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1.
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   

2.
Ambient air pollution and children's lung function in China   总被引:1,自引:0,他引:1  
ObjectiveTo describe the correlations between ambient air pollutants (TSP, SO2, NOx) and the level of children's lung function (FVC, FEV1, MMEF) in China.MethodsWe collected the research articles on ambient air pollution and children's lung function published from 1985 to 2006 and selected 11 articles finally according to the following criteria: (1) Children between the age of 7 and 15 as objects; (2) Local air quality monitoring results were reported; (3) Strict quality control was taken when testing children's lung function; (4) The results were expressed by the average of measured value. Then we analyzed the correlation relationship between the level of ambient air pollutants and children's lung function and compared the effects of ambient air pollutants on children's lung function of boy and girl.ResultsThe selected articles included the results of 7 cities in China. Among them, the results of 6 cities' studies revealed that the levels of children's lung function were significantly lower in the areas with heavy ambient air pollution than those in the areas with light ambient air pollution. According to the articles, the average levels of TSP were at the range of 0.084 mg/m3–0.835 mg/m3, SO2 were 0.013 mg/m3–0.929 mg/m3, NOx were 0.044 mg/m3–0.229 mg/m3. Correlation analysis showed significant negative correlation between the levels of TSP and SO2 and children's FVC and FEV1, as well as the levels of NOx and children's MMEF. The correlation coefficient was ? 0.797 (t = ? 4.384, P = 0.001) between TSP and FVC, ? 0.693 (t = ? 4.190, P < 0.001) between Ln (SO2) and FVC, ? 0.886 (t = ? 5.392, P = 0.001) and ? 0.685 (t = ? 4.101, P = 0.001) between FEV1 and TSP and Ln (SO2), and ? 0.973 (t = ? 5.993, P = 0.027) between NOxNOx and MMEF, respectively. The results also suggested that the decreases of lung function for girl with the increasing of ambient air pollution were significantly greater for boy.ConclusionThe levels of ambient air TSP and SO2 correlated with the damage of the big airway function of children, while NOxNOx affected the small airway function chiefly. Furthermore, lung function of girl was more susceptible to ambient air pollutants than boy.  相似文献   

3.
BackgroundMaternal exposure to air pollution and traffic noise has been suggested to impair fetal growth, but studies have reported inconsistent findings.ObjectiveTo investigate associations between residential air pollution and traffic noise during pregnancy and newborn's size at birth.MethodsFrom a national birth cohort we identified 75,166 live-born singletons born at term with information on the children's size at birth. Residential address history from conception until birth was collected and air pollution (NO2 and NOx) and road traffic noise was modeled at all addresses. Associations between exposures and indicators of newborn's size at birth: birth weight, placental weight and head and abdominal circumference were analyzed by linear and logistic regression, and adjusted for potential confounders.ResultsIn mutually adjusted models we found a 10 μg/m3 higher time-weighted mean exposure to NO2 during pregnancy to be associated with a 0.35 mm smaller head circumference (95% confidence interval (CI): 95% CI: − 0.57; − 0.12); a 0.50 mm smaller abdominal circumference (95% CI: − 0.80; − 0.20) and a 5.02 g higher placental weight (95% CI: 2.93; 7.11). No associations were found between air pollution and birth weight. Exposure to residential road traffic noise was weakly associated with reduced head circumference, whereas none of the other newborn's size indicators were associated with noise, neither before nor after adjustment for air pollution.ConclusionsThis study indicates that air pollution may result in a small reduction in offspring's birth head and abdominal circumference, but not birth weight, whereas traffic noise seems not to affect newborn's size at birth.  相似文献   

4.
Studies of air pollution effects during pregnancy generally only consider exposure in the outdoor air at the home address. We aimed to compare exposure models differing in their ability to account for the spatial resolution of pollutants, space–time activity and indoor air pollution levels. We recruited 40 pregnant women in the Grenoble urban area, France, who carried a Global Positioning System (GPS) during up to 3 weeks; in a subgroup, indoor measurements of fine particles (PM2.5) were conducted at home (n = 9) and personal exposure to nitrogen dioxide (NO2) was assessed using passive air samplers (n = 10). Outdoor concentrations of NO2, and PM2.5 were estimated from a dispersion model with a fine spatial resolution. Women spent on average 16 h per day at home. Considering only outdoor levels, for estimates at the home address, the correlation between the estimate using the nearest background air monitoring station and the estimate from the dispersion model was high (r = 0.93) for PM2.5 and moderate (r = 0.67) for NO2. The model incorporating clean GPS data was less correlated with the estimate relying on raw GPS data (r = 0.77) than the model ignoring space–time activity (r = 0.93). PM2.5 outdoor levels were not to moderately correlated with estimates from the model incorporating indoor measurements and space–time activity (r =  0.10 to 0.47), while NO2 personal levels were not correlated with outdoor levels (r =  0.42 to 0.03). In this urban area, accounting for space–time activity little influenced exposure estimates; in a subgroup of subjects (n = 9), incorporating indoor pollution levels seemed to strongly modify them.  相似文献   

