首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到20条相似文献,搜索用时 15 毫秒
1.

Background

Air pollution exposure has been associated with increased blood pressure in adults.

Objective:

We examined associations of antenatal exposure to ambient air pollution with newborn systolic blood pressure (SBP).

Methods:

We studied 1,131 mother–infant pairs in a Boston, Massachusetts, area pre-birth cohort. We calculated average exposures by trimester and during the 2 to 90 days before birth for temporally resolved fine particulate matter (≤ 2.5 μm; PM2.5), black carbon (BC), nitrogen oxides, nitrogen dioxide, ozone (O3), and carbon monoxide measured at stationary monitoring sites, and for spatiotemporally resolved estimates of PM2.5 and BC at the residence level. We measured SBP at a mean age of 30 ± 18 hr with an automated device. We used mixed-effects models to examine associations between air pollutant exposures and SBP, taking into account measurement circumstances; child’s birth weight; mother’s age, race/ethnicity, socioeconomic position, and third-trimester BP; and time trend. Estimates represent differences in SBP associated with an interquartile range (IQR) increase in each pollutant.

Results:

Higher mean PM2.5 and BC exposures during the third trimester were associated with higher SBP (e.g., 1.0 mmHg; 95% CI: 0.1, 1.8 for a 0.32-μg/m3 increase in mean 90-day residential BC). In contrast, O3 was negatively associated with SBP (e.g., –2.3 mmHg; 95% CI: –4.4, –0.2 for a 13.5-ppb increase during the 90 days before birth).

Conclusions:

Exposures to PM2.5 and BC in late pregnancy were positively associated with newborn SBP, whereas O3 was negatively associated with SBP. Longitudinal follow-up will enable us to assess the implications of these findings for health during later childhood and adulthood.

Citation:

van Rossem L, Rifas-Shiman SL, Melly SJ, Kloog I, Luttmann-Gibson H, Zanobetti A, Coull BA, Schwartz JD, Mittleman MA, Oken E, Gillman MW, Koutrakis P, Gold DR. 2015. Prenatal air pollution exposure and newborn blood pressure. Environ Health Perspect 123:353–359; http://dx.doi.org/10.1289/ehp.1307419  相似文献   

2.
Background: Traffic noise has been associated with prevalence of hypertension, but reports are inconsistent for blood pressure (BP). To ascertain noise effects and to disentangle them from those suspected to be from traffic-related air pollution, it may be essential to estimate people’s noise exposure indoors in bedrooms.Objectives: We analyzed associations between long-term exposure to indoor traffic noise in bedrooms and prevalent hypertension and systolic (SBP) and diastolic (DBP) BP, considering long-term exposure to outdoor nitrogen dioxide (NO2).Methods: We evaluated 1,926 cohort participants at baseline (years 2003–2006; Girona, Spain). Outdoor annual average levels of nighttime traffic noise (Lnight) and NO2 were estimated at postal addresses with a detailed traffic noise model and a land-use regression model, respectively. Individual indoor traffic Lnight levels were derived from outdoor Lnight with application of insulations provided by reported noise-reducing factors. We assessed associations for hypertension and BP with multi-exposure logistic and linear regression models, respectively.Results: Median levels were 27.1 dB(A) (indoor Lnight), 56.7 dB(A) (outdoor Lnight), and 26.8 μg/m3 (NO2). Spearman correlations between outdoor and indoor Lnight with NO2 were 0.75 and 0.23, respectively. Indoor Lnight was associated both with hypertension (OR = 1.06; 95% CI: 0.99, 1.13) and SBP (β = 0.72; 95% CI: 0.29, 1.15) per 5 dB(A); and NO2 was associated with hypertension (OR = 1.16; 95% CI: 0.99, 1.36), SBP (β = 1.23; 95% CI: 0.21, 2.25), and DBP (β⊇= 0.56; 95% CI: –0.03, 1.14) per 10 μg/m3. In the outdoor noise model, Lnight was associated only with hypertension and NO2 with BP only. The indoor noise–SBP association was stronger and statistically significant with a threshold at 30 dB(A).Conclusion: Long-term exposure to indoor traffic noise was associated with prevalent hypertension and SBP, independently of NO2. Associations were less consistent for outdoor traffic Lnight and likely affected by collinearity.Citation: Foraster M, Künzli N, Aguilera I, Rivera M, Agis D, Vila J, Bouso L, Deltell A, Marrugat J, Ramos R, Sunyer J, Elosua R, Basagaña X. 2014. High blood pressure and long-term exposure to indoor noise and air pollution from road traffic. Environ Health Perspect 122:1193–1200; http://dx.doi.org/10.1289/ehp.1307156  相似文献   

