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1.

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   

2.

Background

Prenatal mercury (Hg) exposure is associated with adverse child neurobehavioral outcomes. Because Hg can interfere with placental functioning and cross the placenta to target the fetal brain, prenatal Hg exposure can inhibit fetal growth and development directly and indirectly.

Objectives

We examined potential associations between prenatal Hg exposure assessed through infant toenail Hg, placental DNA methylation changes, and newborn neurobehavioral outcomes.

Methods

The methylation status of > 485,000 CpG loci was interrogated in 192 placental samples using Illumina’s Infinium HumanMethylation450 BeadArray. Hg concentrations were analyzed in toenail clippings from a subset of 41 infants; neurobehavior was assessed using the NICU Network Neurobehavioral Scales (NNNS) in an independent subset of 151 infants.

Results

We identified 339 loci with an average methylation difference > 0.125 between any two toenail Hg tertiles. Variation among these loci was subsequently found to be associated with a high-risk neurodevelopmental profile (omnibus p-value = 0.007) characterized by the NNNS. Ten loci had p < 0.01 for the association between methylation and the high-risk NNNS profile. Six of 10 loci reside in the EMID2 gene and were hypomethylated in the 16 high-risk profile infants’ placentas. Methylation at these loci was moderately correlated (correlation coefficients range, –0.33 to –0.45) with EMID2 expression.

Conclusions

EMID2 hypomethylation may represent a novel mechanism linking in utero Hg exposure and adverse infant neurobehavioral outcomes.

Citation

Maccani JZ, Koestler DC, Lester B, Houseman EA, Armstrong DA, Kelsey KT, Marsit CJ. 2015. Placental DNA methylation related to both infant toenail mercury and adverse neurobehavioral outcomes. Environ Health Perspect 123:723–729; http://dx.doi.org/10.1289/ehp.1408561  相似文献   

3.

Background

The relationship between traffic-related air pollution (TRAP) and risk factors for cardiovascular disease needs to be better understood in order to address the adverse impact of air pollution on human health.

Objective

We examined associations between roadway proximity and traffic exposure zones, as markers of TRAP exposure, and metabolic biomarkers for cardiovascular disease risk in a cohort of patients undergoing cardiac catheterization.

Methods

We performed a cross-sectional study of 2,124 individuals residing in North Carolina (USA). Roadway proximity was assessed via distance to primary and secondary roadways, and we used residence in traffic exposure zones (TEZs) as a proxy for TRAP. Two categories of metabolic outcomes were studied: measures associated with glucose control, and measures associated with lipid metabolism. Statistical models were adjusted for race, sex, smoking, body mass index, and socioeconomic status (SES).

Results

An interquartile-range (990 m) decrease in distance to roadways was associated with higher fasting plasma glucose (β = 2.17 mg/dL; 95% CI: –0.24, 4.59), and the association appeared to be limited to women (β = 5.16 mg/dL; 95% CI: 1.48, 8.84 compared with β = 0.14 mg/dL; 95% CI: –3.04, 3.33 in men). Residence in TEZ 5 (high-speed traffic) and TEZ 6 (stop-and-go traffic), the two traffic zones assumed to have the highest levels of TRAP, was positively associated with high-density lipoprotein cholesterol (HDL-C; β = 8.36; 95% CI: –0.15, 16.9 and β = 5.98; 95% CI: –3.96, 15.9, for TEZ 5 and 6, respectively).

Conclusion

Proxy measures of TRAP exposure were associated with intermediate metabolic traits associated with cardiovascular disease, including fasting plasma glucose and possibly HDL-C.

Citation

Ward-Caviness CK, Kraus WE, Blach C, Haynes CS, Dowdy E, Miranda ML, Devlin RB, Diaz-Sanchez D, Cascio WE, Mukerjee S, Stallings C, Smith LA, Gregory SG, Shah SH, Hauser ER, Neas LM. 2015. Association of roadway proximity with fasting plasma glucose and metabolic risk factors for cardiovascular disease in a cross-sectional study of cardiac catheterization patients. Environ Health Perspect 123:1007–1014; http://dx.doi.org/10.1289/ehp.1306980  相似文献   

4.

Background:

Smoking is a risk factor for many human diseases. DNA methylation has been related to smoking, but genome-wide methylation data for smoking in Chinese populations is limited.

