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1.
Active travel (cycling, walking) is beneficial for the health due to increased physical activity (PA). However, active travel may increase the intake of air pollution, leading to negative health consequences. We examined the risk–benefit balance between active travel related PA and exposure to air pollution across a range of air pollution and PA scenarios.The health effects of active travel and air pollution were estimated through changes in all-cause mortality for different levels of active travel and air pollution. Air pollution exposure was estimated through changes in background concentrations of fine particulate matter (PM2.5), ranging from 5 to 200 μg/m3. For active travel exposure, we estimated cycling and walking from 0 up to 16 h per day, respectively. These refer to long-term average levels of active travel and PM2.5 exposure.For the global average urban background PM2.5 concentration (22 μg/m3) benefits of PA by far outweigh risks from air pollution even under the most extreme levels of active travel. In areas with PM2.5 concentrations of 100 μg/m3, harms would exceed benefits after 1 h 30 min of cycling per day or more than 10 h of walking per day. If the counterfactual was driving, rather than staying at home, the benefits of PA would exceed harms from air pollution up to 3 h 30 min of cycling per day. The results were sensitive to dose–response function (DRF) assumptions for PM2.5 and PA.PA benefits of active travel outweighed the harm caused by air pollution in all but the most extreme air pollution concentrations.  相似文献   

2.
BackgroundThere is growing evidence that chronic exposure to transportation related noise and air pollution affects human health. However, health burden to a country of these two pollutants have been rarely compared.AimsAs an input for external cost quantification, we estimated the cardiorespiratory health burden from transportation related noise and air pollution in Switzerland, incorporating the most recent findings related to the health effects of noise.MethodsSpatially resolved noise and air pollution models for the year 2010 were derived for road, rail and aircraft sources. Average day-evening-night sound level (Lden) and particulate matter (PM10) were selected as indicators, and population-weighted exposures derived by transportation source. Cause-specific exposure–response functions were derived from a meta-analysis for noise and literature review for PM10. Years of life lost (YLL) were calculated using life table methods; population attributable fraction was used for deriving attributable cases for hospitalisations, respiratory illnesses, visits to general practitioners and restricted activity days.ResultsThe mean population weighted exposure above a threshold of 48 dB(A) was 8.74 dB(A), 1.89 dB(A) and 0.37 dB(A) for road, rail and aircraft noise. Corresponding mean exposure contributions were 4.4, 0.54, 0.12 μg/m3 for PM10. We estimated that in 2010 in Switzerland transportation caused 6000 and 14,000 YLL from noise and air pollution exposure, respectively. While there were a total of 8700 cardiorespiratory hospital days attributed to air pollution exposure, estimated burden due to noise alone amounted to 22,500 hospital days.ConclusionsYLL due to transportation related pollution in Switzerland is dominated by air pollution from road traffic, whereas consequences for morbidity and indicators of quality of life are dominated by noise. In terms of total external costs the burden of noise equals that of air pollution.  相似文献   

3.
Recent studies suggest that stress can amplify the harm of air pollution. We examined whether experience of racism and exposure to particulate matter with an aerodynamic diameter of less than 2.5 µm and 10 µm (PM2.5 and PM10) had a synergistic influence on ethnic differences in asthma and lung function across adolescence. Analyses using multilevel models showed lower forced expiratory volume (FEV1), forced vital capacity (FVC) and lower rates of asthma among some ethnic minorities compared to Whites, but higher exposure to PM2.5, PM10 and racism. Racism appeared to amplify the relationship between asthma and air pollution for all ethnic groups, but did not explain ethnic differences in respiratory health.  相似文献   

4.

Introduction and objectives

Air pollution and insufficient physical activity have been associated with inflammation and oxidative stress, molecular mechanisms linked to arterial stiffness and cardiovascular disease. There are no studies on how physical activity modifies the association between air pollution and arterial stiffness. We examined whether the adverse cardiovascular effects of air pollution were modified by individual physical activity levels in 2823 adults aged 50–81 years from the well-characterized Swiss Cohort Study on Air Pollution and Lung and Heart Diseases (SAPALDIA).

