Long-term exposure to traffic-related air pollution and the risk of coronary heart disease hospitalization and mortality

Background

Epidemiologic studies have demonstrated that exposure to road traffic is associated with adverse cardiovascular outcomes.

Objectives

We aimed to identify specific traffic-related air pollutants that are associated with the risk of coronary heart disease (CHD) morbidity and mortality to support evidence-based environmental policy making.

Methods

This population-based cohort study included a 5-year exposure period and a 4-year follow-up period. All residents 45–85 years of age who resided in Metropolitan Vancouver during the exposure period and without known CHD at baseline were included in this study (n = 452,735). Individual exposures to traffic-related air pollutants including black carbon, fine particles [aerodynamic diameter ≤ 2.5 μm (PM_2.5)], nitrogen dioxide (NO₂), and nitric oxide were estimated at residences of the subjects using land-use regression models and integrating changes in residences during the exposure period. CHD hospitalizations and deaths during the follow-up period were identified from provincial hospitalization and death registration records.

Results

An interquartile range elevation in the average concentration of black carbon (0.94 × 10⁻⁵/m filter absorbance, equivalent to approximately 0.8 μg/m³ elemental carbon) was associated with a 3% increase in CHD hospitalization (95% confidence interval, 1–5%) and a 6% increase in CHD mortality (3–9%) after adjusting for age, sex, preexisting comorbidity, neighborhood socioeconomic status, and copollutants (PM_2.5 and NO₂). There were clear linear exposure–response relationships between black carbon and coronary events.

Conclusions

Long-term exposure to traffic-related fine particulate air pollution, indicated by black carbon, may partly explain the observed associations between exposure to road traffic and adverse cardiovascular outcomes.     

Residential exposure to traffic-related air pollution and survival after heart failure

BACKGROUND: Although patients with heart failure (HF) have been identified as particularly susceptible to the acute effects of air pollution, the effects of long-term exposure to air pollution on patients with this increasingly prevalent disease are largely unknown. OBJECTIVE: This study was designed to examine the mortality risk associated with residential exposure to traffic-related air pollution among HF patients. METHODS: A total of 1,389 patients hospitalized with acute HF in greater Worcester, Massachusetts, during 2000 were followed for survival through December 2005. We used daily traffic within 100 and 300 m of residence as well as the distance from residence to major roadways and to bus routes as proxies for residential exposure to traffic-related air pollution. We assessed mortality risks for each exposure variable using Cox proportional hazards models adjusted for prognostic factors. RESULTS: After the 5-year follow-up, only 334 (24%) subjects were still alive. An interquartile range increase in daily traffic within 100 m of home was associated with a mortality hazard ratio (HR) of 1.15 [95% confidence interval (CI), 1.05-1.25], whereas for traffic within 300 m this association was 1.09 (95% CI, 1.01-1.19). The mortality risk decreased with increasing distance to bus routes (HR = 0.88; 95% CI, 0.81-0.96) and was larger for those living within 100 m of a major roadway or 50 m of a bus route (HR = 1.30; 95% CI, 1.13-1.49). Adjustment for area-based income and educational level slightly attenuated these associations. CONCLUSIONS: Residential exposure to traffic-related air pollution increases the mortality risk after hospitalization with acute HF. Reducing exposure to traffic-related emissions may improve the long-term prognosis of HF patients.     

可吸入颗粒物与心血管系统疾病关系研究进展

目的探讨舟山杭州两地空气污染对学龄儿童呼吸系统健康状况的影响,促进采取有效干预措施,减少学龄儿童相关疾病的发生。方法通过整群抽样,将605名杭州市现代实验小学(污染区)和600名舟山市第一、第二小学(清洁区)的三至五年级学生列为研究对象, 进行健康问卷调查和学校因病缺课登记系统统计,并采用t检验、χ²检验和logistic回归进行统计分析。结果2016年杭州市PM_2.5、SO₂、NO₂、PM₁₀的平均质量浓度分别为56.27、11.53、51.58、85.34 μg/m³,均高于舟山市的26.71、8.99、19.86、44.42 μg/m³。杭州市学龄儿童呼吸系统疾病发病率(17.83%)高于舟山市(χ²=103.28,P < 0.05)。logistic分析结果显示,污染区学龄儿童的呼吸系统发病率的危险性为清洁区的32.34倍。结论PM_2.5、SO₂、NO₂、PM₁₀等空气污染成分是影响学龄儿童呼吸系统疾病的发病率的重要影响因素。保护环境,减少污染物排放,注意绿化,控制空气污染,对保护学龄儿童身体健康发育很重要。     