3.
Background: Long-term exposure to air pollution has been hypothesized to elevate arterial blood pressure (BP). The existing evidence is scarce and country specific.Objectives: We investigated the cross-sectional association of long-term traffic-related air pollution with BP and prevalent hypertension in European populations.Methods: We analyzed 15 population-based cohorts, participating in the European Study of Cohorts for Air Pollution Effects (ESCAPE). We modeled residential exposure to particulate matter and nitrogen oxides with land use regression using a uniform protocol. We assessed traffic exposure with traffic indicator variables. We analyzed systolic and diastolic BP in participants medicated and nonmedicated with BP-lowering medication (BPLM) separately, adjusting for personal and area-level risk factors and environmental noise. Prevalent hypertension was defined as ≥ 140 mmHg systolic BP, or ≥ 90 mmHg diastolic BP, or intake of BPLM. We combined cohort-specific results using random-effects meta-analysis.Results: In the main meta-analysis of 113,926 participants, traffic load on major roads within 100 m of the residence was associated with increased systolic and diastolic BP in nonmedicated participants [0.35 mmHg (95% CI: 0.02, 0.68) and 0.22 mmHg (95% CI: 0.04, 0.40) per 4,000,000 vehicles × m/day, respectively]. The estimated odds ratio (OR) for prevalent hypertension was 1.05 (95% CI: 0.99, 1.11) per 4,000,000 vehicles × m/day. Modeled air pollutants and BP were not clearly associated.Conclusions: In this first comprehensive meta-analysis of European population-based cohorts, we observed a weak positive association of high residential traffic exposure with BP in nonmedicated participants, and an elevated OR for prevalent hypertension. The relationship of modeled air pollutants with BP was inconsistent.Citation: Fuks KB, Weinmayr G, Foraster M, Dratva J, Hampel R, Houthuijs D, Oftedal B, Oudin A, Panasevich S, Penell J, Sommar JN, Sørensen M, Tittanen P, Wolf K, Xun WW, Aguilera I, Basagaña X, Beelen R, Bots ML, Brunekreef B, Bueno-de-Mesquita HB, Caracciolo B, Cirach M, de Faire U, de Nazelle A, Eeftens M, Elosua R, Erbel R, Forsberg B, Fratiglioni L, Gaspoz JM, Hilding A, Jula A, Korek M, Krämer U, Künzli N, Lanki T, Leander K, Magnusson PK, Marrugat J, Nieuwenhuijsen MJ, Östenson CG, Pedersen NL, Pershagen G, Phuleria HC, Probst-Hensch NM, Raaschou-Nielsen O, Schaffner E, Schikowski T, Schindler C, Schwarze PE, Søgaard AJ, Sugiri D, Swart WJ, Tsai MY, Turunen AW, Vineis P, Peters A, Hoffmann B. 2014. Arterial blood pressure and long-term exposure to traffic-related air pollution: an analysis in the European Study of Cohorts for Air Pollution Effects (ESCAPE). Environ Health Perspect 122:896–905; http://dx.doi.org/10.1289/ehp.1307725  相似文献   