Methods

We assessed arterial stiffness as the brachial-ankle pulse wave velocity (baPWV [m/s]) with an oscillometric device. We administered a self-reported physical activity questionnaire to classify each subject’s physical activity level. Air pollution exposure was estimated by the annual average individual home outdoor PM10 and PM2.5 (particulate matter <10 μm and <2.5 μm in diameter, respectively) and NO2 (nitrogen dioxide) exposure estimated for the year preceding the survey. Exposure estimates for ultrafine particles calculated as particle number concentration (PNC) and lung deposited surface area (LDSA) were available for a subsample (N = 1353). We used mixed effects logistic regression models to regress increased arterial stiffness (baPWV  14.4 m/s) on air pollution exposure and physical activity while adjusting for relevant confounders.

Results

We found evidence that the association of air pollution exposure with baPWV was different between inactive and active participants. The probability of having increased baPWV was significantly higher with higher PM10, PM2.5, NO2, PNC and LDSA exposure in inactive, but not in physically active participants. We found some evidence of an interaction between physical activity and ambient air pollution exposure for PM10, PM2.5 and NO2 (pinteraction = 0.06, 0.09, and 0.04, respectively), but not PNC and LDSA (pinteraction = 0.32 and 0.35).

Conclusions

Our study provides some indication that physical activity may protect against the adverse vascular effects of air pollution in low pollution settings. Additional research in large prospective cohorts is needed to assess whether the observed effect modification translates to high pollution settings in mega-cities of middle and low-income countries.  相似文献   

5.
IntroductionThe impact of outdoor air pollution exposure on long-term lung development and potential periods of increased lung susceptibility remain unknown. This study assessed associations between early-life and current residential exposure to air pollution and lung function at 15-years of age in two German birth cohorts.MethodsFifteen year-old participants living in an urban and rural area in Germany underwent spirometry before and after bronchodilation (N = 2266). Annual average (long-term) exposure to nitrogen dioxide (NO2), particles with aerodynamic diameters less than 2.5 μg/m3 (PM2.5) mass and less than 10 μg/m3 (PM10) mass, PM2.5 absorbance and ozone were estimated to each participant's birth-, 10- and 15-year home address using land-use regression and kriging (ozone only) modelling. Associations between lung function variables and long-term pollutant concentrations were assessed using linear regression models adjusted for host and environmental covariates and recent short-term air pollution exposures.ResultsLong-term air pollution concentrations assessed to the birth-, 10- and 15-year home addresses were not associated with lung function variables, before and after bronchodilation, in the complete or study area specific populations. However, several lung function variables were negatively associated with long-term NO2 concentrations among asthmatics. For example, NO2 estimated to the 15-year home address was associated with the ratio of forced expiratory volume in one second to forced vital capacity (FEV1/FVC) and the mean flow rate between 25% and 75% of FVC (−3.5%, 95% confidence interval [−6.0, −1.0] and −297.4 ml/s [−592.6, −2.1] per 5.9 μg/m3 increase in NO2, respectively). Nearly all effect estimates for the associations between the short-term PM2.5 mass, PM10 mass and ozone concentrations and the lung function variables were negative in the complete population.ConclusionsEarly-life and current long-term air pollution exposures and lung function at the age of 15 years were not associated in the complete study population. Asthmatics may represent a vulnerable group.  相似文献   

6.
Although traffic emits both air pollution and noise, studies jointly examining the effects of both of these exposures on blood pressure (BP) in children are scarce. We investigated associations between land-use regression modeled long-term traffic-related air pollution and BP in 2368 children aged 10 years from Germany (1454 from Munich and 914 from Wesel). We also studied this association with adjustment of long-term noise exposure (defined as day–evening–night noise indicator “Lden” and night noise indicator “Lnight”) in a subgroup of 605 children from Munich inner city. In the overall analysis including 2368 children, NO2, PM2.5 mass (particles with aerodynamic diameters below 2.5 μm), PM10 mass (particles with aerodynamic diameters below 10 μm) and PM2.5 absorbance were not associated with BP. When restricting the analysis to the subgroup of children with noise information (N = 605), a significant association between NO2 and diastolic BP was observed (−0.88 (95% confidence interval: −1.67, −0.08)). However, upon adjusting the models for noise exposure, only noise remained independently and significantly positively associated with diastolic BP. Diastolic BP increased by 0.50 (−0.03, 1.02), 0.59 (0.05, 1.13), 0.55 (0.03, 1.07), and 0.58 (0.05, 1.11) mmHg for every five decibel increase in Lden and by 0.59 (−0.05, 1.22), 0.69 (0.04, 1.33), 0.64 (0.02, 1.27), and 0.68 (0.05, 1.32) mmHg for every five decibel increase in Lnight, in different models of NO2, PM2.5 mass, PM10 mass and PM2.5 absorbance as the main exposure, respectively. In conclusion, air pollution was not consistently associated with BP with adjustment for noise, noise was independently and positively associated with BP in children.  相似文献   

