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1.
Artigo em Inglês | MEDLINE | ID: mdl-34417545

RESUMO

BACKGROUND: Previous research has revealed links between air pollution exposure and metabolic syndrome in adults; however, these associations are less explored in children. OBJECTIVE: This study aims to investigate the association between traffic-related air pollutants (TRAP) and biomarkers of metabolic dysregulation, oxidative stress, and lung epithelial damage in children. METHODS: We conducted cross-sectional analyses in a sample of predominantly Latinx, low-income children (n = 218) to examine associations between air pollutants (nitrogen dioxide (NO2), nitrogen oxides (NOx), elemental carbon, polycyclic aromatic hydrocarbons, carbon monoxide (CO), fine particulates (PM2.5)) and biomarkers of metabolic function (high-density lipoprotein (HDL), hemoglobin A1c (HbA1c), oxidative stress (8-isoprostane), and lung epithelial damage (club cell protein 16 (CC16)). RESULTS: HDL cholesterol showed an inverse association with NO2 and NOx, with the strongest relationship between HDL and 3-month exposure to NO2 (-15.4 mg/dL per IQR increase in 3-month NO2, 95% CI = -27.4, -3.4). 8-isoprostane showed a consistent pattern of increasing values with 1-day and 1-week exposure across all pollutants. Non-significant increases in % HbA1c were found during 1-month time frames and decreasing CC16 in 3-month exposure time frames. CONCLUSION: Our results suggest that TRAP is significantly associated with decreased HDL cholesterol in longer-term time frames and elevated 8-isoprostane in shorter-term time frames. TRAP could have the potential to influence lifelong metabolic patterns, through metabolic effects in childhood.

2.
Occup Environ Med ; 2021 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-34210793

RESUMO

OBJECTIVE: Despite increasing prevalence of end-stage renal disease (ESRD), little attention has been directed to how occupational exposures may contribute to risk. Our objective was to investigate the relationship between metalworking fluids (MWF) and ESRD in a cohort of 36 703 male autoworkers. METHODS: We accounted for competing risk of death, using the subdistribution hazard approach to estimate subhazard ratios (sHRs) and 95% CIs in models with cubic splines for cumulative exposure to MWF (straight, soluble or synthetic). RESULTS: Based on 501 ESRD cases and 13 434 deaths, we did not observe an association between MWF and ESRD overall. We observed modest associations between MWF and ESRD classification of glomerulonephritis and diabetic nephropathy. For glomerulonephritis, the 60th percentile of straight MWF was associated with an 18% increased subhazard (sHR=1.18, 95% CI: 0.99 to 1.41). For diabetic nephropathy, the subhazard increased 28% at the 60th percentile of soluble MWF (sHR=1.28, 95% CI: 1.00 to 1.64). Differences by race suggest that black males may have higher disease rates following MWF exposure. CONCLUSIONS: Exposure to straight and soluble MWF may be related to ESRD classification, though this relationship should be further examined.

3.
Environ Res ; 195: 110870, 2021 04.
Artigo em Inglês | MEDLINE | ID: mdl-33587949

RESUMO

BACKGROUND: Metabolic syndrome increases the risk of cardiovascular disease in adults. Antecedents likely begin in childhood and whether childhood exposure to air pollution plays a contributory role is not well understood. OBJECTIVES: To assess whether children's exposure to air pollution is associated with markers of risk for metabolic syndrome and oxidative stress, a hypothesized mediator of air pollution-related health effects. METHODS: We studied 299 children (ages 6-8) living in the Fresno, CA area. At a study center visit, questionnaire and biomarker data were collected. Outcomes included hemoglobin A1c (HbA1c), urinary 8-isoprostane, systolic blood pressure (SBP), and BMI. Individual-level exposure estimates for a set of four pollutants that are constituents of traffic-related air pollution (TRAP) - the sum of 4-, 5-, and 6-ring polycyclic aromatic hydrocarbon compounds (PAH456), NO2, elemental carbon, and fine particulate matter (PM2.5) - were modeled at the primary residential location for 1-day lag, and 1-week, 1-month, 3-month, 6-month, and 1-year averages prior to each participant's visit date. Generalized additive models were used to estimate associations between each air pollutant exposure and outcome. RESULTS: The study population was 53% male, 80% Latinx, 11% Black and largely low-income (6% were White and 3% were Asian/Pacific Islander). HbA1c percentage was associated with longer-term increases in TRAP; for example a 4.42 ng/m3 increase in 6-month average PAH456 was associated with a 0.07% increase (95% CI: 0.01, 0.14) and a 3.62 µg/m3 increase in 6-month average PM2.5 was associated with a 0.06% increase (95% CI: 0.01, 0.10). The influence of air pollutants on blood pressure was strongest at 3 months; for example, a 6.2 ppb increase in 3-month average NO2 was associated with a 9.4 mmHg increase in SBP (95% CI: 2.8, 15.9). TRAP concentrations were not significantly associated with anthropometric or adipokine measures. Short-term TRAP exposure averages were significantly associated with creatinine-adjusted urinary 8-isoprostane. DISCUSSION: Our results suggest that both short- and longer-term estimated individual-level outdoor residential exposures to several traffic-related air pollutants, including ambient PAHs, are associated with biomarkers of risk for metabolic syndrome and oxidative stress in children.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Adulto , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Pressão Sanguínea , Criança , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Feminino , Glucose , Humanos , Masculino , Estresse Oxidativo , Material Particulado/análise , Material Particulado/toxicidade
4.
Sci Rep ; 11(1): 4067, 2021 02 18.
Artigo em Inglês | MEDLINE | ID: mdl-33603036

