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1.
BackgroundEpidemiological studies have associated long-term exposure to ambient particulate matter with increased mortality from cardiovascular and respiratory disorders. Systemic inflammation is a plausible biological mechanism behind this association. However, it is unclear how the chemical composition of PM affects inflammatory responses.ObjectivesTo investigate the association between long-term exposure to elemental components of PM and the inflammatory blood markers high-sensitivity C-reactive protein (hsCRP) and fibrinogen as part of the European ESCAPE and TRANSPHORM multi-center projects.MethodsIn total, 21,558 hsCRP measurements and 17,428 fibrinogen measurements from cross-sections of five and four cohort studies were available, respectively. Residential long-term concentrations of particulate matter < 10 μm (PM10) and < 2.5 μm (PM2.5) in diameter and selected elemental components (copper, iron, potassium, nickel, sulfur, silicon, vanadium, zinc) were estimated based on land-use regression models. Associations between components and inflammatory markers were estimated using linear regression models for each cohort separately. Cohort-specific results were combined using random effects meta-analysis. As a sensitivity analysis the models were additionally adjusted for PM mass.ResultsA 5 ng/m3 increase in PM2.5 copper and a 500 ng/m3 increase in PM10 iron were associated with a 6.3% [0.7; 12.3%] and 3.6% [0.3; 7.1%] increase in hsCRP, respectively. These associations between components and fibrinogen were slightly weaker. A 10 ng/m3 increase in PM2.5 zinc was associated with a 1.2% [0.1; 2.4%] increase in fibrinogen; confidence intervals widened when additionally adjusting for PM2.5.ConclusionsLong-term exposure to transition metals within ambient particulate matter, originating from traffic and industry, may be related to chronic systemic inflammation providing a link to long-term health effects of particulate matter.  相似文献   

2.
Indoor air pollution is closely related to children's health. Polybrominated diphenyl ethers (PBDEs) and dechlorane plus (DP) transmitted through indoor PM2.5 and dust, along with carbonyl compounds and black carbon (BC) aerosol were analysed in five Hong Kong kindergartens. The results showed that 60% of the median PM2.5 levels (1.3 × 101 to 2.9 × 101 μg/m3 for indoor; 9.5 to 8.8 × 101 μg/m3 for outdoor) in the five kindergartens were higher than the guidelines set by the World Health Organization (2.5 × 101 μg/m3). Indoor PM2.5 mass concentrations were correlated with outdoor PM2.5 in four of the kindergartens. The PBDEs (0.10–0.64 ng/m3 in PM2.5; 0.30–2.0 × 102 ng/g in dust) and DP (0.05–0.10 ng/m3 in PM2.5; 1.3–8.7 ng/g in dust) were detected in 100% of the PM2.5 and dust samples. Fire retardant levels in the air were not correlated with the levels of dust in this study. The median BC concentrations varied by > 7-fold from 8.8 × 102 ng/m 3 to 6.7 × 103 ng/m 3 and cooking events might have caused BC concentrations to rise both indoors and outdoors. The total concentrations of 16 carbonyls ranged from 4.7 × 101 μg/m3 to 9.3 × 101 μg/m3 indoors and from 1.9 × 101 μg/m3 to 4.3 × 101 μg/m3 outdoors, whilst formaldehyde was the most abundant air carbonyl. Indoor carbonyl concentrations were correlated with outdoor carbonyls in three kindergartens. The health risk assessment showed that hazard indexes (HIs) HIs of non-cancer risks from PBDEs and DPs were all lower than 0.08, whilst non-cancer HIs of carbonyl compounds ranged from 0.77 to 1.85 indoors and from 0.50 to 0.97 outdoors. The human intake of PBDEs and DP through inhalation of PM2.5 accounted for 78% to 92% of the total intake. The cancer hazard quotients (HQs) of formaldehyde ranged from 4.5E  05 to 2.1E  04 indoors and from 1.9E  05 to 6.2E  05 outdoors. In general, the indoor air pollution in the five Hong Kong kindergartens might present adverse effects to children, although different schools showed distinct pollution levels, so indoor air quality might be improved through artificial measures. The data will be useful to developing a feasible management protocol for indoor environments.  相似文献   