Occupational exposure to particulate air pollution and mortality due to ischaemic heart disease and cerebrovascular disease

Objectives

A growing number of epidemiological studies are showing that ambient exposure to particulate matter air pollution is a risk factor for cardiovascular disease; however, whether occupational exposure increases this risk is not clear. The aim of the present study was to examine whether occupational exposure to particulate air pollution increases the risk for ischaemic heart disease and cerebrovascular disease.

Methods

The study population was a cohort of 176 309 occupationally exposed Swedish male construction workers and 71 778 unexposed male construction workers. The definition of exposure to inorganic dust (asbestos, man‐made mineral fibres, dust from cement, concrete and quartz), wood dust, fumes (metal fumes, asphalt fumes and diesel exhaust) and gases and irritants (organic solvents and reactive chemicals) was based on a job‐exposure matrix with focus on exposure in the mid‐1970s. The cohort was followed from 1971 to 2002 with regard to mortality to ischaemic heart disease and cerebrovascular disease. Relative risks (RR) were obtained by the person‐years method and from Poisson regression models adjusting for baseline values of blood pressure, body mass index, age and smoking habits.

Results

Any occupational particulate air pollution was associated with an increased risk for ischemic heart disease (RR 1.13, 95% CI 1.07 to 1.19), but there was no increased risk for cerebrovascular disease (RR 0.97, 95% CI 0.88 to 1.07). There was an increased risk for ischaemic heart disease and exposure to inorganic dust (RR 1.07, 95% CI 1.03 to 1.12) and exposure to fumes (RR 1.05, 95% CI 1.00 to 1.10), especially diesel exhaust (RR 1.18, 95% CI 1.13 to 1.24). There was no significantly increased risk for cerebrovascular disease and exposure to inorganic dust, fumes or wood dust.

Conclusions

Occupational exposure to particulate air pollution, especially diesel exhaust, among construction workers increases the risk for ischaemic heart disease.There are a growing number of epidemiological studies showing that ambient exposure to particulate matter air pollution is a risk factor for cardiovascular disease.^1,2,3,4,5,6 However, regarding the risk for cerebrovascular disease and exposure to air pollution the literature is more scanty, and recent studies have shown conflicting results.^7,8,9 Occupationally exposed groups often have high exposure to particulate air pollution, such as silica dust, asbestos or welding fumes, but whether such dust exposure increases the risk for ischaemic heart disease or cerebrovascular disease is not clear.Our understanding of the underlying pathogenetic mechanisms remains limited, but it has been proposed that inhalation of small particles induces an inflammatory reaction in the airways and subsequent induction of systemic inflammation and coagulation disturbances.^10,11There is also increasing evidence of an association between ambient particulate air pollution and disturbances of the cardiac autonomic nervous system. Several groups have reported changes in heart rate variability associated with ambient particulate air pollution.^12,13,14,15 It has also been shown that acute exposure to particulate air pollution increases the risk of ST‐segment depression among subjects with coronary heart disease and also increases the discharges from pacemakers.^16,17A major methodological problem regarding epidemiological studies on occupationally exposed groups and the risk for cardiovascular diseases is healthy worker selection bias. Exposed cohorts are often compared with national populations, causing an underestimation of the “true” risk, because the general population includes sick and disabled people who are at increased risk of coronary heart disease. For the same reason, most cohort studies of workers who are occupationally exposed to particulate air pollution have also shown a decreased risk for ischaemic heart disease, as they often are compared with general populations. There are some exceptions,^18,19,20,21 but these studies do not make sufficient adjustments for confounders such as smoking, hypertension, sex and body mass index (BMI). However, there is a large case‐referent study with proper adjustments for confounders showing an increased risk for myocardial infarction among those occupationally exposed to combustion products.²²Consequently, to establish the effect of occupational exposure to particulate air pollution and risk for cardiovascular disease there is a need for a large cohort study which, in addition to exposure information, also includes information about relevant confounders. In the following, we report the results of a prospective cohort study of 176 309 Swedish male construction workers exposed to inorganic dust, wood dust, fumes and gases and 71 778 unexposed Swedish construction workers. The specific aim of the study was to elucidate whether occupational exposure to dust, fumes and gases increases the risk for death from cardiovascular disease—that is, ischaemic heart disease and cerebrovascular disease.     