RESUMO

Ambient air pollution exposure is associated with cardiovascular dysregulation and immune system alterations, yet no study has investigated both simultaneously in children. Understanding the multifaceted impacts may provide early clues for clinical intervention prior to actual disease presentation. We therefore determined the associations between exposure to multiple air pollutants and both immunological outcomes (methylation and protein expression of immune cell types associated with immune regulation) and cardiovascular outcomes (blood pressure) in a cohort of school-aged children (6-8 years; n = 221) living in a city with known elevated pollution levels. Exposure to fine particular matter (PM2.5), carbon monoxide (CO), and ozone (O3) was linked to altered methylation of most CpG sites for genes Foxp3, IL-4, IL-10 and IFN-g, all involved in immune regulation (e.g. higher PM2.5 exposure 1 month prior to the study visit was independently associated with methylation of the IL-4 CpG24 site (est = 0.16; P = 0.0095). Also, immune T helper cell types (Th1, Th2 and Th17) were associated with short-term exposure to PM2.5, O3 and CO (e.g. Th1 cells associated with PM2.5 at 30 days: est = - 0.34, P < 0.0001). Both B cells (est = - 0.19) and CD4+ cells (est = 0.16) were associated with 1 day NO2 exposure (P ≤ 0.031), whereas CD4+ and CD8+ cells were associated with chronic exposure to PAH456, NOx and/or NO2 (P ≤ 0.038 for all). Finally, diastolic BP (DBP) was inversely associated with long-term exposures to both CO and PAH456, and both systolic and pulse pressure were associated with short-term NO2 and chronic NOx exposure. Our findings demonstrate links between air pollution exposure and methylation of immunoregulatory genes, immune cell profiles and blood pressure, suggesting that even at a young age, the immune and cardiovascular systems are negatively impacted by exposure to air pollution.

5.
Birth Defects Res ; 113(9): 676-686, 2021 05 15.
Artigo em Inglês | MEDLINE | ID: mdl-33569925

RESUMO

Genetic and environmental factors have been observed to influence risks for birth defects, though few studies have investigated gene-environment interactions. Our aim was to examine the interaction terms of gene variants in biotransformation enzyme pathways and air pollution exposures in relation to risk of several structural birth defects. We evaluated the role of ambient air pollutant exposure (nitrogen dioxide [NO2 ], nitrogen oxide, carbon monoxide, particulate matter <10 [PM10 ] and <2.5 [PM2.5 ] microns) during pregnancy and 104 gene variants of biotransformation enzymes from infant bloodspots or buccal cells in a California population-based case-control study in 1997-2006. Cases included cleft lip with or without cleft palate (N = 206), gastroschisis (N = 94), tetralogy of Fallot (N = 69), and dextro-transposition of the great arteries (d-TGA; N = 40) and were compared to 208 nonmalformed controls. Overall, the results were not consistent, though did highlight some associations for further investigation as indicated by Wald chi-square test p value <.1. Increased risk of cleft lip was associated with exposure to high PM10 and two CYP gene variants. High PM2.5 and the variant of SLCO1B1 was associated with increased risk of teratology of Fallot. Higher NO2 and two gene variants, CYP2A6 and SLC01B1, were associated with increased risk of d-TGA. Results for gastroschisis were inconsistent in direction and across pollutants. These exploratory results suggest that some individuals based on their genetic background may be more susceptible to the adverse effects of air pollution.


Assuntos
Poluição do Ar , Transposição dos Grandes Vasos , Poluição do Ar/efeitos adversos , Biotransformação , Estudos de Casos e Controles , Feminino , Interação Gene-Ambiente , Humanos , Transportador 1 de Ânion Orgânico Específico do Fígado , Mucosa Bucal , Gravidez
6.
Atmos Environ (1994) ; 2422020 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-32982565