4.
5.
Background: Epidemiological evidence of the effects of long-term exposure to air pollution on the chronic processes of atherogenesis is limited.Objective: We investigated the association of long-term exposure to traffic-related air pollution with subclinical atherosclerosis, measured by carotid intima media thickness (IMT) and ankle–brachial index (ABI).Methods: We performed a cross-sectional analysis using data collected during the reexamination (2007–2010) of 2,780 participants in the REGICOR (Registre Gironí del Cor: the Gerona Heart Register) study, a population-based prospective cohort in Girona, Spain. Long-term exposure across residences was calculated as the last 10 years’ time-weighted average of residential nitrogen dioxide (NO2) estimates (based on a local-scale land-use regression model), traffic intensity in the nearest street, and traffic intensity in a 100 m buffer. Associations with IMT and ABI were estimated using linear regression and multinomial logistic regression, respectively, controlling for sex, age, smoking status, education, marital status, and several other potential confounders or intermediates.Results: Exposure contrasts between the 5th and 95th percentiles for NO2 (25 µg/m3), traffic intensity in the nearest street (15,000 vehicles/day), and traffic load within 100 m (7,200,000 vehicle-m/day) were associated with differences of 0.56% (95% CI: –1.5, 2.6%), 2.32% (95% CI: 0.48, 4.17%), and 1.91% (95% CI: –0.24, 4.06) percent difference in IMT, respectively. Exposures were positively associated with an ABI of > 1.3, but not an ABI of < 0.9. Stronger associations were observed among those with a high level of education and in men ≥ 60 years of age.Conclusions: Long-term traffic-related exposures were associated with subclinical markers of atherosclerosis. Prospective studies are needed to confirm associations and further examine differences among population subgroups.  相似文献   

6.
7.
8.

Background

Associations between long-term exposure to air pollution and carotid intima-media thickness (CIMT) have inconsistent findings.

Objectives

In this study we aimed to evaluate association between 1-year average exposure to traffic-related air pollution and CIMT in middle-aged adults in Asia.

Methods

CIMT was measured in Taipei, Taiwan, between 2009 and 2011 in 689 volunteers 35–65 years of age who were recruited as the control subjects of an acute coronary heart disease cohort study. We applied land-use regression models developed by the European Study of Cohorts for Air Pollution Effects (ESCAPE) to estimate each subject’s 1-year average exposure to traffic-related air pollutants with particulate matter diameters ≤ 10 μm (PM10) and ≤ 2.5 μm (PM2.5) and the absorbance levels of PM2.5 (PM2.5abs), nitrogen dioxide (NO2), and nitrogen oxides (NOx) in the urban environment.

Results

One-year average air pollution exposures were 44.21 ± 4.19 μg/m3 for PM10, 27.34 ± 5.12 μg/m3 for PM2.5, and (1.97 ± 0.36) × 10–5/m for PM2.5abs. Multivariate regression analyses showed average percentage increases in maximum left CIMT of 4.23% (95% CI: 0.32, 8.13) per 1.0 × 10–5/m increase in PM2.5abs; 3.72% (95% CI: 0.32, 7.11) per 10-μg/m3 increase in PM10; 2.81% (95% CI: 0.32, 5.31) per 20-μg/m3 increase in NO2; and 0.74% (95% CI: 0.08, 1.41) per 10-μg/m3 increase in NOx. The associations were not evident for right CIMT, and PM2.5 mass concentration was not associated with the outcomes.

Conclusions

Long-term exposures to traffic-related air pollution of PM2.5abs, PM10, NO2, and NOx were positively associated with subclinical atherosclerosis in middle-aged adults.

Citation

Su TC, Hwang JJ, Shen YC, Chan CC. 2015. Carotid intima–media thickness and long-term exposure to traffic-related air pollution in middle-aged residents of Taiwan: a cross-sectional study. Environ Health Perspect 123:773–778; http://dx.doi.org/10.1289/ehp.1408553  相似文献   

9.
10.
Background: Associations between long-term exposure to air pollution and road traffic noise have been established for ischemic heart disease, but findings have been mixed for atrial fibrillation (AF).Objectives: The goal of the study was to examine associations of long-term exposure to road traffic noise and air pollution with AF.Methods: Time-varying Cox regression models were used to estimate associations of 1-, 3-, and 23-y mean road traffic noise and air pollution exposures with AF incidence in 23,528 women enrolled in the Danish Nurse Cohort (age >44y at baseline in 1993 or 1999). AF diagnoses were ascertained via the Danish National Patient Register. Annual mean weighted 24-h average road traffic noise levels (Lden) at the nurses’ residences, since 1970, were estimated using the Nord2000 model, and annual mean levels of particulate matter with a diameter <2.5μm (PM2.5) and nitrogen dioxide (NO2) were estimated using the DEHM/UBM/AirGIS model.Results: Of 23,528 nurses with no prior AF diagnosis at the cohort baseline, 1,522 developed AF during follow-up. In a fully adjusted model (including PM2.5), the estimated risk of AF was 18% higher [hazard ratio (HR); 95% confidence interval (CI): 1.18; 1.02, 1.36] in nurses with residential 3-y mean Lden levels >58 dB vs. <48 dB, with similar findings for 1-y mean exposures. A 3.9-μg/m3 increase in 3-y mean PM2.5 was associated with incident AF before and after adjustment for concurrent exposure to road traffic noise (HR 1.09; 95% CI: 1.00, 1.20 and 1.08; 95% CI: 0.97, 1.19, respectively). Associations with 1-y mean PM2.5 exposures were positive but closer to the null and not significant. Associations with NO2 were null for all time periods before and after adjustment for road traffic noise and inverse when adjusted for concurrent PM2.5.Conclusion: Our analysis of prospective data from a cohort of Danish female nurses followed for up to 14 y provided suggestive evidence of independent associations between incident AF and 1- and 3-y exposures to road traffic noise and PM2.5. https://doi.org/10.1289/EHP8090  相似文献   