Time-space modeling of journey-time exposure to traffic-related air pollution using GIS

Journey-time exposures represent an important, though as yet little-studied, component of human exposure to traffic-related air pollution, potentially with important health effects. Methods for assessing journey-time exposures, either as part of epidemiological studies or for policy assessment, are, however, poorly developed. This paper describes the development and testing of a GIS-based system for modeling human journey-time exposures to traffic-related air pollution: STEMS (Space-Time Exposure Modeling System). The model integrates data on source activity, pollutant dispersion, and travel behavior to derive individual- or group-level exposure measures to atmospheric pollution. The model, which is designed to simulate exposures of people as they move through a changing air pollution field, was developed, validated, and trialed in Northampton, UK. The system currently uses ArcInfo to couple four separate submodels: a source activity/emission model (SATURN), a proprietary atmospheric dispersion model (ADMS-Urban), an empirically derived background air pollution model, and a purposely designed time-activity-based exposure model (TOTEM). This paper describes the structure of the modeling system; presents results of field calibration, validation, and sensitivity analysis; and illustrates the use of the model to analyze journey-time exposures of schoolchildren.     

Reducing personal exposure to particulate air pollution improves cardiovascular health in patients with coronary heart disease

Background: Air pollution exposure increases cardiovascular morbidity and mortality and is a major global public health concern.Objectives: We investigated the benefits of reducing personal exposure to urban air pollution in patients with coronary heart disease.Methods: In an open randomized crossover trial, 98 patients with coronary heart disease walked on a predefined route in central Beijing, China, under different conditions: once while using a highly efficient face mask, and once while not using the mask. Symptoms, exercise, personal air pollution exposure, blood pressure, heart rate, and 12-lead electrocardiography were monitored throughout the 24-hr study period.Results: Ambient air pollutants were dominated by fine and ultrafine particulate matter (PM) that was present at high levels [74 μg/m³ for PM_2.5 (PM with aerodynamic diamater <2.5 µm)]. Consistent with traffic-derived sources, this PM contained organic carbon and polycyclic aromatic hydrocarbons and was highly oxidizing, generating large amounts of free radicals. The face mask was well tolerated, and its use was associated with decreased self-reported symptoms and reduced maximal ST segment depression (–142 vs. –156 μV, p = 0.046) over the 24-hr period. When the face mask was used during the prescribed walk, mean arterial pressure was lower (93 ± 10 vs. 96 ± 10 mmHg, p = 0.025) and heart rate variability increased (high-frequency power: 54 vs. 40 msec², p = 0.005; high-frequency normalized power: 23.5 vs. 20.5 msec, p = 0.001; root mean square successive differences: 16.7 vs. 14.8 msec, p = 0.007). However, mask use did not appear to influence heart rate or energy expenditure.Conclusions: Reducing personal exposure to air pollution using a highly efficient face mask appeared to reduce symptoms and improve a range of cardiovascular health measures in patients with coronary heart disease. Such interventions to reduce personal exposure to PM air pollution have the potential to reduce the incidence of cardiovascular events in this highly susceptible population.     

Occupational noise exposure and ischaemic heart disease mortality

Aims

To investigate the hypothesis that long term exposure to excessive noise can increase the risk of ischaemic heart disease.

Methods

A case‐control design, nested within a cohort of nuclear power workers employed at two sites in England over the period 1950–98, was used. Cases were men who died from ischaemic heart disease (ICD‐9: 410–414) aged 75 or under; each was matched to a surviving control of the nearest age who joined the same site at the same time. Personal noise exposure was assessed retrospectively for each man by hygienists using (1) company work histories, (2) noise survey records from 1965–98, and (3) judgements about likely use of hearing protection devices. Men were classified into four groups according to their cumulative exposure to noise, with men whose exposure at the company never exceeded 85dB(A) for at least one year being considered “unexposed”. Risks were compared via odds ratios (ORs) using conditional logistic regression and adjusted for systolic and diastolic blood pressure, height, BMI, and smoking, as measured at recruitment to the company.