RESUMO

As part of our ongoing research to understand the impact of polycyclic aromatic hydrocarbon (PAH) exposures on health in the San Joaquin Valley, we evaluated airborne PAH concentration data collected over 19 years (2000-2019) at the central air monitoring site in Fresno, California. We found a dramatic decline in outdoor airborne PAH concentrations between 2000 and 2004 that has been maintained through 2019. This decline was present in both the continuous particle-bound PAHs and the filter-based individual PAHs. The decline was more extreme when restricted to winter concentrations. Annual mean PAHs concentrations in 2017- 2018 of particle-bound PAHs were 6.8 ng/m3 or 62% lower than 2000 - 2001. The decline for winter concentrations of continuous particle-bound PAHs between winter 2019 and winter 2001 was 17.2 ng/m3, a drop of 70%. The 2001 to 2018 decline in average wintertime concentrations for filter-based individual PAHs was 82%. We examined industrial emissions, on-road vehicle emissions, residential wood burning, and agricultural and biomass waste burning as possible explanations. The major decline in PAHs from 2000-2004 was coincident with and most likely due to a similar decline in the amount of agricultural and biomass waste burned in Fresno and Madera Counties. On-road vehicle emissions and residential wood burning did not decline until after 2005. Industrial emissions were too low (2% of total) to explain such large decreases in PAH concentrations.

7.
J Pediatr ; 218: 35-41.e1, 2020 03.
Artigo em Inglês | MEDLINE | ID: mdl-31870605

RESUMO

OBJECTIVE: To evaluate a hospital-initiated intervention to reduce tobacco smoke exposure in infants in the neonatal intensive care unit. STUDY DESIGN: A randomized, controlled trial compared motivational interviewing plus financial incentives with conventional care on infant urine cotinine at 1 and 4 months' follow-up. Mothers of infants in the neonatal intensive care unit (N = 360) who reported a smoker living in the home were enrolled. Motivational interviewing sessions were delivered in both the hospital and the home. Financial incentives followed session attendance and negative infant cotinine tests postdischarge. RESULTS: The intervention effect on infant cotinine was not significant, except among mothers who reported high baseline readiness/ability to protect their infant (P ≤ .01) and mothers who completed the study within 6 months postdischarge (per protocol; P ≤ .05). Fewer mothers in the motivational interviewing plus financial incentives condition were smoking postdischarge (P ≤ .01). More mothers in the motivational interviewing plus financial incentives group reported a total home and car smoking ban at follow-up (P ≤ .05). CONCLUSIONS: Motivational interviewing combined with financial incentives reduced infant tobacco smoke exposure in a subset of women who were ready/able to protect their infant. The intervention also resulted in less maternal smoking postpartum. More robust interventions that include maternal and partner/household smoking cessation are likely needed to reduce the costly effects of tobacco smoke exposure on children and their families. TRIAL REGISTRATION: ClinicalTrials.gov: NCT01726062.


Assuntos
Assistência ao Convalescente/métodos , Unidades de Terapia Intensiva Neonatal/estatística & dados numéricos , Entrevista Motivacional/métodos , Abandono do Hábito de Fumar/métodos , Fumar/efeitos adversos , Poluição por Fumaça de Tabaco/efeitos adversos , Adulto , Criança , Pré-Escolar , Feminino , Seguimentos , Humanos , Lactente , Recém-Nascido , Masculino , Estudos Retrospectivos
8.
Artigo em Inglês | MEDLINE | ID: mdl-31783533

RESUMO

Background: Little is known about occupational exposures that occur along fecal sludge collection and resource recovery processes. This study characterizes inhaled endotoxin exposure to workers of a municipal scale fecal sludge-to-fuel processes in Kigali, Rwanda. Methods: Forty-two task-based air samples were collected from workers in five tasks along the fecal sludge collection and resource recovery process. Samples were processed for endotoxin using the limulus amebocyte lysate (LAL) test. To account for exposure variability and compare measured concentrations to established exposure limits, we used Monte Carlo modeling methods to construct distributions representing full eight-hour (8-h) exposures to endotoxin across eight exposure scenarios. Results: Geometric mean (GM) endotoxin concentrations in task-based samples ranged from 11-3700 EU/m3 with exposure concentrations increasing as the dryness of the fecal sludge increased through processing. The thermal dryer task had the highest endotoxin concentrations (GM = 3700 EU/m3) and the inlet task had the lowest (GM = 11 EU/m3). The geometric means (GM) of modeled 8-h exposure concentrations were between 6.7-960 EU/m3 and highest for scenarios which included the thermal dryer task in the exposure scenario. Conclusions: Our data suggest the importance of including worker exposure considerations in the design of nascent fecal sludge management processes. The methods used in this study combine workplace sampling with stochastic modeling and are useful for exposure assessment in resource constrained contexts.


