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1.
Environ Int ; 158: 106898, 2021 Oct 06.
Artigo em Inglês | MEDLINE | ID: mdl-34627014

RESUMO

IMPORTANCE: Previous studies have reported associations between in utero exposure to regional air pollution and autism spectrum disorders (ASD). In utero exposure to components of near-roadway air pollution (NRAP) has been linked to adverse neurodevelopment in animal models, but few studies have investigated NRAP association with ASD risk. OBJECTIVE: To identify ASD risk associated with in utero exposure to NRAP in a large, representative birth cohort. DESIGN, SETTING, AND PARTICIPANTS: This retrospective pregnancy cohort study included 314,391 mother-child pairs of singletons born between 2001 and 2014 at Kaiser Permanente Southern California (KPSC) hospitals. Maternal and child data were extracted from KPSC electronic medical records. Children were followed until: clinical diagnosis of ASD, non-KPSC membership, death, or December 31, 2019, whichever came first. Exposure to the complex NRAP mixture during pregnancy was assessed using line-source dispersion models to estimate fresh vehicle emissions from freeway and non-freeway sources at maternal addresses during pregnancy. Vehicular traffic load exposure was characterized using advanced telematic models combining traditional traffic counts and travel-demand models with cell phone and vehicle GPS data. Cox proportional-hazard models estimated hazard ratios (HR) of ASD associated with near-roadway traffic load and dispersion-modeled NRAP during pregnancy, adjusted for covariates. Non-freeway NRAP was analyzed using quintile distribution due to nonlinear associations with ASD. EXPOSURES: Average NRAP and traffic load exposure during pregnancy at maternal residential addresses. MAIN OUTCOMES: Clinical diagnosis of ASD. RESULTS: A total of 6,291 children (5,114 boys, 1,177 girls) were diagnosed with ASD. The risk of ASD was associated with pregnancy-average exposure to total NRAP [HR(95% CI): 1.03(1.00,1.05) per 5 ppb increase in dispersion-modeled NOx] and to non-freeway NRAP [HR(95% CI) comparing the highest to the lowest quintile: 1.19(1.11, 1.27)]. Total NRAP had a stronger association in boys than in girls, but the association with non-freeway NRAP did not differ by sex. The association of freeway NRAP with ASD risk was not statistically significant. Non-freeway traffic load exposure demonstrated associations with ASD consistent with those of NRAP and ASD. CONCLUSIONS: In utero exposure to near-roadway air pollution, particularly from non-freeway sources, may increase ASD risk in children.

2.
Environ Int ; 133(Pt A): 105110, 2019 12.
Artigo em Inglês | MEDLINE | ID: mdl-31610366

RESUMO

BACKGROUND: Ambient air pollution and maternal diabetes may affect common biological pathways underlying adverse neurodevelopmental effects. However, joint effects of maternal diabetes and air pollution on autism spectrum disorder (ASD) have not been studied. OBJECTIVE: We evaluated whether prenatal and early-life air pollution exposure interacts with maternal diabetes status to affect ASD risk. METHODS: This retrospective cohort study included 246,420 singleton children born in Kaiser Permanente Southern California hospitals in 1999-2009. Children were followed from birth until age 5, during which 2471 ASD cases were diagnosed. Ozone (O3), particulate matter < 2.5 µm (PM2.5) and <10 µm in aerodynamic diameter, and nitrogen dioxide measured at regulatory air monitoring stations were interpolated to estimate exposures during preconception and each pregnancy trimester, and first year of life at each child's birth address. Hazard ratios (HRs) for ASD were estimated adjusting for birth year, KPSC service areas, and relevant maternal and child characteristics. For each exposure window, interactions were tested between pollutants and a 4-category maternal diabetes variable (none, GDM ≥ 24 and <24 weeks' gestation, and pre-existing type 2 diabetes). For an exposure window with statistically significant global interaction between pollutant and diabetes (p < 0.05), pollutant-associated HRs were estimated separately for each category of maternal diabetes. RESULTS: There were associations of ASD with preconception, first and third trimesters, and first year of life PM2.5, but not with other pollutants. There were, however, interactions of maternal diabetes with first trimester and first year of life O3. Increased ASD risk was associated with first trimester O3 among mothers with GDM < 24 weeks' gestation [adjusted HR 1.50 per 15.7 ppb O3 (95% CI: 1.08-2.09)]. No O3 associations with ASD were observed in other categories of maternal diabetes. CONCLUSIONS: GDM onset early in pregnancy may increase children's susceptibility to prenatal O3-associated ASD risk. These novel findings merit further investigation.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Transtorno do Espectro Autista/etiologia , Diabetes Gestacional/etiologia , Exposição Materna , Adulto , Poluentes Atmosféricos/análise , California , Pré-Escolar , Estudos de Coortes , Diabetes Mellitus Tipo 2/complicações , Feminino , Humanos , Lactente , Recém-Nascido , Masculino , Dióxido de Nitrogênio/análise , Ozônio/efeitos adversos , Ozônio/análise , Material Particulado/efeitos adversos , Material Particulado/análise , Gravidez , Trimestres da Gravidez , Modelos de Riscos Proporcionais , Estudos Retrospectivos
3.
Environ Pollut ; 254(Pt A): 113010, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31554142

