Synergistic Association of House Endotoxin Exposure and Ambient Air Pollution with Asthma Outcomes.
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ABSTRACT:
SUBMITTER: Mendy A
PROVIDER: S-EPMC6775869 | biostudies-literature |
REPOSITORIES: biostudies-literature
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| S-EPMC6775880 | biostudies-literature
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.
| S-EPMC8099301 | biostudies-literature
Project description:PURPOSE:Maternal asthma increases adverse neonatal respiratory outcomes, and pollution may further increase risk. Air quality in relation to neonatal respiratory health has not been studied. METHODS:Transient tachypnea of the newborn (TTN), asphyxia, and respiratory distress syndrome (RDS) were identified using medical records among 223,375 singletons from the Consortium on Safe Labor (2002-2008). Community Multiscale Air Quality models estimated pollutant exposures. Multipollutant Poisson regression models calculated adjusted relative risks of outcomes for interquartile range increases in average exposure. Maternal asthma and preterm delivery were evaluated as effect modifiers. RESULTS:TTN risk increased after particulate matter (PM) less than or equal to 10-micron exposure during preconception and trimester one (9-10%), and whole-pregnancy exposure to PM less than or equal to 2.5 microns (PM2.5; 17%) and carbon monoxide (CO; 10%). Asphyxia risk increased after exposure to PM2.5 in trimester one (48%) and whole pregnancy (84%), CO in trimester two and whole pregnancy (28-32%), and consistently for ozone (34%-73%). RDS risk was associated with increased concentrations of nitrogen oxides (33%-42%) and ozone (9%-21%) during all pregnancy windows. Inverse associations were observed with several pollutants, particularly sulfur dioxide. No interaction with maternal asthma was observed. Restriction to term births yielded similar results. CONCLUSIONS:Several pollutants appear to increase neonatal respiratory outcome risks.
| S-EPMC6232679 | biostudies-literature
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.
| S-EPMC6806433 | biostudies-literature
Project description:Environmental factors may play roles in the development of rheumatoid arthritis (RA), and some studies have shown that air pollution was associated with the development of autoimmune disease. This study was designed to investigate the effect of air pollutants on the development of adult RA. A nested case-control cohort study was performed using the National Health Insurance Service-National Sample Cohort during 2002⁻2014 in Korea. Air pollution data were collected from the National Ambient Air Monitoring System (NAMIS), and exposure levels were extrapolated using geographic information systems. The group with RA (n = 444) was compared with a propensity score-matched control group (n = 1776), and one-year average concentrations of air pollution were predicted at each patient's residence. The adjusted binary logistic regression analysis showed a positive association between O₃ exposure and the incidence risk of RA for the third (odds ratios (OR) = 1.45, 95% confidence intervals (CI): 1.08⁻1.96) and fourth (OR = 1.35, 95% CI: 1.00⁻1.83) quartiles in adults over 20 years of age. The third quartile CO exposure was also associated with an increased risk of RA (OR = 1.57, 95% CI: 1.16⁻2.12). The results of this nationwide population-based study showed that a one-year exposure to CO and O₃ in adults was associated with an increased risk of RA.
| S-EPMC6480037 | biostudies-literature
Project description:ObjectiveAlthough exposure to air pollution and pollen is associated with asthma exacerbation and increased health care use, longitudinal effects of fine particulate matter 2.5 (PM2.5), ozone (O3), and pollen exposure on asthma control status in pediatric patients are understudied. This study investigated effects of exposure to PM2.5, O3, and pollen on asthma control status among pediatric patients with asthma.MethodsA total of 229 dyads of pediatric patients with asthma and their parents were followed for 15 months. The Asthma Control and Communication Instrument was used to measure asthma control, which was reported weekly by parents during a 26-week period. PM2.5 and O3 data were collected from the US Environmental Protection Agency Air Quality System. Pollen data were obtained from Intercontinental Marketing Services Health. Mean air pollutant and pollen exposures within 7 days before the reporting of asthma control were used to estimate weekly exposures for each participant. Linear mixed-effects models were performed to test associations of PM2.5, O3, and pollen exposure with asthma control status. Sensitivity analyses were performed to evaluate the robustness of findings by different exposure monitoring days per week and distances between monitoring sites and participants' residences.ResultsElevated PM2.5 concentration and pollen severity were associated with poorer asthma control status (P < .05), yet elevated O3 concentration was marginally associated with better asthma control (P < .1).ConclusionsPoorer asthma control status was associated with elevated PM2.5 and pollen severity. Reducing harmful outdoor environmental ambient exposure may improve asthma outcomes in children and adolescents.