Assuntos
Poluentes Ocupacionais do Ar/análise , Endotoxinas/análise , Exposição Ocupacional/análise , Esgotos , Inquéritos Epidemiológicos , Humanos , Exposição por Inalação , Ruanda
9.
Environ Health Perspect ; 127(9): 97001, 2019 09.
Artigo em Inglês | MEDLINE | ID: mdl-31487206

RESUMO

BACKGROUND: Lung cancer rates among never-smoking women in Xuanwei and Fuyuan in China are among the highest in the world and have been attributed to the domestic use of smoky (bituminous) coal for heating and cooking. However, the key components of coal that drive lung cancer risk have not been identified. OBJECTIVES: We aimed to investigate the relationship between lifelong exposure to the constituents of smoky coal (and other fuel types) and lung cancer. METHODS: Using a population-based case-control study of lung cancer among 1,015 never-smoking female cases and 485 controls, we examined the association between exposure to 43 household air pollutants and lung cancer. Pollutant predictions were derived from a comprehensive exposure assessment study, which included methylated polycyclic aromatic hydrocarbons (PAHs), which have never been directly evaluated in an epidemiological study of any cancer. Hierarchical clustering and penalized regression were applied in order to address high colinearity in exposure variables. RESULTS: The strongest association with lung cancer was for a cluster of 25 PAHs [odds ratio (OR): 2.21; 95% confidence interval (CI): 1.67, 2.87 per 1 standard deviation (SD) change], within which 5-methylchrysene (5-MC), a mutagenic and carcinogenic PAH, had the highest individual observed OR (5.42; 95% CI: 0.94, 27.5). A positive association with nitrogen dioxide ([Formula: see text]) was also observed (OR: 2.06; 95% CI: 1.19, 3.49). By contrast, neither benzo(a)pyrene (BaP) nor fine particulate matter with aerodynamic diameter [Formula: see text] ([Formula: see text]) were associated with lung cancer in the multipollutant models. CONCLUSIONS: To our knowledge, this is the first study to comprehensively evaluate the association between lung cancer and household air pollution (HAP) constituents estimated over the entire life course. Given the global ubiquity of coal use domestically for indoor cooking and heating and commercially for electric power generation, our study suggests that more extensive monitoring of coal combustion products, including methylated PAHs, may be warranted to more accurately assess health risks and develop prevention strategies from this exposure. https://doi.org/10.1289/EHP4913.


Assuntos
Poluição do Ar em Ambientes Fechados/estatística & dados numéricos , Neoplasias Pulmonares/epidemiologia , Adulto , Carcinógenos , China/epidemiologia , Culinária , Características da Família , Feminino , Calefação , Humanos , Pessoa de Meia-Idade , Hidrocarbonetos Policíclicos Aromáticos , Fumaça/análise
10.
J Occup Environ Hyg ; 16(11): 735-744, 2019 11.
Artigo em Inglês | MEDLINE | ID: mdl-31545144

RESUMO

Wildland firefighters engaged in fire suppression activities are often exposed to hazardous air pollutants such as polycyclic aromatic hydrocarbons (PAHs) and particulate matter (PM2.5) during wildfires with no respiratory protection. Although the most significant exposures to smoke likely occur on the fireline, wildland firefighters may also be exposed at the incident command post (ICP), an area designated for wildfire suppression support operations. Our objective was to characterize exposures of PAHs and PM2.5 near an ICP during a wildfire event in California. We collected area air samples for PAHs and PM2.5, during the first 12 days of a wildfire event. PAH area air samples were actively collected in 12-hr shifts (day and night) using XAD4-coated quartz fiber filters and XAD2 sorbent tubes and analyzed for 17 individual PAHs. Hourly area PM2.5 concentrations were measured with an Environmental Beta Attenuation Monitor. Most PAH concentrations generally had similar concentrations during the day and night. PM2.5 concentrations were higher during the day, due to increased fire activity, than at night. The highest concentrations of the 17 PAHs measured were for naphthalene, phenanthrene, and retene. The location of an ICP may be a critical factor in reducing these potential exposures to firefighters during wildfire events. Additionally, exposures could be reduced by utilizing clean air tents or sleeping trailers with HEPA filtration or setting up smaller camps in less smokey areas closer to the fireline for firefighters. Although measured exposures to PAHs for firefighters from smoke are lower at an ICP, these exposures still contribute to the overall cumulative work exposures.


Assuntos
Poluentes Ocupacionais do Ar/análise , Exposição por Inalação/análise , Exposição Ocupacional/análise , Material Particulado/análise , Hidrocarbonetos Policíclicos Aromáticos/análise , Monitoramento Ambiental/métodos , Bombeiros , Humanos , Fumaça/análise , Incêndios Florestais
11.
Neurotoxicology ; 75: 24-29, 2019 12.
Artigo em Inglês | MEDLINE | ID: mdl-31445054

RESUMO

Automotive technicians are commonly exposed to organic and chlorinated solvents, particularly through use of cleaning products. Mainly during the period 1989-2002, n-hexane was a component of some of these products. In other occupational contexts, n-hexane has been shown to be a cause of peripheral neuropathy. The purpose of the present study was to investigate whether previous exposures to low concentrations of n-hexane were a cause of persistent peripheral neuropathy in automotive technicians. Enrolled in the study were 830 San Francisco Bay Area automotive technicians. Each participant underwent a battery of tests to investigate peripheral nervous system impairment. Test results regressed against estimated hexane and total solvent exposures showed only limited evidence of association with solvent exposures. Exposures to both hexane and general solvents were well below their occupational exposure limits. Generally, our results provide reassurance about persistent peripheral neuropathic effects in automotive technicians who previously used hexane-containing automotive cleaning products. This may reflect repair processes, since the exposures occurred some years previous to the study. However, we cannot exclude the possibility that the absence of observed effect in this study may be attributable to low exposures, exposure misclassification and/or the healthy worker survivor effect.