7.
Most previous studies which have investigated the short-term effects of air pollution on airway inflammation, assessed by an increase of exhaled nitric oxide (eNO), have been conducted among asthmatic children. Few studies have considered this potential association among non-asthmatics. Furthermore, although both short- and long-term effects of air pollution on eNO had been reported separately, studies which include both are scarce. We explored associations between 24 h NO2 and PM10 (particles with aerodynamic diameters below 10 μm) mass with eNO in 1985 children (192 asthmatics and 1793 non-asthmatics) aged 10 years and accounted for the long-term effects of air pollution by adjusting for annual averages of NO2, PM10 mass, PM2.5 mass (particles with aerodynamic diameters below 2.5 μm) and PM2.5 absorbance, using data from two German birth cohorts in Munich and Wesel. In total, robust associations between 24 h NO2 and eNO were observed in both single-pollutant (percentage change: 18.30%, 95% confidence interval: 11.63–25.37) and two-pollutant models (14.62%, 6.71–23.11). The association between 24 h PM10 mass and eNO was only significant in the single-pollutant model (9.59%, 4.80–14.61). The same significant associations were also observed in non-asthmatic children, while they did not reach significant levels in asthmatic children. Associations between annual averages of ambient air pollution (NO2, PM10 mass, PM2.5 mass and PM2.5 absorbance) and eNO were consistently null. In conclusion, significantly positive associations were observed between short-term ambient air pollution and eNO. No long-term effects of air pollution on eNO were found in this study.  相似文献   

8.
BackgroundShort-term exposure to increased particulate matter (PM) concentration has been reported to trigger myocardial infarction (MI). However, the association with ultrafine particles remains unclear.ObjectivesWe aimed to assess the effects of short-term air pollution and especially ultrafine particles on registry-based MI events and coronary deaths in the area of Augsburg, Germany.MethodsBetween 1995 and 2009, the MONICA/KORA myocardial infarction registry recorded 15,417 cases of MI and coronary deaths. Concentrations of PM < 10 μm (PM10), PM < 2.5 μm (PM2.5), particle number concentration (PNC) as indicator for ultrafine particles, and meteorological parameters were measured in the study region. Quasi-Poisson regression adjusting for time trend, temperature, season, and weekday was used to estimate immediate, delayed and cumulative effects of air pollutants on the occurrence of MI. The daily numbers of total MI, nonfatal and fatal events as well as incident and recurrent events were analysed.ResultsWe observed a 1.3% risk increase (95%-confidence interval: [−0.9%; 3.6%]) for all events and a 4.4% [−0.4%; 9.4%] risk increase for recurrent events per 24.3 μg/m3 increase in same day PM10 concentrations. Nonfatal events indicated a risk increase of 3.1% [−0.1%; 6.5%] with previous day PM10. No association was seen for PM2.5 which was only available from 1999 on. PNC showed a risk increase of 6.0% [0.6%; 11.7%] for recurrent events per 5529 particles/cm3 increase in 5-day average PNC.ConclusionsOur results suggested an association between short-term PM10 concentration and numbers of MI, especially for nonfatal and recurrent events. For ultrafine particles, risk increases were notably high for recurrent events. Thus, persons who already suffered a MI seemed to be more susceptible to air pollution.  相似文献   

9.