5.
BackgroundParticulate air pollution is a risk factor for cardiovascular diseases and thrombosis. Long-term exposure to particulate matter with a diameter < 10 μm (PM10) has been associated with an increased risk of venous thrombosis.ObjectivesThe aim of this study was to investigate whether or not particulate air pollution alters fibrin clot structure and thus modulates thrombosis risk.MethodsWe investigated fibrin polymerization by turbidity (maximum absorbance mOD), clot structure by confocal microscopy (fibre number per μm) and fibrin pore size by permeability (Ks × 10 10 cm2) in 103 patients with deep vein thrombosis and 121 healthy controls, for whom levels of air pollution exposure had been recorded. Exposure groups were defined by mean PM10 concentrations over the 730 days before the event.ResultsWe found a higher average number of fibres per clot area in patients than controls, but no difference in Ks or fibre thickness. When the two groups were divided into high or low exposure to PM10, a significantly denser fibrin clot network structure with thicker fibres (higher maximum absorbance, p < 0.05), decreased permeability (lower Ks value, p < 0.05) and higher average fibre numbers per clot area (p < 0.05) was observed in patients in the high exposure group compared to those with low exposure. There were no significant differences in fibrin clot structure between the two exposure levels in healthy subjects.ConclusionsPM10 levels are associated with altered fibrin clot structure in patients with deep vein thrombosis but not in controls, suggesting that air pollution may trigger differences in fibrin clot structure only in patients predisposed to thrombotic disease.  相似文献   

6.
BackgroundWe investigated the associations between daily sales of respiratory medication and air pollutants in the Brussels-Capital Region between 2005 and 2011.MethodsWe used over-dispersed Poisson Generalized Linear Models to regress daily individual reimbursement data of prescribed asthma and COPD medication from the social security database against each subject's residential exposure to outdoor particulate matter (PM10) or NO2 estimated, by interpolation from monitoring stations. We calculated cumulative risk ratios (RR) and their 95% confidence intervals (CI) for interquartile ranges (IQR) of exposure for different windows of past exposure for the entire population and for seven age groups.ResultsMedian daily concentrations of PM10 and NO2 were 25 μg/m3 (IQR = 17.1) and 38 μg/m3 (IQR = 20.5), respectively. PM10 was associated with daily medication sales among individuals aged 13 to 64 y. For NO2, significant associations were observed among all age groups except > 84 y. The highest RR were observed for NO2, among adolescents, including three weeks lags (RR = 1.187 95%CI: 1.097–1.285).ConclusionThe associations found between temporal changes in exposure to air pollutants and daily sales of respiratory medication in Brussels indicate that urban air pollution contributes to asthma and COPD morbidity in the general population.  相似文献   

7.
BackgroundExposure to traffic noise and air pollution have both been associated with cardiovascular disease, though the mechanisms behind are not yet clear.ObjectivesWe aimed to investigate whether the two exposures were associated with levels of cholesterol in a cross-sectional design.MethodsIn 1993–1997, 39,863 participants aged 50–64 year and living in the Greater Copenhagen area were enrolled in a population-based cohort study. For each participant, non-fasting total cholesterol was determined in whole blood samples on the day of enrolment. Residential addresses 5-years preceding enrolment were identified in a national register and road traffic noise (Lden) were modeled for all addresses. For air pollution, nitrogen dioxide (NO2) was modeled at all addresses using a dispersion model and PM2.5 was modeled at all enrolment addresses using a land-use regression model. Analyses were done using linear regression with adjustment for potential confounders as well as mutual adjustment for the three exposures.ResultsBaseline residential exposure to the interquartile range of road traffic noise, NO2 and PM2.5 was associated with a 0.58 mg/dl (95% confidence interval: − 0.09; 1.25), a 0.68 mg/dl (0.22; 1.16) and a 0.78 mg/dl (0.22; 1.34) higher level of total cholesterol in single pollutant models, respectively. In two pollutant models with adjustment for noise in air pollution models and vice versa, the association between air pollution and cholesterol remained for both air pollution variables (NO2: 0.72 (0.11; 1.34); PM2.5: 0.70 (0.12; 1.28) mg/dl), whereas there was no association for noise (− 0.08 mg/dl). In three-pollutant models (NO2, PM2.5 and road traffic noise), estimates for NO2 and PM2.5 were slightly diminished (NO2: 0.58 (− 0.05; 1.22); PM2.5: 0.57 (− 0.02; 1.17) mg/dl).ConclusionsAir pollution and possibly also road traffic noise may be associated with slightly higher levels of cholesterol, though associations for the two exposures were difficult to separate.  相似文献   

