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1.
Epidemiology ; 31(6): 779-787, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-33003149

RESUMO

BACKGROUND: Air conditioning has been proposed as one of the key factors explaining reductions of heat-related mortality risks observed in the last decades. However, direct evidence is still limited. METHODS: We used a multi-country, multi-city, longitudinal design to quantify the independent role of air conditioning in reported attenuation in risk. We collected daily time series of mortality, mean temperature, and yearly air conditioning prevalence for 311 locations in Canada, Japan, Spain, and the USA between 1972 and 2009. For each city and sub-period, we fitted a quasi-Poisson regression combined with distributed lag non-linear models to estimate summer-only temperature-mortality associations. At the second stage, we used a novel multilevel, multivariate spatio-temporal meta-regression model to evaluate effect modification of air conditioning on heat-mortality associations. We computed relative risks and fractions of heat-attributable excess deaths under observed and fixed air conditioning prevalences. RESULTS: Results show an independent association between increased air conditioning prevalence and lower heat-related mortality risk. Excess deaths due to heat decreased during the study periods from 1.40% to 0.80% in Canada, 3.57% to 1.10% in Japan, 3.54% to 2.78% in Spain, and 1.70% to 0.53% in the USA. However, increased air conditioning explains only part of the observed attenuation, corresponding to 16.7% in Canada, 20.0% in Japan, 14.3% in Spain, and 16.7% in the USA. CONCLUSIONS: Our findings are consistent with the hypothesis that air conditioning represents an effective heat adaptation strategy, but suggests that other factors have played an equal or more important role in increasing the resilience of populations.

2.
Epidemiology ; 2020 Sep 28.
Artigo em Inglês | MEDLINE | ID: mdl-33009251

RESUMO

BACKGROUND: Fine particulate matter (PM2.5) has been consistently linked to cardiovascular disease (CVD). Although studies have reported modification by income, to our knowledge no study to date has examined this relationship among adults in Medicaid, which provides health coverage to low-income and/or disabled Americans. METHODS: We estimated the association between short-term PM2.5 exposure (average of PM2.5 on the day of hospitalization and the preceding day) and CVD admissions rates among adult Medicaid enrollees in the continental US (2000-2012) using a time-stratified case-crossover design. We repeated this analysis at PM2.5 concentrations below the World Health Organization daily guideline of 25 µg/m. We compared the PM2.5 - CVD association in the Medicaid ≥65 years old vs. non-Medicaid-eligible Medicare enrollees (≥65 years old). RESULTS: Using information on 3,666,657 CVD hospitalizations among Medicaid adults we observed a 0.9% (95%CI: 0.6, 1.1%) increase in CVD admission rates per 10 µg/m PM2.5 increase. The association was stronger at low PM2.5 levels (1.3%; 95%CI: 0.9, 1.6%).Among Medicaid enrollees ≥65 years old, the association was 0.9% (95%CI: 0.6, 1.3%) vs. 0.8% (95%CI: 0.6, 0.9%) among non-Medicaid-eligible Medicare enrollees ≥65 years old. CONCLUSION: We found robust evidence of an association between short-term PM2.5 and CVD hospitalizations among the vulnerable subpopulation of adult Medicaid enrollees. Importantly, this association persisted even at PM2.5 levels below the current national standards.

3.
Artigo em Inglês | MEDLINE | ID: mdl-33027507

RESUMO

One-carbon metabolism is an important contributor to aging-related diseases; nevertheless, relationships of one-carbon metabolites with novel DNA methylation-based measures of biological aging remain poorly characterized. We examined relationships of one-carbon metabolites with three DNA methylation-based measures of biological aging: DNAmAge, GrimAge, and PhenoAge. We measured plasma levels of four common one-carbon metabolites (vitamin B6, vitamin B12, folate, and homocysteine) in 715 VA Normative Aging Study participants with at least one visit between 1999 and 2008 (observations = 1153). DNA methylation age metrics were calculated using the HumanMethylation450 BeadChip. We utilized Bayesian Kernel Machine Regression (BKMR) models adjusted for chronological age, lifestyle factors, age-related diseases, and study visits to determine metabolites important to the aging outcomes. BKMR models allowed for the estimation of the relationships of single metabolites and the cumulative metabolite mixture with methylation age. Log vitamin B6 was selected as important to PhenoAge (ß = -1.62-years, 95%CI: -2.28, -0.96). Log folate was selected as important to GrimAge (ß = 0.75-years, 95%CI: 0.41, 1.09) and PhenoAge (ß = 1.62-years, 95%CI: 0.95, 2.29). Compared to a model where each metabolite in the mixture is set to its 50 th percentile, the log cumulative mixture with each metabolite at its 30 th (ß = -0.13-years, 95%CI: -0.26, -0.005) and 40 th percentile (ß = -0.06-years, 95%CI: -0.11, -0.005) was associated with decreased GrimAge. Our results provide novel characterizations of the relationships between one-carbon metabolites and DNA methylation age in a human population study. Further research is required to confirm these findings and establish their generalizability.