Objectives:

We aimed to investigate epigenome-wide methylation in relation to smoking in a Chinese population.

Methods:

We measured the methylation levels at > 485,000 CpG sites (CpGs) in DNA from leukocytes using a methylation array and conducted a genome-wide meta-analysis of DNA methylation and smoking in a total of 596 Chinese participants. We further evaluated the associations of smoking-related CpGs with internal polycyclic aromatic hydrocarbon (PAH) biomarkers and their correlations with the expression of corresponding genes.

Results:

We identified 318 CpGs whose methylation levels were associated with smoking at a genome-wide significance level (false discovery rate < 0.05), among which 161 CpGs annotated to 123 genes were not associated with smoking in recent studies of Europeans and African Americans. Of these smoking-related CpGs, methylation levels at 80 CpGs showed significant correlations with the expression of corresponding genes (including RUNX3, IL6R, PTAFR, ANKRD11, CEP135 and CDH23), and methylation at 15 CpGs was significantly associated with urinary 2-hydroxynaphthalene, the most representative internal monohydroxy-PAH biomarker for smoking.

Conclusion:

We identified DNA methylation markers associated with smoking in a Chinese population, including some markers that were also correlated with gene expression. Exposure to naphthalene, a byproduct of tobacco smoke, may contribute to smoking-related methylation.

Citation:

Zhu X, Li J, Deng S, Yu K, Liu X, Deng Q, Sun H, Zhang X, He M, Guo H, Chen W, Yuan J, Zhang B, Kuang D, He X, Bai Y, Han X, Liu B, Li X, Yang L, Jiang H, Zhang Y, Hu J, Cheng L, Luo X, Mei W, Zhou Z, Sun S, Zhang L, Liu C, Guo Y, Zhang Z, Hu FB, Liang L, Wu T. 2016. Genome-wide analysis of DNA methylation and cigarette smoking in Chinese. Environ Health Perspect 124:966–973; http://dx.doi.org/10.1289/ehp.1509834  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

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   

7.

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   

8.

Background

Although binge drinking and high resting heart rate independently affect cardiovascular and all-cause mortality risk, the combined effect of these two risk factors and their interaction has rarely been studied. This study examined the association between binge drinking and cardiovascular and all-cause mortality and evaluated the potential modifying effect on this association of resting heart rate in Korean men.

Methods

Men aged 55 years or older in 1985 (n = 2600) were followed for cardiovascular and all-cause mortality for 20.8 years, until 2005. We estimated hazard ratios (HRs) for cardiovascular and all-cause mortality by binge drinking and resting heart rate using the Cox proportional hazard model.

Results

Heavy binge drinkers (≥12 drinks on one occasion) with elevated resting heart rate (≥80 bpm) had a HR of 2.25 (95% confidence interval [CI], 1.47–3.45) for death from cardiovascular disease and 1.37 (95% CI, 0.87–2.14) for all-cause mortality compared to the reference group (non-drinking and resting heart rate 61–79 bpm). The HRs of dying from cardiovascular disease increased linearly from 1.36 to 1.52, 1.71, and 2.25 among individuals with resting heart rate greater than or equal to 80 bpm within the four alcohol consumption categories (non-drinking, non-binge, moderate binge, and heavy binge), respectively.

Conclusions

Our findings suggest that, among older Korean men, heavy binge drinkers with an elevated resting heart rate are at high risk for cardiovascular and all-cause mortality.Key words: alcohol drinking, binge drinking, cardiovascular disease, mortality, resting heart rate  相似文献   

9.

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   

10.

Background

Traffic noise has been associated with cardiovascular and metabolic disorders. Potential modes of action are through stress and sleep disturbance, which may lead to endocrine dysregulation and overweight.

Objectives

We aimed to investigate the relationship between residential traffic and railway noise and adiposity.

Methods

In this cross-sectional study of 57,053 middle-aged people, height, weight, waist circumference, and bioelectrical impedance were measured at enrollment (1993–1997). Body mass index (BMI), body fat mass index (BFMI), and lean body mass index (LBMI) were calculated. Residential exposure to road and railway traffic noise exposure was calculated using the Nordic prediction method. Associations between traffic noise and anthropometric measures at enrollment were analyzed using general linear models and logistic regression adjusted for demographic and lifestyle factors.