RESUMO

Autism spectrum disorder (ASD) affects more boys than girls. Recent animal studies found that early life exposure to ambient particles caused autism-like behaviors only in males. However, there has been little study of sex-specificity of effects on ASD in humans. We evaluated ASD risk associated with prenatal and first year of life exposures to particulate matter less than 2.5 µm in aerodynamic diameter (PM2.5) by child sex. This retrospective cohort study included 246,420 singleton children born in Kaiser Permanente Southern California (KPSC) hospitals between 1999 and 2009. The cohort was followed from birth through age five to identify 2471 ASD cases from the electronic medical record. Ambient PM2.5 and other regional air pollution measurements (PM less than 10 µm, ozone, nitrogen dioxide) from regulatory air monitoring stations were interpolated to estimate exposure during each trimester and first year of life at each geocoded birth address. Hazard ratios (HRs) were estimated using Cox regression models to adjust for birth year, KPSC medical center service areas, and relevant maternal and child characteristics. Adjusted HRs per 6.5 µg/m3 PM2.5 were elevated during entire pregnancy [1.17 (95% confidence interval (CI), 1.04-1.33)]; first trimester [1.10 (95% CI, 1.02-1.19)]; third trimester [1.08 (1.00-1.18)]; and first year of life [1.21 (95% CI, 1.05-1.40)]. Only the first trimester association remained robust to adjustment for other exposure windows, and was specific to boys only (HR = 1.18; 95% CI, 1.08-1.27); there was no association in girls (HR = 0.90; 95% CI, 0.76-1.07; interaction p-value 0.03). There were no statistically significant associations with other pollutants. PM2.5-associated ASD risk was stronger in boys, consistent with findings from recent animal studies. Further studies are needed to better understand these sexually dimorphic neurodevelopmental associations.


Assuntos
Poluentes Atmosféricos/toxicidade , Poluição do Ar/análise , Transtorno do Espectro Autista/induzido quimicamente , Material Particulado/toxicidade , Poluentes Atmosféricos/análise , California , Criança , Estudos de Coortes , Feminino , Humanos , Masculino , Dióxido de Nitrogênio/análise , Ozônio/análise , Material Particulado/análise , Gravidez , Primeiro Trimestre da Gravidez , Modelos de Riscos Proporcionais , Estudos Retrospectivos , Fatores Sexuais
4.
Environ Int ; 126: 363-376, 2019 05.
Artigo em Inglês | MEDLINE | ID: mdl-30826615

RESUMO

BACKGROUND: Prenatal air pollution exposure has been linked to many adverse health conditions in the offspring. However, little is known about the mechanisms underlying these associations. Epigenetics may be one plausible biologic link. Here, we sought to identify site-specific and global DNA methylation (DNAm) changes, in developmentally relevant tissues, associated with prenatal exposure to nitrogen dioxide (NO2) and ozone (O3). Additionally, we assessed whether sex-specific changes in methylation exist and whether DNAm changes are consistently observed across tissues. METHODS: Genome-scale DNAm measurements were obtained using the Infinium HumanMethylation450k platform for 133 placenta and 175 cord blood specimens from Early Autism Risk Longitudinal Investigation (EARLI) neonates. Ambient NO2 and O3 exposure levels were based on prenatal address locations of EARLI mothers and the Environmental Protection Agency's AirNOW monitoring network using inverse distance weighting. We computed sample-level aggregate methylation measures for each of 5 types of genomic regions including genome-wide, open sea, shelf, shore, and island regions. Linear regression was performed for each genomic region; per-sample aggregate methylation measures were modeled as a function of quantitative exposure level with covariate adjustment. In addition, bumphunting was performed to identify differentially methylated regions (DMRs) associated with prenatal O3 and NO2 exposures in each tissue and by sex, with adjustment for technical and biological sources of variation. RESULTS: We identified global and locus-specific changes in DNA methylation related to prenatal exposure to NO2 and O3 in 2 developmentally relevant tissues. Neonates with increased prenatal O3 exposure had lower aggregate levels of DNAm at CpGs located in open sea and shelf regions of the genome. We identified 6 DMRs associated with prenatal NO2 exposure, including 3 sex-specific. An additional 3 sex-specific DMRs were associated with prenatal O3 exposure levels. DMRs initially detected in cord blood samples (n = 4) showed consistent exposure-related changes in DNAm in placenta. However, the DMRs initially detected in placenta (n = 5) did not show DNAm differences in cord blood and, thus, they appear to be tissue-specific. CONCLUSIONS: We observed global, locus, and sex-specific methylation changes associated with prenatal NO2 and O3 exposures. Our findings support DNAm is a biologic target of prenatal air pollutant exposures and highlight epigenetic involvement in sex-specific differential susceptibility to environmental exposure effects in 2 developmentally relevant tissues.


