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J Allergy Clin Immunol ; 144(3): 839-845.e10, 2019 09.
Artigo em Inglês | MEDLINE | ID: mdl-31247265


BACKGROUND: Telomere length (TL) can serve as a potential biomarker for conditions associated with chronic oxidative stress and inflammation, such as asthma. Air pollution can induce oxidative stress. Understanding the relationship between TL, asthma, and air pollution is important for identifying risk factors contributing to unhealthy aging in children. OBJECTIVES: We sought to investigate associations between exposures to ambient air pollutants and TL in African American children and adolescents and to examine whether African ancestry, asthma status, and steroid medication use alter the association. METHODS: Linear regression was used to examine associations between absolute telomere length (aTL) and estimated annual average residential ozone (O3) and fine particulate matter with a diameter of 2.5 µm or less (PM2.5) exposures in a cross-sectional analysis of 1072 children in an existing asthma case-control study. African ancestry, asthma status, and use of steroid medications were examined as effect modifiers. RESULTS: Participants' aTLs were measured by using quantitative PCR. A 1-ppb and 1 µg/m3 increase in annual average exposure to O3 and PM2.5 were associated with a decrease in aTL of 37.1 kilo-base pair (kb; 95% CI, -66.7 to -7.4 kb) and 57.1 kb (95% CI, -118.1 to 3.9 kb), respectively. African ancestry and asthma were not effect modifiers; however, exposure to steroid medications modified the relationships between TL and pollutants. Past-year exposure to O3 and PM2.5 was associated with shorter TLs in patients without steroid use. CONCLUSION: Exposure to air pollution was associated with shorter TLs in nonasthmatic children and adolescents. This was not the case for asthmatic children as a group, but those receiving steroid medication had less shortening than those not using steroids. Reduced exposure to air pollution in childhood might help to preserve TL.

Afro-Americanos , Poluição do Ar , Asma/tratamento farmacológico , Exposição Ambiental , Esteroides/uso terapêutico , Telômero , Adolescente , Adulto , Poluentes Atmosféricos , Asma/etnologia , Criança , Humanos , Ozônio , Material Particulado , Adulto Jovem
Autism Res ; 11(1): 69-80, 2018 01.
Artigo em Inglês | MEDLINE | ID: mdl-29120534


Independent studies report that periconceptional folic acid (FA) may decrease the risk of autism spectrum disorder (ASD) while exposure to air pollution may increase ASD risk. We examined the joint effects of gestational FA and air pollution exposures in association with ASD. We studied 346 ASD cases and 260 typically developing controls from the CHARGE case-control study. Self-reported FA intake for each month of pregnancy was quantified. Estimates of exposure to near roadway air pollution (NRP) and criteria air pollutant measures were assigned based on maternal residential history. Among mothers with high FA intake (>800 µg) in the first pregnancy month, exposure to increasing levels of all air pollutants, except ozone, during the first trimester was associated with decreased ASD risk, while increased ASD risk was observed for the same pollutant among mothers with low FA intake (≤800 µg). This difference was statistically significant for NO2 (e.g., NO2 and low FA intake: OR = 1.53 (0.91, 2.56) vs NO2 and high FA intake: OR = 0.74 (0.46, 1.19), P-interaction = 0.04). Mothers exposed to higher levels (≥ median) of any air pollutant during the first trimester of pregnancy and who reported low FA intake were at a higher ASD risk compared to mothers exposed to lower levels of that air pollutant and who reported high first month FA intake. Joint effects showed significant (alpha < 0.10) departures from expected interaction for NRP and NO2 . Our results suggest that periconceptional FA intake may reduce ASD risk in those with high prenatal air pollution exposure. Further study is needed to replicate these findings in larger sample sizes and to understand mechanisms of this potential relationship.. Autism Res 2018, 11: 69-80. © 2017 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: We examined interactions between periconceptional folic acid (FA) and air pollution exposure on risk of ASD. Mothers exposed to higher levels of air pollution during the first trimester of pregnancy and who reported low supplemental FA intake during the first pregnancy month were at a higher ASD risk compared to mothers exposed to lower levels of air pollution and who reported high first month FA intake. Our results suggest that periconceptional FA intake may reduce ASD risk in those with high prenatal air pollution exposure.