Results

Linear regression models adjusted for age, sex, and socioeconomic factors showed that 5-year mean road traffic noise exposure preceding enrollment was associated with a 0.35-cm wider waist circumference (95% CI: 0.21, 0.50) and a 0.18-point higher BMI (95% CI: 0.12, 0.23) per 10 dB. Small, significant increases were also found for BFMI and LBMI. All associations followed linear exposure–response relationships. Exposure to railway noise was not linearly associated with adiposity measures. However, exposure > 60 dB was associated with a 0.71-cm wider waist circumference (95% CI: 0.23, 1.19) and a 0.19-point higher BMI (95% CI: 0.0072, 0.37) compared with unexposed participants (0–20 dB).

Conclusions

The present study finds positive associations between residential exposure to road traffic and railway noise and adiposity.

Citation

Christensen JS, Raaschou-Nielsen O, Tjønneland A, Overvad K, Nordsborg RB, Ketzel M, Sørensen TI, Sørensen M. 2016. Road traffic and railway noise exposures and adiposity in adults: a cross-sectional analysis of the Danish Diet, Cancer, and Health cohort. Environ Health Perspect 124:329–335; http://dx.doi.org/10.1289/ehp.1409052  相似文献   

11.
Mind the Gap     

Background

Recent analysis has demonstrated a remarkably consistent, nonlinear relationship between estimated inhaled dose of combustion particles measured as PM2.5 (particulate matter with aerodynamic diameter ≤ 2.5 μm) and cardiovascular disease mortality over several orders of magnitude of dose—from cigarette smoking, environmental tobacco smoke (ETS) exposure, and ambient air pollution exposure.

Objectives

Here we discuss the implications of this relationship and point out the gaps in our knowledge that it reveals.

Discussion

The nonlinear exposure–response relationship that is revealed—much steeper at lower than at higher doses—explains the seemingly inconsistent risks observed from ambient air pollution and cigarette smoking but also raises important questions about the relative benefits of control at different points along the curve. This analysis also reveals a gap in the evidence base along the dose–response curve between ETS and active smoking, which is the dose range experienced by half the world’s population from indoor biomass and coal burning for cooking and heating.

Conclusions

The shape of the exposure–response relationship implies much larger public health benefits of reductions at the lower end of the dose spectrum (e.g., from reductions in outdoor air pollution) than from reducing the rate of active smoking, which seems counterintuitive and deserving of further study because of its importance for control policies. In addition, given the potential risks and consequent global disease burden, epidemiologic studies are urgently needed to quantify the cardiovascular risks of particulate matter exposures from indoor biomass burning in developing countries, which lie in the dose gap of current evidence.  相似文献   

12.

Background

It has recently been postulated that low mortality levels in the previous winter may increase the proportion of vulnerable individuals in the pool of people at risk of heat-related death during the summer months.

Objectives

We explored the sensitivity of heat-related mortality in summer (June–August) to mortality in the previous winter (December–February) in Seoul, Daegu, and Incheon in South Korea, from 1992 through 2007, excluding the summer of 1994.

Methods

Poisson regression models adapted for time-series data were used to estimate associations between a 1°C increase in average summer temperature (on the same day and the previous day) above thresholds specific for city, age, and cause of death, and daily mortality counts. Effects were estimated separately for summers preceded by winters with low and high mortality, with adjustment for secular trends.

Results

Temperatures above city-specific thresholds were associated with increased mortality in all three cities. Associations were stronger in summers preceded by winters with low versus high mortality levels for all nonaccidental deaths and, to a lesser extent, among persons ≥ 65 years of age. Effect modification by previous-winter mortality was not evident when we restricted deaths to cardiovascular disease outcomes in Seoul.

Conclusions

Our results suggest that low winter all-cause mortality leads to higher mortality during the next summer. Evidence of a relation between increased summer heat-related mortality and previous wintertime deaths has the potential to inform public health efforts to mitigate effects of hot weather.  相似文献   

13.

Background

Fatty acids (FAs) are essential for fetal growth. Exposure to perfluorinated chemicals (PFCs) may disrupt FA homeostasis, but there are no epidemiological data regarding associations of PFCs and FA concentrations.

Objectives

We estimated associations between perfluorooctane sulfonate (PFOS)/perfluorooctanoate (PFOA) concentrations and maternal levels of FAs and triglyceride (TG) and birth size of the offspring.