Background

Existing studies exploring the association between low birth weight (LBW) and maternal fine particulate matter (aerodynamic diameter < 2.5 μm, PM2.5) exposure have presented equivocal results, and one of the possible reasons for this finding might be due to relatively low maternal exposures. In addition, relatively narrow maternal exposure windows to PM2.5 have not been well established for LBW.

Methods

We employed a nested matched case-control design among 43,855 term births in a large maternity and child care hospital in Jinan, China. A total of 369 cases were identified, and four controls per case matched by maternal age were randomly selected among those with normal birth weight (n = 1,476) from 2014 to 2016. Ambient air monitoring data on continuous measures of PM2.5, nitrogen dioxide (NO2), and sulfur dioxide (SO2) (24-h average concentrations) from 2013 to 2016 were collected from thirteen local monitoring stations. An inverse distance weighting method based on both home and work addresses was adopted to estimate the individual daily exposures to these air pollutants during pregnancy by weighting the average of the twelve nearest monitoring stations within 30 km of each 100 m × 100 m grid cell by an inverse squared distance, and then the average exposure concentrations for gestational months, trimesters and the entire pregnancy were calculated. Adjusted conditional logistic regression models were used to estimate the odds ratios (ORs) per 10 μg/m3 increment in PM2.5 and by PM2.5 quartiles during different gestational periods.

Results

In this study, the estimated mean values of PM2.5, NO2, and SO2 exposure during the entire pregnancy were 88.0, 54.6, and 63.1 μg/m3, respectively. Term low birth weight (TLBW) increased in association with per 10 μg/m3 increment in PM2.5 for the 8th month [OR = 1.13, 95% confidence interval (CI): 1.04, 1.22], the 9th month (OR = 1.06, 95% CI: 0.99, 1.15), the third trimester (OR = 1.17, 95% CI: 1.05, 1.29), and the entire pregnancy (OR = 1.38, 95% CI: 1.07, 1.77) in models adjusted for one pollutant (PM2.5). In models categorizing the PM2.5 exposure by quartiles, comparing the second, third, and highest with the lowest PM2.5 exposure quartile, the PM2.5 was positively associated with TLBW during the 8th month (OR: 1.77, 95% CI: 1.09, 2.88; OR: 1.77, 95% CI: 1.03, 3.04; OR: 1.92, 95% CI: 1.04, 3.55, respectively) and for the 9th month, only association for exposure in the third versus the lowest quartile was significant (OR: 1.91, 95% CI: 1.02, 3.58).

Conclusions

The study provides evidence that exposure to PM2.5 during pregnancy might be associated with the risk of TLBW in the context of very high pollution level of PM2.5, and the 8th and 9th months were identified as potentially relevant exposure windows.  相似文献   

10.
Epidemiological studies have shown associations between ambient air pollution and changes in heart rate variability (HRV). However, studies using personal air pollution measurements, especially with exposure averages <24 h, are still rare.Between February and March 2008 HRV data as well as personal exposure to particulate matter <2.5 μm (PM2.5), and particle number concentrations (PNC) were collected in five volunteers for up to 8.3 h on a 5 min resolution. Information about the participant's whereabouts was also collected. Mixed models were used to analyze concurrent and up to 30 min delayed effects of air pollutants as well as being in traffic on 5 min-averages of heart rate (HR), high and low frequency power (HF and LF), standard deviation of all normal-to-normal intervals (SDNN), and the root mean square of successive interval differences (RMSSD). Results are presented as %-change from the mean per increase in interquartile range of air pollutant.In total, 474 5-min segments were available for analysis. We observed concurrent and delayed reductions in SDNN of about 0.8–1.0% in association with a 5.4 μg/m3 increase in PM2.5. However, being in traffic by car led to an increase of about 20% 10–14 min and 15–19 min later. An increase in PM2.5 or PNC was associated with lagged decreases for RMSSD and HF. We detected concurrent reductions in RMSSD (−17.6% [95%-confidence interval: 29.1; −4.3]) when being in traffic by bike/foot. Being in traffic by car was associated with an immediate reduction in LF while more delayed increases in LF were observed when being in traffic by bike/foot. Air pollution and traffic effects on HR were less consistent.These rapid changes in HRV within 30 min might be mediated by the autonomic nervous system in response to direct reflexes from receptors in the lungs.  相似文献   