4.
Nat Commun ; 11(1): 5002, 2020 10 13.
Artigo em Inglês | MEDLINE | ID: mdl-33051463

RESUMO

Unconventional oil and natural gas development (UOGD) expanded extensively in the United States from the early 2000s. However, the influence of UOGD on the radioactivity of ambient particulate is not well understood. We collected the ambient particle radioactivity (PR) measurements of RadNet, a nationwide environmental radiation monitoring network. We obtained the information of over 1.5 million wells from the Enverus database. We investigated the association between the upwind UOGD well count and the downwind gross-beta radiation with adjustment for environmental factors governing the natural emission and transport of radioactivity. Our statistical analysis found that an additional 100 upwind UOGD wells within 20 km is associated with an increase of 0.024 mBq/m3 (95% confidence interval [CI], 0.020, 0.028 mBq/m3) in the gross-beta particle radiation downwind. Based on the published health analysis of PR, the widespread UOGD could induce adverse health effects to residents living close to UOGD by elevating PR.

5.
Sci Total Environ ; 755(Pt 2): 142524, 2020 Oct 03.
Artigo em Inglês | MEDLINE | ID: mdl-33065503

RESUMO

BACKGROUND: Although long-term exposure to particulate matter<2.5 µm (PM2.5) has been linked to chronic debilitating brain disorders (CDBD), the role of short-term exposure in health care demand, and increased susceptibility for PM2.5-related health conditions, among Medicare enrollees with CDBD has received little attention. We used a causal modeling approach to assess the effect of short-term high PM2.5 exposure on all-cause admissions, and prevalent cause-specific admissions among Medicare enrollees with CDBD (Parkinson's disease-PD, Alzheimer's disease-AD and other dementia). METHODS: We constructed daily zipcode counts of hospital admissions of Medicare beneficiaries older than 65 across the United-States (2000-2014). We obtained daily PM2.5 estimates from a satellite-based model. A propensity score matching approach was applied to match high-pollution (PM2.5 > 17.4 µg/m3) to low-pollution zip code-days with similar background characteristics. Then, we estimated the percent change in admissions attributable to high pollution. We repeated the models restricting the analysis to zipcode-days with PM2.5 below of 35 µg/m3. RESULTS: We observed significant increases in all-cause hospital admissions (2.53% in PD and 2.49% in AD/dementia) attributable to high PM2.5 exposure. The largest observed effect for common causes was for pneumonia and urinary tract infection. All the effects were larger in CDBD compared to the general Medicare population, and similarly strong at levels of exposure considered safe by the EPA. CONCLUSION: We found Medicare beneficiaries with CDBD to be at higher risk of being admitted to the hospital following acute exposure to PM2.5 levels well below the National Ambient Air Quality Standard defined as safe by the EPA.