3.
RationaleExposure to ambient particulate matter (PM) and ozone has been associated with cardiovascular disease (CVD). However, the mechanisms linking PM and ozone exposure to CVD remain poorly understood.ObjectiveThis study explored associations between short-term exposures to PM with a diameter < 2.5 μm (PM2.5) and ozone with plasma metabolite concentrations.Methods and resultsWe used cross-sectional data from a cardiac catheterization cohort at Duke University, North Carolina (NC), USA, accumulated between 2001 and 2007. Amino acids, acylcarnitines, ketones and total non-esterified fatty acid plasma concentrations were determined in fasting samples. Daily concentrations of PM2.5 and ozone were obtained from a Bayesian space-time hierarchical model, matched to each patient's residential address. Ten metabolites were selected for the analysis based on quality criteria and cluster analysis. Associations between metabolites and PM2.5 or ozone were analyzed using linear regression models adjusting for long-term trend and seasonality, calendar effects, meteorological parameters, and participant characteristics.We found delayed associations between PM2.5 or ozone and changes in metabolite levels of the glycine-ornithine-arginine metabolic axis and incomplete fatty acid oxidation associated with mitochondrial dysfunction. The strongest association was seen for an increase of 8.1 μg/m3 in PM2.5 with a lag of one day and decreased mean glycine concentrations (− 2.5% [95% confidence interval: − 3.8%; − 1.2%]).ConclusionsShort-term exposures to ambient PM2.5 and ozone is associated with changes in plasma concentrations of metabolites in a cohort of cardiac catheterization patients. Our findings might help to understand the link between air pollution and cardiovascular disease.  相似文献   

4.
IntroductionLong-term exposure to air pollution (AP) has been shown to have an impact on mortality in numerous countries, but since 2005 no data exists for France.ObjectivesWe analyzed the association between long-term exposure to air pollution and mortality at the individual level in a large French cohort followed from 1989 to 2013.MethodsThe study sample consisted of 20,327 adults working at the French national electricity and gas company EDF-GDF. Annual exposure to PM10, PM10–2.5, PM2.5, NO2, O3, SO2, and benzene was assessed for the place of residence of participants using a chemistry-transport model and taking residential history into account. Hazard ratios were estimated using a Cox proportional-hazards regression model, adjusted for selected individual and contextual risk factors. Hazard ratios were computed for an interquartile range (IQR) increase in air pollutant concentrations.ResultsThe cohort recorded 1967 non-accidental deaths. Long-term exposures to baseline PM2.5, PM10-25, NO2 and benzene were associated with an increase in non-accidental mortality (Hazard Ratio, HR = 1.09; 95% CI: 0.99, 1.20 per 5.9 μg/m3, PM10-25; HR = 1.09;95% CI: 1.04, 1.15 per 2.2 μg/m3, NO2: HR = 1.14; 95% CI: 0.99, 1.31 per 19.3 μg/m3 and benzene: HR = 1.10; 95% CI: 1.00, 1.22 per 1.7 μg/m3).The strongest association was found for PM10: HR = 1.14; 95% CI: 1.05, 1.25 per 7.8 μg/m3. PM10, PM10-25 and SO2 were associated with non-accidental mortality when using time varying exposure. No significant associations were observed between air pollution and cardiovascular and respiratory mortality.ConclusionLong-term exposure to fine particles, nitrogen dioxide, sulfur dioxide and benzene is associated with an increased risk of non-accidental mortality in France. Our results strengthen existing evidence that outdoor air pollution is a significant environmental risk factor for mortality. Due to the limited sample size and the nature of our study (occupational), further investigations are needed in France with a larger representative population sample.  相似文献   