Assuntos
Poluição do Ar/análise , Metilação de DNA , Troca Materno-Fetal , Poluentes Atmosféricos/análise , Saúde da Criança , Epigenômica , Feminino , Humanos , Saúde do Lactente , Recém-Nascido , Masculino , Exposição Materna , Dióxido de Nitrogênio/análise , Ozônio/análise , Placenta/química , Gravidez
5.
JAMA Netw Open ; 1(5): e182172, 2018 09 07.
Artigo em Inglês | MEDLINE | ID: mdl-30646156

RESUMO

Importance: Thyroid hormones are critical for fetal growth and development. Prenatal particulate matter (PM) air pollution exposure has been associated with altered newborn thyroid function, but other air pollutants have not been evaluated, and critical windows of exposure are unknown. Objectives: To investigate the association of prenatal exposure to ambient and traffic-related air pollutants with newborn thyroid function and identify critical windows of exposure. Design, Setting, and Participants: This cohort study used data from 2050 participants in the Children's Health Study. Statistical analyses were conducted from 2017 to 2018 using pregnancy and birth data from 1994 to 1997 for a subset of participants recruited from schools in 13 southern California communities in 2002 to 2003 when participants were 5 to 7 years of age. Participants were included in statistical analyses if they could be linked to their newborn blood spot and had complete monthly exposure measures for at least 1 air pollutant across pregnancy. Exposures: Prenatal monthly averages of ambient (PM diameter <2.5 µm [PM2.5] or <10 µm [PM10], nitrogen dioxide, and ozone) and traffic-related (freeway, nonfreeway, and total nitrogen oxides) air pollutant exposures were determined using inverse distance-squared weighting of central monitoring data and the California Line Source Dispersion model, respectively. Main Outcomes and Measures: Newborn heel-stick blood spot total thyroxine (TT4) measures were acquired retrospectively from the California Department of Public Health. Results: Participants included 2050 newborns (50.5% male), with a median (interquartile range) age of 20 (15-29) hours. The majority of newborns were Hispanic white (1202 [58.6%]) or non-Hispanic white (638 [31.1%]). Sixty-six (3.2%) were black and 144 (7.0%) were from other racial/ethnic groups. The mean (SD) newborn TT4 measure was 16.2 (4.3) µg/dL. A 2-SD increase in prenatal PM2.5 (16.3 µg/m3) and PM10 (22.2 µg/m3) was associated with a 1.2-µg/dL (95% CI, 0.5-1.8 µg/dL) and 1.5-µg/dL (95% CI, 0.9-2.1 µg/dL) higher TT4 measure, respectively, in covariate-adjusted linear regression models. Other pollutants were not consistently associated with newborn TT4. Distributed lag models revealed that PM2.5 exposure during months 3 to 7 of pregnancy and PM10 exposure during months 1 to 8 of pregnancy were associated with significantly higher newborn TT4 concentrations (P < .05). Conclusions and Relevance: Prenatal PM exposure, particularly in early pregnancy and midpregnancy, is associated with higher newborn TT4 concentrations. Future studies should assess the health implications of PM-associated differences in newborn TT4 concentrations.


Assuntos
Poluição do Ar/efeitos adversos , Exposição Ambiental/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Poluentes Atmosféricos/análise , Poluição do Ar/estatística & dados numéricos , California/epidemiologia , Estudos de Coortes , Exposição Ambiental/estatística & dados numéricos , Feminino , Desenvolvimento Fetal , Humanos , Recém-Nascido , Masculino , Material Particulado/análise , Gravidez , Estudos Retrospectivos , Testes de Função Tireóidea/métodos , Testes de Função Tireóidea/estatística & dados numéricos , Tiroxina/análise , Tiroxina/sangue
6.
Int J Cancer ; 141(4): 744-749, 2017 08 15.
Artigo em Inglês | MEDLINE | ID: mdl-28589567

RESUMO

Particulate matter (PM) air pollution exposure has been associated with cancer incidence and mortality especially with lung cancer. The liver is another organ possibly affected by PM due to its role in detoxifying xenobiotics absorbed from PM. Various studies have investigated the mechanistic pathways between inhaled pollutants and liver damage, cancer incidence, and tumor progression. However, little is known about the effects of PM on liver cancer survival. Twenty thousand, two hundred and twenty-one California Cancer Registry patients with hepatocellular carcinoma (HCC) diagnosed between 2000 and 2009 were used to examine the effect of exposure to ambient PM with diameter <2.5 µm (PM2.5 ) on HCC survival. Cox proportional hazards models were used to estimate hazard ratios (HRs) relating PM2.5 to all-cause and liver cancer-specific mortality linearly and nonlinearly-overall and stratified by stage at diagnosis (local, regional and distant)-adjusting for potential individual and geospatial confounders.PM2.5 exposure after diagnosis was statistically significantly associated with HCC survival. After adjustment for potential confounders, the all-cause mortality HR associated with a 1 standard deviation (5.0 µg/m3 ) increase in PM2.5 was 1.18 (95% CI: 1.16-1.20); 1.31 (95% CI:1.26-1.35) for local stage, 1.19 (95% CI:1.14-1.23) for regional stage, and 1.05 (95% CI:1.01-1.10) for distant stage. These associations were nonlinear, with substantially larger HRs at higher exposures. The associations between liver cancer-specific mortality and PM2.5 were slightly attenuated compared to all-cause mortality, but with the same patterns.Exposure to elevated PM2.5 after the diagnosis of HCC may shorten survival, with larger effects at higher concentrations.