Results

Analysis was based on 1101 case‐control pairs. There was little difference between the exposure groups at recruitment. There was no evidence of increased risk at site A: the ORs for ischaemic heart disease mortality among low, medium, and high exposure categories, compared to unexposed men, being 1.04, 1.00, and 0.77. The corresponding ORs (95% CIs) at site B were 1.15 (0.81–1.65) 1.45 (1.02–2.06), and 1.37 (0.96–1.96). When the comparison was confined to men with at least five years of employment, these dropped to 1.07 (0.64–1.77), 1.33 (0.88–2.01), and 1.21 (0.82–1.79) respectively.

Conclusions

The authors did not find statistically robust evidence of increased risk but the estimates at site B are consistent with those in a major cohort study. A strength of the present study is that the validity of noise estimation at site B has been demonstrated elsewhere.Excessive noise, at work or in the wider environment, has been linked with increased blood pressure and risk of ischaemic heart disease. A meta‐analysis¹ of nine cross sectional, “well matched” occupational studies concluded that an increase of 5dB(A) on the 8‐hour A‐weighted scale was associated with an increase of 0.51 mmHg (95% CI 0.01 to 1.00) in systolic blood pressure and of 14% (1%–29%) in the prevalence of hypertension. However, the authors noted that the results of the studies were inconsistent and there was some evidence of a publication bias against small negative studies. An earlier review of occupational exposure² concluded that there was considerable evidence that noise has short term effects on cardiovascular function and catecholamine levels but that, although there was a suggestion that chronic noise exposure might lead to sustained increases in blood pressure, there was a lack of convincing evidence that it caused cardiovascular disease. This was, in part, due to poor quantification of noise exposures and inadequate consideration of confounders.Another problem is that there have been few longitudinal studies: although some of the reviewed studies incorporated estimates of cumulative exposure, they were essentially cross sectional with the emphasis on prevalence. One longitudinal study³ of miners with high exposures who remained in work for at least 10 years found no evidence of a link with blood pressure. Lang et al⁴ found effects on blood pressure only among those exposed at work to levels above 85dB(A) for at least 20 years, but there may have been insufficient power at lower durations. Recently, the findings from a large cohort study⁵ of lumber mill workers, including workers with 20 or more years at levels over 85dB(A), have been reported. Among workers who terminated employment before the introduction of hearing protection devices, there was a exposure‐response relation between ischaemic heart disease mortality and years of exposure above 85dB(A), with a relative risk of 1.3 (p = 0.04) in those with 20 or more years'' exposure above 85dB(A) compared to less than three years, after adjustment for age, calendar year, and ethnicity. Twenty or more years above 95dB(A) produced an RR of 1.5 (95% CI 1.1 to 2.2).According to the Netherlands Health Council committee on Noise and Health, the “no adverse effect level” for industrial workers is at most 85dB(A) on the 8‐hour A‐weighted scale and, for general environmental noise, 70dB(A) on the 24‐hour L_dn scale.^6,7 A large cohort study⁸ of road traffic noise and incidence of ischaemic heart disease found no statistically significant effects, perhaps because the maximum L_dn was less than 70 dB(A). On the other hand, a recent, large case‐control study⁹ found an OR of 1.8 (95% CI 1.0 to 3.2) for myocardial infarction among men who lived for at least 10 years in homes with daytime traffic noise levels above 70dB(A). Other cross sectional studies^10,11 found a relation between aircraft noise, up to 76dB(A) on the L_dn scale, and use of medication for cardiovascular diseases.Given these results and the ubiquity of noise exposure, there is a need for further longitudinal studies. We report here on a longitudinal study of occupational exposure and mortality from ischaemic heart disease among a cohort of nuclear power workers in England.     

Medium-term exposure to traffic-related air pollution and markers of inflammation and endothelial function

Background

Exposure to traffic-related air pollution (TRAP) contributes to increased cardiovascular risk. Land-use regression models can improve exposure assessment for TRAP.

Objectives

We examined the association between medium-term concentrations of black carbon (BC) estimated by land-use regression and levels of soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1), both markers of inflammatory and endothelial response.