5.
The effects of air pollution on health have been studied worldwide. Given that air pollution triggers oxidative stress and inflammation, it is plausible that high levels of air pollutants cause higher number of hospitalisations. This study aimed to assess the impact of air pollution on the emergency hospitalisation for respiratory disease in Rio de Janeiro, Brazil. The study was divided in two parts: Part I specifically addressing the air pollution assessment and Part II addressing the health assessment. Accordingly, this Part II aimed to estimate the association between the concentrations of PM10, SO2 and CO observed in Rio de Janeiro and the number of emergency hospitalisations at a central hospital due to respiratory diseases. The pollutant concentrations were measured at two different sites in Rio de Janeiro, but the excess relative risks were calculated based on the concentrations observed at one of the sites, where limits were generally exceeded more frequently, between September 2000 and December 2005. A time series analysis was performed using the number of hospitalisations, divided in three categories (children until 1 year old, children aged between 1 and 5 years old and elderly with 65 years old or more) as independent variable, the concentrations of pollutants as dependent variables and temperature, relative humidity, long term trend, and seasonality as confounders. Data were analysed using generalised additive models with smoothing for some of the dependent variables. Results showed an excess risk of hospitalisation for respiratory disease higher than 2% per 10 μg m 3 increase in PM10 concentrations for children under 5 years old, of 2% per 10 μg m 3 increase in SO2 for elderly above 65 years old and around 0.1% per 10 μg m 3 increase in CO for children under 1 year and elderly. Other studies have found associations that are in agreement with the results achieved in this study.The study suggests that the ambient levels of air pollutants experienced in Rio de Janeiro between 2000 and 2005 were linked to the number of hospitalisations for respiratory diseases among children and elderly.  相似文献   

6.
Primary Biologic Atmospheric Particles (PBAPs) constitute an interesting and poorly investigated component of the atmospheric aerosol. We have developed and validated a method for evaluating the contribution of overall PBAPs to the mass concentration of atmospheric particulate matter (PM). The method is based on PM sampling on polycarbonate filters, staining of the collected particles with propidium iodide, observation at epifluorescence microscope and calculation of the bioaerosol mass using a digital image analysis software. The method has been also adapted to the observation and quantification of size-segregated aerosol samples collected by multi-stage impactors.Each step of the procedure has been individually validated. The relative repeatability of the method, calculated on 10 pairs of atmospheric PM samples collected side-by-side, was 16%.The method has been applied to real atmospheric samples collected in the vicinity of Rome, Italy. Size distribution measurements revealed that PBAPs was mainly in the coarse fraction of PM, with maxima in the range 5.6–10 μm. 24-h samples collected during different period of the year have shown that the concentration of bioaerosol was in the range 0.18–5.3 μg m 3 (N = 20), with a contribution to the organic matter in PM10 in the range 0.5–31% and to the total mass concentration of PM10 in the range 0.3–18%.The possibility to determine the concentration of total PBAPs in PM opens up interesting perspectives in terms of studying the health effects of these components and of increasing our knowledge about the composition of the organic fraction of the atmospheric aerosol.  相似文献   

7.
Cooking and heating with coal and biomass is the main source of household air pollution in China and a leading contributor to disease burden. As part of a baseline assessment for a household energy intervention program, we enrolled 205 adult women cooking with biomass fuels in Sichuan, China and measured their 48-h personal exposure to fine particulate matter (PM2.5) and carbon monoxide (CO) in winter and summer. We also measured the indoor 48-h PM2.5 concentrations in their homes and conducted outdoor PM2.5 measurements during 101 (74) days in summer (winter). Indoor concentrations of CO and nitrogen oxides (NO, NO2) were measured over 48-h in a subset of ~ 80 homes. Women's geometric mean 48-h exposure to PM2.5 was 80 μg/m3 (95% CI: 74, 87) in summer and twice as high in winter (169 μg/m3 (95% CI: 150, 190), with similar seasonal trends for indoor PM2.5 concentrations (winter: 252 μg/m3; 95% CI: 215, 295; summer: 101 μg/m3; 95% CI: 91, 112). We found a moderately strong relationship between indoor PM2.5 and CO (r = 0.60, 95% CI: 0.46, 0.72), and a weak correlation between personal PM2.5 and CO (r = 0.41, 95% CI: − 0.02, 0.71). NO2/NO ratios were higher in summer (range: 0.01 to 0.68) than in winter (range: 0 to 0.11), suggesting outdoor formation of NO2 via reaction of NO with ozone is a more important source of NO2 than biomass combustion indoors. The predictors of women's personal exposure to PM2.5 differed by season. In winter, our results show that primary heating with a low-polluting fuel (i.e., electric stove or wood-charcoal) and more frequent kitchen ventilation could reduce personal PM2.5 exposures. In summer, primary use of a gaseous fuel or electricity for cooking and reducing exposure to outdoor PM2.5 would likely have the greatest impacts on personal PM2.5 exposure.  相似文献   