8.
BackgroundElevated temperature and air pollution have been associated with increased mortality. Exposure to heat and air pollution, as well as the density of vulnerable groups varies within cities. The objective was to investigate the extent of neighbourhood differences in mortality risk due to heat and air pollution in a city with a temperate maritime climate.MethodsA case-crossover design was used to study associations between heat, air pollution and mortality. Different thermal indicators and air pollutants (PM10, NO2, O3) were reconstructed at high spatial resolution to improve exposure classification. Daily exposures were linked to individual mortality cases over a 15 year period.ResultsSignificant interaction between maximum air temperature (Tamax) and PM10 was observed. During “summer smog” days (Tamax > 25 °C and PM10 > 50 μg/m3), the mortality risk at lag 2 was 7% higher compared to the reference (Tamax 15 °C and PM10 15 μg/m3). Persons above age 85 living alone were at highest risk.ConclusionWe found significant synergistic effects of high temperatures and air pollution on mortality. Single living elderly were the most vulnerable group. Due to spatial differences in temperature and air pollution, mortality risks varied substantially between neighbourhoods, with a difference up to 7%.  相似文献   

9.
IntroductionEvidence has accumulated on the association between ambient air pollution and adverse birth outcomes. However, most of the previous studies were conducted in geographically distinct areas and suffer from lack of important potential covariates. We examined the effect of ambient air pollution on term low birth weight (LBW) using data from a nationwide population-based longitudinal survey in Japan that began in 2001.MethodsWe restricted participants to term singletons (n = 44,109). Air pollution concentrations during the 9 months before birth were obtained at the municipality level and were assigned to the participants who were born in the corresponding municipality. We conducted multilevel logistic regression analyses adjusting for individual and municipality-level variables.ResultsWe found that air pollution exposure during pregnancy was positively associated with the risk of term LBW. In the fully adjusted models, odds ratios following one interquartile range increase in each pollutant were 1.09 (95% confidence interval: 1.00, 1.19) for suspended particulate matter (SPM), 1.11 (0.99, 1.26) for nitrogen dioxide (NO2), and 1.71 (1.18, 2.46) for sulfur dioxide (SO2). Specifically, effect estimates for SPM and NO2 exposure at the first trimester were higher than those at other trimesters, while SO2 was associated with the risk at all trimesters. Nonsmoking mothers were more susceptible to SPM and NO2 exposure compared with smoking mothers.ConclusionsAmbient air pollution increases the risk of term LBW in a nationally representative sample in Japan.  相似文献   

10.
BackgroundShort telomeres are associated with chronic disease and early mortality. Recent studies in adults suggest an association between telomere length and exposure to particulate matter, and that ethnicity may modify the relationship. However associations in children are unknown.ObjectivesWe examined associations between air pollution and telomere length in an ethnically diverse group of children exposed to high levels of traffic derived pollutants, particularly diesel exhaust, and to environmental tobacco smoke.MethodsOral DNA from 333 children (8–9 years) participating in a study on air quality and respiratory health in 23 inner city London schools was analysed for relative telomere length using monochrome multiplex qPCR. Annual, weekly and daily exposures to nitrogen oxides and particulate matter were obtained from urban dispersion models (2008–10) and tobacco smoke by urinary cotinine. Ethnicity was assessed by self-report and continental ancestry by analysis of 28 random genomic markers. We used linear mixed effects models to examine associations with telomere length.ResultsTelomere length increased with increasing annual exposure to NOx (model coefficient 0.003, [0.001, 0.005], p < 0.001), NO2 (0.009 [0.004, 0.015], p < 0.001), PM2.5 (0.041, [0.020, 0.063], p < 0.001) and PM10 (0.096, [0.044, 0.149], p < 0.001). There was no association with environmental tobacco smoke. Telomere length was increased in children reporting black ethnicity (22% [95% CI 10%, 36%], p < 0.001)ConclusionsPollution exposure is associated with longer telomeres in children and genetic ancestry is an important determinant of telomere length. Further studies should investigate both short and long-term associations between pollutant exposure and telomeres in childhood and assess underlying mechanisms.  相似文献   