Methods

We analyzed 306 mother–child pairs in this birth cohort between 2002 and 2005 in Japan. The prenatal PFOS and PFOA levels were measured in maternal serum samples by liquid chromatography–tandem mass spectrometry. Maternal blood levels of nine FAs and TG were measured by gas chromatography–mass spectrometry and TG E-Test Wako kits, respectively. Information on infants’ birth size was obtained from participant medical records.

Results

The median PFOS and PFOA levels were 5.6 and 1.4 ng/mL, respectively. In the fully adjusted model, including maternal age, parity, annual household income, blood sampling period, alcohol consumption, and smoking during pregnancy, PFOS but not PFOA had a negative association with the levels of palmitic, palmitoleic, oleic, linoleic, α-linolenic, and arachidonic acids (p < 0.005) and TG (p-value = 0.016). Female infants weighed 186.6 g less with mothers whose PFOS levels were in the fourth quartile compared with the first quartile (95% CI: –363.4, –9.8). We observed no significant association between maternal levels of PFOS and birth weight of male infants.

Conclusions

Our data suggest an inverse association between PFOS exposure and polyunsaturated FA levels in pregnant women. We also found a negative association between maternal PFOS levels and female birth weight.

Citation

Kishi R, Nakajima T, Goudarzi H, Kobayashi S, Sasaki S, Okada E, Miyashita C, Itoh S, Araki A, Ikeno T, Iwasaki Y, Nakazawa H. 2015. The association of prenatal exposure to perfluorinated chemicals with maternal essential and long-chain polyunsaturated fatty acids during pregnancy and the birth weight of their offspring: the Hokkaido Study. Environ Health Perspect 123:1038–1045; http://dx.doi.org/10.1289/ehp.1408834  相似文献   

14.

Background

The temperature–mortality relationship has repeatedly been found, mostly in large cities, to be U/J-shaped, with higher minimum mortality temperature (MMT) at low latitudes being interpreted as indicating human adaptation to climate.

Objectives

Our aim was to partition space with a high-resolution grid to assess the temperature–mortality relationship in a territory with wide climate diversity, over a period with notable climate warming.

Methods

The 16,487,668 death certificates of persons > 65 years of age who died of natural causes in continental France (1968–2009) were analyzed. A 30-km × 30-km grid was placed over the map of France. Generalized additive model regression was used to assess the temperature–mortality relationship for each grid square, and extract the MMT and the RM25 and RM25/18 (respectively, the ratios of mortality at 25°C/MMT and 25°C/18°C). Three periods were considered: 1968–1981 (P1), 1982–1995 (P2), and 1996–2009 (P3).

Results

All temperature–mortality curves computed over the 42-year period were U/J-shaped. MMT and mean summer temperature were strongly correlated. Mean MMT increased from 17.5°C for P1 to 17.8°C for P2 and to 18.2°C for P3 and paralleled the summer temperature increase observed between P1 and P3. The temporal MMT rise was below that expected from the geographic analysis. The RM25/18 ratio of mortality at 25°C versus that at 18°C declined significantly (p = 5 × 10–5) as warming increased: 18% for P1, 16% for P2, and 15% for P3.

Conclusions

Results of this spatiotemporal analysis indicated some human adaptation to climate change, even in rural areas.

Citation:

Todd N, Valleron AJ. 2015. Space–time covariation of mortality with temperature: a systematic study of deaths in France, 1968–2009. Environ Health Perspect 123:659–664; http://dx.doi.org/10.1289/ehp.1307771  相似文献   

15.

Background

Long-term exposure to air pollution has been associated with mortality in urban cohort studies. Few studies have investigated this association in large-scale population registries, including non-urban populations.

Objectives

The aim of the study was to evaluate the associations between long-term exposure to air pollution and nonaccidental and cause-specific mortality in the Netherlands based on existing national databases.

Methods

We used existing Dutch national databases on mortality, individual characteristics, residence history, neighborhood characteristics, and national air pollution maps based on land use regression (LUR) techniques for particulates with an aerodynamic diameter ≤ 10 μm (PM10) and nitrogen dioxide (NO2). Using these databases, we established a cohort of 7.1 million individuals ≥ 30 years of age. We followed the cohort for 7 years (2004–2011). We applied Cox proportional hazard models adjusting for potential individual and area-specific confounders.

