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1.

Background

The International Agency for Research on Cancer (IARC) recently declared air pollution carcinogenic to humans. However, no study of air pollution and lung cancer to date has incorporated adjustment for exposure measurement error, and few have examined specific histological subtypes.

Objectives

Our aim was to assess the association of air pollution and incident lung cancer in the Netherlands Cohort Study on Diet and Cancer and the impact of measurement error on these associations.

Methods

The cohort was followed from 1986 through 2003, and 3,355 incident cases were identified. Cox proportional hazards models were used to estimate hazard ratios and 95% confidence intervals, for long-term exposures to nitrogen dioxide (NO2), black smoke (BS), PM2.5 (particulate matter with diameter ≤ 2.5 μm), and measures of roadway proximity and traffic volume, adjusted for potential confounders. Information from a previous validation study was used to correct the effect estimates for measurement error.

Results

We observed elevated risks of incident lung cancer with exposure to BS [hazard ratio (HR) = 1.16; 95% CI: 1.02, 1.32, per 10 μg/m3], NO2 (HR = 1.29; 95% CI: 1.08, 1.54, per 30 μg/m3), PM2.5 (HR = 1.17; 95% CI: 0.93, 1.47, per 10 μg/m3), and with measures of traffic at the baseline address. The exposures were positively associated with all lung cancer subtypes. After adjustment for measurement error, the HRs increased and the 95% CIs widened [HR = 1.19 (95% CI: 1.02, 1.39) for BS and HR = 1.37 (95% CI: 0.86, 2.17) for PM2.5].

Conclusions

These findings add support to a growing body of literature on the effects of air pollution on lung cancer. In addition, they highlight variation in measurement error by pollutant and support the implementation of measurement error corrections when possible.

Citation

Hart JE, Spiegelman D, Beelen R, Hoek G, Brunekreef B, Schouten LJ, van den Brandt P. 2015. Long-term ambient residential traffic–related exposures and measurement error–adjusted risk of incident lung cancer in the Netherlands Cohort Study on Diet and Cancer. Environ Health Perspect 123:860–866; http://dx.doi.org/10.1289/ehp.1408762  相似文献   

2.

Background

Physical activity reduces, whereas exposure to air pollution increases, the risk of premature mortality. Physical activity amplifies respiratory uptake and deposition of air pollutants in the lung, which may augment acute harmful effects of air pollution during exercise.

Objectives

We aimed to examine whether benefits of physical activity on mortality are moderated by long-term exposure to high air pollution levels in an urban setting.

Methods

A total of 52,061 subjects (50–65 years of age) from the Danish Diet, Cancer, and Health cohort, living in Aarhus and Copenhagen, reported data on physical activity in 1993–1997 and were followed until 2010. High exposure to air pollution was defined as the upper 25th percentile of modeled nitrogen dioxide (NO2) levels at residential addresses. We associated participation in sports, cycling, gardening, and walking with total and cause-specific mortality by Cox regression, and introduced NO2 as an interaction term.

Results

In total, 5,534 subjects died: 2,864 from cancer, 1,285 from cardiovascular disease, 354 from respiratory disease, and 122 from diabetes. Significant inverse associations of participation in sports, cycling, and gardening with total, cardiovascular, and diabetes mortality were not modified by NO2. Reductions in respiratory mortality associated with cycling and gardening were more pronounced among participants with moderate/low NO2 [hazard ratio (HR) = 0.55; 95% CI: 0.42, 0.72 and 0.55; 95% CI: 0.41, 0.73, respectively] than with high NO2 exposure (HR = 0.77; 95% CI: 0.54, 1.11 and HR = 0.81; 95% CI: 0.55, 1.18, p-interaction = 0.09 and 0.02, respectively).

Conclusions

In general, exposure to high levels of traffic-related air pollution did not modify associations, indicating beneficial effects of physical activity on mortality. These novel findings require replication in other study populations.

Citation

Andersen ZJ, de Nazelle A, Mendez MA, Garcia-Aymerich J, Hertel O, Tjønneland A, Overvad K, Raaschou-Nielsen O, Nieuwenhuijsen MJ. 2015. A study of the combined effects of physical activity and air pollution on mortality in elderly urban residents: the Danish Diet, Cancer, and Health cohort. Environ Health Perspect 123:557–563; http://dx.doi.org/10.1289/ehp.1408698  相似文献   

3.

Background

Long-term exposure to fine particles (particulate matter ≤ 2.5 μm; PM2.5) has been consistently linked to heart and lung disease. Recently, there has been increased interest in examining the effects of air pollution on the nervous system, with evidence showing potentially harmful effects on neurodegeneration.

Objective

Our objective was to assess the potential impact of long-term PM2.5 exposure on event time, defined as time to first admission for dementia, Alzheimer’s (AD), or Parkinson’s (PD) diseases in an elderly population across the northeastern United States.

Methods

We estimated the effects of PM2.5 on first hospital admission for dementia, AD, and PD among all Medicare enrollees ≥ 65 years in 50 northeastern U.S. cities (1999–2010). For each outcome, we first ran a Cox proportional hazards model for each city, adjusting for prior cardiopulmonary-related hospitalizations and year, and stratified by follow-up time, age, sex, and race. We then pooled the city-specific estimates by employing a random effects meta-regression.