11.
Dusts are one of the main air pollutants emitted during cement manufacturing. A substantial part of these are breathable particles that are less than 10 μm in diameter (PM10), which represent a potential threat for the health of the exposed population. This study aimed at evaluating the short-term effects of PM10 concentrations on the health of children, aged 6–14 years, who attended the schools in Fumane (Italy), in proximity (1.2 km) to a large cement plant. School absenteeism was used as a proxy indicator of child morbidity. Time series of daily school absences and PM10 concentrations were collected for 3 school-years from 2007 to 2010 (541 school-days, 462 children on average). The associations between PM10 concentrations and school absence rates in the same day (lag0) and in the following 4 days (lag1 to lag4) were evaluated using generalised additive models, smoothed for medium/long term trends and adjusted for day of the week, influenza outbreaks, daily temperature and rain precipitations. The average concentration of PM10 in the period was 34 (range: 4–183) μg/m3. An average 10 μg/m3 increase of PM10 concentration in the previous days (lag0–4) was associated with a statistically significant 2.5% (95%CI: 1.1–4.0%) increase in the rate of school absences. The highest increase in the absence rates (2.4%; 95%CI: 1.2–3.5%) was found 2 days after exposure (lag2). These findings provide epidemiological evidence of the acute health effects of PM10 in areas with annual concentrations that are lower than the legal European Union limit of 40 μg/m3, and support the need to establish more restrictive legislative standards.  相似文献   

12.
Negative associations between bone turnover markers and bone mineral density have been reported. In order to study the association between ambient air pollution and bone turnover markers, as indicators of bone loss, we investigated associations between land-use regression modeled air pollution (NO2, PM2.5 mass, PM2.5 – 10 [coarse particles], PM10 mass and PM2.5 absorbance) and bone turnover markers in 2264 children aged 10 years. Serum osteocalcin and C-terminal telopeptide of type I collagen (CTx), measured by Modular-System (Roche), were the two bone turnover markers considered in this analysis. In total population, NO2, PM2.5 – 10 and PM10 mass exposure were positively and significantly associated with both osteocalcin and CTx. A 2.5 (95% CI: 0.6, 4.4) ng/ml increase in osteocalcin and a 24.0 (95% CI: 6.7, 41.3) ng/L increase in CTx were observed per IQR (6.7 μg/m3) increase in NO2, independent of socioeconomic status, sex, age, pubertal status, fasting status and total physical activity. The estimated coefficients were 3.0 (95% CI: 0.1, 5.8) for osteocalcin and 32.3 (95% CI: 6.1, 58.5) for CTx with PM2.5 – 10; 3.2 (95% CI: 0.0, 6.4) for osteocalcin and 30.7 (95% CI: 1.7, 59.7) for CTx with PM10. Children living close to a major road (≤ 350 m) had higher levels of both osteocalcin (1.4 [−1.2, 4.0] ng/ml) and CTx (16.2 [−7.4, 39.8] ng/L). The adverse impact of ambient air pollution on bone turnover rates observed in one of the study areas showed stimulation of more such studies.  相似文献   

13.
Agricultural work is a major contributor to California's and the nation's economy and employs a large number of workers. However, agricultural work can have numerous risks, such as exposure to elevated levels of particulate matter (PM) and other airborne pollutants with potential adverse health effects. To determine the magnitude of occupational exposures, PM levels were assessed for 89 workers from three major crops in California; almonds, melons and tomatoes. Personal samples were collected for PM2.5 and inhalable PM using personal sampling equipment. Geometric mean concentrations from personal exposure for workers in almonds (inhalable PM = 4368 μg/m3, PM2.5 = 122 μg/m3, N = 5), tomatoes (inhalable PM = 1410 μg/m3, PM2.5 = 12 μg/m3, N = 33), and melons (inhalable PM = 1118 μg/m3, PM2.5 = 19 μg/m3, N = 51) showed high PM exposure when working with these three crops. Large exposure differences by crop were more common than by task (i.e. harvesting, packing and weeding) among the three crops studied. This is the largest study of agricultural workers engaged in hand harvesting, a significant employer of farm labor, and relatively high levels of exposure to PM were measured.  相似文献   

14.