6.
Environ Res ; : 110201, 2020 Sep 13.
Artigo em Inglês | MEDLINE | ID: mdl-32937174

RESUMO

Accumulating evidence suggests that air pollution increases pregnancy loss; however, most previous studies have focused on case identification from medical records, which may underrepresent early pregnancy losses. Our objective was to investigate the association between acute and chronic exposure to ambient air pollution and time to pregnancy loss among women undergoing assisted reproductive technologies (ART) who are closely followed throughout early pregnancy. We included 275 women (345 human chorionic gonadotropin (hCG)-confirmed pregnancies) undergoing ART at a New England academic fertility center. We estimated daily nitrogen dioxide (NO2), ozone (O3), fine particulate matter <2.5 µm (PM2.5), and black carbon (BC) exposures using validated spatiotemporal models estimated from first positive hCG test until day of failure or live birth. Air pollution exposures were averaged over the past week and the whole pregnancy. Multivariable Cox proportional hazards models were used to estimate the hazards ratio (HR) for pregnancy loss for an interquartile range (IQR) increase in pollutant exposure. We tested for violation of proportional hazards by considering an interaction between time (in days) since positive hCG (<30 days vs. ≥30 days) and air pollution. The incidence of pregnancy loss was 29 per 100 confirmed pregnancies (n=99). Among pregnancies not resulting in live birth, the median (IQR) time to loss was 21 (11, 30) days following positive hCG. Average past week exposures to NO2, O3, PM2.5, and BC were not associated with time to pregnancy loss. Exposure throughout pregnancy to NO2 was not associated with pregnancy loss; however, there was a statistically significant interaction with time (p-for-interaction<0.001). Specifically, an IQR increase in exposure to NO2 was positively associated with pregnancy loss after 30 days (HR=1.34, 95% CI: 1.13, 1.58), but not in the first 30 days after positive hCG (HR=0.83, 95% CI: 0.57, 1.20). Overall pregnancy exposure to O3, PM2.5, and BC were not associated with pregnancy loss regardless of timing. Models evaluating joint effects of all pollutants yielded similar findings. In conclusion, acute and chronic exposure to NO2, O3, PM2.5, and BC were not associated with risk of pregnancy loss; however, higher exposure to NO2 throughout pregnancy was associated with increased risk of loss 30 days after positive hCG. In this cohort, later pregnancy losses appeared more susceptible to the detrimental effects of air pollution exposure.

8.
Innovation (N Y) ; : 100047, 2020 Sep 21.
Artigo em Inglês | MEDLINE | ID: mdl-32984861

RESUMO

Background: The novel human coronavirus disease 2019 (COVID-19) pandemic has claimed more than 600,000 lives worldwide, causing tremendous public health, social, and economic damages. While the risk factors of COVID-19 are still under investigation, environmental factors, such as urban air pollution, may play an important role in increasing population susceptibility to COVID-19 pathogenesis. Methods: We conducted a cross-sectional nationwide study using zero-inflated negative binomial models to estimate the association between long-term (2010-2016) county-level exposures to NO2, PM2.5 and O3 and county-level COVID-19 case-fatality and mortality rates in the US. We used both single and multipollutant models and controlled for spatial trends and a comprehensive set of potential confounders, including state-level test positive rate, county-level healthcare capacity, phase-of-epidemic, population mobility, population density, sociodemographics, socioeconomic status, race and ethnicity, behavioral risk factors, and meteorology. Results: 3,659,828 COVID-19 cases and 138,552 deaths were reported in 3,076 US counties from January 22, 2020 to July 17, 2020, with an overall observed case-fatality rate of 3.8%. County-level average NO2 concentrations were positively associated with both COVID-19 case-fatality rate and mortality rate in single-, bi-, and tri-pollutant models. When adjusted for co-pollutants, per inter-quartile range (IQR) increase in NO2 (4.6 ppb), COVID-19 case-fatality rate and mortality rate were associated with an increase of 11.3% (95% CI 4.9% to 18.2%) and 16.2% (95% CI 8.7% to 24.0%), respectively. We did not observe significant associations between COVID-19 case-fatality rate and long-term exposure to PM2.5 or O3, although per IQR increase in PM2.5 (2.6 ug/m3) was marginally associated with 14.9% (95% CI: 0.0% to 31.9%) increase in COVID-19 mortality rate when adjusted for co-pollutants. Discussion: Long-term exposure to NO2, which largely arises from urban combustion sources such as traffic, may enhance susceptibility to severe COVID-19 outcomes, independent of long-term PM2.5 and O3 exposure. The results support targeted public health actions to protect residents from COVID-19 in heavily polluted regions with historically high NO2 levels. Continuation of current efforts to lower traffic emissions and ambient air pollution may be an important component of reducing population-level risk of COVID-19 case-fatality and mortality.