Poluentes Atmosféricos/efeitos adversos , Transtorno do Espectro Autista/epidemiologia , Suplementos Nutricionais , Ácido Fólico/administração & dosagem , Exposição Materna/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Adulto , California/epidemiologia , Estudos de Casos e Controles , Causalidade , Pré-Escolar , Feminino , Humanos , Masculino , Mães , Gravidez , Risco
Am J Respir Crit Care Med ; 193(10): 1143-50, 2016 May 15.
Artigo em Inglês | MEDLINE | ID: mdl-26681363


RATIONALE: The contribution of air pollution to the risk of acute respiratory distress syndrome (ARDS) is unknown. METHODS: We studied 1,558 critically ill patients enrolled in a prospective observational study at a tertiary medical center who lived less than 50 km from an air quality monitor and had an ARDS risk factor. Pollutant exposures (ozone, NO2, SO2, particulate matter < 2.5 µm, particulate matter < 10 µm) were assessed by weighted average of daily levels from the closest monitors for the prior 3 years. Associations between pollutant exposure and ARDS risk were evaluated by logistic regression controlling for age, race, sex, smoking, alcohol, insurance status, rural versus urban residence, distance to study hospital, and Acute Physiology and Chronic Health Evaluation II. MEASUREMENTS AND MAIN RESULTS: The incidence of ARDS increased with increasing ozone exposure: 28% in the lowest exposure quartile versus 32, 40, and 42% in the second, third, and fourth quartiles (P < 0.001). In a logistic regression model controlling for potential confounders, ozone exposure was associated with risk of ARDS in the entire cohort (odds ratio, 1.58 [95% confidence interval, 1.27-1.96]) and more strongly associated in the subgroup with trauma as their ARDS risk factor (odds ratio, 2.26 [95% confidence interval, 1.46-3.50]). There was a strong interaction between ozone exposure and current smoking status (P = 0.007). NO2 exposure was also associated with ARDS but not independently of ozone exposure. SO2, particulate matter less than 2.5 µm, and particulate matter less than 10 µm were not associated with ARDS. CONCLUSIONS: Long-term ozone exposure is associated with development of ARDS in at-risk critically ill patients, particularly in trauma patients and current smokers. Ozone exposure may represent a previously unrecognized environmental risk factor for ARDS.

Poluentes Atmosféricos/análise , Poluição do Ar/estatística & dados numéricos , Exposição Ambiental/estatística & dados numéricos , Ozônio/análise , Síndrome do Desconforto Respiratório/epidemiologia , Adulto , Idoso , Poluição do Ar/análise , Exposição Ambiental/análise , Feminino , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Modelos de Riscos Proporcionais , Estudos Prospectivos , Risco , Tempo , Estados Unidos/epidemiologia
Environ Res ; 135: 221-6, 2014 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-25282280


BACKGROUND: Preterm birth is an important marker of health and has a prevalence of 12-13% in the U.S. Polycyclic aromatic hydrocarbons (PAHs) are a group of organic contaminants that form during the incomplete combustion of hydrocarbons, such as coal, diesel and gasoline. Studies suggest that exposure to PAHs during pregnancy is related to adverse birth outcomes. The aim of this study is to evaluate the association between exposure to PAHs during the pregnancy and preterm birth. METHODS: The study population included births from years 2001 to 2006 of women whose maternal residence was within 20km of the primary monitoring site in Fresno, California. Data in the Fresno area were used to form a spatio-temporal model to assign daily exposure to PAHs with 4, 5, or 6 rings at the maternal residence throughout pregnancy of all of the births in the study area. Gestational age at birth and relevant covariates were extracted from the birth certificate. RESULTS: We found an association between PAHs during the last 6 weeks of pregnancy and birth at 20-27 weeks (OR=2.74; 95% CI: 2.24-3.34) comparing the highest quartile to the lower three. The association was consistent when each quartile was compared to the lowest (OR2nd=1.49, 95% CI: 1.08-2.06; OR3rd=2.63, 95% CI:1.93-3.59; OR4th=3.94, 95% CI:3.03-5.12). Inverse associations were also observed for exposure to PAHs during the entire pregnancy and the first trimester and birth at 28-31 weeks and 20-27 weeks. CONCLUSION: An association between PAH exposure during the 6 weeks before delivery and early preterm birth was observed. However, the inverse association with early preterm birth offers an unclear, and potentially complex, inference of these associations.