Assuntos
Poluição do Ar/efeitos adversos , Carcinoma Hepatocelular/mortalidade , Neoplasias Hepáticas/mortalidade , Material Particulado/efeitos adversos , Idoso , Estudos de Coortes , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Modelos de Riscos Proporcionais , Análise de Sobrevida
7.
Diabetes ; 66(7): 1789-1796, 2017 07.
Artigo em Inglês | MEDLINE | ID: mdl-28137791

RESUMO

Evidence suggests that ambient air pollution (AAP) exposure may contribute to the development of obesity and type 2 diabetes. The objective of this study was to determine whether exposure to elevated concentrations of nitrogen dioxide (NO2) and particulate matter with aerodynamic diameter <2.5 (PM2.5) had adverse effects on longitudinal measures of insulin sensitivity (SI), ß-cell function, and obesity in children at high risk for developing diabetes. Overweight and obese Latino children (8-15 years; n = 314) were enrolled between 2001 and 2012 from Los Angeles, CA, and followed for an average of 3.4 years (SD 3.1 years). Linear mixed-effects models were fitted to assess relationships between AAP exposure and outcomes after adjusting for covariates including body fat percent. Higher NO2 and PM2.5 were associated with a faster decline in SI and a lower SI at age 18 years, independent of adiposity. NO2 exposure negatively affected ß-cell function, evidenced by a faster decline in disposition index (DI) and a lower DI at age 18 years. Higher NO2 and PM2.5 exposures over follow-up were also associated with a higher BMI at age 18 years. AAP exposure may contribute to development of type 2 diabetes through direct effects on SI and ß-cell function.


Assuntos
Poluição do Ar/estatística & dados numéricos , Exposição Ambiental/estatística & dados numéricos , Hispano-Americanos/estatística & dados numéricos , Resistência à Insulina , Células Secretoras de Insulina/metabolismo , Dióxido de Nitrogênio , Material Particulado , Obesidade Pediátrica/epidemiologia , Adiposidade , Adolescente , Glicemia/metabolismo , Índice de Massa Corporal , Criança , Diabetes Mellitus Tipo 2/epidemiologia , Diabetes Mellitus Tipo 2/metabolismo , Feminino , Humanos , Insulina/metabolismo , Modelos Lineares , Estudos Longitudinais , Los Angeles/epidemiologia , Masculino , Obesidade Pediátrica/metabolismo
8.
Thorax ; 71(10): 891-8, 2016 10.
Artigo em Inglês | MEDLINE | ID: mdl-27491839

RESUMO

RATIONALE: Exposure to ambient air pollutants has been associated with increased lung cancer incidence and mortality, but due to the high case fatality rate, little is known about the impacts of air pollution exposures on survival after diagnosis. This study aimed to determine whether ambient air pollutant exposures are associated with the survival of patients with lung cancer. METHODS: Participants were 352 053 patients with newly diagnosed lung cancer during 1988-2009 in California, ascertained by the California Cancer Registry. Average residential ambient air pollutant concentrations were estimated for each participant's follow-up period. Cox proportional hazards models were used to estimate HRs relating air pollutant exposures to all-cause mortality overall and stratified by stage (localised only, regional and distant site) and histology (squamous cell carcinoma, adenocarcinoma, small cell carcinoma, large cell carcinoma and others) at diagnosis, adjusting for potential individual and area-level confounders. RESULTS: Adjusting for histology and other potential confounders, the HRs associated with 1 SD increases in NO2, O3, PM10, PM2.5 for patients with localised stage at diagnosis were 1.30 (95% CI 1.28 to 1.32), 1.04 (95% CI 1.02 to 1.05), 1.26 (95% CI 1.25 to 1.28) and 1.38 (95% CI 1.35 to 1.41), respectively. Adjusted HRs were smaller in later stages and varied by histological type within stage (p<0.01, except O3). The largest associations were for patients with early-stage non-small cell cancers, particularly adenocarcinomas. CONCLUSIONS: These epidemiological findings support the hypothesis that air pollution exposures after lung cancer diagnosis shorten survival. Future studies should evaluate the impacts of exposure reduction.


Assuntos
Poluição do Ar/efeitos adversos , Neoplasias Pulmonares/mortalidade , Idoso , Idoso de 80 Anos ou mais , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , Poluição do Ar/análise , California/epidemiologia , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Monitoramento Ambiental/métodos , Feminino , Mapeamento Geográfico , Humanos , Neoplasias Pulmonares/etiologia , Masculino , Pessoa de Meia-Idade , Dióxido de Nitrogênio/efeitos adversos , Dióxido de Nitrogênio/análise , Material Particulado/efeitos adversos , Material Particulado/análise , Sistema de Registros , Fatores Socioeconômicos , Análise de Sobrevida
9.
J Expo Sci Environ Epidemiol ; 25(3): 295-302, 2015 May.
Artigo em Inglês | MEDLINE | ID: mdl-24938508

RESUMO

Few studies have examined the relationship between ambient polycyclic aromatic hydrocarbons (PAHs) and pulmonary function in children. Major sources include vehicular emissions, home heating, wildland fires, agricultural burning, and power plants. PAHs are an important component of fine particulate matter that has been linked to respiratory health. This cross-sectional study examines the relationship between estimated individual exposures to the sum of PAHs with 4, 5, or 6 rings (PAH456) and pulmonary function tests (forced expiratory volume in one second (FEV1) and forced expiratory flow between 25% and 75% of vital capacity) in asthmatic and non-asthmatic children. We applied land-use regression to estimate individual exposures to ambient PAHs for averaging periods ranging from 1 week to 1 year. We used linear regression to estimate the relationship between exposure to PAH456 with pre- and postbronchodilator pulmonary function tests in children in Fresno, California (N=297). Among non-asthmatics, there was a statistically significant association between PAH456 during the previous 3 months, 6 months, and 1 year and postbronchodilator FEV1. The magnitude of the association increased with the length of the averaging period ranging from 60 to 110 ml decrease in FEV1 for each 1 ng/m(3) increase in PAH456. There were no associations with PAH456 observed among asthmatic children. We identified an association between annual PAHs and chronic pulmonary function in children without asthma. Additional studies are needed to further explore the association between exposure to PAHs and pulmonary function, especially with regard to differential effects between asthmatic and non-asthmatic children.