Methods

We studied 642 elderly men participating in the Veterans Administration (VA) Normative Aging Study with repeated measurements of sICAM-1 and sVCAM-1 during 1999–2008. Daily estimates of BC exposure at each geocoded participant address were derived using a validated spatiotemporal model and averaged to form 4-, 8-, and 12-week exposures. We used linear mixed models to estimate associations, controlling for confounders. We examined effect modification by statin use, obesity, and diabetes.

Results

We found statistically significant positive associations between BC and sICAM-1 for averages of 4, 8, and 12 weeks. An interquartile-range increase in 8-week BC exposure (0.30 μg/m³) was associated with a 1.58% increase in sICAM-1 (95% confidence interval, 0.18–3.00%). Overall associations between sVCAM-1 and BC exposures were suggestive but not statistically significant. We found a significant interaction with diabetes—where diabetics were more susceptible to the effect of BC—for both sICAM-1 and sVCAM-1. We also observed an interaction with statin use, which was statistically significant for sVCAM-1 and suggestive for sICAM-1. We found no evidence of an interaction with obesity.

Conclusion

Our results suggest that medium-term exposure to TRAP may induce an increased inflammatory/endothelial response, especially among diabetics and those not using statins.     

Association of long-term PM2.5 exposure with mortality using different air pollution exposure models: impacts in rural and urban California

Most PM2.5-associated mortality studies are not conducted in rural areas where mortality rates may differ when population characteristics, health care access, and PM2.5 composition differ. PM2.5-associated mortality was investigated in the elderly residing in rural–urban zip codes. Exposure (2000–2006) was estimated using different models and Poisson regression was performed using 2006 mortality data. PM2.5 models estimated comparable exposures, although subtle differences were observed in rate ratios (RR) within areas by health outcomes. Cardiovascular disease (CVD), ischemic heart disease (IHD), and cardiopulmonary disease (CPD), mortality was significantly associated with rural, urban, and statewide chronic PM2.5 exposures. We observed larger effect sizes in RRs for CVD, CPD, and all-cause (AC) with similar sizes for IHD mortality in rural areas compared to urban areas. PM2.5 was significantly associated with AC mortality in rural areas and statewide; however, in urban areas, only the most restrictive exposure model showed an association. Given the results seen, future mortality studies should consider adjusting for differences with rural–urban variables.     

PM2.5的污染特征及其生物效应研究进展

目的探讨维生素E(VE)对PM_2.5急性染毒致大鼠心血管损伤的干预作用。方法将36只雄性SD大鼠随机分为玉米油对照组(溶剂对照组)、VE对照组、PM_2.5染毒组(8.0 mg/kg,以体重计,下同)、PM_2.5+VE低、中、高给药组,剂量分别为15.0、30.0、60.0 mg/kg。VE给药组均经VE灌胃28 d后,气管滴注PM_2.5悬浊液染毒,隔天1次,共3次。末次染毒24 h后,腹主动脉取血,分析测定血清中白细胞介素1-β(IL-1β)、白细胞介素6(IL-6)、肿瘤坏死因子α(TNF-α)、超敏C反应蛋白(HS-CRP);谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA)、总超氧化物歧化酶(T-SOD)、血清一氧化氮(NO)、内皮素1(ET-1)和心肌缝隙连接蛋白(Cx43)的含量。结果溶剂对照组IL-1β、IL-6、TNF-α、HS-CRP、GSH、GSH-Px、MDA、T-SOD、NO、ET-1及Cx43分别为(68.73±6.21)μg/L、(15.86±0.45)μg/L、(41.12±7.66)μg/L、(1.29±0.26)μg/L、(15.30±2.52)μmol/L、(492.29±28.28)、(10.19±0.74)μmol/L、(272.98±8.59)U/mL,(3.22±0.22)μmol/L、(0.28±0.021)μg/L、(0.42±0.04)μg/L。PM_2.5染毒组IL-1β[(1 155.98±100.28)μg/L]、IL-6[(24.94±2.06)μg/L]、TNF-α[(821.45±14.26)μg/L ]、HS-CRP[(3.10±0.28)μg/L]、MDA[(15.88±1.41)μmol/L]和ET-1[(0.38±0.03)μg/L]的释放量升高,GSH[(4.62±0.37)μmol/L]、GSH-Px[(289.28±30.65)]、NO[(0.97±0.074)μmol/L]、Cx43[(0.26±0.10)μg/L和T-SOD[(239.26±4.97)U/mL]含量降低,差异有统计学意义(P < 0.05);与PM_2.5染毒组相比,VE给药组的各项指标均有一定缓解作用,差异均有统计学意义(P < 0.05),且存在一定的剂量反应关系。结论急性PM_2.5染毒可引起大鼠心血管损伤,导致炎性因子、氧化应激指标、血管内皮功能和心肌缝隙链接蛋白的变化,而VE喂饲对PM_2.5引起的大鼠急性肺部损伤具有一定的保护作用。     