Assuntos
Automóveis , Hexanos/toxicidade , Doenças Profissionais/induzido quimicamente , Exposição Ocupacional/efeitos adversos , Doenças do Sistema Nervoso Periférico/induzido quimicamente , Adulto , California , Hemoglobina A Glicada/análise , Humanos , Masculino , Pessoa de Meia-Idade , Exposição Ocupacional/estatística & dados numéricos , Fatores Socioeconômicos , Inquéritos e Questionários
12.
Environ Res ; 173: 306-317, 2019 06.
Artigo em Inglês | MEDLINE | ID: mdl-30951957

RESUMO

Previous studies found associations between impairments of immune functions and exposure to polycyclic aromatic hydrocarbons (PAHs) in ambient air pollution in the U. S. and China. However, the results remain inconclusive due to the limitations of these studies. In this study, we aimed to examine the direction and magnitude of immune changes related to PAH exposure from household air pollution among rural women living in Gansu, China. Healthy village women (n = 34) were recruited and enrolled in the study. Questionnaires were administered. Blood and urine samples were collected and analyzed during non-heating (September 2017, "summer") and heating (January 2018, "winter") seasons. Urinary 1-hydroxypyrene (1-OHP) was quantified as the biomarker of PAH exposure. To evaluate Treg cell related immune functions, we examined immunoglobulin E (IgE), percent of T-regulatory (Treg) cells, and gene expression of following: forkhead box transcription factor 3 (Foxp3), transforming growth factor-ß (TGF-ß), interleukin 10 (IL-10), and interleukin 35 (IL-35), composed of interleukin-12 alpha (IL-12α) and Epstein-Barr-virus-induced gene 3 (EBi3). Urinary 8-hydroxy-2-deoxyguanosine (8-OHdG) was measured to evaluate oxidative DNA damage. The results showed that the concentration of 1-OHP increased from 0.90 to 17.4 µmol mol-Cr -1 from summer to winter (p < 0.001). Meanwhile, average percent of Treg cells decreased from 5.01% to 1.15% (p < 0.001); IgE and mRNA expressions of Foxp3, TGF-ß, IL-10, IL-12α and EBi3 all significantly decreased (p < 0.001); Urinary 8-OHdG increased from 12.7 to 30.3 ng mg-Cr -1 (p < 0.001). The changes in 8-OHdG, Foxp3 and TGF-ß were significantly associated with the increase of 1-OHP. The results suggested that we observed a substantial increase of PAH exposure in winter, which was significantly associated with the repression on Treg cell function and oxidative DNA damage. Exposure to PAHs in household air pollution possibly induced immune impairments among rural women in northwest China.


Assuntos
Poluentes Atmosféricos/toxicidade , Poluição do Ar em Ambientes Fechados/estatística & dados numéricos , Exposição Ambiental/estatística & dados numéricos , Imunidade/efeitos dos fármacos , Hidrocarbonetos Policíclicos Aromáticos/toxicidade , Poluição do Ar , China , Desoxiguanosina , Feminino , Humanos , Projetos Piloto , Pirenos , Linfócitos T Reguladores
13.
Environ Epidemiol ; 3(5)2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32051927

RESUMO

Background: Air pollution has been associated with hypertension and preterm birth. We examined if prenatal exposure to air pollutants was associated with gestational hypertension and if its association with preterm birth was modified by maternal hypertension. Methods: Data were from birth certificates and hospital discharge records of 252,205 women in San Joaquin Valley of California from 2000-2006. Air quality data were assigned from 24-hour averages of nitrogen dioxide (NO2), particulate matter <10µm (PM10) and <2.5µm (PM2.5), and carbon monoxide (CO) for different averaging periods over pregnancy. We estimated odds of preterm birth and multiplicative interaction between each pollutant and hypertensive disorder. Results: Among normotensive women, odds of preterm birth were slightly higher for higher exposure to all pollutants over the entire pregnancy. Patterns were similar among women with a hypertensive disorder. Among 32-36 week births there was effect modification for exposure to NO2 and CO during the first trimester with higher odds among hypertensive women, and PM2.5 and CO during the last six weeks with higher odds among normotensive women. For 28-31 week births, there was effect modification by hypertensive status for PM10 exposure for entire pregnancy, first, and second trimester with hypertensive women consistently having lower odds of preterm birth than normotensive. Conclusion: There was some evidence of effect modification in the direction counter to our hypothesis for exposure to PM10 and early preterm birth, and CO and PM2.5 at the end of pregnancy, but overall, hypertension did not modify the relationship between pollution and preterm birth.