Assuntos
Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Exposição por Inalação/efeitos adversos , Pulmão/efeitos dos fármacos , Hidrocarbonetos Policíclicos Aromáticos/toxicidade , Adolescente , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Poluição do Ar/estatística & dados numéricos , Asma/fisiopatologia , California , Criança , Estudos Transversais , Monitoramento Ambiental , Feminino , Fluxo Expiratório Forçado/efeitos dos fármacos , Volume Expiratório Forçado/efeitos dos fármacos , Humanos , Exposição por Inalação/análise , Exposição por Inalação/estatística & dados numéricos , Modelos Lineares , Pulmão/fisiopatologia , Masculino , Hidrocarbonetos Policíclicos Aromáticos/análise , Espirometria , Capacidade Vital/efeitos dos fármacos
10.
Ann Epidemiol ; 24(12): 888-95e4, 2014 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-25453347

RESUMO

PURPOSE: To evaluate associations between traffic-related air pollution during pregnancy and preterm birth in births in four counties in California during years 2000 to 2006. METHODS: We used logistic regression to examine the association between the highest quartile of ambient air pollutants (carbon monoxide, nitrogen dioxide, particulate matter <10 and 2.5 µm) and traffic density during pregnancy and each of five levels of prematurity based on gestational age at birth (20-23, 24-27, 28-31, 32-33, and 34-36 weeks) versus term (37-42 weeks). We examined trimester averages and the last month and the last 6 weeks of pregnancy. Models were adjusted for birthweight, maternal age, race/ethnicity, education, prenatal care, and birth costs payment. Neighborhood socioeconomic status (SES) was evaluated as a potential effect modifier. RESULTS: There were increased odds ratios (ORs) for early preterm birth for those exposed to the highest quartile of each pollutant during the second trimester and the end of pregnancy (adjusted OR, 1.4-2.8). Associations were stronger among mothers living in low SES neighborhoods (adjusted OR, 2.1-4.3). We observed exposure-response associations for multiple pollutant exposures and early preterm birth. Inverse associations during the first trimester were observed. CONCLUSIONS: The results confirm associations between traffic-related air pollution and prematurity, particularly among very early preterm births and low SES neighborhoods.


Assuntos
Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Resultado da Gravidez/epidemiologia , Nascimento Prematuro/induzido quimicamente , Emissões de Veículos/toxicidade , Adulto , Poluentes Atmosféricos/análise , Peso ao Nascer/efeitos dos fármacos , California/epidemiologia , Monóxido de Carbono/análise , Monóxido de Carbono/toxicidade , Feminino , Idade Gestacional , Humanos , Recém-Nascido , Modelos Logísticos , Masculino , Idade Materna , Exposição Materna , Óxidos de Nitrogênio/análise , Óxidos de Nitrogênio/toxicidade , Material Particulado/análise , Material Particulado/toxicidade , Gravidez , Nascimento Prematuro/epidemiologia , Características de Residência , Medição de Risco , Emissões de Veículos/análise , Adulto Jovem
11.
Thorax ; 69(6): 540-7, 2014 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-24253832

RESUMO

BACKGROUND: Previous studies have reported adverse effects of either regional or near-roadway air pollution (NRAP) on lung function. However, there has been little study of the joint effects of these exposures. OBJECTIVES: To assess the joint effects of NRAP and regional pollutants on childhood lung function in the Children's Health Study. METHODS: Lung function was measured on 1811 children from eight Southern Californian communities. NRAP exposure was assessed based on (1) residential distance to the nearest freeway or major road and (2) estimated near-roadway contributions to residential nitrogen dioxide (NO2), nitric oxide (NO) and total nitrogen oxides (NOx). Exposure to regional ozone (O3), NO2, particulate matter with aerodynamic diameter <10 µm (PM10) and 2.5 µm (PM2.5) was measured continuously at community monitors. RESULTS: An increase in near-roadway NOx of 17.9 ppb (2 SD) was associated with deficits of 1.6% in forced vital capacity (FVC) (p=0.005) and 1.1% in forced expiratory volume in 1 s (FEV1) (p=0.048). Effects were observed in all communities and were similar for NO2 and NO. Residential proximity to a freeway was associated with a reduction in FVC. Lung function deficits of 2-3% were associated with regional PM10 and PM2.5 (FVC and FEV1) and with O3 (FEV1), but not NO2 across the range of exposure between communities. Associations with regional pollution and NRAP were independent in models adjusted for each. The effects of NRAP were not modified by regional pollutant concentrations. CONCLUSIONS: The results indicate that NRAP and regional air pollution have independent adverse effects on childhood lung function.