Results

After adjustment for individual and area-specific confounders, for each 10-μg/m3 increase, PM10 and NO2 were associated with nonaccidental mortality [hazard ratio (HR) = 1.08; 95% CI: 1.07, 1.09 and HR = 1.03; 95% CI: 1.02, 1.03, respectively], respiratory mortality (HR = 1.13; 95% CI: 1.10, 1.17 and HR = 1.02; 95% CI: 1.01, 1.03, respectively), and lung cancer mortality (HR = 1.26; 95% CI: 1.21, 1.30 and HR = 1.10 95% CI: 1.09, 1.11, respectively). Furthermore, PM10 was associated with circulatory disease mortality (HR = 1.06; 95% CI: 1.04, 1.08), but NO2 was not (HR = 1.00; 95% CI: 0.99, 1.01). PM10 associations were robust to adjustment for NO2; NO2 associations remained for nonaccidental mortality and lung cancer mortality after adjustment for PM10.

Conclusions

Long-term exposure to PM10 and NO2 was associated with nonaccidental and cause-specific mortality in the Dutch population of ≥ 30 years of age.

Citation

Fischer PH, Marra M, Ameling CB, Hoek G, Beelen R, de Hoogh K, Breugelmans O, Kruize H, Janssen NA, Houthuijs D. 2015. Air pollution and mortality in seven million adults: the Dutch Environmental Longitudinal Study (DUELS). Environ Health Perspect 123:697–704; http://dx.doi.org/10.1289/ehp.1408254  相似文献   

16.

Background

Although from a societal point of view a modal shift from car to bicycle may have beneficial health effects due to decreased air pollution emissions, decreased greenhouse gas emissions, and increased levels of physical activity, shifts in individual adverse health effects such as higher exposure to air pollution and risk of a traffic accident may prevail.

Objective

We describe whether the health benefits from the increased physical activity of a modal shift for urban commutes outweigh the health risks.

Data sources and extraction

We have summarized the literature for air pollution, traffic accidents, and physical activity using systematic reviews supplemented with recent key studies.

Data synthesis

We quantified the impact on all-cause mortality when 500,000 people would make a transition from car to bicycle for short trips on a daily basis in the Netherlands. We have expressed mortality impacts in life-years gained or lost, using life table calculations. For individuals who shift from car to bicycle, we estimated that beneficial effects of increased physical activity are substantially larger (3–14 months gained) than the potential mortality effect of increased inhaled air pollution doses (0.8–40 days lost) and the increase in traffic accidents (5–9 days lost). Societal benefits are even larger because of a modest reduction in air pollution and greenhouse gas emissions and traffic accidents.

Conclusions

On average, the estimated health benefits of cycling were substantially larger than the risks relative to car driving for individuals shifting their mode of transport.  相似文献   

17.

Background

Climate change may lead to more severe and extreme heat waves in the future, but its potential impact on sudden infant death—a leading cause of infant mortality—is unclear.

Objectives

We sought to determine whether risk of sudden infant death syndrome (SIDS) is elevated during hot weather.

Methods

We undertook a case-crossover analysis of all sudden infant deaths during warm periods in metropolitan Montreal, Quebec, Canada, from 1981 through 2010. Our analysis included a total of 196 certified cases of SIDS, including 89 deaths at 1–2 months of age, and 94 at 3–12 months. We estimated associations between maximum outdoor temperatures and SIDS by comparing outdoor temperatures on the day of or day before a SIDS event with temperatures on control days during the same month, using cubic splines to model temperature and adjusting for relative humidity.

Results

Maximum daily temperatures of ≥ 29°C on the same day were associated with 2.78 times greater odds of sudden infant death relative to 20°C (95% CI: 1.64, 4.70). The likelihood of sudden death increased steadily with higher temperature. Associations were stronger for infants 3–12 months of age than for infants 1–2 months of age, with odds ratios of 3.90 (95% CI: 1.87, 8.13) and 1.73 (95% CI: 0.80, 3.73), respectively, for 29°C compared with 20°C on the day of the event.

Conclusions

High ambient temperature may be a novel risk factor for SIDS, especially at ≥ 3 months of age. Climate change and the higher temperatures that result may account for a potentially greater proportion of sudden infant deaths in the future.