11.
农村地区空气污染人群暴露评价研究   总被引:8,自引:4,他引:8  
目的了解我国农村欠发达地区空气污染的状况及农村人群对空气污染的实际暴露水平。方法选择安庆市所属两个县18个乡镇的189个家庭,对其室内、外空气污染水平进行环境监测 ,同时对上述家庭中年龄在15~65岁之间的488名调查对象进行入户问卷调查。结果被调查地区存在严重的室内外空气污染 ,污染物以可吸入颗粒物PM10 为主 ,厨房、卧室、庭院、田间分别为(518±27)μg/m3,(340±9)μg/m3,(287±9)μg/m3,(270±10)μg/m3,室内污染水平显著高于室外 (P<0.01) ;SO2 和CO的污染水平较低 (P>0.05)。结合个体暴露时间和环境暴露浓度对个体的综合空气污染暴露进行综合评价的结果显示 ,该地区农村居民冬季对PM10 的实际暴露水平明显高于国家卫生标准 ,而其室内外空气污染主要来源是由于做饭和取暖的燃料燃烧引起。结论该地区农村室内空气污染严重 ,污染物以PM10 为主  相似文献   

12.

Background

Limited information is available regarding long-term effects of air pollution on blood pressure (BP) and hypertension.

Objective

We studied whether 1-year exposures to particulate matter (PM) and nitrogen oxides (NOx) were correlated with BP and hypertension in the elderly.

Methods

We analyzed cross-sectional data from 27,752 Taipei City residents > 65 years of age who participated in a health examination program in 2009. Land-use regression models were used to estimate participants’ 1-year exposures to particulate matter with aerodynamic diameter ≤ 10 μm (PM10), coarse particles (PM2.5–10), fine particles (≤ 2.5 μm; PM2.5), PM2.5 absorbance, NOx, and nitrogen dioxide (NO2). Generalized linear regressions and logistic regressions were used to examine the association between air pollution and BP and hypertension, respectively.

Results

Diastolic BP was associated with 1-year exposures to air pollution, with estimates of 0.73 [95% confidence interval (CI): 0.44, 1.03], 0.46 (95% CI: 0.30, 0.63), 0.62 (95% CI: 0.24, 0.99), 0.34 (95% CI: 0.19, 0.50), and 0.65 (95% CI: 0.44, 0.85) mmHg for PM10 (10 μg/m3), PM2.5–10 (5 μg/m3), PM2.5 absorbance (10–5/m), NOx (20 μg/m3), and NO2 (10 μg/m3), respectively. PM2.5 was not associated with diastolic BP, and none of the air pollutants was associated with systolic BP. Associations of diastolic BP with PM10 and PM2.5 absorbance were stronger among participants with hypertension, diabetes, or a body mass index ≥ 25 kg/m2 than among participants without these conditions. One-year air pollution exposures were not associated with hypertension.

Conclusions

One-year exposures to PM10, PM2.5–10, PM2.5 absorbance, and NOx were associated with higher diastolic BP in elderly residents of Taipei.