9.
Environ Epidemiol ; 4(4): e0108, 2020 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-32832843

RESUMO

Background: General cognitive function deteriorates with aging, a change that has been linked to outdoor temperature. Older individuals have reduced ability to adapt to changes in outdoor temperature than younger people. However, to what extent short-term changes in outdoor temperature interact with mitochondria to affect cognition in older people has not yet been determined. Methods: Our study included 591 participants of the Normative Aging Study who underwent multiple examinations between 2000 and 2013. Cognitive function was evaluated via the Mini-Mental State Examination. Outdoor temperature was estimated at residential addresses 1 day before the examination using on a validated spatiotemporal temperature model. Mitochondrial DNA copy number (mtDNAcn) was determined using buffy coat samples. Results: We found an interaction between temperature, age, mtDNAcn, and cognition. In individuals 84 years of age or older, cooler temperature was associated with low cognition (odds ratio = 1.2; 95% confidence interval = 1.05, 1.35 for a 1°C decrease in temperature; P = 0.007). We found higher odds ratio per 1°C decrease in temperature among individuals with lower mtDNAcn (ß3 = 0.12; 95% confidence interval = 0.01, 0.22; P interaction = 0.02). Conclusions: Our findings, albeit potentially underpowered, suggest that older individuals may be more susceptible to the influence of short-term temperature exposure on cognition. Moreover, the level of mtDNAcn may also modify the association between temperature and cognitive function, indicating a possible role of these cellular elements in this relationship.

10.
Environ Res ; 190: 110022, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32791250

RESUMO

BACKGROUND: Lead (Pb) is widespread and exposure to this non-essential heavy metal can cause multiple negative health effects; however the mechanisms underlying these effects remain incompletely understood. OBJECTIVES: To identify plasma metabolomic signatures of Pb exposure, as measured in blood and toenails. METHODS: In a subset of men from the VA Normative Aging Study, mass-spectrometry based plasma metabolomic profiling was performed. Pb levels were measured in blood samples and toenail clippings collected concurrently. Multivariable linear regression models, smoothing splines and Pathway analyses were employed to identify metabolites associated with Pb exposure. RESULTS: In 399 men, 858 metabolites were measured and passed QC, of which 154 (17.9%) were significantly associated with blood Pb (p < 0.05). Eleven of these passed stringent correction for multiple testing, including pro-hydroxy-pro (ß(95%CI): 1.52 (0.93,2.12), p = 7.18x10-7), N-acetylglycine (ß(95%CI): 1.44 (0.85,2.02), p = 1.12x10-6), tartarate (ß(95%CI): 0.68 (0.35,1.00), p = 4.84x10-5), vanillylmandelate (ß(95%CI): 1.05 (0.47,1.63), p = 4.44x10-7), and lysine (ß(95%CI): 1.88 (-2.8,-0.95), p = 9.10x10-5). A subset of 48 men had a second blood sample collected a mean of 6.1 years after their first. Three of the top eleven metabolites were also significant in this second blood sample. Furthermore, we identified 70 plasma metabolites associated with Pb as measured in toenails. Twenty-three plasma metabolites were significantly associated with both blood and toenail measures, while others appeared to be specific to the biosample in which Pb was measured. For example, benzanoate metabolism appeared to be of importance with the longer-term exposure assessed by toenails. DISCUSSION: Pb exposure is responsible for 0.6% of the global burden of disease and metabolomics is particularly well-suited to explore its pathogenic mechanisms. In this study, we identified metabolites and metabolomic pathways associated with Pb exposure that suggest that Pb exposure acts through oxidative stress and immune dysfunction. These findings help us to better understand the biology of this important public health burden.

11.
Hypertension ; 76(4): 1289-1298, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-32816598

RESUMO

Ambient air pollution, specifically particulate matter of diameter <2.5 µm, is reportedly associated with cardiovascular disease risk. However, evidence linking particulate matter of diameter <2.5 µm and blood pressure (BP) is largely from cross-sectional studies and from settings with lower concentrations of particulate matter of diameter <2.5 µm, with exposures not accounting for myriad time-varying and other factors such as built environment. This study aimed to study the association between long- and short-term ambient particulate matter of diameter <2.5 µm exposure from a hybrid spatiotemporal model at 1-km×1-km spatial resolution with longitudinally measured systolic and diastolic BP and incident hypertension in 5342 participants from urban Delhi, India, within an ongoing representative urban adult cohort study. Median annual and monthly exposure at baseline was 92.1 µg/m3 (interquartile range, 87.6-95.7) and 82.4 µg/m3 (interquartile range, 68.4-107.0), respectively. We observed higher average systolic BP (1.77 mm Hg [95% CI, 0.97-2.56] and 3.33 mm Hg [95% CI, 1.12-5.52]) per interquartile range differences in monthly and annual exposures, respectively, after adjusting for covariates. Additionally, interquartile range differences in long-term exposures of 1, 1.5, and 2 years increased the risk of incident hypertension by 1.53× (95% CI, 1.19-1.96), 1.59× (95% CI, 1.31-1.92), and 1.16× (95% CI, 0.95-1.43), respectively. Observed effects were larger in individuals with higher waist-hip ratios. Our data strongly support a temporal association between high levels of ambient air pollution, higher systolic BP, and incident hypertension. Given that high BP is an important risk factor of cardiovascular disease, reducing ambient air pollution is likely to have meaningful clinical and public health benefits.