Synergistic effects of traffic-related air pollution and exposure to violence on urban asthma etiology

BACKGROUND: Disproportionate life stress and consequent physiologic alteration (i.e., immune dysregulation) has been proposed as a major pathway linking socioeconomic position, environmental exposures, and health disparities. Asthma, for example, disproportionately affects lower-income urban communities, where air pollution and social stressors may be elevated. OBJECTIVES: We aimed to examine the role of exposure to violence (ETV), as a chronic stressor, in altering susceptibility to traffic-related air pollution in asthma etiology. METHODS: We developed geographic information systems (GIS)-based models to retrospectively estimate residential exposures to traffic-related pollution for 413 children in a community-based pregnancy cohort, recruited in East Boston, Massachusetts, between 1987 and 1993, using monthly nitrogen dioxide measurements for 13 sites over 18 years. We merged pollution estimates with questionnaire data on lifetime ETV and examined the effects of both on childhood asthma etiology. RESULTS: Correcting for potential confounders, we found an elevated risk of asthma with a 1-SD (4.3 ppb) increase in NO(2) exposure solely among children with above-median ETV [odds ratio (OR) = 1.63; 95% confidence interval (CI), 1.14-2.33)]. Among children always living in the same community, with lesser exposure measurement error, this association was magnified (OR = 2.40; 95% CI, 1.48-3.88). Of multiple exposure periods, year-of-diagnosis NO(2) was most predictive of asthma outcomes. CONCLUSIONS: We found an association between traffic-related air pollution and asthma solely among urban children exposed to violence. Future studies should consider socially patterned susceptibility, common spatial distributions of social and physical environmental factors, and potential synergies among these. Prospective assessment of physical and social exposures may help determine causal pathways and critical exposure periods.     

Association between maternal exposure to ambient air pollution and congenital heart disease: A register-based spatiotemporal analysis

Recent studies have linked maternal exposure to air pollution with a range of adverse pregnancy outcomes. However, the available evidence linking this exposure to congenital anomalies is still limited and controversial. The present case-control study tested the hypothesis that maternal exposure to ambient black smoke and sulfur dioxide is a risk factor for the occurrence of congenital heart disease. The authors used registry-based data on congenital heart disease for the population of the northeast of England in 1985-1996. A 2-stage spatiotemporal model was developed to predict weekly black smoke and sulfur dioxide levels at each maternal place of residence. Controls were frequency-matched to cases by year of birth (control-to-case ratio of 4:1). Two sets of analyses were performed, using predicted mean values of exposure and 1,000 simulated scenarios of exposure. The analyses were adjusted for birth year, socioeconomic status, infant sex, season of conception, and degree of urbanity. The authors found a weak association between maternal exposure to black smoke and congenital malformations of cardiac chambers and connections only when using exposure as a continuous variable. When the authors used quartiles of exposure, odds ratios did not show a dose-response relation for consecutive quartiles. For sulfur dioxide, the results were not indicative of any association.     

Cardio-respiratory morbidity and long-term exposure to particulate air pollution

To explore the long-term influence of particulate air pollution on cardio-respiratory morbidity in the UK, a cross-sectional postal survey was conducted. Women were randomly selected from the electoral rolls of 11 wards in which Black Smoke measurements had been collected over at least 30 years. Our analyses included 1166 women aged 45 years or older who had lived within 5 miles of their current address for at least 30 years. After adjustment for potential confounders there was no clear increase in prevalence of productive cough or medically diagnosed ischaemic heart disease with long-term residence in places with higher levels of particulate pollution. The prevalence of asthma was lower in wards with the highest Black Smoke measurements (prevalence ratio 0.7, 95% CI 0.5 - 1.0). Our findings provide no indication that prolonged residence in places with relatively high levels of particulate pollution causes an important increase in cardio-respiratory morbidity. This is in contrast to observations in US studies. In view of this discordance, there is a need for further evaluation of the long-term impact of particulate pollution on health in the UK.     