Results

We followed approximately 9.8 million subjects and observed significant associations of long-term PM2.5 city-wide exposure with all three outcomes. Specifically, we estimated a hazard ratio (HR) of 1.08 (95% CI: 1.05, 1.11) for dementia, an HR of 1.15 (95% CI: 1.11, 1.19) for AD, and an HR of 1.08 (95% CI: 1.04, 1.12) for PD admissions per 1-μg/m3 increase in annual PM2.5 concentrations.

Conclusions

To our knowledge, this is the first study to examine the relationship between long-term exposure to PM2.5 and time to first hospitalization for common neurodegenerative diseases. We found strong evidence of association for all three outcomes. Our findings provide the basis for further studies, as the implications of such exposures could be crucial to public health.

Citation

Kioumourtzoglou MA, Schwartz JD, Weisskopf MG, Melly SJ, Wang Y, Dominici F, Zanobetti A. 2016. Long-term PM2.5 exposure and neurological hospital admissions in the northeastern United States. Environ Health Perspect 124:23–29; http://dx.doi.org/10.1289/ehp.1408973  相似文献   

4.

Background

Few studies examining the associations between long-term exposure to ambient air pollution and mortality have considered multiple pollutants when assessing changes in exposure due to residential mobility during follow-up.

Objective

We investigated associations between cause-specific mortality and ambient concentrations of fine particulate matter (≤ 2.5 μm; PM2.5), ozone (O3), and nitrogen dioxide (NO2) in a national cohort of about 2.5 million Canadians.

Methods

We assigned estimates of annual concentrations of these pollutants to the residential postal codes of subjects for each year during 16 years of follow-up. Historical tax data allowed us to track subjects’ residential postal code annually. We estimated hazard ratios (HRs) for each pollutant separately and adjusted for the other pollutants. We also estimated the product of the three HRs as a measure of the cumulative association with mortality for several causes of death for an increment of the mean minus the 5th percentile of each pollutant: 5.0 μg/m3 for PM2.5, 9.5 ppb for O3, and 8.1 ppb for NO2.

Results

PM2.5, O3, and NO2 were associated with nonaccidental and cause-specific mortality in single-pollutant models. Exposure to PM2.5 alone was not sufficient to fully characterize the toxicity of the atmospheric mix or to fully explain the risk of mortality associated with exposure to ambient pollution. Assuming additive associations, the estimated HR for nonaccidental mortality corresponding to a change in exposure from the mean to the 5th percentile for all three pollutants together was 1.075 (95% CI: 1.067, 1.084). Accounting for residential mobility had only a limited impact on the association between mortality and PM2.5 and O3, but increased associations with NO2.

Conclusions

In this large, national-level cohort, we found positive associations between several common causes of death and exposure to PM2.5, O3, and NO2.

Citation

Crouse DL, Peters PA, Hystad P, Brook JR, van Donkelaar A, Martin RV, Villeneuve PJ, Jerrett M, Goldberg MS, Pope CA III, Brauer M, Brook RD, Robichaud A, Menard R, Burnett RT. 2015. Ambient PM2.5, O3, and NO2 exposures and associations with mortality over 16 years of follow-up in the Canadian Census Health and Environment Cohort (CanCHEC). Environ Health Perspect 123:1180–1186; http://dx.doi.org/10.1289/ehp.1409276  相似文献   

5.

Background

Exposure to air pollution has been consistently associated with cardiovascular morbidity and mortality, but mechanisms remain uncertain. Associations with blood pressure (BP) may help to explain the cardiovascular effects of air pollution.

Objective

We examined the cross-sectional relationship between long-term (annual average) residential air pollution exposure and BP in the National Institute of Environmental Health Sciences’ Sister Study, a large U.S. cohort study investigating risk factors for breast cancer and other outcomes.

Methods

This analysis included 43,629 women 35–76 years of age, enrolled 2003–2009, who had a sister with breast cancer. Geographic information systems contributed to satellite-based nitrogen dioxide (NO2) and fine particulate matter (≤ 2.5 μm; PM2.5) predictions at participant residences at study entry. Generalized additive models were used to examine the relationship between pollutants and measured BP at study entry, adjusting for cardiovascular disease risk factors and including thin plate splines for potential spatial confounding.

Results

A 10-μg/m3 increase in PM2.5 was associated with 1.4-mmHg higher systolic BP (95% CI: 0.6, 2.3; p < 0.001), 1.0-mmHg higher pulse pressure (95% CI: 0.4, 1.7; p = 0.001), 0.8-mmHg higher mean arterial pressure (95% CI: 0.2, 1.4; p = 0.01), and no significant association with diastolic BP. A 10-ppb increase in NO2 was associated with a 0.4-mmHg (95% CI: 0.2, 0.6; p < 0.001) higher pulse pressure.

Conclusions

Long-term PM2.5 and NO2 exposures were associated with higher blood pressure. On a population scale, such air pollution–related increases in blood pressure could, in part, account for the increases in cardiovascular disease morbidity and mortality seen in prior studies.

Citation

Chan SH, Van Hee VC, Bergen S, Szpiro AA, DeRoo LA, London SJ, Marshall JD, Kaufman JD, Sandler DP. 2015. Long-term air pollution exposure and blood pressure in the Sister Study. Environ Health Perspect 123:951–958; http://dx.doi.org/10.1289/ehp.1408125  相似文献   

6.