12.
Environ Sci Technol ; 54(19): 11780-11788, 2020 Oct 06.
Artigo em Inglês | MEDLINE | ID: mdl-32786555

RESUMO

The adverse effects of ambient particulate matter (PM) on human health have been well demonstrated, but the underlying properties responsible for its toxicity are still unclear. We hypothesized that particulate radioactivity, which is due to the attachment of radioactive nuclides on particle surfaces, may be responsible for part of PM toxicity. We measured the gross α- and ß-activities for daily PM2.5 and PM10 filters collected at the Harvard Supersite in downtown Boston from 2005 to 2006 and calculated the radioactivities at the time of air sampling retrospectively based on a previously established formula. We examined the relationship between different radioactivities and compared our measurements to those measured at the Boston EPA RadNet Station. The results showed that the majority of PM10 radioactivity is associated with that of PM2.5 samples for both α-activity (98%) and ß-activity (83%). A strong linear relationship was observed between the α- and ß-activities for both PM2.5 [slope = 0.47 (±0.03); p-value < 0.0001] and PM10 [slope = 0.46 (±0.09); p-value < 0.0001] samples. Measurements at the Harvard Supersite and at EPA RadNet sites are highly correlated for both α-activities [slope = 0.17 (±0.02), p-value < 0.0001] and ß-activities [slope = 0.30 (±0.05), p-value < 0.0001]. Additionally, we identified several significant predictors for PM2.5 α-activities. This novel method we developed to measure α- and ß-activities from archived filters will make it possible to assess the retrospective particle radioactivity exposure for future epidemiological studies.

13.
Circulation ; 142(9): 858-867, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32795087

RESUMO

BACKGROUND: Individuals are exposed to air pollution and ionizing radiation from natural sources through inhalation of particles. This study investigates the association between cardiac arrhythmias and short-term exposures to fine particulate matter (particulate matter ≤2.5 µm aerodynamic diameter; PM2.5) and particle radioactivity. METHODS: Ventricular arrhythmic events were identified among 176 patients with dual-chamber implanted cardioverter-defibrillators in Boston, Massachusetts between September 2006 and June 2010. Patients were assigned exposures based on residential addresses. Daily PM2.5 levels were estimated at 1-km×1-km grid cells from a previously validated prediction model. Particle gross ß activity was used as a surrogate for particle radioactivity and was measured from several monitoring sites by the US Environmental Protection Agency's monitoring network. The association of the onset of ventricular arrhythmias (VA) with 0- to 21-day moving averages of PM2.5 and particle radioactivity (2 single-pollutant models and a 2-pollutant model) before the event was examined using time-stratified case-crossover analyses, adjusted for dew point and air temperatures. RESULTS: A total of 1,050 VA were recorded among 91 patients, including 123 sustained VA among 25 of these patients. In the single-pollutant model of PM2.5, each interquartile range increase in daily PM2.5 levels for a 21-day moving average was associated with 39% higher odds of a VA event (95% CI, 12%-72%). In the single-pollutant model of particle radioactivity, each interquartile range increase in particle radioactivity for a 2-day moving average was associated with 13% higher odds of a VA event (95% CI, 1%-26%). In the 2-pollutant model, for the same averaging window of 21 days, each interquartile range increase in daily PM2.5 was associated with an 48% higher odds of a VA event (95% CI, 15%-90%), and each interquartile range increase of particle radioactivity with a 10% lower odds of a VA event (95% CI, -29% to 14%). We found that with higher levels of particle radioactivity, the effect of PM2.5 on VAs is reduced. CONCLUSIONS: In this high-risk population, intermediate (21-day) PM2.5 exposure was associated with higher odds of a VA event onset among patients with known cardiac disease and indication for implanted cardioverter-defibrillator implantation independently of particle radioactivity.