8.
In India, more than a billion population is at risk of exposure to ambient fine particulate matter (PM2.5) concentration exceeding World Health Organization air quality guideline, posing a serious threat to health. Cause-specific premature death from ambient PM2.5 exposure is poorly known for India. Here we develop a non-linear power law (NLP) function to estimate the relative risk associated with ambient PM2.5 exposure using satellite-based PM2.5 concentration (2001  2010) that is bias-corrected against coincident direct measurements. We show that estimate of annual premature death in India is lower by 14.7% (19.2%) using NLP (integrated exposure risk function, IER) for assumption of uniform baseline mortality across India (as considered in the global burden of disease study) relative to the estimate obtained by adjusting for state-specific baseline mortality using GDP as a proxy. 486,100 (811,000) annual premature death in India is estimated using NLP (IER) risk functions after baseline mortality adjustment. 54.5% of premature death estimated using NLP risk function is attributed to chronic obstructive pulmonary disease (COPD), 24.0% to ischemic heart disease (IHD), 18.5% to stroke and the remaining 3.0% to lung cancer (LC). 44,900 (5900–173,300) less premature death is expected annually, if India achieves its present annual air quality target of 40 μg m 3. Our results identify the worst affected districts in terms of ambient PM2.5 exposure and resulting annual premature death and call for initiation of long-term measures through a systematic framework of pollution and health data archive.  相似文献   

9.
BackgroundEvidence on health effects of ultrafine particles (UFP) is still limited as they are usually not monitored routinely. The few epidemiological studies on UFP and (cause-specific) mortality so far have reported inconsistent results.ObjectivesThe main objective of the UFIREG project was to investigate the short-term associations between UFP and fine particulate matter (PM) < 2.5 μm (PM2.5) and daily (cause-specific) mortality in five European Cities. We also examined the effects of PM < 10 μm (PM10) and coarse particles (PM2.5–10).MethodsUFP (20–100 nm), PM and meteorological data were measured in Dresden and Augsburg (Germany), Prague (Czech Republic), Ljubljana (Slovenia) and Chernivtsi (Ukraine). Daily counts of natural and cardio-respiratory mortality were collected for all five cities. Depending on data availability, the following study periods were chosen: Augsburg and Dresden 2011–2012, Ljubljana and Prague 2012–2013, Chernivtsi 2013–March 2014. The associations between air pollutants and health outcomes were assessed using confounder-adjusted Poisson regression models examining single (lag 0–lag 5) and cumulative lags (lag 0–1, lag 2–5, and lag 0–5). City-specific estimates were pooled using meta-analyses methods.ResultsResults indicated a delayed and prolonged association between UFP and respiratory mortality (9.9% [95%-confidence interval: − 6.3%; 28.8%] increase in association with a 6-day average increase of 2750 particles/cm3 (average interquartile range across all cities)). Cardiovascular mortality increased by 3.0% [− 2.7%; 9.1%] and 4.1% [0.4%; 8.0%] in association with a 12.4 μg/m3 and 4.7 μg/m3 increase in the PM2.5- and PM2.5–10-averages of lag 2–5.ConclusionsWe observed positive but not statistically significant associations between prolonged exposures to UFP and respiratory mortality, which were independent of particle mass exposures. Further multi-centre studies are needed investigating several years to produce more precise estimates on health effects of UFP.  相似文献   

10.
Burning candles and incense generate particulate matter (PM) that produces poor indoor air quality and may cause human pulmonary problems. This study physically characterised combustion particles collected in a church during services. In addition, the emissions from five types of candles and two types of incense were investigated using a combustion chamber. The plasmid scission assay was used to determine the oxidative capacities of these church particles. The corresponding risk factor (CRf) was derived from the emission factor (Ef) and the oxidative DNA damage, and used to evaluate the relative respiratory exposure risks. Real-time PM measurements in the church during candle–incense burning services showed that the levels (91.6 μg/m3 for PM10; 38.9 μg/m3 for PM2.5) exceeded the European Union (EU) air quality guidelines. The combustion chamber testing, using the same environmental conditions, showed that the incense Ef for both PM10 (490.6–587.9 mg/g) and PM2.5 (290.1–417.2 mg/g) exceeded that of candles; particularly the PM2.5 emissions. These CRf results suggested that the exposure to significant amounts of incense PM could result in a higher risk of oxidative DNA adducts (27.4–32.8 times) than tobacco PM. The generation and subsequent inhalation of PM during church activities may therefore pose significant risks in terms of respiratory health effects.  相似文献   