11.
BackgroundStudies have found long-term exposure to traffic noise to be associated with higher risk for hypertension, ischemic heart disease and stroke. We aimed to investigate the novel hypothesis that traffic noise increases the risk of atrial fibrillation (A-fib).MethodsIn a population-based cohort of 57,053 people aged 50–64 years at enrolment in 1993–1997, we identified 2692 cases of first-ever hospital admission of A-fib from enrolment to end of follow-up in 2011 using a nationwide registry. The mean follow-up time was 14.7 years. Present and historical residential addresses were identified for all cohort members from 1987 to 2011. For all addresses, exposure to road traffic and railway noise was estimated using the Nordic prediction method and exposure to air pollution was estimated using a validated dispersion model. We used Cox proportional hazard model for the analyses with adjustment for lifestyle, socioeconomic position and air pollution.ResultsA 10 dB higher 5-year time-weighted mean exposure to road traffic noise was associated with a 6% higher risk of A-fib (incidence rate ratio (IRR): 1.06; 95% confidence interval (95% CI): 1.00–1.12) in models adjusted for factors related to lifestyle and socioeconomic position. The association followed a monotonic exposure–response relationship. In analyses with adjustment for air pollution, NOx or NO2, there were no statistically significant associations between exposure to road traffic noise and risk of A-fib; IRR: 1.04; (95% CI: 0.96–1.11) and IRR: 1.01; (95% CI: 0.94–1.09), respectively. Exposure to railway noise was not associated with A-fib.ConclusionExposure to residential road traffic noise may be associated with higher risk of A-fib, though associations were difficult to separate from exposure to air pollution.  相似文献   

12.
Air pollution is an important risk factor for global burden of disease. There has been recent interest in its possible role in the etiology of diabetes mellitus. Experimental evidence is suggestive, but epidemiological evidence is limited and mixed. We therefore explored the association between air pollution and prevalent diabetes, in a population-based Swiss cohort.We did cross-sectional analyses of 6392 participants of the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults [SAPALDIA], aged between 29 and 73 years. We used estimates of average individual home outdoor PM10 [particulate matter <10 μm in diameter] and NO2 [nitrogen dioxide] exposure over the 10 years preceding the survey. Their association with diabetes was modeled using mixed logistic regression models, including participants' study area as random effect, with incremental adjustment for confounders.There were 315 cases of diabetes (prevalence: 5.5% [95% confidence interval (CI): 2.8, 7.2%]). Both PM10 and NO2 were associated with prevalent diabetes with respective odds ratios of 1.40 [95% CI: 1.17, 1.67] and 1.19 [95% CI: 1.03, 1.38] per 10 μg/m3 increase in the average home outdoor level. Associations with PM10 were generally stronger than with NO2, even in the two-pollutant model. There was some indication that beta blockers mitigated the effect of PM10. The associations remained stable across different sensitivity analyses.Our study adds to the evidence that long term air pollution exposure is associated with diabetes mellitus. PM10 appears to be a useful marker of aspects of air pollution relevant for diabetes. This association can be observed at concentrations below air quality guidelines.  相似文献   

13.
ObjectiveRheumatoid arthritis (RA) has been associated with inhaled pollutants in several studies, and it is a disease of chronic inflammation. The association between air pollution and the risk of RA remains unclear. Therefore, we conducted this nationwide, retrospective, sex-stratification study to evaluate this association.MethodsWe collected data from the Longitudinal Health Insurance Database (LHID), maintained by the Taiwan Bureau of National Health Insurance, and the Taiwan Air Quality-Monitoring Database (TAQMD), released by the Taiwan Environmental Protection Agency. The TAQMD provides the daily concentrations of particulate matter with the aerodynamic diameter < 2.5 μm (PM2.5) and nitrogen dioxide (NO2) from 74 ambient air quality-monitoring stations distributed all over Taiwan during 1998–2010. The LHID and TAQMD were linked according to the residential areas of insurants and the areas where the air quality-monitoring stations were located. A residential area was defined according to the location of the clinic and hospital that treated acute upper respiratory tract infections. The yearly average air pollutant concentrations were categorized into 4 levels based on quartiles. We evaluated the risk of RA in residents exposed to 4 levels of PM2.5 and NO2 concentrations.ResultsWe detected an increased risk of RA in participants exposed to PM2.5 and NO2. Among four quartiles of NO2 concentration, namely Q1, Q2, Q3, and Q4, the adjusted hazard ratios (aHRs) in Q2, Q3, and Q4 compared with that in Q1 were 1.07 (95% confidence interval [CI] = 0.76–1.50), 1.63 (95% CI = 1.16–2.31),and 1.49 (95% CI = 1.05–2.12), respectively. Regarding the PM2.5 concentrations, the aHRs after exposure to the Q2, Q3, and Q4 levels were 1.22 (95% CI = 0.85–1.74), 1.15 (95% CI = 0.82–1.62), and 0.79 (95% CI = 0.53–1.16), respectively.ConclusionThe results of this nationwide study suggest an increased risk of RA in residents exposed to NO2.  相似文献   