14.
Aging (Albany NY) ; 12(16): 16539-16554, 2020 08 03.
Artigo em Inglês | MEDLINE | ID: mdl-32747609

RESUMO

Chronic obstructive pulmonary disease (COPD) is a frequent diagnosis in older individuals and contributor to global morbidity and mortality. Given the link between lung disease and aging, we need to understand how molecular indicators of aging relate to lung function and disease. Using data from the population-based KORA (Cooperative Health Research in the Region of Augsburg) surveys, we associated baseline epigenetic (DNA methylation) age acceleration with incident COPD and lung function. Models were adjusted for age, sex, smoking, height, weight, and baseline lung disease as appropriate. Associations were replicated in the Normative Aging Study. Of 770 KORA participants, 131 developed incident COPD over 7 years. Baseline accelerated epigenetic aging was significantly associated with incident COPD. The change in age acceleration (follow-up - baseline) was more strongly associated with COPD than baseline aging alone. The association between the change in age acceleration between baseline and follow-up and incident COPD replicated in the Normative Aging Study. Associations with spirometric lung function parameters were weaker than those with COPD, but a meta-analysis of both cohorts provide suggestive evidence of associations. Accelerated epigenetic aging, both baseline measures and changes over time, may be a risk factor for COPD and reduced lung function.

15.
Environ Int ; 144: 106021, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32791345

RESUMO

BACKGROUND: Post-transcriptional modifications of RNA constitute fundamental mechanisms of gene regulation. N6-methyladenosine (m6A) is critical for health and disease and is modulated by cellular stressors. However, associations between environmental exposures and m6A have not been studied in humans. We aimed to examine associations between tobacco smoking and particulate air pollution with m6A and mRNA expression levels of its reader, writer and eraser (RWE) genes in blood. METHODS: Using the Beijing Truck Driver Air Pollution Study, we investigated global m6A in RNA from peripheral blood collected from 106 human subjects in Beijing, China, in 2008. We measured m6A with nano-flow liquid chromatography-tandem mass spectrometry and investigated gene expression of six m6A RWEs with real-time-quantitative PCR. Using linear models, we examined associations with smoking status, pack-years, and smoking on day of visit in men, and with environmental tobacco smoke in nonsmokers. We also examined associations with ambient PM10 (particulate matter ≤ 10 µm in diameter), and personal black carbon (BC) and PM2.5 measured with a portable monitor. RESULTS: Smoking in men was significantly associated with a relative 10.7% decrease in global m6A levels in comparison to nonsmokers (p = 0.02). In men, smoking greater than 3.8 pack-years was associated with a 14.9% lower m6A than in nonsmokers. BC exposure trended towards positive associations with m6A (5.95% per 10 µg/m3 increase in BC; 95% CI: -0.96, 13.3). Global m6A levels were not correlated with RWE gene expression levels. No associations were detected between smoking or air pollutants and m6A RWE gene expression. DISCUSSION: m6A was negatively associated with long-term smoking, yet positively associated with short-term BC exposure. These results indicate variable m6A responses to environmental stressors, providing early evidence into the impacts of toxicants on RNA modifications and suggesting potential for m6A as a biomarker or mechanism in environmental health research.

16.
Environ Sci Technol ; 54(18): 11037-11047, 2020 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-32808786

RESUMO

In this paper, we integrated multiple types of predictor variables and three types of machine learners (neural network, random forest, and gradient boosting) into a geographically weighted ensemble model to estimate the daily maximum 8 h O3 with high resolution over both space (at 1 km × 1 km grid cells covering the contiguous United States) and time (daily estimates between 2000 and 2016). We further quantify monthly model uncertainty for our 1 km × 1 km gridded domain. The results demonstrate high overall model performance with an average cross-validated R2 (coefficient of determination) against observations of 0.90 and 0.86 for annual averages. Overall, the model performance of the three machine learning algorithms was quite similar. The overall model performance from the ensemble model outperformed those from any single algorithm. The East North Central region of the United States had the highest R2, 0.93, and performance was weakest for the western mountainous regions (R2 of 0.86) and New England (R2 of 0.87). For the cross validation by season, our model had the best performance during summer with an R2 of 0.88. This study can be useful for the environmental health community to more accurately estimate the health impacts of O3 over space and time, especially in health studies at an intra-urban scale.