Introduction

The use of a waterpipe to smoke tobacco has emerged as a popular trend in the United States. Waterpipe smoking establishments have had an increasing presence in the U.S., despite smoke-free air legislation. Dangers of waterpipe smoking have been documented, but less data has been gathered about the waterpipe café itself. This project sought to determine a waterpipe-specific calibration factor (CF) for measuring waterpipe aerosol, and field-test this CF by conducting surveillance on the existing waterpipe cafés of western and central New York.

Methods

Nine laboratory-controlled experiments were conducted to determine a waterpipe-specific CF. In the lab, two TSI SidePak AM510 Personal Aerosol Monitors and two sampling trains for gravimetric PM2.5 sampling were present during waterpipe smoking sessions (lasting 1–3 h). Indoor air quality was assessed in 7 waterpipe cafés in three counties of New York, and real-time measurements of particulate matter (PM2.5) and carbon monoxide (CO) were obtained.

Results

Results from the 9 controlled waterpipe experiments determined a calibration factor of 0.38 (SD 0.08), which should be used to convert SidePak measurements to true PM2.5 measurements. When applying the CF to the measurements taken in the 7 public waterpipe venues, the mean PM2.5 concentration was 515 μg/m3 micrograms per cubic meter (SD = 338.8) while the mean ambient CO was 20.5 ppm (SD = 18.3). The mean active smoking density was 2.41 waterpipes per 100 m3 of air. The PM2.5 levels increased with increasing active smoking density (rho = 0.68, p = 0.09).

Conclusions

Applying the waterpipe-specific CF for the SidePak, 0.38, allowed for field assessments to be conducted in locations with waterpipe smoke to determine accurate particle exposure concentrations. The concentrations of both particulate matter and carbon monoxide were above established air quality standards and therefore increase the health risks of both patrons and workers of these establishments.  相似文献   

15.
The association between traffic-related air pollution and adverse cardiovascular effects has been well documented; however, little is known about whether different commuting modes can modify the effects of air pollution on the cardiovascular system in human subjects in urban areas with heavy traffic. We recruited 120 young, healthy subjects in Taipei, Taiwan. Each participant was classified with different commuting modes according to his/her own commuting style. Three repeated measurements of heart rate variability (HRV) indices {standard deviation of NN intervals (SDNN) and the square root of the mean of the sum of the squares of differences between adjacent NN intervals (r-MSSD)}, particulate matter with an aerodynamic diameter ≤2.5 μm (PM2.5), temperature, humidity and noise level were conducted for each subject during 1-h morning commutes (0900–1000 h) in four different commuting modes, including an electrically powered subway, a gas-powered bus, a gasoline-powered car, and walking. Linear mixed-effects models were used to investigate the association of PM2.5 with HRV indices. The results showed that decreases in the HRV indices were associated with increased levels of PM2.5. The personal exposure levels to PM2.5 were the highest in the walking mode. The effects of PM2.5 on cardiovascular endpoints were the lowest in the subway mode compared to the effects in the walking mode. The participants in the car and bus modes had reduced effects on their cardiovascular endpoints compared to the participants in the walking mode. We concluded that traffic-related PM2.5 is associated with autonomic alteration. Commuting modes can modify the effects of PM2.5 on HRV indices among young, healthy subjects.  相似文献   