14.
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   

15.
Human exposure to ambient ozone (O3) has been linked to a variety of adverse health effects. The ozone level at a location is contributed by local production, regional transport, and background ozone. This study combines detailed emission inventory, air quality modeling, and census data to investigate the source–receptor relationships between nitrogen oxides (NOx) emissions and population exposure to ambient O3 in 48 states over the continental United States. By removing NOx emissions from each state one at a time, we calculate the change in O3 exposures by examining the difference between the base and the sensitivity simulations. Based on the 49 simulations, we construct state-level and census region-level source–receptor matrices describing the relationships among these states/regions. We find that, for 43 receptor states, cumulative NOx emissions from upwind states contribute more to O3 exposures than the state's own emissions. In-state emissions are responsible for less than 15% of O3 exposures in 90% of U.S. states. A state's NOx emissions can influence 2 to 40 downwind states by at least a 0.1 ppbv change in population-averaged O3 exposure. The results suggest that the U.S. generally needs a regional strategy to effectively reduce O3 exposures. But the current regional emission control program in the U.S. is a cap-and-trade program that assumes the marginal damage of every ton of NOx is equal. In this study, the average O3 exposures caused by one ton of NOx emissions ranges from ? 2.0 to 2.3 ppm-people-hours depending on the state. The actual damage caused by one ton of NOx emissions varies considerably over space.  相似文献   

16.
Studies in a number of countries have reported associations between exposure to ambient air pollutants and adverse birth outcomes, including low birth weight, preterm birth (PTB) and, less commonly, small for gestational age (SGA). Despite their growing number, the available studies have significant limitations, e.g., incomplete control of temporal trends in exposure, modest sample sizes, and a lack of information regarding individual risk factors such as smoking. No study has yet examined large numbers of susceptible individuals.We investigated the association between ambient air pollutant concentrations and term SGA and PTB outcomes among 164,905 singleton births in Detroit, Michigan occurring between 1990 and 2001. SO2, CO, NO2, O3 and PM10 exposures were used in single and multiple pollutant logistic regression models to estimate odds ratios (OR) for these outcomes, adjusted for the infant's sex and gestational age, the mother's race, age group, education level, smoking status and prenatal care, birth season, site of residence, and long-term exposure trends.Term SGA was associated with CO levels exceeding 0.75 ppm (OR = 1.14, 95% confidence interval = 1.02–1.27) and NO2 exceeding 6.8 ppb (1.11, 1.03–1.21) exposures in the first month, and with PM10 exceeding 35 μg/m3 (1.22, 1.03–1.46) and O3 (1.11, 1.02–1.20) exposure in the third trimester. PTB was associated with SO2 (1.07, 1.01–1.14) exposure in the last month, and with (hourly) O3 exceeding 92 ppb (1.08, 1.02–1.14) exposure in the first month.Exposure to several air pollutants at modest concentrations was associated with adverse birth outcomes. This study, which included a large Black population, suggests the importance of the early period of pregnancy for associations between term SGA with CO and NO2, and between O3 with PTB; and the late pregnancy period for associations between term SGA and O3 and PM10, and between SO2 with PTB. It also highlights the importance of accounting for individual risk factors such as maternal smoking, maternal race, and long-term trends in air pollutant levels and adverse birth outcomes in evaluating relationships between pollutant exposures and adverse birth outcomes.  相似文献   