Background

Pulmonary embolism (PE) is the most serious manifestation of venous thromboembolism and a leading cause of sudden death. Several studies have suggested associations of venous thromboembolism with short-term particulate matter (PM) exposure; evidence on long-term PM and traffic exposure is mixed.

Objectives

We examined the association of long-term exposure to PM2.5, PM2.5–10, and PM10 (PM with diameter of ≤ 2.5, 2.5–10, and ≤ 10 μm) and distance to roadways with overall incident PE and with PE subtypes in a cohort of U.S. women.

Methods

The study included 115,745 women from the Nurses’ Health Study, followed from 1992 through 2008. Incident PE cases were self-reported biennially. Nonidiopathic PE were cases for which the medical record revealed an underlying health condition related to PE (i.e., surgery, trauma, or malignancy); idiopathic PE were cases with no such history. We used spatiotemporal models combining spatial smoothing and geographic covariates to quantify exposure at residential addresses, and Cox proportional hazards models to calculate hazard ratios (HR) and 95% confidence intervals (CIs).

Results

PM2.5 averaged over 1 month (HR = 1.22; 95% CI: 1.04, 1.44) or 12 months (HR = 1.17; 95% CI: 0.93, 1.48) was associated with incident PE, after adjusting for known risk factors and PM2.5–10. Equivalent analyses restricted to PE subtypes showed a positive association for PM2.5 with nonidiopathic PE, but not with idiopathic PE. We did not find evidence of an association between distance to roadways and PE risk.

Conclusions

We provide evidence that PM in the prior 1 and 12 months is associated with PE risk. Our results also suggest that women with underlying health conditions may be more susceptible to PE after PM exposure.

Citation

Pun VC, Hart JE, Kabrhel C, Camargo CA Jr, Baccarelli AA, Laden F. 2015. Prospective study of ambient particulate matter exposure and risk of pulmonary embolism in the Nurses’ Health Study cohort. Environ Health Perspect 123:1265–1270; http://dx.doi.org/10.1289/ehp.1408927  相似文献   

7.

Background

The relationship of fine particulate matter < 2.5 μm in diameter (PM2.5) air pollution with mortality and cardiovascular disease is well established, with more recent long-term studies reporting larger effect sizes than earlier long-term studies. Some studies have suggested the coarse fraction, particles between 2.5 and 10 μm (PM10–2.5), may also be important. With respect to mortality and cardiovascular events, questions remain regarding the relative strength of effect sizes for chronic exposure to fine and coarse particles.

Objectives

We examined the relationship of chronic PM2.5 and PM10–2.5 exposures with all-cause mortality and fatal and nonfatal incident coronary heart disease (CHD), adjusting for time-varying covariates.

Methods

The current study included women from the Nurses’ Health Study living in metropolitan areas of the northeastern and midwestern United States. Follow-up was from 1992 to 2002. We used geographic information systems–based spatial smoothing models to estimate monthly exposures at each participant’s residence.

Results

We found increased risk of all-cause mortality [hazard ratio (HR), 1.26; 95% confidence interval (CI), 1.02–1.54] and fatal CHD (HR = 2.02; 95% CI, 1.07–3.78) associated with each 10-μg/m3 increase in annual PM2.5 exposure. The association between fatal CHD and PM10–2.5 was weaker.

Conclusions

Our findings contribute to growing evidence that chronic PM2.5 exposure is associated with risk of all-cause and cardiovascular mortality.  相似文献   

8.

Background

Both short- and long-term exposures to fine particulate matter (≤ 2.5 μm; PM2.5) are associated with mortality. However, whether the associations exist at levels below the new U.S. Environmental Protection Agency (EPA) standards (12 μg/m3 of annual average PM2.5, 35 μg/m3 daily) is unclear. In addition, it is not clear whether results from previous time series studies (fit in larger cities) and cohort studies (fit in convenience samples) are generalizable.

Objectives

We estimated the effects of low-concentration PM2.5 on mortality.

Methods

High resolution (1 km × 1 km) daily PM2.5 predictions, derived from satellite aerosol optical depth retrievals, were used. Poisson regressions were applied to a Medicare population (≥ 65 years of age) in New England to simultaneously estimate the acute and chronic effects of exposure to PM2.5, with mutual adjustment for short- and long-term exposure, as well as for area-based confounders. Models were also restricted to annual concentrations < 10 μg/m3 or daily concentrations < 30 μg/m3.

Results

PM2.5 was associated with increased mortality. In the study cohort, 2.14% (95% CI: 1.38, 2.89%) and 7.52% (95% CI: 1.95, 13.40%) increases were estimated for each 10-μg/m3 increase in short- (2 day) and long-term (1 year) exposure, respectively. The associations held for analyses restricted to low-concentration PM2.5 exposure, and the corresponding estimates were 2.14% (95% CI: 1.34, 2.95%) and 9.28% (95% CI: 0.76, 18.52%). Penalized spline models of long-term exposure indicated a larger effect for mortality in association with exposures ≥ 6 μg/m3 versus those < 6 μg/m3. In contrast, the association between short-term exposure and mortality appeared to be linear across the entire exposure distribution.