11.
To investigate the assumed association between indoor air pollution with monoterpenes (MTps) and the internal MTp exposure of occupants, a comparative study was performed in daycare centers in two federal states of Germany. Three well-known monoterpenoid air pollutants, viz. α-pinene (αPN), Δ3-carene (CRN), and R-limonene (LMN), were measured in indoor air in 45 daycare centers. Additionally, urine samples of 222 children visiting these facilities were collected in the evening after a full-day stay. Altogether 11 MTp metabolites were analyzed in the urine samples using a novel highly sensitive and selective gas chromatographic–tandem-mass spectrometric procedure. The medians (95th percentiles) of the MTp levels in indoor air were 9.1 μg m 3 (94 μg m 3) for LMN, 2.6 μg m 3 (13 μg m 3) for αPN, and < 1.0 μg m 3 (3.2 μg m 3) for CRN. None of the day care centers exceeded the German health precaution or hazard guide value. In spite of the low MTp air exposure, the urine analyses revealed an exposure to the three monoterpenes in almost all children. The median levels of MTp metabolites in urine were 0.11 mg L 1 for LMN-8,9-OH, 0.10 mg L 1 for LMN-1,2-OH, 49 μg L 1 for PA, 2.9 μg L 1 for POH, 5.2 μg L 1 for tCAR, and 4.1 μg L 1 for cCAR (LMN metabolites), 7.2 μg L 1 for MYR, 19 μg L 1 for tVER, and 19 μg L 1 for cVER (αPN metabolites), as well as 8.2 μg L 1 for CRN-10-COOH (CRN metabolite). Statistically significant and strong correlations among the urinary metabolites of each MTp were found. Moreover, statistical associations between LMN metabolites and the LMN indoor air levels were revealed. However, the weakness of the associations indicates a considerable impact of other MTp sources, e.g. diet and consumer products, on the internal exposure.  相似文献   

12.
Levels of eight potentially toxic heavy metals in indoor dust from homes and offices in Istanbul were investigated. The concentrations of heavy metals in indoor dust from homes + office ranged from 62 to 1800 μg g 1 for Cu, 3–200 μg g 1 for Pb, 0.4–20 μg g 1 for Cd, 210–2800 μg g 1 for Zn, 2.8–460 μg g 1 for Cr, 8–1300 μg g 1 for Mn, 2.4–25 μg g 1 for Co, 120–2600 μg g 1 for Ni. Results of the study were comparable to other studies conducted on indoor dust and street dust from a variety of cities globally. Considering only ingestion + inhalation, the carcinogenic risk level of Cr for adults and children (3.7 × 10 5 and 2.7 × 10 5) in Istanbul was in the range of EPA's safe limits (1 × 10 6 and 1 × 10 4), indicating that cancer risk of Cr due to exposure to indoor dust in Istanbul can be acceptable. According to calculated Hazard Quotient (HQ), for non-cancer effects, the ingestion of indoor dust appears to be the major route of exposure to the indoor dust that results in a higher risk for heavy metals, followed by dermal contact and inhalation pathways. However, compared to ingestion and dermal contact exposure, exposure through inhalation is almost negligible. Hazard Index (HI) values for all studied elements were lower than safe limit of 1 and this result suggested that none of the population groups would likely to experience potential health risk due to exposure to heavy metals from indoor dust in the study area.  相似文献   