17.
JAMA Netw Open ; 3(7): e2010350, 2020 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-32658288

RESUMO

Importance: Chronic obstructive pulmonary disease (COPD) is a critical public health burden. The neutrophil to lymphocyte ratio (NLR), an inflammation biomarker, has been associated with COPD morbidity and mortality; however, its associations with lung function decline and COPD development are poorly understood. Objective: To explore the associations of NLR with lung function decline and COPD risks. Design, Setting, and Participants: This longitudinal cohort study included white male veterans in the US with more than 30 years of follow-up to investigate the associations of NLR with lung function, COPD, and hypomethylation of cg05575921, the top DNA methylation marker of lung function changes in response to tobacco smoking. This study included 7466 visits from 1549 participants, each examined up to 13 times between 1982 and 2018. A subgroup of 1411 participants without COPD at baseline were selected to analyze the association of NLR with incident COPD. Data were analyzed from September 2019 to January 2020. Exposures: The primary exposure was NLR, which was estimated using automated whole blood cell counts based on a blood sample collected at each visit. The methylation level of cg05575921 was measured in blood DNA from a subgroup of 1228 visits. Main Outcomes and Measures: The outcomes of interest were lung function, measured as forced respiratory volume in the first second (FEV1) in liters, forced vital capacity (FVC) in liters, percentage of FVC exhaled in the first second (FEV1/FVC), and maximal midexpiratory flow rate (MMEF) in liters per minute and COPD status, defined as meeting the Global Initiative for Chronic Obstructive Lung Diseases stage II (or higher) criteria. Both outcomes were measured as each visit. Results: Among 1549 included men (mean [SD] age, 68.3 [9.3] years) with 7466 visits from 1982 to 2018, a 1-unit increase in NLR was associated with statistically significant mean (SE) decreases of 0.021 (0.004) L in FEV1, 0.016 (0.005) L in FVC, 0.290% (0.005) L in FVC, 0.290% (0.065%) in FEV1/FVC, and 3.65 (0.916) L/min MMEF. Changes in NLR up to approximately 10 years were associated with corresponding longitudinal changes in lung function. Furthermore, this increase in NLR was associated with 9% higher odds of COPD (odds ratio, 1.09 [95% CI, 1.03-1.15]) for all visits and 27% higher risk of incident COPD (odds ratio, 1.07 [95% CI, 1.07-1.51]) for participants without COPD at baseline. Additionally, a 1-unit increase in NLR was associated with a mean (SE) decrease of 0.0048 (0.0021 in cg05575921 hypomethylation, which may mediate the adverse association of NLR-related inflammation on lung function. Conclusions and Relevance: These findings suggest that NLR may be a clinically relevant biomarker associated with high risk of lung function impairment and COPD alone or in combination with DNA methylation profiles.

18.
Brief Bioinform ; 2020 Jul 07.
Artigo em Inglês | MEDLINE | ID: mdl-32632436

RESUMO

Epigenome-wide mediation analysis aims to identify DNA methylation CpG sites that mediate the causal effects of genetic/environmental exposures on health outcomes. However, DNA methylations in the peripheral blood tissues are usually measured at the bulk level based on a heterogeneous population of white blood cells. Using the bulk level DNA methylation data in mediation analysis might cause confounding bias and reduce study power. Therefore, it is crucial to get fine-grained results by detecting mediation CpG sites in a cell-type-specific way. However, there is a lack of methods and software to achieve this goal. We propose a novel method (Mediation In a Cell-type-Specific fashion, MICS) to identify cell-type-specific mediation effects in genome-wide epigenetic studies using only the bulk-level DNA methylation data. MICS follows the standard mediation analysis paradigm and consists of three key steps. In step1, we assess the exposure-mediator association for each cell type; in step 2, we assess the mediator-outcome association for each cell type; in step 3, we combine the cell-type-specific exposure-mediator and mediator-outcome associations using a multiple testing procedure named MultiMed [Sampson JN, Boca SM, Moore SC, et al. FWER and FDR control when testing multiple mediators. Bioinformatics 2018;34:2418-24] to identify significant CpGs with cell-type-specific mediation effects. We conduct simulation studies to demonstrate that our method has correct FDR control. We also apply the MICS procedure to the Normative Aging Study and identify nine DNA methylation CpG sites in the lymphocytes that might mediate the effect of cigarette smoking on the lung function.