Assuntos
Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Exposição Ambiental/efeitos adversos , Pulmão/efeitos dos fármacos , Material Particulado/toxicidade , Emissões de Veículos/toxicidade , California , Criança , Pré-Escolar , Feminino , Volume Expiratório Forçado/efeitos dos fármacos , Volume Expiratório Forçado/fisiologia , Humanos , Pulmão/fisiopatologia , Masculino , Óxido Nítrico/toxicidade , Dióxido de Nitrogênio/toxicidade , Óxidos de Nitrogênio/toxicidade , Ozônio/toxicidade , Características de Residência , Transportes , Capacidade Vital/efeitos dos fármacos , Capacidade Vital/fisiologia
12.
Birth Defects Res A Clin Mol Teratol ; 97(11): 730-5, 2013 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-24108522

RESUMO

BACKGROUND: Birth defects are a leading cause of infant morbidity and mortality. Studies suggest associations between environmental contaminants and some structural anomalies, although evidence is limited and several anomalies have not been investigated previously. METHODS: We used data from the California Center of the National Birth Defects Prevention Study and the Children's Health and Air Pollution Study to estimate the odds of 26 congenital birth defect phenotypes with respect to quartiles of seven ambient air pollutant and traffic exposures in California during the first 2 months of pregnancy, 1997 to 2006 (874 cases and 849 controls). We calculated odds ratios (adjusted for maternal race/ethnicity, education, and vitamin use; aOR) for 11 phenotypes that had at least 40 cases. RESULTS: Few odds ratios had confidence intervals that did not include 1.0. Odds of esophageal atresia were increased for the highest versus lowest of traffic density (aOR = 2.8, 95% confidence interval [CI], 1.1-7.4) and PM10 exposure (aOR 4.9; 95% CI, 1.4-17.2). PM10 was associated with a decreased risk of hydrocephaly (aOR= 0.3; 95% CI, 0.1-0.9) and CO with decreased risk of anotia/microtia (aOR = 0.4; 95% CI, 0.2-0.8) and transverse limb deficiency (aOR = 0.4; 95% CI, 0.2-0.9), again reflecting highest versus lowest quartile comparisons. CONCLUSION: Most analyses showed no substantive association between air pollution and the selected birth defects with few exceptions of mixed results.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Poluição do Ar/efeitos adversos , Anormalidades Congênitas , Orelha/anormalidades , Hidrocefalia , Exposição Materna/efeitos adversos , Adulto , California/epidemiologia , Anormalidades Congênitas/epidemiologia , Anormalidades Congênitas/etiologia , Microtia Congênita , Feminino , Humanos , Hidrocefalia/epidemiologia , Hidrocefalia/etiologia , Gravidez , Estudos Retrospectivos
13.
Environ Health Perspect ; 118(10): 1497-502, 2010 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-20570778

RESUMO

BACKGROUND: Although studies have demonstrated that air pollution is associated with exacerbation of asthma symptoms in children with asthma, little is known about the susceptibility of subgroups, particularly those with atopy. OBJECTIVE: This study was designed to evaluate our a priori hypothesis that identifiable subgroups of asthmatic children are more likely to wheeze with exposure to ambient air pollution. METHODS: A cohort of 315 children with asthma, 6-11 years of age, was recruited for longitudinal follow-up in Fresno, California (USA). During the baseline visit, children were administered a respiratory symptom questionnaire and allergen skin-prick test. Three times a year, participants completed 14-day panels during which they answered symptom questions twice daily. Ambient air quality data from a central monitoring station were used to assign exposures to the following pollutants: particulate matter ≤ 2.5 µm in aerodynamic diameter, particulate matter between 2.5 and 10 µm in aerodynamic diameter (PM10-2.5), elemental carbon, nitrogen dioxide (NO2), nitrate, and O3. RESULTS: For the group as a whole, wheeze was significantly associated with short-term exposures to NO2 [odds ratio (OR) = 1.10 for 8.7-ppb increase; 95% confidence interval (CI), 1.02-1.20] and PM10-2.5 (OR = 1.11 for 14.7-µg/m3 increase; 95% CI, 1.01-1.22). The association with wheeze was stronger for these two pollutants in children who were skin-test positive to cat or common fungi and in boys with mild intermittent asthma. CONCLUSION: A pollutant associated with traffic emissions, NO2, and a pollutant with bioactive constituents, PM10-2.5, were associated with increased risk of wheeze in asthmatic children living in Fresno, California. Children with atopy to cat or common fungi and boys with mild intermittent asthma were the subgroups for which we observed the largest associations.


Assuntos
Poluentes Atmosféricos/toxicidade , Asma/fisiopatologia , Sons Respiratórios/etiologia , Asma/complicações , California , Criança , Humanos , Inquéritos e Questionários
14.
Environ Health Perspect ; 118(10): 1490-6, 2010 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-20494854