14.
Environ Res ; 170: 160-167, 2019 03.
Artigo em Inglês | MEDLINE | ID: mdl-30579990

RESUMO

Prenatal exposure to ambient air pollution has been associated with preterm birth in several studies. Associations between air pollution and gestational or pre-existing diabetes have been hypothesized but are not well established. We examined the association between air pollution exposure in pregnancy and gestational diabetes and whether the association between air pollution and preterm birth is modified by diabetes (gestational or pre-existing) in a highly polluted area of California. Birth certificates and hospital discharge data from all singleton births from 2000 to 2006 to women living in four counties in the San Joaquin Valley of California were linked to criteria air pollution and traffic density measurements at the geocoded maternal residence. Air pollutants were dichotomized at the highest quartile and compared to the lower three quartiles. Logistic regression models were adjusted for maternal race-ethnicity, age, education, payment of birth expenses, and prenatal care. There were consistent inverse associations between exposure to air pollution during the first two trimesters and gestational diabetes (statistically significant odds ratios (OR) less than 1). When stratified by any diabetes (gestational or pre-existing), associations between air pollution exposure during pregnancy and categories of preterm birth (20-27, 28-31, 32-33, 34-36 weeks) were generally similar with few exceptions of exposures to carbon monoxide (CO) and particulate matter < 2.5 µm (PM2.5). Those with diabetes and exposure higher levels of CO (in first trimester or entire pregnancy) or PM2.5 (in first trimester) had higher risk of extremely preterm birth (20-27 weeks) compared with those without diabetes. The associations between traffic-related air pollution and gestational diabetes were in the unexpected ("protective") direction. Among those with any diabetes, associations were stronger between CO and PM2.5 and extremely preterm birth.


Assuntos
Poluição do Ar/estatística & dados numéricos , Diabetes Mellitus/epidemiologia , Exposição Materna/estatística & dados numéricos , Nascimento Prematuro/epidemiologia , Poluentes Atmosféricos , California , Cesárea , Feminino , Humanos , Recém-Nascido , Material Particulado , Gravidez , Efeitos Tardios da Exposição Pré-Natal
15.
Environ Sci Technol ; 52(19): 11267-11275, 2018 10 02.
Artigo em Inglês | MEDLINE | ID: mdl-30200753

RESUMO

Traditional methods for measuring personal exposure to fine particulate matter (PM2.5) are cumbersome and lack spatiotemporal resolution; methods that are time-resolved are limited to a single species/component of PM. To address these limitations, we developed an automated microenvironmental aerosol sampler (AMAS), capable of resolving personal exposure by microenvironment. The AMAS is a wearable device that uses a GPS sensor algorithm in conjunction with a custom valve manifold to sample PM2.5 onto distinct filter channels to evaluate home, school, and other (e.g., outdoors, in transit, etc.) exposures. Pilot testing was conducted in Fresno, CA where 25 high-school participants ( n = 37 sampling events) wore an AMAS for 48-h periods in November 2016. Data from 20 (54%) of the 48-h samples collected by participants were deemed valid and the filters were analyzed for PM2.5 black carbon (BC) using light transmissometry and aerosol oxidative potential (OP) using the dithiothreitol (DTT) assay. The amount of inhaled PM2.5 was calculated for each microenvironment to evaluate the health risks associated with exposure. On average, the estimated amount of inhaled PM2.5 BC (µg day-1) and OP [(µM min-1) day-1] was greatest at home, owing to the proportion of time spent within that microenvironment. Validation of the AMAS demonstrated good relative precision (8.7% among collocated instruments) and a mean absolute error of 22% for BC and 33% for OP when compared to a traditional personal sampling instrument. This work demonstrates the feasibility of new technology designed to quantify personal exposure to PM2.5 species within distinct microenvironments.


Assuntos
Poluentes Atmosféricos , Monitoramento Ambiental , Aerossóis , Carbono , Estresse Oxidativo , Material Particulado
16.
Am J Med Genet A ; 176(5): 1055-1090, 2018 05.
Artigo em Inglês | MEDLINE | ID: mdl-29681089

RESUMO

Spina bifida is a birth defect characterized by incomplete closure of the embryonic neural tube. Genetic factors as well as environmental factors have been observed to influence risks for spina bifida. Few studies have investigated possible gene-environment interactions that could contribute to spina bifida risk. The aim of this study is to examine the interaction between gene variants in biotransformation enzyme pathways and ambient air pollution exposures and risk of spina bifida. We evaluated the role of air pollution exposure during pregnancy and gene variants of biotransformation enzymes from bloodspots and buccal cells in a California population-based case-control (86 cases of spina bifida and 208 non-malformed controls) study. We considered race/ethnicity and folic acid vitamin use as potential effect modifiers and adjusted for those factors and smoking. We observed gene-environment interactions between each of the five pollutants and several gene variants: NO (ABCC2), NO2 (ABCC2, SLC01B1), PM10 (ABCC2, CYP1A1, CYP2B6, CYP2C19, CYP2D6, NAT2, SLC01B1, SLC01B3), PM2.5 (CYP1A1 and CYP1A2). These analyses show positive interactions between air pollution exposure during early pregnancy and gene variants associated with metabolizing enzymes. These exploratory results suggest that some individuals based on their genetic background may be more susceptible to the adverse effects of pollution.