16.
Evidence for a role of long-term particulate matter exposure on acute respiratory infections is growing. However, which components of particulate matter may be causative remains largely unknown. We assessed associations between eight particulate matter elements and early-life pneumonia in seven birth cohort studies (Ntotal = 15,980): BAMSE (Sweden), GASPII (Italy), GINIplus and LISAplus (Germany), INMA (Spain), MAAS (United Kingdom) and PIAMA (The Netherlands). Annual average exposure to copper, iron, potassium, nickel, sulfur, silicon, vanadium and zinc, each respectively derived from particles with aerodynamic diameters  10 μm (PM10) and 2.5 μm (PM2.5), were estimated using standardized land use regression models and assigned to birth addresses. Cohort-specific associations between these exposures and parental reports of physician-diagnosed pneumonia between birth and two years were assessed using logistic regression models adjusted for host and environmental covariates and total PM10 or PM2.5 mass. Combined estimates were calculated using random-effects meta-analysis. There was substantial within and between-cohort variability in element concentrations. In the adjusted meta-analysis, pneumonia was weakly associated with zinc derived from PM10 (OR: 1.47 (95% CI: 0.99, 2.18) per 20 ng/m3 increase). No other associations with the other elements were consistently observed. The independent effect of particulate matter mass remained after adjustment for element concentrations. In conclusion, associations between particulate matter mass exposure and pneumonia were not explained by the elements we investigated. Zinc from PM10 was the only element which appeared independently associated with a higher risk of early-life pneumonia. As zinc is primarily attributable to non-tailpipe traffic emissions, these results may suggest a potential adverse effect of non-tailpipe emissions on health.  相似文献   

17.

Background

The association between exposure to air pollutants and mental disorders among adults has been suggested, although results are not consistent.

Objective

To analyze the association between long-term exposure to air pollution and history of anxiety and depression disorders and of medication use (benzodiazepines and antidepressants) in adults living in Barcelona.

Methods

A total of 958 adults (45–74 years old) residents in Barcelona, most of them having at least one of their parents diagnosed with dementia (86%), and participating in the ALFA (Alzheimer and Families) study, were included. We used Land Use Regression (LUR) models to estimate long-term residential exposure (period 2009–2014) to PM2.5, PM2.5 absorbance (PM2.5 abs), PM10, PM coarse, NO2 and NOx. Between 2013 and 2014 participants self-reported their history of anxiety and depression disorders and related medication use. The analysis was focused on those participants reporting outcome occurrence from 2009 onwards (until 2014).

Results

We observed an increased odds of history of depression disorders with increasing concentrations of all air pollutants [e.g. an increased odds of depression of 2.00 (95% CI; 1.37, 2.93) for each 10 μg/m3 NO2 increase]. Such associations were consistent with an increased odds of medication use in relation to higher concentrations of air pollutants [e.g. an increased odds of antidepressants use of 1.23 (1.04, 1.44) for each 20 μg/m3 NOx increase]. Associations regarding anxiety disorders did not reach statistical significance.

Conclusions

Our study shows that increasing long-term exposure to air pollution may increase the odds of depression and the use of antidepressants and benzodiazepines. Further studies are needed to replicate our results and confirm this association.  相似文献   

18.
《Vaccine》2016,34(50):6316-6322
ObjectiveAir pollution, weather condition and influenza are known risk factors of acute coronary syndrome (ACS) among elderly people. The influenza vaccine (IV) has been shown to reduce major cardiovascular events. The purpose of this study was to compare resistance to air pollution and weather factors causing ACS between vaccinated and less-vaccinated elderly people.MethodsA case–crossover design was applied to 1835 elderly ACS patients who were obtained from the 1-million sample of Taiwan National Health Insurance Research Data with inclusion criteria: (1) the first diagnosis of ACS was in cold season and at age 68 or more, (2) had received the free IV program at least once during the period 3 years before the ACS. They were stratified into two groups: 707 had received flu vaccinations for all the 3 years and the remaining 1128 had not. The measurements of air pollutants, temperature, and humidity corresponding to each of the 3 days prior to the ACS diagnosis date were retrieved from the data banks of the Taiwan Environmental Protection Administration and Central Weather Bureau.FindingsIncreases in air pollution concentrations of CO, NO2, PM10 or PM2.5 and decreases in temperature significantly influenced the risk of ACS for the non-continuously vaccinated elderly population; however, less significant effects were observed for the continuously vaccinated population.ConclusionConsecutive influenza vaccination may potentially offer resistance against the detrimental effects of air pollution and changes in temperature in frail elderly adults with ACS. Future studies are needed to directly assess the interaction effect between the vaccination and environmental factors on ACS.  相似文献   