RESUMO

BACKGROUND: Endotoxins are found in indoor dust generated by human activity and pets, in soil, and adsorbed onto the surfaces of ambient combustion particles. Endotoxin concentrations have been associated with respiratory symptoms and the risk of atopy and asthma in children. OBJECTIVE: We characterized the temporal and spatial variability of ambient endotoxin in Fresno/Clovis, California, located in California's Central Valley, to identify correlates and potential predictors of ambient endotoxin concentrations in a cohort of children with asthma [Fresno Asthmatic Children's Environment Study (FACES)]. METHODS: Between May 2001 and October 2004, daily ambient endotoxin and air pollutants were collected at the central ambient monitoring site of the California Air Resources Board in Fresno and, for shorter time periods, at 10 schools and indoors and outdoors at 84 residences in the community. Analyses were restricted to May-October, the dry months during which endotoxin concentrations are highest. RESULTS: Daily endotoxin concentration patterns were determined mainly by meteorologic factors, particularly the degree of air stagnation. Overall concentrations were lowest in areas distant from agricultural activities. Highest concentrations were found in areas immediately downwind from agricultural/pasture land. Among three other measured air pollutants [fine particulate matter, elemental carbon (a marker of traffic in Fresno), and coarse particulate matter (PMc)], PMc was the only pollutant correlated with endotoxin. Endotoxin, however, was the most spatially variable. CONCLUSIONS: Our data support the need to evaluate the spatial/temporal variability of endotoxin concentrations, rather than relying on a few measurements made at one location, in studies of exposure and and respiratory health effects, particularly in children with asthma and other chronic respiratory diseases.


Assuntos
Poluentes Atmosféricos/análise , Endotoxinas/análise , Poluentes Atmosféricos/toxicidade , Asma/fisiopatologia , California , Criança , Estudos de Coortes , Endotoxinas/toxicidade , Humanos
15.
Int J Environ Health Res ; 19(2): 139-55, 2009 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-19370464

RESUMO

Cross-sectional analyses were conducted to evaluate the effects of exposure to highway traffic on pulmonary function in Fresno, California. Traffic and spirometry data were available for 214 children (enrollment ages six to 11 years). Multiple linear regression was used to evaluate the relations between pulmonary function and traffic parameters. Heavy-duty vehicle count was used as a surrogate measure for diesel-related exposures. Pulmonary function was non-significantly associated with longer distance-to-road and non-significantly associated with higher traffic intensity. Evaluation of effect modification by FEF(25-75)/FVC (a measure of intrinsic airway size) showed that all pulmonary function measures of flow were significantly inversely related to a traffic metric that incorporates traffic intensity and roadway proximity. The results indicate that residence proximity to highway traffic is associated with lower pulmonary function among children with asthma, and smaller airway size is an important modifier of the effect of traffic exposure on pulmonary function and a marker of increased susceptibility.


Assuntos
Asma/fisiopatologia , Exposição Ambiental , Pulmão/fisiopatologia , Emissões de Veículos/toxicidade , Criança , Estudos Transversais , Feminino , Humanos , Masculino , Análise de Regressão , Características de Residência , Testes de Função Respiratória
16.
J Environ Manage ; 88(4): 1003-15, 2008 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-17590260

RESUMO

Many regions worldwide are experiencing rapid urbanization, and often along with growth in the local economy and population comes worsening air quality. Such regions typically find that addressing the additional challenge of polluted air is difficult. This paper reports the results of an assessment of the present health and related economic costs of poor air quality in the San Joaquin Valley of California. Further, it suggests how such assessments can support strategies to pursue pollution reductions that offer the largest near-term gains, by rigorously modeling the associations between pollution levels, demographic groups, and recognized adverse health effects.


Assuntos
Poluentes Atmosféricos/análise , Adolescente , Adulto , Poluentes Atmosféricos/toxicidade , California , Criança , Pré-Escolar , Exposição Ambiental , Humanos , Lactente , Pessoa de Meia-Idade , Urbanização
17.
J Air Waste Manag Assoc ; 56(9): 1267-77, 2006 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-17004682

RESUMO

Air quality monitoring was conducted at a rural site with a tower in the middle of California's San Joaquin Valley (SJV) and at elevated sites in the foothills and mountains surrounding the SJV for the California Regional PM10/ PM2.5 Air Quality Study. Measurements at the surface and n a tower at 90 m were collected in Angiola, CA, from December 2000 through February 2001 and included hourly black carbon (BC), particle counts from optical particle counters, nitric oxide, ozone, temperature, relative humidity, wind speed, and direction. Boundary site measurements were made primarily using 24-hr integrated particulate matter (PM) samples. These measurements were used to understand the vertical variations of PM and PM precursors, the effect of stratification in the winter on concentrations and chemistry aloft and at the surface, and the impact of aloft-versus-surface transport on PM concentrations. Vertical variations of concentrations differed among individual species. The stratification may be important to atmospheric chemistry processes, particularly nighttime nitrate formation aloft, because NO2 appeared to be oxidized by ozone in the stratified aloft layer. Additionally, increases in accumulation-mode particle concentrations in the aloft layer during a fine PM (PM2.5) episode corresponded with increases in aloft nitrate, demonstrating the likelihood of an aloft nighttime nitrate formation mechanism. Evidence of local transport at the surface and regional transport aloft was found; transport processes also varied among the species. The distribution of BC appeared to be regional, and BC was often uniformly mixed vertically. Overall, the combination of time-resolved tower and surface measurements provided important insight into PM stratification, formation, and transport.