Long-term exposure to traffic-related air pollution associated with blood pressure and self-reported hypertension in a Danish cohort

Background: Short-term exposure to air pollution has been associated with changes in blood pressure (BP) and emergency department visits for hypertension, but little is known about the effects of long-term exposure to traffic-related air pollution on BP and hypertension.Objectives: We studied whether long-term exposure to air pollution is associated with BP and hypertension.Methods: In 1993–1997, 57,053 participants 50–64 years of age were enrolled in a population-based cohort study. Systolic and diastolic BP (SBP and DBP, respectively) were measured at enrollment. Self-reported incident hypertension during a mean follow-up of 5.3 years was assessed by questionnaire. We used a validated dispersion model to estimate residential long-term nitrogen oxides (NO_x), a marker of traffic-related air pollution, for the 1- and 5-year periods prior to enrollment and before a diagnosis of hypertension. We conducted a cross-sectional analysis of associations between air pollution and BP at enrollment with linear regression, adjusting for traffic noise, measured short-term NO_x, temperature, relative humidity, and potential lifestyle confounders (n = 44,436). We analyzed incident hypertension with Cox regression, adjusting for traffic noise and potential confounders.Results: A doubling of NO_x exposure during 1- and 5-year periods preceding enrollment was associated with 0.53-mmHg decreases [95% confidence interval (CI): –0.88, –0.19 mmHg] and 0.50-mmHg decreases (95% CI: –0.84, –0.16 mmHg) in SBP, respectively. Long-term exposure also was associated with a lower prevalence of baseline self-reported hypertension (per doubling of 5-year mean NO_x: odds ratio = 0.96; 95% CI: 0.91, 1.00), whereas long-term NO_x exposure was not associated with incident self-reported hypertension during follow-up.Conclusions: Long-term exposure to traffic-related air pollution was associated with a slightly lower prevalence of BP at baseline, but was not associated with incident hypertension.     

孕期环境空气污染物暴露和先天性心脏病关系的Meta分析

目的 探讨孕期空气污染物暴露与先天性心脏病（先心病）发生的关系,为先心病的一级预防提供循证医学证据。方法 收集国内外发表的有关孕期空气污染物暴露与先心病有关的流行病学研究文章,对连续性增长和高浓度对比低浓度的污染物与先心病亚型的关系效应值分别进行合并。使用Stata 12.0软件对文献进行Meta分析。结果 共纳入20篇英文文献。Meta分析结果显示,CO暴露增加法洛四联症的发生风险（高浓度对比低浓度OR=1.22,95%CI：1.03~1.44））;NO₂暴露增加主动脉缩窄的发生风险（浓度每升高10 mm³/m³ OR=1.01,95%CI：1.01~1.20）;O₃暴露增加房间隔缺损的发生风险（浓度每升高10 mm³/m³ OR=1.14,95%CI：1.03~1.26）;PM₁₀暴露增加房间隔缺损的发生风险（浓度每升高10 μg/m³ OR=1.10,95%CI：1.03~1.19）。此外,还发现CO暴露和房间隔缺损的发生,PM₁₀暴露和室间隔缺损的发生存在负相关。结论 孕期暴露于空气污染物CO、O₃、NO₂、PM₁₀可能会增加先心病的发生风险。     

Traffic-related air pollution in relation to incidence and prognosis of coronary heart disease