Citation

Chen SY, Wu CF, Lee JH, Hoffmann B, Peters A, Brunekreef B, Chu DC, Chan CC. 2015. Associations between long-term air pollutant exposures and blood pressure in elderly residents of Taipei City: a cross-sectional study. Environ Health Perspect 123:779–784; http://dx.doi.org/10.1289/ehp.1408771  相似文献   

13.
A portable personal air pollution sampler was used to measure the exposure of twenty children to respirable particulates, sulfur dioxide, and nitrogen dioxide over a 24-hour period. Particulate exposures were significantly higher among children who lived with one or more smokers, and exceeded the primary air quality standard in nineteen of the twenty subjects. To a large extent, an individual’s respirable particulate load appears to be determined by exposure to indoor rather than outdoor pollutants.  相似文献   

14.
15.
Background: Few European studies have investigated the effects of long-term exposure to both fine particulate matter (≤ 2.5 µm; PM2.5) and nitrogen dioxide (NO2) on mortality.Objectives: We studied the association of exposure to NO2, PM2.5, and traffic indicators on cause-specific mortality to evaluate the form of the concentration–response relationship.Methods: We analyzed a population-based cohort enrolled at the 2001 Italian census with 9 years of follow-up. We selected all 1,265,058 subjects ≥ 30 years of age who had been living in Rome for at least 5 years at baseline. Residential exposures included annual NO2 (from a land use regression model) and annual PM2.5 (from a Eulerian dispersion model), as well as distance to roads with > 10,000 vehicles/day and traffic intensity. We used Cox regression models to estimate associations with cause-specific mortality adjusted for individual (sex, age, place of birth, residential history, marital status, education, occupation) and area (socioeconomic status, clustering) characteristics.Results: Long-term exposures to both NO2 and PM2.5 were associated with an increase in nonaccidental mortality [hazard ratio (HR) = 1.03 (95% CI: 1.02, 1.03) per 10-µg/m3 NO2; HR = 1.04 (95% CI: 1.03, 1.05) per 10-µg/m3 PM2.5]. The strongest association was found for ischemic heart diseases (IHD) [HR = 1.10 (95% CI: 1.06, 1.13) per 10-µg/m3 PM2.5], followed by cardiovascular diseases and lung cancer. The only association showing some deviation from linearity was that between NO2 and IHD. In a bi-pollutant model, the estimated effect of NO2 on mortality was independent of PM2.5.Conclusions: This large study strongly supports an effect of long-term exposure to NO2 and PM2.5 on mortality, especially from cardiovascular causes. The results are relevant for the next European policy decisions regarding air quality.  相似文献   

16.
Background: Phthalate exposure is ubiquitous and may affect biological pathways related to regulators of blood pressure. Given the profound changes in vasculature during pregnancy, pregnant women may be particularly susceptible to the potential effects of phthalates on blood pressure.Objectives: We examined associations of phthalate exposure during pregnancy with maternal blood pressure trajectories from mid-pregnancy through 72 months postpartum.Methods: Women with singleton pregnancies delivering a live birth in Mexico City were enrolled during the second trimester (n=892). Spot urine samples from the second and third trimesters were analyzed for 15 phthalate metabolites. Blood pressure and covariate data were collected over nine visits through 72 months postpartum. We used linear, logistic, and linear mixed models; latent class growth models (LCGMs); and Bayesian kernel machine regression to estimate the relationship of urinary phthalate biomarkers with maternal blood pressure.Results: As a joint mixture, phthalate biomarker concentrations during pregnancy were associated with higher blood pressure rise during mid-to-late gestation. With respect to individual biomarkers, second trimester concentrations of monobenzyl phthalate (MBzP) and di(2-ethylhexyl) phthalate biomarkers (ΣDEHP) were associated with higher third trimester blood pressure. Two trajectory classes were identified by LCGM, characterized by increasing blood pressure through 72 months postpartum (“increase–increase”) or decreased blood pressure through 18 months postpartum with a gradual increase thereafter (“decrease–increase”). Increasing exposure to phthalate mixtures during pregnancy was associated with higher odds of being in the increase–increase class. Similar associations were observed for mono-2-ethyl-5-carboxypentyl terephthalate (MECPTP) and dibutyl phthalate (ΣDBP) biomarkers. When specific time periods were examined, we observed specific temporal relationships were observed for ΣDEHP, MECPTP, MBzP, and ΣDBP.Discussion: In our cohort of pregnant women from Mexico City, exposure to phthalates and phthalate biomarkers was associated with higher blood pressure during late pregnancy, as well as with long-term changes in blood pressure trajectories. https://doi.org/10.1289/EHP8562  相似文献   