| S-EPMC8981069 | biostudies-literature
Project description:ImportanceIncreased levels of ambient fine particulate matter (PM2.5) air pollution are associated with increased risks for detrimental health outcomes, but risks for patients with kidney transplants (KTs) remain unknown.ObjectiveTo investigate the association of PM2.5 exposure with KT outcomes.Design, setting, and participantsThis retrospective cohort study was conducted using data on patients who received KTs from 2004 to 2016 who were identified in the national US transplant registry and followed up through March 2021. Multiple databases were linked to obtain data on PM2.5 concentration, KT outcomes, and patient clinical, transplant, and contextual factors. Data were analyzed from April 2020 through July 2021.ExposuresExposures included post-KT time-dependent annual mean PM2.5 level (in 10 μg/m3) and mean PM2.5 level in the year before KT (ie, baseline levels) in quartiles, as well as baseline annual mean PM2.5 level (in 10 μg/m3).Main outcomes and measuresAcute kidney rejection (ie, rejection within 1 year after KT), time to death-censored graft failure, and time to all-cause death. Multivariable logistic regression for kidney rejection and Cox analyses with nonlinear assessment of exposure-response for death-censored graft failure and all-cause death were performed. The national burden of graft failure associated with PM2.5 levels greater than the Environmental Protection Agency recommended level of 12 μg/m3 was estimated.ResultsAmong 112 098 patients with KTs, 70 522 individuals (62.9%) were older than age 50 years at the time of KT, 68 117 (60.8%) were men, and the median (IQR) follow-up was 6.0 (3.9-8.9) years. There were 37 265 Black patients (33.2%), 17 047 Hispanic patients (15.2%), 48 581 White patients [43.3%]), and 9205 patients (8.2%) of other race or ethnicity. The median (IQR) baseline PM2.5 level was 9.8 (8.3-11.9) μg/m3. Increased baseline PM2.5 level, compared with quartile 1 baseline PM2.5 level, was not associated with higher odds of acute kidney rejection for quartile 2 (adjusted odds ratio [aOR], 0.99; 95% CI, 0.92-1.06) but was associated with increased odds for quartile 3 (aOR, 1.11; 95% CI, 1.04-1.20) and quartile 4 (aOR, 1.13; 95% CI, 1.05-1.23). Nonlinear assessment of exposure-response for graft failure and death showed no evidence for nonlinearity. Increased PM2.5 levels were associated with increased risk of death-censored graft failure (adjusted hazard ratio [aHR] per 10 μg/m3 increase, 1.17; 95% CI, 1.09-1.25) and all-cause death (aHR per 10 μg/m3 increase, 1.21; 95% CI, 1.14-1.28). The national burden of death-censored graft failure associated with PM2.5 above 12 μg/m3 was 57 failures (95% uncertainty interval, 48-67 failures) per year among patients with KTs.Conclusions and relevanceThis cohort study found that PM2.5 level was an independent risk factor associated with acute rejection, graft failure, and death among patients with KTs. These findings suggest that efforts toward decreasing levels of PM2.5 concentration may be associated with improved outcomes after KT.
| S-EPMC8498852 | biostudies-literature
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.
| S-EPMC9646727 | biostudies-literature
Project description:Exposure to higher levels of ambient air pollution is a known risk factor for cardiovascular disease but long-term effects of pollution exposure on the pulmonary vessels are unknown.MethodsAmong 2428 Framingham Heart Study participants who underwent chest computed tomography (CT) between 2008 and 2011, pulmonary vascular volumes were calculated by image analysis, including the total vascular volume and small vessel volume (cross-sectional area <5 mm2; BV5 defined as small vessel volume). Using spatiotemporal models and participant home address, we assigned 1-year (2008) and 5-year (2004-2008) average concentrations of fine particulate matter (PM2.5), elemental carbon (EC), and ground-level ozone (O3), and distance to major roadway. We examined associations of 1- and 5-year exposures, and distance to road, with CT vascular volumes using multivariable linear regression models.ResultsThere was a consistent negative association of higher O3 with lower small vessel volumes, which persisted after adjustment for distance to road. Per interquartile range (IQR) of 2008 O3, BV5 was 0.34 mL lower (95% confidence intervals [CI], -0.61 to -0.06; P = 0.02), with similar results for 5-year exposure. One-year EC exposure and closer proximity to road were weakly associated with small vessel volumes; BV5 was 0.18 mL higher per IQR of 2008 EC (95% CI, -0.05 to 0.42; P = 0.13) and 0.40 mL higher per IQR closer proximity to road (95% CI: -0.10 to 0.89; P = 0.12). PM2.5 was not associated with small vascular volumes; BV5 was 0.26 mL lower per IQR of 2008 PM2.5 (95% CI: -0.68 to 0.16; P = 0.22).ConclusionsAmong community-dwelling adults living in the northeastern United States, higher exposure to O3 was associated with lower small pulmonary vessel volumes on CT.
| S-EPMC8043731 | biostudies-literature
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.
| S-EPMC11234239 | biostudies-literature