007 to February 2008; and for Project Viva, April 1999 to November 2002. Statistical analyses were conducted from January 2018 to April 2019. Main Outcomes and Measures:Residential air pollution concentrations (ie, nitrogen oxide and particulate matter [PM]) during the first trimester of pregnancy were estimated using land-use regression and satellite-derived aerosol optical depth models. Free thyroxine, thyrotropin, and thyroid peroxidase antibody levels were measured across gestation. Hypothyroxinemia was defined as free thyroxine below the fifth percentile of the cohort distribution with normal thyrotropin levels, following the American Thyroid Association guidelines. Results:Among 9931 participants, the mean (SD) age was 31.2 (4.8) years, 4853 (48.9%) had more than secondary educational levels, 5616 (56.6%) were nulliparous, 404 (4.2%) had hypothyroxinemia, and 506 (6.7%) tested positive for thyroid peroxidase antibodies. Concentrations of nitrogen dioxide and PM with an aerodynamic diameter of 2.5 ?m or less (PM2.5) were lower and had less variation in women in the US cohort than those in European cohorts. No associations of nitrogen oxide with thyroid function were found. Higher exposures to PM2.5 were associated with higher odds of hypothyroxinemia in pregnant women (odds ratio per 5-?g/m3 change, 1.21; 95% CI, 1.00-1.47). Although exposure to PM with an aerodynamic diameter of 10 ?m or less was not significantly associated with hypothyroxinemia, the coefficient was similar to that for the association of PM2.5 with hypothyroxinemia (odds ratio per 10-?g/m3 change, 1.18; 95% CI, 0.93-1.48). Absorbances of PM2.5 and PM with aerodynamic diameter from 2.5 to 10 ?g and were not associated with hypothyroxinemia. There was substantial heterogeneity among cohorts with respect to thyroid peroxidase antibodies (P for heterogeneity, <.001), showing associations of nitrogen oxide and PM with thyroid autoimmunity only in the women in the Generation R Study. Conclusions and Relevance:The findings of this study suggest that first-trimester exposures to PM2.5 were associated with mild thyroid dysfunction throughout pregnancy. The association of PM2.5 exposure with thyroid function during pregnancy is of global health importance because air pollution exposure is widespread and hypothyroxinemia may adversely influence the brain development of offspring.

Project description:Ambient air pollution was known to cause central nervous system diseases and depressive symptoms. In this study, we examined the associations between air pollution exposure and the prevalence of insomnia in Taipei City of Taiwan. We applied the health information system of electrical medical records of Taipei City Hospital to collect a total of 5108 study subjects (insomniacs N = 912 and non-insomniacs N = 4196) over 18 years old from the family medicine and internal medicine outpatients of six branches of Taipei City Hospital. These patients were grouped into insomniacs and non-insomniacs following the primary insomnia diagnosis (ICD9:780.52, 780.54, 307.41, 307.42, ICD10: G47.00, G47.01, G47.09, F51.01, F51.09) and the prescription times of anxiolytics and hypnotics. We estimated one-year average concentrations of PM2.5, ozone, and NOx before the first date of insomnia diagnosis and the last date of outpatient visit for insomniacs and non-insomniacs, respectively, by using the data of nearest air quality monitoring stations relative to study subjects' residential addresses. Logistic regression analysis was employed to examine the independent effects of air pollution concentrations on the risk of insomnia. One-year average PM2.5, ozone, and NOx levels for insomniacs was significantly higher than those of non-insomniacs. After adjusting for confounding factors, increase each 1(μg/m3) in one-year average PM2.5 showed a statistically significant association with insomnia (the odds ratio 1.610, 95% CI [1.562,1.660]). As to multi pollutants, one-year average PM2.5 (1.624, [1.570, 1.681] and ozone (1.198, [1.094, 1.311]) exposure showed a significant association with insomnia. Subgroup analysis revealed that the influence of PM2.5 and ozone on insomnia have significant risks in people with major chronic disease. This study demonstrated a positive association between PM2.5 and ozone exposure and the prevalence of hypnotic-treated insomnia. Especially, the people with major chronic diseases were with obvious effect of PM2.5 and ozone on risk of insomnia.

Project description:ImportanceAir pollution is associated with structural brain changes, disruption of neurogenesis, and neurodevelopmental disorders. The association between prenatal exposure to ambient air pollution and risk of cerebral palsy (CP), which is the most common motor disability in childhood, has not been thoroughly investigated.ObjectiveTo evaluate the associations between prenatal residential exposure to ambient air pollution and risk of CP among children born at term gestation in a population cohort in Ontario, Canada.Design, setting, and participantsPopulation-based cohort study in Ontario, Canada using linked, province-wide health administrative databases. Participants were singleton full term births (≥37 gestational weeks) born in Ontario hospitals between April 1, 2002, and March 31, 2017. Data were analyzed from January to December 2022.ExposuresWeekly average concentrations of ambient fine particulate matter with a diameter 2.5 μm (PM2.5) or smaller, nitrogen dioxide (NO2), and ozone (O3) during pregnancy assigned by maternal residence reported at delivery from satellite-based estimates and ground-level monitoring data.Main outcome and measuresCP cases were ascertained by a single inpatient hospitalization diagnosis or at least 2 outpatient diagnoses for children from birth to age 18 years.ResultsThe present study included 1 587 935 mother-child pairs who reached term gestation, among whom 3170 (0.2%) children were diagnosed with CP. The study population had a mean (SD) maternal age of 30.1 (5.6) years and 811 745 infants (51.1%) were male. A per IQR increase (2.7 μg/m3) in prenatal ambient PM2.5 concentration was associated with a cumulative hazard ratio (CHR) of 1.12 (95% CI, 1.03-1.21) for CP. The CHR in male infants (1.14; 95% CI, 1.02-1.26) was higher compared with the CHR in female infants (1.08; 95% CI, 0.96-1.22). No specific window of susceptibility was found for prenatal PM2.5 exposure and CP in the study population. No associations or windows of susceptibility were found for prenatal NO2 or O3 exposure and CP risk.Conclusions and relevanceIn this large cohort study of singleton full term births in Canada, prenatal ambient PM2.5 exposure was associated with an increased risk of CP in offspring. Further studies are needed to explore this association and its potential biological pathways, which could advance the identification of environmental risk factors of CP in early life.

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Synergistic Association of House Endotoxin Exposure and Ambient Air Pollution with Asthma Outcomes.

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