Conclusions

Using a mutually adjusted model, we estimated significant acute and chronic effects of PM2.5 exposure below the current U.S. EPA standards. These findings suggest that improving air quality with even lower PM2.5 than currently allowed by U.S. EPA standards may benefit public health.

Citation

Shi L, Zanobetti A, Kloog I, Coull BA, Koutrakis P, Melly SJ, Schwartz JD. 2016. Low-concentration PM2.5 and mortality: estimating acute and chronic effects in a population-based study. Environ Health Perspect 124:46–52; http://dx.doi.org/10.1289/ehp.1409111  相似文献   

9.

Background

Preeclampsia is a major complication of pregnancy that can lead to substantial maternal and perinatal morbidity, mortality, and preterm birth. Increasing evidence suggests that air pollution adversely affects pregnancy outcomes. Yet few studies have examined how local traffic-generated emissions affect preeclampsia in addition to preterm birth.

Objectives

We examined effects of residential exposure to local traffic-generated air pollution on preeclampsia and preterm delivery (PTD).

Methods

We identified 81,186 singleton birth records from four hospitals (1997–2006) in Los Angeles and Orange Counties, California (USA). We used a line-source dispersion model (CALINE4) to estimate individual exposure to local traffic-generated nitrogen oxides (NOx) and particulate matter < 2.5 μm in aerodynamic diameter (PM2.5) across the entire pregnancy. We used logistic regression to estimate effects of air pollution exposures on preeclampsia, PTD (gestational age < 37 weeks), moderate PTD (MPTD; gestational age < 35 weeks), and very PTD (VPTD; gestational age < 30 weeks).

Results

We observed elevated risks for preeclampsia and preterm birth from maternal exposure to local traffic-generated NOx and PM2.5. The risk of preeclampsia increased 33% [odds ratio (OR) = 1.33; 95% confidence interval (CI), 1.18–1.49] and 42% (OR = 1.42; 95% CI, 1.26–1.59) for the highest NOx and PM2.5 exposure quartiles, respectively. The risk of VPTD increased 128% (OR = 2.28; 95% CI, 2.15–2.42) and 81% (OR = 1.81; 95% CI, 1.71–1.92) for women in the highest NOx and PM2.5 exposure quartiles, respectively.

Conclusion

Exposure to local traffic-generated air pollution during pregnancy increases the risk of preeclampsia and preterm birth in Southern California women. These results provide further evidence that air pollution is associated with adverse reproductive outcomes.  相似文献   

10.

Background

Ambient air pollution has been linked to the development of gestational diabetes mellitus (GDM). However, evidence of the association is very limited, and no study has estimated the effects of ozone.

Objective

Our aim was to determine the association of prenatal exposures to particulate matter ≤ 2.5 μm (PM2.5) and ozone (O3) with GDM.

Methods

We used Florida birth vital statistics records to investigate the association between the risk of GDM and two air pollutants (PM2.5 and O3) among 410,267 women who gave birth in Florida between 2004 and 2005. Individual air pollution exposure was assessed at the woman’s home address at time of delivery using the hierarchical Bayesian space–time statistical model. We further estimated associations between air pollution exposures during different trimesters and GDM.

Results

After controlling for nine covariates, we observed increased odds of GDM with per 5-μg/m3 increase in PM2.5 (ORTrimester1 = 1.16; 95% CI: 1.11, 1.21; ORTrimester2 = 1.15; 95% CI: 1.10, 1.20; ORPregnancy = 1.20; 95% CI: 1.13, 1.26) and per 5-ppb increase in O3 (ORTrimester1 = 1.09; 95% CI: 1.07, 1.11; ORTrimester2 = 1.12; 95% CI: 1.10, 1.14; ORPregnancy = 1.18; 95% CI: 1.15, 1.21) during both the first trimester and second trimester as well as the full pregnancy in single-pollutant models. Compared with the single-pollutant model, the ORs for O3 were almost identical in the co-pollutant model. However, the ORs for PM2.5 during the first trimester and the full pregnancy were attenuated, and no association was observed for PM2.5 during the second trimester in the co-pollutant model (OR = 1.02; 95% CI: 0.98, 1.07).

Conclusion

This population-based study suggests that exposure to air pollution during pregnancy is associated with increased risk of GDM in Florida, USA.

Citation

Hu H, Ha S, Henderson BH, Warner TD, Roth J, Kan H, Xu X. 2015. Association of atmospheric particulate matter and ozone with gestational diabetes mellitus. Environ Health Perspect 123:853–859; http://dx.doi.org/10.1289/ehp.1408456  相似文献   

11.

Background

Air pollution is associated with morbidity and premature mortality. Satellite remote sensing provides globally consistent decadal-scale observations of ambient nitrogen dioxide (NO2) pollution.

Objective

We determined global population-weighted annual mean NO2 concentrations from 1996 through 2012.

Methods

We used observations of NO2 tropospheric column densities from three satellite instruments in combination with chemical transport modeling to produce a global 17-year record of ground-level NO2 at 0.1° × 0.1° resolution. We calculated linear trends in population-weighted annual mean NO2 (PWMNO2) concentrations in different regions around the world.