13.
BackgroundResearchers and policymakers are increasingly focused on combined exposures to social and environmental stressors, especially given how often these stressors tend to co-locate. Such exposures are equally relevant in urban and rural areas and may accrue disproportionately to particular communities or specific subpopulations.ObjectivesTo estimate relationships between racial isolation (RI), a measure of the extent to which minority racial/ethnic group members are exposed to only one another, and long-term particulate matter with an aerodynamic diameter of < 2.5 μ (PM2.5) and ozone (O3) levels in urban and nonurban areas of the eastern two-thirds of the US.MethodsLong-term (5 year average) census tract-level PM2.5 and O3 concentrations were calculated using output from a downscaler model (2002–2006). The downscaler uses a linear regression with additive and multiplicative bias coefficients to relate ambient monitoring data with gridded output from the Community Multi-scale Air Quality (CMAQ) model. A local, spatial measure of RI was calculated at the tract level, and tracts were classified by urbanicity, RI, and geographic region. We examined differences in estimated pollutant exposures by RI, urbanicity, and demographic subgroup (e.g., race/ethnicity, education, socioeconomic status, age), and used linear models to estimate associations between RI and air pollution levels in urban, suburban, and rural tracts.ResultsHigh RI tracts (≥ 80th percentile) had higher average PM2.5 levels in each category of urbanicity compared to low RI tracts (< 20th percentile), with the exception of the rural West. Patterns in O3 levels by urbanicity and RI differed by region. Linear models indicated that PM2.5 concentrations were significantly and positively associated with RI. The largest association between PM2.5 and RI was observed in the rural Midwest, where a one quintile increase in RI was associated with a 0.90 μg/m3 (95% confidence interval: 0.83, 0.99 μg/m3) increase in PM2.5 concentration. Associations between O3 and RI in the Northeast, Midwest and West were positive and highest in suburban and rural tracts, even after controlling for potential confounders such as percentage in poverty.ConclusionRI is associated with higher 5 year estimated PM2.5 concentrations in urban, suburban, and rural census tracts, adding to evidence that segregation is broadly associated with disparate air pollution exposures. Disproportionate burdens to adverse exposures such as air pollution may be a pathway to racial/ethnic disparities in health.  相似文献   

14.
Organosiloxanes are widely used in the formulation of a broad range of cosmetic and personal care products (PCPs), including creams and lotions, bath soaps, shampoo and hair care products to soften, smooth, and moisten. In fact, the intensive and widespread use of organosiloxanes combined with their lipophilic nature, makes them interesting targets for future research, particularly in the toxicology area.This study focused on determining the concentration levels of these compounds in the bestselling brands of PCPs in the Oporto region (Portugal), allowing the estimation of dermal and inhalation exposure to siloxanes and the evaluation of the quantities released to the environment “down-the-drain” and to air. To accomplish this task, a QuEChERS technique (“Quick, Easy, Cheap, Effective, Rugged, and Safe”) was employed to extract the siloxanes from the target PCPs, which has never been tested before. The resulting extract was analysed by gas chromatography–mass spectrometry (GC–MS). The limits of detection varied between 0.17 (L2) and 3.75 ng g 1 (L5), being much lower than any values reported in the literature for this kind of products. In general, satisfactory precision (< 10%) and accuracy values (average recovery of 84%) were obtained.123 PCPs were analysed (moisturizers, deodorants, body and hair washes, toilet soaps, toothpastes and shaving products) and volatile methylsiloxanes were detected in 96% of the samples, in concentrations between 0.003 μg g 1 and 1203 μg g 1. Shampoo exhibited the highest concentration for cyclic and aftershaves for linear siloxanes. Combining these results with the daily usage amounts, an average daily dermal exposure of 25.04 μg kgbw 1 day 1 for adults and 0.35 μg kgbw 1 day 1 for baby/children was estimated. The main contributors for adult dermal exposure were body moisturizers, followed by facial creams and aftershaves, while for babies/children were body moisturizers, followed by shower gel and shampoo. Similarly, the average daily inhalation exposure was also estimated. Values of 1.56 μg kgbw 1 day 1 for adults and 0.03 μg kgbw 1 day 1 for babies/children were calculated. An estimate of the siloxanes amount released “down-the-drain” into the sewage systems through the use of toiletries was also performed. An emission per capita between 49.25 and 9574 μg day 1 (mean: 1817 μg day 1) is expected and shampoo and shower gel presented the higher mean total values (1008 μg day 1 and 473.3 μg day 1, respectively). In the worst-case scenario, D5 and D3 were the predominant siloxanes in the effluents with 3336 μg day 1 and 3789 μg day 1, respectively. Regarding the air emissions per capita, values between 8.33 and 6109 μg day 1 (mean: 1607 μg day 1) are expected and D5 and D6 were the predominant siloxanes.  相似文献   