19.
Environ Int ; 143: 105933, 2020 Jul 10.
Artigo em Inglês | MEDLINE | ID: mdl-32659528

RESUMO

BACKGROUND: Emerging findings have increased concern that exposure to fine particulate matter air pollution (aerodynamic diameter ≤ 2.5 µm; PM2.5) may be neurotoxic, even at lower levels of exposure. Yet, additional studies are needed to determine if exposure to current PM2.5 levels may be linked to hemispheric and regional patterns of brain development in children across the United States. OBJECTIVES: We examined the cross-sectional associations between geocoded measures of concurrent annual average outdoor PM2.5 exposure, regional- and hemisphere-specific differences in brain morphometry and cognition in 10,343 9- and 10- year-old children. METHODS: High-resolution structural T1-weighted brain magnetic resonance imaging (MRI) and NIH Toolbox measures of cognition were collected from children at ages 9-10 years. FreeSurfer was used to quantify cortical surface area, cortical thickness, as well as subcortical and cerebellum volumes in each hemisphere. PM2.5 concentrations were estimated using an ensemble-based model approach and assigned to each child's primary residential address collected at the study visit. We used mixed-effects models to examine regional- and hemispheric- effects of PM2.5 exposure on brain estimates and cognition after considering nesting of participants by familial relationships and study site, adjustment for socio-demographic factors and multiple comparisons. RESULTS: Annual residential PM2.5 exposure (7.63 ± 1.57 µg/m3) was associated with hemispheric specific differences in gray matter across cortical regions of the frontal, parietal, temporal and occipital lobes as well as subcortical and cerebellum brain regions. There were hemispheric-specific associations between PM2.5 exposures and cortical surface area in 9/31 regions; cortical thickness in 22/27 regions; and volumes of the thalamus, pallidum, and nucleus accumbens. We found neither significant associations between PM2.5 and task performance on individual measures of neurocognition nor evidence that sex moderated the observed associations. DISCUSSION: Even at relatively low-levels, current PM2.5 exposure across the U.S. may be an important environmental factor influencing patterns of structural brain development in childhood. Prospective follow-up of this cohort will help determine how current levels of PM2.5 exposure may affect brain development and subsequent risk for cognitive and emotional problems across adolescence.

20.
PLoS One ; 15(7): e0236479, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32716950

RESUMO

BACKGROUND: Many studies have identified an inequitable distribution of exposure to PM2.5 (particulate matter less than 2.5 microns) by race. We investigated the association of PM2.5 and cardiovascular mortality considering both the decedents' race and neighborhood racial composition as potential modifiers. METHODS: We obtained geocoded cardiovascular mortality records of all black and white decedents from urban block-groups in Massachusetts between 2001 and 2011 (n = 130,863). We examined the association between PM2.5 and cardiovascular mortality, and assessed effect modification by three types of racial modifiers: decedents' race, census block-group percent black and white, and two novel measures of racial segregation. The Racial Residential Segregation (RRS) quantifies the concentration of non-Hispanic blacks and whites in each block-group. The Index of Racial Dissimilarity measures dissimilarity in non-Hispanic black and white racial distribution between the smaller census block-group and larger tract. RESULTS: We found a 2.35%(95%CI: 0.92%;3.79%) increase in mortality for each 10µg/m3 increase in two-day average exposure to PM2.5. The effect was modified by the block-group racial composition, with higher risks in block-groups with the highest percentage of black residents (interaction p-value = 0.04), and in block-groups with the lowest RRS (i.e. higher black to white resident ratio, interaction p-value = 0.072). Racial dissimilarity did not modify the associations. CONCLUSION: Current levels of PM2.5 are associated with increased cardiovascular deaths in Massachusetts, with different risks between areas with different racial composition and segregation. This suggests that pollution reductions in neighborhoods with the highest percentage of non-Hispanic blacks would be most beneficial in reducing cardiovascular mortality and disparities.


Assuntos
Doenças Cardiovasculares/etnologia , Doenças Cardiovasculares/mortalidade , Grupos de Populações Continentais , Tamanho da Partícula , Material Particulado/efeitos adversos , Material Particulado/química , Segregação Social , Idoso de 80 Anos ou mais , Feminino , Humanos , Masculino , Fatores de Risco , Estatística como Assunto , População Urbana
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