Results

We found that PWMNO2 in high-income North America (Canada and the United States) decreased more steeply than in any other region, having declined at a rate of –4.7%/year [95% confidence interval (CI): –5.3, –4.1]. PWMNO2 decreased in western Europe at a rate of –2.5%/year (95% CI: –3.0, –2.1). The highest PWMNO2 occurred in high-income Asia Pacific (predominantly Japan and South Korea) in 1996, with a subsequent decrease of –2.1%/year (95% CI: –2.7, –1.5). In contrast, PWMNO2 almost tripled in East Asia (China, North Korea, and Taiwan) at a rate of 6.7%/year (95% CI: 6.0, 7.3). The satellite-derived estimates of trends in ground-level NO2 were consistent with regional trends inferred from data obtained from ground-station monitoring networks in North America (within 0.7%/year) and Europe (within 0.3%/year). Our rankings of regional average NO2 and long-term trends differed from the satellite-derived estimates of fine particulate matter reported elsewhere, demonstrating the utility of both indicators to describe changing pollutant mixtures.

Conclusions

Long-term trends in satellite-derived ambient NO2 provide new information about changing global exposure to ambient air pollution. Our estimates are publicly available at http://fizz.phys.dal.ca/~atmos/martin/?page_id=232.

Citation

Geddes JA, Martin RV, Boys BL, van Donkelaar A. 2016. Long-term trends worldwide in ambient NO2 concentrations inferred from satellite observations. Environ Health Perspect 124:281–289; http://dx.doi.org/10.1289/ehp.1409567  相似文献   

12.

Background

Particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5) has been consistently associated with preterm birth (PTB) to varying degrees, but roles of PM2.5 species have been less studied.

Objective

We estimated risk differences (RD) of PTB (reported per 106 pregnancies) associated with change in ambient concentrations of elemental carbon (EC), organic carbon (OC), nitrates (NO3), and sulfates (SO4).

Methods

From live birth certificates from three states, we constructed a cohort of singleton pregnancies at or beyond 20 weeks of gestation from 2000 through 2005 (n = 1,771,225; 8% PTB). We estimated mean species exposures for each week of gestation from monitor-corrected Community Multi-Scale Air Quality modeling data. RDs and 95% confidence intervals (CIs) for four PTB categories were estimated for each exposure using linear regression, adjusted for maternal race/ethnicity, marital status, education, age, smoking, maximum temperature, ozone, and season of conception. We also adjusted for other species in multi-species models.

Results

RDs varied by exposure window and outcome period. EC was positively associated with PTB after 27 and before 35 weeks of gestation. For example, for a 0.25-μg/m3 increase in EC exposure during gestational week 9, RD = 96 (95% CI: –20, 213) and RD = 145 (95% CI: –50, 341) for PTB during weeks 28–31 and 32–34, respectively. Associations with OCs were null or negative. RDs for NO3 were elevated with exposure in early weeks of gestation, and null in later weeks. RDs for SO4 exposure were positively associated with PTB, though magnitude varied across gestational weeks. We observed effect measure modification for associations between EC and PTB by race/ethnicity and smoking status.

Conclusion

EC and SO4 may contribute to associations between PM2.5 and PTB. Associations varied according to the timing of exposure and the timing of PTB.

Citation

Rappazzo KM, Daniels JL, Messer LC, Poole C, Lobdell DT. 2015. Exposure to elemental carbon, organic carbon, nitrate, and sulfate fractions of fine particulate matter and risk of preterm birth in New Jersey, Ohio, and Pennsylvania (2000–2005). Environ Health Perspect 123:1059–1065; http://dx.doi.org/10.1289/ehp.1408953  相似文献   

13.

Background

Toxicological research suggests that coarse particles (PM10–2.5) are inflammatory, but responses are complex and may be best summarized by multiple inflammatory markers. Few human studies have investigated associations with PM10–2.5 and, of those, none have explored long-term exposures. Here we examine long-term associations with inflammation and coagulation in the Multi-Ethnic Study of Atherosclerosis.

Methods

Participants included 3,295 adults (45–84 years of age) from three metropolitan areas. Site-specific spatial models were used to estimate 5-year concentrations of PM10–2.5 mass and copper, zinc, phosphorus, silicon, and endotoxin found in PM10–2.5. Outcomes included interleukin-6, C-reactive protein, fibrinogen, total homocysteine, D-dimer, factor VIII, plasmin–antiplasmin complex, and inflammation and coagulation scores. We used multivariable regression with multiply imputed data to estimate associations while controlling for potential confounders, including co-pollutants such as fine particulate matter.

Results

Some limited evidence was found of relationships between inflammation and coagulation and PM10–2.5. Endotoxin was the PM10–2.5 component most strongly associated with inflammation, with an interquartile range (IQR) increase (0.08 EU/m3) associated with 0.15 (95% CI: 0.01, 0.28; p = 0.03) and 0.08 (95% CI: –0.07, 0.23; p = 0.28) higher inflammation scores before and after control for city, respectively. Copper was the component with the strongest association with coagulation, with a 4-ng/m3 increase associated with 0.19 (95% CI: 0.08, 0.30; p = 0.0008) and 0.12 (95% CI: –0.05, 0.30; p = 0.16) unit higher coagulation scores before and after city adjustment, respectively.

Conclusions

Our cross-sectional analysis provided some evidence that long-term PM10–2.5 exposure was associated with inflammation and coagulation, but associations were modest and depended on particle composition.