BACKGROUND: Long-term air pollution exposure is associated with increased mortality, but the association with incidence of fatal and nonfatal coronary heart disease is less certain. Moreover, it is unknown how chronic exposure to air pollution affects prognosis among survivors of a first coronary event. This study evaluated the association between long-term traffic-related air pollution exposure and incidence of nonfatal and fatal coronary events, as well as subsequent hospital readmission and mortality among myocardial infarction survivors. METHODS: The study population comprised all residents of Rome aged 35-84 years during the period 1998-2000. Residential nitrogen dioxide (NO2) exposure as a marker of traffic pollution was assessed by a land-use regression model in 1995-1996 (R = 0.69). A total of 11,167 incident coronary events were observed (4654 fatal, including 3598 out-of-hospital coronary deaths, and 6513 nonfatal). The cohort of 6513 survivors was followed 4.0-7.5 years for readmission or mortality, starting 28 days from the date of first event. Relative risks per 10 mug/m of NO2 exposure, adjusted for age, sex, and socioeconomic status, were calculated by Poisson regression (population-based incidence) and Cox regression (cohort analysis). RESULTS: The relative risk for incidence in coronary events per 10 mug/m of NO2 was 1.03 (95% confidence interval = 1.00-1.07). Stronger associations were found for fatal cases (1.07; 1.02-1.12) and out-of-hospital deaths (1.08; 1.02-1.13). Using NO2 exposure at the time of the first event, there was no association of air pollution exposure with either subsequent hospital readmission or mortality among survivors of the first coronary event. CONCLUSIONS: Long-term air pollution exposure increases the risk of coronary heart disease, particularly fatal events. Hospital readmission or subsequent mortality among survivors was not associated with traffic air pollution.     

The temporal pattern of respiratory and heart disease mortality in response to air pollution

Short-term changes in ambient particulate matter with aerodynamic diameters < 10 micro m (PM10) have been associated with short-term fluctuations in mortality or morbidity in many studies. In this study, we tested whether those deaths are just advanced by a few days or weeks using a multicity hierarchical modeling approach for all-cause, respiratory, and cardiovascular deaths, for all ages and stratifying by age groups, within the APHEA-2 (Air Pollution and Health: A European Approach) project. We fit a Poisson regression and used an unconstrained distributed lag to model the effect of PM10 exposure on deaths up to 40 days after the exposure. In baseline models using PM10 the day of and day before the death, we found that the overall PM10 effect (per 10 micro g/m3) was 0.74% [95% confidence interval (95% CI), -0.17 to 1.66] for respiratory deaths and 0.69% (95% CI, 0.31-1.08) for cardiovascular deaths. In unrestricted distributed lag models, the effect estimates increased to 4.2% (95% CI, 1.08-7.42) for respiratory deaths and to 1.97% (95% CI, 1.38-2.55) for cardiovascular deaths. Our study confirms that most of the effect of air pollution is not simply advanced by a few weeks and that effects persist for more than a month after exposure. The effect size estimate for PM10 doubles when we considered longer-term effects for all deaths and for cardiovascular deaths and becomes five times higher for respiratory deaths. We found similar effects when stratifying by age groups. These larger effects are important for risk assessment.     

Estimation of long-term average exposure to outdoor air pollution for a cohort study on mortality.

Recent prospective cohort studies have suggested that long-term exposure to low levels of particulate matter (PM) air pollution is associated with increased mortality due to, especially, cardio-pulmonary disease. Exposure to ambient air pollution was estimated mostly as city average concentrations, assuming homogenous exposure within the city. We used an ongoing cohort study - The Netherlands Cohort Study (NLCS) on diet and cancer - to investigate the relationship between traffic-related air pollution and mortality. The baseline data collection took place in 1986. A study was conducted to develop methods for exposure assessment and evaluate the contrast in exposure to air pollution within the cohort. Assessment of long-term exposure to two traffic-related air pollutants, Black Smoke (BS) and Nitrogen Dioxide (NO(2)), consisted of separate estimation of regional background, urban background, and local traffic contributions at the home address. Interpolation of concentration data from a routine monitoring network was used to estimate the regional background concentration. A regression model relating degree of urbanization to air pollution was used to allow for differences between different towns/neighborhoods of cities. Distance to major roads was calculated to characterize local traffic contributions, using a Geographic Information System (GIS). Interpolation resulted in reasonably precise regional background estimation when distant sites were not used and distance squared was used as the weight. Cross-validation showed that prediction errors were about 15% of the range in regional background concentration. Urban and local scales contributed significantly to the contrast within the cohort. Prediction errors for estimating the urban background were about 25% of the range in background concentrations. When the developed model was applied to the study cohort, there was substantial contrast in estimated exposure to BS and NO(2). About 90% of the study population lived 10 years or more at its 1986 home address - supporting the use of the estimated concentration at the 1986 address as a relevant exposure variable.