17.
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   

18.
BackgroundSpatially resolved exposure models are increasingly used in epidemiology. We previously reported that, although exhibiting a moderate correlation, pregnancy nitrogen dioxide (NO2) levels estimated by the nearest air quality monitoring station (AQMS) model and a geostatistical model, showed similar associations with infant birth weight.ObjectivesWe extended this study by comparing a total of four exposure models, including two highly spatially resolved models: a land-use regression (LUR) model and a dispersion model. Comparisons were made in terms of predicted NO2 and particle (aerodynamic diameter < 10 μm, PM10) exposure and adjusted association with birth weight.MethodsThe four exposure models were implemented in two French metropolitan areas where 1026 pregnant women were followed as part of the EDEN mother–child cohort.ResultsCorrelations between model predictions were high (≥ 0.70), except for NO2 between the AQMS and both the LUR (r = 0.54) and dispersion models (r = 0.63). Spatial variations as estimated by the AQMS model were greater for NO2 (95%) than for PM10 (22%). The direction of effect estimates of NO2 on birth weight varied according to the exposure model, while PM10 effect estimates were more consistent across exposure models.ConclusionsFor PM10, highly spatially resolved exposure model agreed with the poor spatial resolution AQMS model in terms of estimated pollutant levels and health effects. For more spatially heterogeneous pollutants like NO2, although predicted levels from spatially resolved models (all but AQMS) agreed with each other, our results suggest that some may disagree with each other as well as with the AQMS regarding the direction of the estimated health effects.  相似文献   

19.
BackgroundMiscarriages are an important indicator of reproductive health but only few studies have analyzed their association with exposure to emissions from municipal solid waste incinerators.This study analyzed the occurrence of miscarriages in women aged 15–49 years residing near seven incinerators of the Emilia-Romagna Region (Northern Italy) in the period 2002–2006.MethodsWe considered all pregnancies occurring in women residing during the first trimester of pregnancy within a 4 km radius of each incinerator. Addresses were geocoded and exposures were characterized by a dispersion model (ADMS Urban model) producing pollution maps for incinerators based on PM10 stack measurements and for other pollution sources based on NOx ground measurements. Information on pregnancies and their outcomes was obtained from the Hospital Discharge Database. Simplified True Abortion Risks (STAR) × 100 estimated pregnancies were calculated. We ran logistic regressions adjusting for maternal characteristics, exposure to other sources of pollution, and sites, considering the whole population and stratifying by miscarriage history.ResultsThe study analyzed 11,875 pregnancies with 1375 miscarriages. After adjusting for confounders, an increase of PM10 due to incinerator emissions was associated with an increased risk of miscarriage (test for trend, p = 0.042). The odds ratio for the highest quartile of exposed versus not exposed women was 1.29, 95% CI 0.97–1.72. The effect was present only for women without previous miscarriages (highest quartile of exposed versus not exposed women 1.44, 95% CI 1.06–1.96; test for trend, p = 0.009).ConclusionExposure to incinerator emissions is associated with an increased risk of miscarriage. This result should be interpreted with those of a previous study on reproductive health conducted in the same area that observed an association between incinerator exposure and preterm births.  相似文献   

20.
Robust methods to estimate historic population air pollution exposures are important tools for epidemiological studies evaluating long-term health effects. We developed land use regression (LUR) models for NO2 exposure in Great Britain for 1991 and explored whether the choice of year-specific or back-extrapolated LUR yields 1) similar LUR variables and model performance, and 2) similar national and regional address-level and small-area concentrations. We constructed two LUR models for 1991using NO2 concentrations from the diffusion tube monitoring network, one using 75% of all available measurement sites (that over-represent industrial areas), and the other using 75% of a subset of sites proportionate to population by region to study the effects of monitoring site selection bias. We compared, using the remaining (hold-out) 25% of monitoring sites, the performance of the two 1991 models with back-extrapolation of a previously published 2009 model, developed using NO2 concentrations from automatic chemiluminescence monitoring sites and predictor variables from 2006/2007. The 2009 model was back-extrapolated to 1991 using the same predictors (1990 & 1995) used to develop 1991 models. The 1991 models included industrial land use variables, not present for 2009. The hold-out performance of 1991 models (mean-squared-error-based-R2: 0.62–0.64) was up to 8% higher and ~ 1 μg/m3 lower in root mean squared error than the back-extrapolated 2009 model, with best performance from the subset of sites representing population exposures. Year-specific and back-extrapolated exposures for residential addresses (n = 1.338,399) and small areas (n = 10.518) were very highly linearly correlated for Great Britain (r > 0.83). This study suggests that year-specific model for 1991 and back-extrapolation of the 2009 LUR yield similar exposure assessment.  相似文献   

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