15.
ObjectiveWe used log-linear and log-log exposure-response (E-R) functions to model the association between PM2.5 exposure and non-elective hospitalizations for pneumonia, and estimated the attributable hospital costs by using the effect estimates obtained from both functions.MethodsWe used hospital discharge data on 3519 non-elective pneumonia admissions from UZ Brussels between 2007 and 2012 and we combined a case-crossover design with distributed lag models. The annual averted pneumonia hospitalization costs for a reduction in PM2.5 exposure from the mean (21.4 μg/m3) to the WHO guideline for annual mean PM2.5 (10 μg/m3) were estimated and extrapolated for Belgium.ResultsNon-elective hospitalizations for pneumonia were significantly associated with PM2.5 exposure in both models. Using a log-linear E-R function, the estimated risk reduction for pneumonia hospitalization associated with a decrease in mean PM2.5 exposure to 10 μg/m3 was 4.9%. The corresponding estimate for the log-log model was 10.7%. These estimates translate to an annual pneumonia hospital cost saving in Belgium of €15.5 million and almost €34 million for the log-linear and log-log E-R function, respectively.DiscussionAlthough further research is required to assess the shape of the association between PM2.5 exposure and pneumonia hospitalizations, we demonstrated that estimates for health effects and associated costs heavily depend on the assumed E-R function. These results are important for policy making, as supra-linear E-R associations imply that significant health benefits may still be obtained from additional pollution control measures in areas where PM levels have already been reduced.  相似文献   

16.
Few studies have explored the relationship between coarse particles (PM10-2.5) and adverse birth outcomes. We examined associations between gestational exposure of PM10-2.5 and birth weight. U.S. birth certificates data (1999–2007) were acquired for 8,017,865 births. Gestational and trimester exposures of PM10-2.5 were estimated using co-located PM10 and PM2.5 monitors  35 km from the population-weighted centroid of mothers' residential counties. A linear regression model was applied, adjusted by potential confounders. As sensitivity analyses, we explored alternative PM10-2.5 estimations, adjustment for PM2.5, and stratification by regions. Gestational exposure to PM10-2.5 was associated with 6.6 g (95% Confidence Interval: 5.9, 7.2) lower birth weight per interquartile range increase (7.8 μg/m3) in PM10-2.5 exposures. All three trimesters showed associations. Under different exposure methods for PM10-2.5, associations remained consistent but with different magnitudes. Results were robust after adjusting for PM2.5, and regional analyses showed associations in all four regions with larger estimates in the South. Our results suggest that PM10-2.5 is associated with birth weight in addition to PM2.5. Regional heterogeneity may reflect differences in population, measurement error, region-specific emission pattern, or different chemical composition within PM10-2.5. Most countries do not set health-based standards for PM10-2.5, but our findings indicate potentially important health effects of PM10-2.5.  相似文献   

17.
BackgroundAmbient particulate matter (PM) exposure has been associated with short- and long-term effects on cardiovascular disease (CVD). Telomere length (TL) is a biomarker of CVD risk that is modified by inflammation and oxidative stress, two key pathways for PM effects. Whether PM exposure modifies TL is largely unexplored.ObjectivesTo investigate effects of PM on blood TL in a highly-exposed population.MethodsWe measured blood TL in 120 blood samples from truck drivers and 120 blood samples from office workers in Beijing, China. We measured personal PM2.5 and Elemental Carbon (EC, a tracer of traffic particles) using light-weight monitors. Ambient PM10 was obtained from local monitoring stations. We used covariate-adjusted regression models to estimate percent changes in TL per an interquartile-range increase in exposure.ResultsCovariate-adjusted TL was higher in drivers (mean = 0.87, 95%CI: 0.74; 1.03) than in office workers (mean = 0.79, 95%CI: 0.67; 0.93; p = 0.001). In all participants combined, TL increased in association with personal PM2.5 (+ 5.2%, 95%CI: 1.5; 9.1; p = 0.007), personal EC (+ 4.9%, 95%CI: 1.2; 8.8; p = 0.01), and ambient PM10 (+ 7.7%, 95%CI: 3.7; 11.9; p < 0.001) on examination days. In contrast, average ambient PM10 over the 14 days before the examinations was significantly associated with shorter TL (− 9.9%, 95%CI: − 17.6; − 1.5; p = 0.02).ConclusionsShort-term exposure to ambient PM is associated with increased blood TL, consistent with TL roles during acute inflammatory responses. Longer exposures may shorten TL as expected after prolonged pro-oxidant exposures. The observed TL alterations may participate in the biological pathways of short- and long-term PM effects.  相似文献   