19.
Chronic particulate matter less than 2.5 μm in diameter (PM2.5) exposure can leave infants more susceptible to illness. Our objective is to estimate associations of the chronic PM2.5 exposure with infant bronchiolitis and otitis media (OM) clinical encounters. We obtained all first time bronchiolitis (n = 18,029) and OM (n = 40,042) clinical encounters among children less than 12 and 36 months of age, respectively, diagnosed from 2001 to 2009 and two controls per case matched on birthdate and gestational age from the Pregnancy to Early Life Longitudinal data linkage system in Massachusetts. We applied conditional logistic regression to estimate odds ratios (OR) and confidence intervals (CI) per 2-μg/m3 increase in lifetime average satellite based PM2.5 exposure. Effect modification was assessed by age, gestational age, frequency of clinical encounter, and income. We examined associations between residential distance to roadways, traffic density, and infant bronchiolitis and OM risk. PM2.5 was not associated with infant bronchiolitis (OR = 1.02, 95% CI = 1.00, 1.04) and inversely associated with OM (OR = 0.97, 95% CI = 0.95, 0.99). There was no evidence of effect modification. Compared to infants living near low traffic density, infants residing in high traffic density had elevated risk of bronchiolitis (OR = 1.23, 95% CI = 1.14, 1.31) but not OM (OR = 0.98, 95% CI = 0.93, 1.02) clinical encounter. We did not find strong evidence to support an association between early-life long-term PM2.5 exposure and infant bronchiolitis or OM. Bronchiolitis risk was increased among infants living near high traffic density.  相似文献   

20.

Background

Air quality indices based on the maximum of sub-indices of pollutants are easy to produce and help quantify the degree of air pollution. However, they discount the additive effects of multiple pollutants and are only sensitive to changes in highest sub-index.

Objectives

We propose a simple and concise method to construct an air quality index that takes into account additive effects of multiple pollutants and evaluate the extent to which this index predicts health effects.

Materials and methods

We obtained concentrations of four criteria pollutants: particulate matter with aerodynamic diameter ≤ 10 μm (PM10), sulphur dioxide (SO2), nitrogen dioxide (NO2) and ozone (O3) and daily admissions to Hong Kong hospitals for cardiovascular and respiratory diseases for all ages and those 65 years or older for years 2001–2012. We derived sub-indices of the four criteria pollutants, calculated by normalizing pollutant concentrations to their respective short-term WHO Air Quality Guidelines (WHO AQG). We aggregated the sub-indices using the root-mean-power function with an optimal power to form an overall air quality index. The optimal power was determined by minimizing the sum of over- and under-estimated days. We then assessed associations between the pollution bands of the index and cardiovascular and respiratory admissions using a time-stratified case-crossover design adjusted for ambient temperature, relative humidity and influenza epidemics. Further, we conducted case-crossover analyses using the Hong Kong air quality data with the respective standards and classification of pollution bands of the China Air Quality Index (AQI), the United Kingdom Daily AQI (DAQI), and the United States Environmental Protection Agency (USEPA) AQI.

Results

The mean concentrations of PM10 and SO2 based on maximum 3-h mean exceeded the WHO AQG by 37% and 50%, respectively. We identified the combined condition of observed high-pollution days as either at least one pollutant > 1.5 × WHO AQG or at least two pollutants > 1.0 × WHO AQG to characterize the typical pollution profiles over the study period, which resulted in the optimal power = 3.0. The distribution of days in different pollution bands of the index was: 5.8% for “Low” (0–50), 37.6% for “Moderate” (51–100), 31.1% for “High” (101–150), 14.7% for “Very High” (151–200), and 10.8% for “Serious” (201+). For cardiovascular and respiratory admissions, there were significant associations with the pollution bands of the index for all ages and those 65 years or older. The trends of increasing pollution bands in relation to increasing excess risks of cardiovascular and respiratory admissions were significant for the proposed index, the China AQI, the UK DAQI and the USEPA AQI (P value for test for linear trend < 0.0001), suggesting a dose-response relation.

Conclusions

We have developed a simple and concise method to construct an air quality index that accounts for multiple pollutants to quantify air quality conditions for Hong Kong. Further developments are needed in order to support the extension of the method to other settings.  相似文献   

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