Assuntos
Poluição do Ar/efeitos adversos , Biotransformação/genética , Regulação Enzimológica da Expressão Gênica , Predisposição Genética para Doença , Variação Genética , Disrafismo Espinal/etiologia , Adulto , Alelos , Monóxido de Carbono/efeitos adversos , Estudos de Casos e Controles , Bases de Dados Genéticas , Exposição Ambiental , Feminino , Interação Gene-Ambiente , Estudos de Associação Genética , Testes Genéticos , Humanos , Masculino , Pessoa de Meia-Idade , Óxidos de Nitrogênio/efeitos adversos , Razão de Chances , Material Particulado/efeitos adversos , Medição de Risco , Fatores de Risco , Adulto Jovem
17.
Pediatrics ; 141(Suppl 1): S63-S74, 2018 01.
Artigo em Inglês | MEDLINE | ID: mdl-29292307

RESUMO

BACKGROUND AND OBJECTIVES: Secondhand smoke (SHS) directly increases exposure to airborne nicotine, tobacco's main psychoactive substance. When exposed to SHS, nonsmokers inhale 60% to 80% of airborne nicotine, absorb concentrations similar to those absorbed by smokers, and display high levels of nicotine biomarkers. Social modeling, or observing other smokers, is a well-established predictor of smoking during adolescence. Observing smokers also leads to increased pharmacological exposure to airborne nicotine via SHS. The objective of this study is to investigate whether greater exposure to airborne nicotine via SHS increases the risk for smoking initiation precursors among never-smoking adolescents. METHODS: Secondary students (N = 406; never-smokers: n = 338, 53% girls, mean age = 12.9, SD = 0.4) participated in the AdoQuest II longitudinal cohort. They answered questionnaires about social exposure to smoking (parents, siblings, peers) and known smoking precursors (eg, expected benefits and/or costs, SHS aversion, smoking susceptibility, and nicotine dependence symptoms). Saliva and hair samples were collected to derive biomarkers of cotinine and nicotine. Adolescents wore a passive monitor for 1 week to measure airborne nicotine. RESULTS: Higher airborne nicotine was significantly associated with greater expected benefits (R2 = 0.024) and lower expected costs (R2 = 0.014). Higher social exposure was significantly associated with more temptation to try smoking (R2 = 0.025), lower aversion to SHS (R2 = 0.038), and greater smoking susceptibility (R2 = 0.071). Greater social exposure was significantly associated with more nicotine dependence symptoms; this relation worsened with higher nicotine exposure (cotinine R2 = 0.096; airborne nicotine R2 = 0.088). CONCLUSIONS: Airborne nicotine exposure via SHS is a plausible risk factor for smoking initiation during adolescence. Public health implications include limiting airborne nicotine through smoking bans in homes and cars, in addition to stringent restrictions for e-cigarettes.


Assuntos
Comportamento do Adolescente , Nicotina/efeitos adversos , Poluição por Fumaça de Tabaco/efeitos adversos , Fumar Tabaco/epidemiologia , Adolescente , Criança , Cotinina/análise , Exposição Ambiental , Feminino , Cabelo/química , Humanos , Estudos Longitudinais , Masculino , Nicotina/análise , Quebeque/epidemiologia , Fatores de Risco , Saliva/química , Política Antifumo , Comportamento Social , Inquéritos e Questionários , Fumar Tabaco/psicologia
18.
Clin Epigenetics ; 10: 2, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29317916

RESUMO

Background: DNA methylation of CpG sites on genetic loci has been linked to increased risk of asthma in children exposed to elevated ambient air pollutants (AAPs). Further identification of specific CpG sites and the pollutants that are associated with methylation of these CpG sites in immune cells could impact our understanding of asthma pathophysiology. In this study, we sought to identify some CpG sites in specific genes that could be associated with asthma regulation (Foxp3 and IL10) and to identify the different AAPs for which exposure prior to the blood draw is linked to methylation levels at these sites. We recruited subjects from Fresno, California, an area known for high levels of AAPs. Blood samples and responses to questionnaires were obtained (n = 188), and in a subset of subjects (n = 33), repeat samples were collected 2 years later. Average measures of AAPs were obtained for 1, 15, 30, 90, 180, and 365 days prior to each blood draw to estimate the short-term vs. long-term effects of the AAP exposures. Results: Asthma was significantly associated with higher differentially methylated regions (DMRs) of the Foxp3 promoter region (p = 0.030) and the IL10 intronic region (p = 0.026). Additionally, at the 90-day time period (90 days prior to the blood draw), Foxp3 methylation was positively associated with NO2, CO, and PM2.5 exposures (p = 0.001, p = 0.001, and p = 0.012, respectively). In the subset of subjects retested 2 years later (n = 33), a positive association between AAP exposure and methylation was sustained. There was also a negative correlation between the average Foxp3 methylation of the promoter region and activated Treg levels (p = 0.039) and a positive correlation between the average IL10 methylation of region 3 of intron 4 and IL10 cytokine expression (p = 0.030). Conclusions: Short-term and long-term exposures to high levels of CO, NO2, and PM2.5 were associated with alterations in differentially methylated regions of Foxp3. IL10 methylation showed a similar trend. For any given individual, these changes tend to be sustained over time. In addition, asthma was associated with higher differentially methylated regions of Foxp3 and IL10.