Citation

Adar SD, D’Souza J, Mendelsohn-Victor K, Jacobs DR Jr, Cushman M, Sheppard L, Thorne PS, Burke GL, Daviglus ML, Szpiro AA, Diez Roux AV, Kaufman JD, Larson TV. 2015. Markers of inflammation and coagulation after long-term exposure to coarse particulate matter: a cross-sectional analysis from the Multi-Ethnic Study of Atherosclerosis. Environ Health Perspect 123:541–548; http://dx.doi.org/10.1289/ehp.1308069  相似文献   

14.

Background

Previous studies have reported decreased birth weight associated with increased air pollutant concentrations during pregnancy. However, it is not clear when during pregnancy increases in air pollution are associated with the largest differences in birth weight.

Objectives

Using the natural experiment of air pollution declines during the 2008 Beijing Olympics, we evaluated whether having specific months of pregnancy (i.e., 1st…8th) during the 2008 Olympics period was associated with larger birth weights, compared with pregnancies during the same dates in 2007 or 2009.

Methods

Using n = 83,672 term births to mothers residing in four urban districts of Beijing, we estimated the difference in birth weight associated with having individual months of pregnancy during the 2008 Olympics (8 August–24 September 2008) compared with the same dates in 2007 and 2009. We also estimated the difference in birth weight associated with interquartile range (IQR) increases in mean ambient particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5), sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide (CO) concentrations during each pregnancy month.

Results

Babies whose 8th month of gestation occurred during the 2008 Olympics were, on average, 23 g larger (95% CI: 5 g, 40 g) than babies whose 8th month occurred during the same calendar dates in 2007 or 2009. IQR increases in PM2.5 (19.8 μg/m3), CO (0.3 ppm), SO2 (1.8 ppb), and NO2 (13.6 ppb) concentrations during the 8th month of pregnancy were associated with 18 g (95% CI: –32 g, –3 g), 17 g (95% CI: –28 g, –6 g), 23 g (95% CI: –36 g, –10 g), and 34 g (95% CI: –70 g, 3 g) decreases in birth weight, respectively. We did not see significant associations for months 1–7.

Conclusions

Short-term decreases in air pollution late in pregnancy in Beijing during the 2008 Summer Olympics, a normally heavily polluted city, were associated with higher birth weight.

Citation

Rich DQ, Liu K, Zhang J, Thurston SW, Stevens TP, Pan Y, Kane C, Weinberger B, Ohman-Strickland P, Woodruff TJ, Duan X, Assibey-Mensah V, Zhang J. 2015. Differences in birth weight associated with the 2008 Beijing Olympics air pollution reduction: results from a natural experiment. Environ Health Perspect 123:880–887; http://dx.doi.org/10.1289/ehp.1408795  相似文献   

15.

Background

PM2.5 (particulate matter ≤ 2.5 μm) has been associated with adverse cardiovascular outcomes, but it is unclear whether specific PM2.5 components, particularly metals, may be responsible for cardiovascular effects.

Objectives

We aimed to determine which PM2.5 components are associated with blood pressure in a longitudinal cohort.

Methods

We fit linear mixed-effects models with the adaptive LASSO penalty to longitudinal data from 718 elderly men in the Veterans Affairs Normative Aging Study, 1999–2010. We controlled for PM2.5 mass, age, body mass index, use of antihypertensive medication (ACE inhibitors, non-ophthalmic beta blockers, calcium channel blockers, diuretics, and angiotensin receptor antagonists), smoking status, alcohol intake, years of education, temperature, and season as fixed effects in the models, and additionally applied the adaptive LASSO method to select PM2.5 components associated with blood pressure. Final models were identified by the Bayesian Information Criterion (BIC).

Results

For systolic blood pressure (SBP), nickel (Ni) and sodium (Na) were selected by the adaptive LASSO, whereas only Ni was selected for diastolic blood pressure (DBP). An interquartile range increase (2.5 ng/m3) in 7-day moving-average Ni was associated with 2.48-mmHg (95% CI: 1.45, 3.50 mmHg) increase in SBP and 2.22-mmHg (95% CI: 1.69, 2.75 mmHg) increase in DBP, respectively. Associations were comparable when the analysis was restricted to study visits with PM2.5 below the 75th percentile of the distribution (12 μg/m3).

Conclusions

Our study suggested that exposure to ambient Ni was associated with increased blood pressure independent of PM2.5 mass in our study population of elderly men. Further research is needed to confirm our findings, assess generalizability to other populations, and identify potential mechanisms for Ni effects.

Citation

Dai L, Koutrakis P, Coull BA, Sparrow D, Vokonas PS, Schwartz JD. 2016. Use of the adaptive LASSO method to identify PM2.5 components associated with blood pressure in elderly men: the Veterans Affairs Normative Aging Study. Environ Health Perspect 124:120–125; http://dx.doi.org/10.1289/ehp.1409021  相似文献   

16.

Background

Autism spectrum disorder (ASD) is a developmental disorder with increasing prevalence worldwide, yet has unclear etiology.

Objective

We explored the association between maternal exposure to particulate matter (PM) air pollution and odds of ASD in her child.