18.
Ambient PM2.5 pollution is a substantial threat to public health in global megacities. This paper reviews the PM2.5 pollution of 45 global megacities in 2013, based on mass concentration from official monitoring networks and composition data reported in the literature. The results showed that the five most polluted megacities were Delhi, Cairo, Xi'an, Tianjin and Chengdu, all of which had an annual average concentration of PM2.5 greater than 89 μg/m3. The five cleanest megacities were Miami, Toronto, New York, Madrid and Philadelphia, the annual averages of which were less than 10 μg/m3. Spatial distribution indicated that the highly polluted megacities are concentrated in east-central China and the Indo-Gangetic Plain. Organic matter and SNA (sum of sulfate, nitrate and ammonium) contributed 30% and 36%, respectively, of the average PM2.5 mass for all megacities. Notable seasonal variation of PM2.5 polluted days was observed, especially for the polluted megacities of China and India, resulting in frequent heavy pollution episodes occurring during more polluted seasons such as winter. Marked differences in PM2.5 pollution between developing and developed megacities require more effort on local emissions reduction as well as global cooperation to address the PM2.5 pollution of those megacities mainly in Asia.  相似文献   

19.
BackgroundThe underlying intermediate mechanisms about the association between fine particulate matter (PM2.5) air pollution and blood pressure (BP) were unclear. Few epidemiological studies have explored the potential mediation effects of angiotensin-converting enzyme (ACE) and its DNA methylation.MethodsWe designed a longitudinal panel study with 4 follow-ups among 36 healthy college students in Shanghai, China from December 17, 2014 to July 11, 2015. We measured personal real-time exposure to PM2.5, serum ACE level, and blood methylation of ACE gene and the repetitive elements. We applied linear mixed-effects models to examine the effects of PM2.5 on ACE protein, DNA methylation and BP markers. Furthermore, we conducted mediation analyses to evaluate the potential pathways.ResultsAn interquartile range increase (26.78 μg/m3) in 24-h average exposure to PM2.5 was significantly associated with 1.12 decreases in ACE average methylation (%5mC), 13.27% increase in ACE protein, and increments of 1.13 mmHg in systolic BP, 0.66 mmHg in diastolic BP and 0.82 mmHg in mean arterial pressure. ACE hypomethylation mediated 11.78% (P = 0.03) of the elevated ACE protein by PM2.5. Increased ACE protein accounted for 3.90 ~ 13.44% (P = 0.35 ~ 0.68) of the elevated BP by PM2.5. Repetitive-element methylation was also decreased but did not significantly mediate the association between PM2.5 and BP.ConclusionsThis investigation provided strong evidence that short-term exposure to PM2.5 was significantly associated with BP, ACE protein and ACE methylation. Our findings highlighted a possible involvement of ACE and ACE methylation in the effects of PM2.5 on elevating BP.  相似文献   

20.
BackgroundPrenatal exposure to air pollutants has recently been identified as a potential risk factor for neuropsychological impairment.ObjectivesTo assess whether prenatal exposure to fine particulate matter (PM2.5), nitrogen dioxide (NO2) and benzene were associated with impaired development in infants during their second year of life.MethodsRegression analyses, based on 438 mother–child pairs, were performed to estimate the association between mother exposure to air pollutants during pregnancy and neurodevelopment of the child. The average exposure to PM2.5, NO2 and benzene over the whole pregnancy was calculated for each woman. During the second year of life, infant neuropsychological development was assessed using the Bayley Scales of Infant Development. Regression analyses were performed to estimate the association between exposure and outcomes, accounting for potential confounders.ResultsWe estimated that a 1 μg/m3 increase during pregnancy in the average levels of PM2.5 was associated with a − 1.14 point decrease in motor score (90% CI: − 1.75; − 0.53) and that a 1 μg/m3 increase of NO2 exposure was associated with a − 0.29 point decrease in mental score (90% CI: − 0.47; − 0.11). Benzene did not show any significant association with development. Considering women living closer (≤ 100 m) to metal processing activities, we found that motor scores decreased by − 3.20 (90% CI: − 5.18; − 1.21) for PM2.5 and − 0.51 (− 0.89; − 0.13) for NO2, while mental score decreased by − 2.71 (90% CI: − 4.69; − 0.74) for PM2.5, and − 0.41 (9% CI: − 0.76; − 0.06) for NO2.ConclusionsOur findings suggest that prenatal residential exposure to PM2.5 and NO2 adversely affects infant motor and cognitive developments. This negative effect could be higher in the proximity of metal processing plants.  相似文献   

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