Citation

Auger N, Fraser WD, Smargiassi A, Kosatsky T. 2015. Ambient heat and sudden infant death: a case-crossover study spanning 30 years in Montreal, Canada. Environ Health Perspect 123:712–716; http://dx.doi.org/10.1289/ehp.1307960  相似文献   

18.

Background

Population pharmacokinetic models combined with multiple sets of age–concentration biomonitoring data facilitate back-calculation of chemical uptake rates from biomonitoring data.

Objectives

We back-calculated uptake rates of PBDEs for the Australian population from multiple biomonitoring surveys (top-down) and compared them with uptake rates calculated from dietary intake estimates of PBDEs and PBDE concentrations in dust (bottom-up).

Methods

Using three sets of PBDE elimination half-lives, we applied a population pharmacokinetic model to the PBDE biomonitoring data measured between 2002–2003 and 2010–2011 to derive the top-down uptake rates of four key PBDE congeners and six age groups. For the bottom-up approach, we used PBDE concentrations measured around 2005.

Results

Top-down uptake rates of Σ4BDE (the sum of BDEs 47, 99, 100, and 153) varied from 7.9 to 19 ng/kg/day for toddlers and from 1.2 to 3.0 ng/kg/day for adults; in most cases, they were—for all age groups—higher than the bottom-up uptake rates. The discrepancy was largest for toddlers with factors up to 7–15 depending on the congener. Despite different elimination half-lives of the four congeners, the age–concentration trends showed no increase in concentration with age and were similar for all congeners.

Conclusions

In the bottom-up approach, PBDE uptake is underestimated; currently known pathways are not sufficient to explain measured PBDE concentrations, especially in young children. Although PBDE exposure of toddlers has declined in the past years, pre- and postnatal exposure to PBDEs has remained almost constant because the mothers’ PBDE body burden has not yet decreased substantially.

Citation

Gyalpo T, Toms LM, Mueller JF, Harden FA, Scheringer M, Hungerbühler K. 2015. Insights into PBDE uptake, body burden, and elimination gained from Australian age–concentration trends observed shortly after peak exposure. Environ Health Perspect 123:978–984; http://dx.doi.org/10.1289/ehp.1408960  相似文献   

19.

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   

20.

Background

Epidemiologic studies of postnatal PCB exposure and behavior have not reported consistent evidence of adverse associations, possibly because of challenges in exposure estimation. We previously developed a pharmacokinetic model to improve estimation of children’s PCB exposure.

Objectives

We aimed to assess whether estimated serum PCB levels in infancy are associated with attention deficit/hyperactivity disorder (ADHD)–related behaviors at 8 years of age among children whose cord serum PCB levels were previously shown to be associated with ADHD-related behaviors.

Methods

We used a pharmacokinetic model to estimate monthly serum polychlorinated biphenyl (PCB)–153 levels in 441 infants (ages 1–12 months) based on parameters such as breastfeeding and cord serum PCB-153 levels. Behavior was evaluated at age 8 using the Conners’ Rating Scale for Teachers (CRS-T). Associations between PCB-153 levels and ADHD-related CRS-T indices were assessed using multivariable quantile regression at the 50th and 75th percentiles of CRS-T scores, where higher percentiles reflect more adverse behaviors.

Results

Cord serum PCB-153 levels (median, 38 ng/g lipids) were associated with ADHD-related behaviors, although statistical significance was observed with quantile regression models only at the 75th percentile. Associations with postnatal exposure estimates were attenuated. For example, hyperactive-impulsive behavior scores at age 8 years were 0.9 points (95% CI: 0.2, 2.5), 0.5 points (95% CI: 0.3, 2.3), and 0.3 points (95% CI: –0.2, 1.5) higher in association with interquartile range increases in serum PCB-153 at birth, 2 months, and 12 months of age, respectively.

Conclusions

Associations between estimated postnatal PCB-153 exposures and ADHD-related behaviors at 8 years of age were weaker than associations with PCB-153 concentrations measured in cord serum at birth.

Citation

Verner MA, Hart JE, Sagiv SK, Bellinger DC, Altshul LM, Korrick SA. 2015. Measured prenatal and estimated postnatal levels of polychlorinated biphenyls (PCBs) and ADHD-related behaviors in 8-year-old children. Environ Health Perspect 123:888–894; http://dx.doi.org/10.1289/ehp.1408084  相似文献   

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