Methods

We conducted a nested case–control study of participants in the Nurses’ Health Study II (NHS II), a prospective cohort of 116,430 U.S. female nurses recruited in 1989, followed by biennial mailed questionnaires. Subjects were NHS II participants’ children born 1990–2002 with ASD (n = 245), and children without ASD (n = 1,522) randomly selected using frequency matching for birth years. Diagnosis of ASD was based on maternal report, which was validated against the Autism Diagnostic Interview-Revised in a subset. Monthly averages of PM with diameters ≤ 2.5 μm (PM2.5) and 2.5–10 μm (PM10–2.5) were predicted from a spatiotemporal model for the continental United States and linked to residential addresses.

Results

PM2.5 exposure during pregnancy was associated with increased odds of ASD, with an adjusted odds ratio (OR) for ASD per interquartile range (IQR) higher PM2.5 (4.42 μg/m3) of 1.57 (95% CI: 1.22, 2.03) among women with the same address before and after pregnancy (160 cases, 986 controls). Associations with PM2.5 exposure 9 months before or after the pregnancy were weaker in independent models and null when all three time periods were included, whereas the association with the 9 months of pregnancy remained (OR = 1.63; 95% CI: 1.08, 2.47). The association between ASD and PM2.5 was stronger for exposure during the third trimester (OR = 1.42 per IQR increase in PM2.5; 95% CI: 1.09, 1.86) than during the first two trimesters (ORs = 1.06 and 1.00) when mutually adjusted. There was little association between PM10–2.5 and ASD.

Conclusions

Higher maternal exposure to PM2.5 during pregnancy, particularly the third trimester, was associated with greater odds of a child having ASD.

Citation

Raz R, Roberts AL, Lyall K, Hart JE, Just AC, Laden F, Weisskopf MG. 2015. Autism spectrum disorder and particulate matter air pollution before, during, and after pregnancy: a nested case–control analysis within the Nurses’ Health Study II cohort. Environ Health Perspect 123:264–270; http://dx.doi.org/10.1289/ehp.1408133  相似文献   

17.

Background

Prenatal exposure to air pollutants has been suggested as a possible etiologic factor for the occurrence of autism spectrum disorder.

Objectives

We aimed to assess whether prenatal air pollution exposure is associated with childhood autistic traits in the general population.

Methods

Ours was a collaborative study of four European population-based birth/child cohorts—CATSS (Sweden), Generation R (the Netherlands), GASPII (Italy), and INMA (Spain). Nitrogen oxides (NO2, NOx) and particulate matter (PM) with diameters of ≤ 2.5 μm (PM2.5), ≤ 10 μm (PM10), and between 2.5 and 10 μm (PMcoarse), and PM2.5 absorbance were estimated for birth addresses by land-use regression models based on monitoring campaigns performed between 2008 and 2011. Levels were extrapolated back in time to exact pregnancy periods. We quantitatively assessed autistic traits when the child was between 4 and 10 years of age. Children were classified with autistic traits within the borderline/clinical range and within the clinical range using validated cut-offs. Adjusted cohort-specific effect estimates were combined using random-effects meta-analysis.

Results

A total of 8,079 children were included. Prenatal air pollution exposure was not associated with autistic traits within the borderline/clinical range (odds ratio = 0.94; 95% CI: 0.81, 1.10 per each 10-μg/m3 increase in NO2 pregnancy levels). Similar results were observed in the different cohorts, for the other pollutants, and in assessments of children with autistic traits within the clinical range or children with autistic traits as a quantitative score.

Conclusions

Prenatal exposure to NO2 and PM was not associated with autistic traits in children from 4 to 10 years of age in four European population-based birth/child cohort studies.

Citation

Guxens M, Ghassabian A, Gong T, Garcia-Esteban R, Porta D, Giorgis-Allemand L, Almqvist C, Aranbarri A, Beelen R, Badaloni C, Cesaroni G, de Nazelle A, Estarlich M, Forastiere F, Forns J, Gehring U, Ibarluzea J, Jaddoe VW, Korek M, Lichtenstein P, Nieuwenhuijsen MJ, Rebagliato M, Slama R, Tiemeier H, Verhulst FC, Volk HE, Pershagen G, Brunekreef B, Sunyer J. 2016. Air pollution exposure during pregnancy and childhood autistic traits in four European population-based cohort studies: the ESCAPE Project. Environ Health Perspect 124:133–140; http://dx.doi.org/10.1289/ehp.1408483  相似文献   

18.

Background

Although several cohort studies report associations between chronic exposure to fine particles (PM2.5) and mortality, few have studied the effects of chronic exposure to ultrafine (UF) particles. In addition, few studies have estimated the effects of the constituents of either PM2.5 or UF particles.

Methods

We used a statewide cohort of > 100,000 women from the California Teachers Study who were followed from 2001 through 2007. Exposure data at the residential level were provided by a chemical transport model that computed pollutant concentrations from > 900 sources in California. Besides particle mass, monthly concentrations of 11 species and 8 sources or primary particles were generated at 4-km grids. We used a Cox proportional hazards model to estimate the association between the pollutants and all-cause, cardiovascular, ischemic heart disease (IHD), and respiratory mortality.

Results

We observed statistically significant (p < 0.05) associations of IHD with PM2.5 mass, nitrate, elemental carbon (EC), copper (Cu), and secondary organics and the sources gas- and diesel-fueled vehicles, meat cooking, and high-sulfur fuel combustion. The hazard ratio estimate of 1.19 (95% CI: 1.08, 1.31) for IHD in association with a 10-μg/m3 increase in PM2.5 is consistent with findings from the American Cancer Society cohort. We also observed significant positive associations between IHD and several UF components including EC, Cu, metals, and mobile sources.