Assuntos
Asma/genética , Monóxido de Carbono/análise , Metilação de DNA , Fatores de Transcrição Forkhead/genética , Interleucina-10/genética , Dióxido de Nitrogênio/análise , Material Particulado/análise , Adolescente , Asma/sangue , Asma/induzido quimicamente , California , Monóxido de Carbono/efeitos adversos , Ilhas de CpG/efeitos dos fármacos , Metilação de DNA/efeitos dos fármacos , Epigênese Genética/efeitos dos fármacos , Feminino , Regulação da Expressão Gênica , Estudos de Associação Genética , Humanos , Íntrons , Masculino , Dióxido de Nitrogênio/efeitos adversos , Material Particulado/efeitos adversos , Regiões Promotoras Genéticas
19.
Environ Int ; 112: 41-48, 2018 03.
Artigo em Inglês | MEDLINE | ID: mdl-29247842

RESUMO

Firefighters are exposed to chemicals during fire events and we previously demonstrated that fire station dust has high levels of polybrominated diphenyl ethers (PBDEs). In conducting the Fire Station Dust Study, we sought to further characterize the chemicals to which firefighters could be exposed - measuring the emerging class of phosphorous-containing flame retardants (PFRs) in fire stations, for the first time, as well as PBDEs. Dust samples from 26 fire stations in five states were collected from vacuum-cleaner bags and analyzed for PFRs and PBDEs. PFR concentrations were found to be on the same order of magnitude as PBDE concentrations (maximum PFR: 218,000ng/g; maximum PBDE: 351,000ng/g). Median concentrations of tri-n-butyl phosphate (TNBP), tris (2-chloroisopropyl) phosphate (TCIPP), and tris(1,3-dichloroisopropyl)phosphate (TDCIPP) in dust from fire stations were higher than those previously reported in homes and other occupational settings around the world. Total PFR levels did not vary significantly among states. Levels of TDCIPP were higher in stations where vacuum cleaners were used to clean surfaces other than the floor. PBDE levels were comparable to those found in our previous study of 20 California fire stations and much higher than levels in California residences. PFR and PBDE levels in fire station dust are higher than in other occupational and residential settings, underscoring the need to identify and control sources of this contamination.


Assuntos
Poeira/análise , Poluentes Ambientais/análise , Retardadores de Chama/análise , Organofosfatos/análise , Bombeiros , Humanos
20.
Sci Rep ; 7(1): 15473, 2017 11 13.
Artigo em Inglês | MEDLINE | ID: mdl-29133798

RESUMO

We tested the effectiveness of a program consisting of motivational interviewing (MI) and feedback of urine cotinine to stop passive smoking (PS) in children at risk for asthma. Fifty-eight families with children 0-13 years with a high risk of asthma and PS exposure were randomised in a one-year follow-up study. The intervention group received the intervention program during 6 sessions (1/month) and the control group received measurements (questionnaires, urine cotinine, and lung function) only. The primary outcome measure was the percentage of families stopping PS (parental report verified and unverified with the child's urine cotinine concentration <10 µg/l) in children during the intervention program. The analyses were performed with Mixed Logistic Regression. After 6 months, a significant group difference was observed for the unverified parental report of stopping PS in children: 27% of parents in the intervention group versus 7% in the control group. For the verified parental report, the difference was similar (23% versus 7%) but was not statistically significant. Despite a limited sample size, the results suggest that the intervention program is probably an effective strategy to stop PS in children. A program longer than 6 months might be necessary for a longer lasting intervention effect.


Assuntos
Asma/prevenção & controle , Cotinina/urina , Entrevista Motivacional , Pais/psicologia , Poluição por Fumaça de Tabaco/prevenção & controle , Adulto , Asma/diagnóstico , Asma/etiologia , Asma/urina , Criança , Pré-Escolar , Aconselhamento , Suscetibilidade a Doenças , Feminino , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , Avaliação de Programas e Projetos de Saúde , Testes de Função Respiratória , Inquéritos e Questionários/estatística & dados numéricos , Poluição por Fumaça de Tabaco/efeitos adversos , Resultado do Tratamento
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