Assuntos
Poluentes Atmosféricos/análise , Carbono/análise , Poeira/análise , Óxido Nítrico/análise , Ozônio/análise , California , Monitoramento Ambiental , Tamanho da Partícula , Estações do Ano
18.
J Air Waste Manag Assoc ; 56(12): 1679-93, 2006 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-17195487

RESUMO

Air quality data collected in the California Regional PM10/ PM(2.5) Air Quality Study (CRPAQS) are analyzed to qualitatively assess the processes affecting secondary aerosol formation in the San Joaquin Valley (SJV). This region experiences some of the highest fine particulate matter (PM(2.5)) mass concentrations in California (< or = 188 microg/m3 24-hr average), and secondary aerosol components (as a group) frequently constitute over half of the fine aerosol mass in winter. The analyses are based on 15 days of high-frequency filter and canister measurements and several months of wintertime continuous gas and aerosol measurements. The phase-partitioning of nitrogen oxide (NO(x))-related nitrogen species and carbonaceous species shows that concentrations of gaseous precursor species are far more abundant than measured secondary aerosol nitrate or estimated secondary organic aerosols. Comparisons of ammonia and nitric acid concentrations indicate that ammonium nitrate formation is limited by the availability of nitric acid rather than ammonia. Time-resolved aerosol nitrate data collected at the surface and on a 90-m tower suggest that both the daytime and nighttime nitric acid formation pathways are active, and entrainment of aerosol nitrate formed aloft at night may explain the spatial homogeneity of nitrate in the SJV. NO(x) and volatile organic compound (VOC) emissions plus background O3 levels are expected to determine NO(x) oxidation and nitric acid production rates, which currently control the ammonium nitrate levels in the SJV. Secondary organic aerosol formation is significant in winter, especially in the Fresno urban area. Formation of secondary organic aerosol is more likely limited by the rate of VOC oxidation than the availability of VOC precursors in winter.


Assuntos
Aerossóis/análise , Poluentes Atmosféricos/análise , Material Particulado/análise , Amônia/análise , California , Monitoramento Ambiental , Humanos , Luminescência , Modelos Teóricos , Nitratos/análise , Ácido Nítrico/análise , Oxidantes Fotoquímicos , Fotoquímica , Estações do Ano , Termodinâmica , Fatores de Tempo , Volatilização
19.
Sci Total Environ ; 363(1-3): 166-74, 2006 Jun 15.
Artigo em Inglês | MEDLINE | ID: mdl-16095670

RESUMO

Oxides of nitrogen in fresh traffic exhaust are known to scavenge ambient ozone. However, there has only been little study of local variation in ozone resulting from variation in vehicular traffic patterns within communities. Homes of 78 children were selected from a sample of participants in 3 communities in the southern California Children's Health Study. Twenty-four hour ozone measurements were made simultaneously at a home and at a community central site monitor on two occasions between February and November 1994. Homes were geo-coded, and local residential nitrogen oxides (NOx) above regional background due to nearby traffic at each participant's home were estimated using a line source dispersion model. Measured home ozone declined in a predictable manner as modeled residential NOx increased. NOx modeled from local traffic near homes accounted for variation in ozone concentrations of as much as 17 parts per billion. We conclude that residential ozone concentrations may be over- or underestimated by measurements at a community monitor, depending on the variation in local traffic in the community. These findings may have implications for studies of health effects of traffic-related pollutants.


Assuntos
Poluentes Atmosféricos/análise , Dióxido de Nitrogênio/análise , Ozônio/análise , Saúde da População Urbana , Emissões de Veículos/análise , California , Criança , Monitoramento Ambiental , Previsões , Habitação , Humanos , Oxidantes Fotoquímicos/análise , Características de Residência
20.
Environ Health Perspect ; 113(11): 1638-44, 2005 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-16263524

RESUMO

Exposures to ambient air pollutants have been associated with adverse birth outcomes. We investigated the effects of air pollutants on birth weight mediated by reduced fetal growth among term infants who were born in California during 1975-1987 and who participated in the Children's Health Study. Birth certificates provided maternal reproductive history and residence location at birth. Sociodemographic factors and maternal smoking during pregnancy were collected by questionnaire. Monthly average air pollutant levels were interpolated from monitors to the ZIP code of maternal residence at childbirth. Results from linear mixed-effects regression models showed that a 12-ppb increase in 24-hr ozone averaged over the entire pregnancy was associated with 47.2 g lower birth weight [95% confidence interval (CI), 27.4-67.0 g], and this association was most robust for exposures during the second and third trimesters. A 1.4-ppm difference in first-trimester carbon monoxide exposure was associated with 21.7 g lower birth weight (95% CI, 1.1-42.3 g) and 20% increased risk of intrauterine growth retardation (95% CI, 1.0-1.4). First-trimester CO and third-trimester O3 exposures were associated with 20% increased risk of intrauterine growth retardation. A 20-microg/m3 difference in levels of particulate matter < or = 10 microm in aerodynamic diameter (PM10) during the third trimester was associated with a 21.7-g lower birth weight (95% CI, 1.1-42.2 g), but this association was reduced and not significant after adjusting for O3. In summary, O3 exposure during the second and third trimesters and CO exposure during the first trimester were associated with reduced birth weight.


Assuntos
Poluentes Atmosféricos/toxicidade , Monóxido de Carbono/toxicidade , Retardo do Crescimento Fetal/induzido quimicamente , Recém-Nascido de Baixo Peso , Ozônio/toxicidade , Adulto , Peso ao Nascer , California , Poeira , Feminino , Humanos , Recém-Nascido , Masculino , Exposição Materna , Dióxido de Nitrogênio/toxicidade , Tamanho da Partícula , Gravidez
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