Poluentes Atmosféricos/efeitos adversos , Exposição Materna/efeitos adversos , Modelos Biológicos , Hidrocarbonetos Policíclicos Aromáticos/efeitos adversos , Nascimento Prematuro/epidemiologia , Estações do Ano , California/epidemiologia , Feminino , Humanos , Razão de Chances , Gravidez , Nascimento Prematuro/induzido quimicamente , Prevalência
Environ Res ; 129: 1-10, 2014 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-24528996


BACKGROUND: While exposure to outdoor particulate matter (PM) has been associated with poor asthma outcomes, few studies have investigated the combined effects of outdoor and indoor PM (including secondhand tobacco smoke). OBJECTIVE: To examine the associations between PM and asthma outcomes. METHODS: We analyzed data from a cohort of adults with asthma and rhinitis (n=302; 82% both conditions; 13% asthma only; 5% rhinitis alone) including measures of home PM, tobacco smoke exposure (hair nicotine and self-report), ambient PM from regional monitoring, distance to roadway, and season (wet or dry). The outcomes of interest were frequent respiratory symptoms and forced expiratory volume in 1 second (FEV1) below the lower limit of normal (NHANES reference values). Multivariable regression analyses examined the associations (Odds Ratio [OR] and 95% Confidence Interval [95%CI]) between exposures and these outcomes, adjusted by sociodemographic characteristics. RESULTS: In adjusted analyses of each exposure, the highest tertile of home PM and season of interview were associated with increased odds for more frequent respiratory symptoms (OR=1.64 95%CI: [1.00, 2.69] and OR=1.66 95%CI: [1.09, 2.51]). The highest tertile of hair nicotine was significantly associated with FEV1 below the lower limit of normal (OR=1.80 95%CI: [1.00, 3.25]). In a model including home PM, ambient PM, hair nicotine, and season, only two associations remained strong: hair nicotine with FEV1 below the lower limit of normal and season of measurement (dry, April-October) with increased respiratory symptoms (OR=1.85 95%CI: [1.00, 3.41] and OR=1.54 95%CI: [1.0, 2.37]). When that model was stratified by sex, the highest tertiles of ambient PM and hair nicotine were associated with FEV1 below the lower limit of normal among women (OR=2.23 95%CI: [1.08, 4.61] and OR=2.90 95%CI: [1.32, 6.38]), but not men. The highest tertile of hair nicotine was also associated with increased respiratory symptoms in women but not men (OR=2.38 95%CI: [1.26, 4.49]). When stratified by age, the middle quartile of ambient PM and the highest hair nicotine tertile were associated with increased respiratory symptoms (OR=2.07 95%CI: [1.01, 4.24] and OR=2.55 95%CI: [1.21, 5.36]) in those under 55 but not in the older stratum. CONCLUSIONS: Exposure to PM from both home and ambient sources is associated with increased symptoms and lower lung function in adults with asthma, although these associations vary by type of PM, the respiratory outcome studied, sex and age.

Poluentes Atmosféricos/análise , Poluição do Ar em Ambientes Fechados/análise , Asma/epidemiologia , Exposição por Inalação/análise , Nicotina/análise , Material Particulado/análise , Poluição por Fumaça de Tabaco/análise , Adolescente , Adulto , Poluentes Atmosféricos/efeitos adversos , Poluição do Ar em Ambientes Fechados/efeitos adversos , Asma/induzido quimicamente , Asma/fisiopatologia , California , Estudos de Coortes , Interpretação Estatística de Dados , Monitoramento Ambiental/métodos , Monitoramento Ambiental/estatística & dados numéricos , Feminino , Volume Expiratório Forçado/efeitos dos fármacos , Cabelo/química , Humanos , Exposição por Inalação/efeitos adversos , Exposição por Inalação/estatística & dados numéricos , Masculino , Pessoa de Meia-Idade , Material Particulado/efeitos adversos , Rinite/induzido quimicamente , Rinite/epidemiologia , Rinite/fisiopatologia , Estações do Ano , Fatores Socioeconômicos , Inquéritos e Questionários , Poluição por Fumaça de Tabaco/efeitos adversos , Adulto Jovem