17.
自贡市空气污染及人群暴露量研究   总被引:2,自引:0,他引:2  
为研究空气污染与人群健康的关系,对1061例不同职业人群暴露在不同微环境的暴露时间及该环境中主要污染物如可吸入尘(IP)、二氧化硫(SO2)、氮氧化物(NOx)、硫化氢(H2S)和一氧化碳(CO)暴露水平进行调查。结果表明,人群一日中平均暴露时间最长为卧室,长达14.33h/d,占59.74%,厨房暴露1.63h/d,占6.75%。人群平均总暴露量为54.838mg/d,退休人员最高(59.065  相似文献   

18.
ObjectivesTo evaluate the incidence of deprescribing of antihypertensive medication among older adults residing in Veterans Affairs (VA) nursing homes for long-term care and rates of deprescribing after potentially triggering events.DesignRetrospective cohort study.Setting and ParticipantsLong-term care residents aged 65 years and older admitted to a VA nursing home from 2006 to 2019 and using blood pressure medication at admission.MethodsData were extracted from the VA electronic health record, and Centers for Medicare & Medicaid Services Minimum Data Set and Bar Code Medication Administration. Deprescribing was defined on a rolling basis as a reduction in the number or dose of antihypertensive medications, sustained for ≥2 weeks. We examined potentially triggering events for deprescribing, including low blood pressure (<90/60 mmHg), acute renal impairment (creatinine increase of 50%), electrolyte imbalance (potassium below 3.5 mEq/L, sodium decrease by 5 mEq/L), and falls.ResultsAmong 31,499 VA nursing home residents on antihypertensive medication, 70.4% had ≥1 deprescribing event (median length of stay = 6 months), and 48.7% had a net reduction in antihypertensive medications over their stay. Deprescribing events were most common in the first 4 weeks after admission and the last 4 weeks of life. Among potentially triggering events, a 50% increase in serum creatinine was associated with the greatest increase in the likelihood of deprescribing over the subsequent 4 weeks: residents with this event had a 41.7% chance of being deprescribed compared with 11.5% in those who did not (risk difference = 30.3%, P < .001). A fall in the past 30 days was associated with the smallest magnitude increased risk of deprescribing (risk difference = 3.8%, P < .001) of the events considered.Conclusions and ImplicationsDeprescribing of antihypertensive medications is common among VA nursing home residents, especially after a potential renal adverse event.  相似文献   

19.
Background: Epidemiological studies have assessed T-wave alternans (TWA) as a possible mechanism of cardiac arrhythmias related to air pollution in high-risk subjects and have reported associations with increased TWA magnitude.Objective: In this controlled human exposure study, we assessed the impact of exposure to concentrated ambient particulate matter (CAP) and ozone (O3) on T-wave alternans in resting volunteers without preexisting cardiovascular disease.Methods: Seventeen participants without preexisting cardiovascular disease were randomized to filtered air (FA), CAP (150 μg/m3), O3 (120 ppb), or combined CAP + O3 exposures for 2 hr. Continuous electrocardiograms (ECGs) were recorded at rest and T-wave alternans (TWA) was computed by modified moving average analysis with QRS alignment for the artifact-free intervals of 20 beats along the V2 and V5 leads. Exposure-induced changes in the highest TWA magnitude (TWAMax) were estimated for the first and last 5 min of each exposure (TWAMax_Early and TWAMax_Late respectively). ΔTWAMax (Late-Early) were compared among exposure groups using analysis of variance.Results: Mean ± SD values for ΔTWAMax were -2.1 ± 0.4, -2.7 ± 1.1, -1.9 ± 1.5, and -1.2 ± 1.5 in FA, CAP, O3, and CAP + O3 exposure groups, respectively. No significant differences were observed between pollutant exposures and FA.Conclusion: In our study of 17 volunteers who had no preexisting cardiovascular disease, we did not observe significant changes in T-wave alternans after 2-hr exposures to CAP, O3, or combined CAP + O3. This finding, however, does not preclude the possibility of pollution-related effects on TWA at elevated heart rates, such as during exercise, or the possibility of delayed responses.  相似文献   

20.
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号