Conclusions

Using an emissions-based model with a 4-km spatial scale, we observed significant positive associations between IHD mortality and both fine and ultrafine particle species and sources. Our results suggest that the exposure model effectively measured local exposures and facilitated the examination of the relative toxicity of particle species.

Citation

Ostro B, Hu J, Goldberg D, Reynolds P, Hertz A, Bernstein L, Kleeman MJ. 2015. Associations of mortality with long-term exposures to fine and ultrafine particles, species and sources: results from the California Teachers Study cohort. Environ Health Perspect 123:549–556; http://dx.doi.org/10.1289/ehp.1408565  相似文献   

19.

Background

There is substantial evidence that mortality increases in low temperatures. Less is known about the role of prolonged cold periods denoted as cold spells.

Objective

We conducted the first systematic review and meta-analysis to summarize the evidence on the adverse health effects of cold spells in varying climates.

Data sources and extraction

Four databases (Ovid Medline, PubMed, Scopus, Web of Science) were searched for all years and languages available. “Cold spell” was defined as an event below a temperature threshold lasting for a minimum duration of 2 days. Of 1,527 identified articles, 26 satisfied our eligibility criteria for the systematic review, and 9 were eligible for meta-analyses. The articles were grouped by the three main study questions into Overall-effect Group, Added-effect Group, and Temperature-change-effect Group.

Data synthesis

Based on random-effects models in the meta-analyses, cold spells were associated with increased mortality from all or all nonaccidental causes (summary rate ratio = 1.10; 95% CI: 1.04, 1.17 based on 9 estimates from five studies), cardiovascular diseases (1.11; 95% CI: 1.03, 1.19; 12 estimates from eight studies), and respiratory diseases (1.21; 95% CI: 0.97, 1.51; 8 estimates from four studies). Estimated associations were stronger for people ≥ 65 years of age (1.06; 95% CI: 1.00, 1.12) than for people 0–64 years of age (1.01; 95% CI: 1.00, 1.03). Study-specific effect estimates from a limited number of studies suggested an increased morbidity related to cold spells, but it was not possible to quantitatively summarize the evidence.

Conclusions

Cold spells are associated with increased mortality rates in populations around the world. The body of evidence suggests that cold spells also have other adverse health effects. There was substantial heterogeneity among the studies, which should be taken into account in the interpretation of the results.

Citation

Ryti NR, Guo Y, Jaakkola JJ. 2016. Global association of cold spells and adverse health effects: a systematic review and meta-analysis. Environ Health Perspect 124:12–22; http://dx.doi.org/10.1289/ehp.1408104  相似文献   

20.

Background:

In four European cohorts, we investigated the cross-sectional association between long-term exposure to air pollution and intima-media thickness of the common carotid artery (CIMT), a preclinical marker of atherosclerosis.

Methods:

Individually assigned levels of nitrogen dioxide, nitrogen oxides, particulate matter ≤ 2.5 μm (PM2.5), absorbance of PM2.5 (PM2.5abs), PM10, PMcoarse, and two indicators of residential proximity to highly trafficked roads were obtained under a standard exposure protocol (European Study of Cohorts for Air Pollution Effects—ESCAPE study) in the Stockholm area (Sweden), the Ausburg and Ruhr area (Germany), and the Girona area (Spain). We used linear regression and meta-analyses to examine the association between long-term exposure to air pollution and CIMT.

Results:

The meta-analysis with 9,183 individuals resulted in an estimated increase in CIMT (geometric mean) of 0.72% (95% CI: –0.65%, 2.10%) per 5-μg/m3 increase in PM2.5 and 0.42% (95% CI: –0.46%, 1.30%) per 10–5/m increase in PM2.5abs. Living in proximity to high traffic was also positively but not significantly associated with CIMT. Meta-analytic estimates for other pollutants were inconsistent. Results were similar across different adjustment sets and sensitivity analyses. In an extended meta-analysis for PM2.5 with three other previously published studies, a 0.78% (95% CI: –0.18%, 1.75%) increase in CIMT was estimated for a 5-μg/m3 contrast in PM2.5.

Conclusions:

Using a standardized exposure and analytical protocol in four European cohorts, we found that cross-sectional associations between CIMT and the eight ESCAPE markers of long-term residential air pollution exposure did not reach statistical significance. The additional meta-analysis of CIMT and PM2.5 across all published studies also was positive but not significant.

Citation:

Perez L, Wolf K, Hennig F, Penell J, Basagaña X, Foraster M, Aguilera I, Agis D, Beelen R, Brunekreef B, Cyrys J, Fuks KB, Adam M, Baldassarre D, Cirach M, Elosua R, Dratva J, Hampel R, Koenig W, Marrugat J, de Faire U, Pershagen G, Probst-Hensch NM, de Nazelle A, Nieuwenhuijsen MJ, Rathmann W, Rivera M, Seissler J, Schindler C, Thiery J, Hoffmann B, Peters A, Künzli N. 2015. Air pollution and atherosclerosis: a cross-sectional analysis of four European cohort studies in the ESCAPE Study. Environ Health Perspect 123:597–605; http://dx.doi.org/10.1289/ehp.1307711  相似文献   

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