• article

    Association of Traffic-Related Air Pollution with Children’s Neurobehavioral Functions in Quanzhou, China

    Abstract

    Background

    With the increase of motor vehicles, ambient air pollution related to traffic exhaust has become an important environmental issue in China. Because of their fast growth and development, children are more susceptible to ambient air pollution exposure. Many chemicals from traffic exhaust, such as carbon monoxide, nitrogen dioxide, and lead, have been reported to show adverse effects on neurobehavioral functions. Several studies in China have suggested that traffic exhaust might affect neurobehavioral functions of adults who have occupational traffic exhaust exposure. However, few data have been reported on the effects on neurobehavioral function in children.

    Objectives

    The objective of this study was to explore the association between traffic-related air pollution exposure and its effects on neurobehavioral function in children.

    Methods

    This field study was conducted in Quanzhou, China, where two primary schools were chosen based on traffic density and monitoring data of ambient air pollutants. School A was located in a clear area and school B in a polluted area. We monitored NO2 and particulate matter with aerodynamic diameter ≤ 10 μm as indicators for traffic-related air pollution on the campuses and in classrooms for 2 consecutive days in May 2005. The children from second grade (8–9 years of age) and third grade (9–10 years of age) of the two schools (n = 928) participated in a questionnaire survey and manual-assisted neurobehavioral testing. We selected 282 third-grade children (school A, 136; school B, 146) to participate in computer-assisted neurobehavioral testing. We conducted the fieldwork between May and June 2005. We used data from 861 participants (school A, 431; school B, 430) with manual neurobehavioral testing and from all participants with computerized testing for data analyses.

    Results

    Media concentrations of NO2 in school A and school B campus were 7 μg/m and 36 μg/m, respectively (p < 0.05). The ordinal logistic regression analyses showed that, after controlling the potential confounding factors, participants living in the polluted area showed poor performance on all testing; differences in results for six of nine tests (66.7%) achieved statistical significance: Visual Simple Reaction Time with preferred hand and with nonpreferred hand, Continuous Performance, Digit Symbol, Pursuit Aiming, and Sign Register.

    Conclusion

    We found a significant relationship between chronic low-level traffic-related air pollution exposure and neurobehavioral function in exposed children. More studies are needed to explore the effects of traffic exhaust on neurobehavioral function and development.

  • article

    Ambient Fine Particulate Matter Exposure and Myocardial Ischemia in the Environmental Epidemiology of Arrhythmogenesis in the Women’s Health Initiative (EEAWHI) Study

    Abstract

    Background

    Ambient particulate matter (PM) air pollution is associated with coronary heart disease, but the pathways underlying the association remain to be elucidated.

    Methods

    We studied the association between PM and ischemia among 57,908 Women’s Health Initiative clinical trial participants from 1999–2003. We used the Minnesota Code criteria to identify ST-segment and T-wave abnormalities, and estimated T amplitude (microvolt) from resting, standard 12-lead electrocardiogram (ECG). We used U.S. Environmental Protection Agency’s monitor data to estimate concentrations of PM < 2.5 μm (PM2.5) at geocoded participant addresses over 6 days before the ECGs (lag0 through lag5). We excluded 2,379 women with ECG QRS duration ≥ 120 msec.

    Results

    Overall, 6% of the remaining 55,529 women (52–90 years of age; 83% non-Hispanic white) had ST abnormalities and 16% had T abnormalities. Lead-specific T amplitude was normally distributed (range of means from −14 to 349 μV). PM2.5 (mean ± SD) averaged over lag0–2 was 14 ± 7 μg/m. In logistic and linear regression models adjusted for demographic, clinical, temporal, and climatic factors, a 10-μg/m increase in lag0–2 PM2.5 was associated with a 4% [95% confidence interval (CI), −3%, to 10%] increase in the odds of ST abnormality and a 5% (95% CI, 0% to 9%) increase in the odds of T abnormality. We observed corresponding decreases in T amplitude in all exam sites and leads except lead V1, reaching a minimum of −2 μV (95% CI, −5 to 0 μV) in lead V3.

    Conclusions

    Short-term PM2.5 exposure is associated with ECG evidence of myocardial ischemia among postmenopausal women. The principal manifestations include subclinical but potentially arrhythmogenic ST–T abnormalities and decreases in T amplitude.

  • article

    California Wildfires of 2008: Coarse and Fine Particulate Matter Toxicity

    Abstract

    Background

    During the last week of June 2008, central and northern California experienced thousands of forest and brush fires, giving rise to a week of severe fire-related particulate air pollution throughout the region. California experienced PM10–2.5 (particulate matter with mass median aerodynamic diameter > 2.5 μm to < 10 μm; coarse ) and PM2.5 (particulate matter with mass median aerodynamic diameter < 2.5 μm; fine) concentrations greatly in excess of the air quality standards and among the highest values reported at these stations since data have been collected.

    Objectives

    These observations prompt a number of questions about the health impact of exposure to elevated levels of PM10–2.5 and PM2.5 and about the specific toxicity of PM arising from wildfires in this region.

    Methods

    Toxicity of PM10–2.5 and PM2.5 obtained during the time of peak concentrations of smoke in the air was determined with a mouse bioassay and compared with PM samples collected under normal conditions from the region during the month of June 2007.

    Results

    Concentrations of PM were not only higher during the wildfire episodes, but the PM was much more toxic to the lung on an equal weight basis than was PM collected from normal ambient air in the region. Toxicity was manifested as increased neutrophils and protein in lung lavage and by histologic indicators of increased cell influx and edema in the lung.

    Conclusions

    We conclude that the wildfire PM contains chemical components toxic to the lung, especially to alveolar macrophages, and they are more toxic to the lung than equal doses of PM collected from ambient air from the same region during a comparable season.

  • article

    Association between GIS-Based Exposure to Urban Air Pollution during Pregnancy and Birth Weight in the INMA Sabadell Cohort

    Abstract

    Background

    There is growing evidence that traffic-related air pollution reduces birth weight. Improving exposure assessment is a key issue to advance in this research area.

    Objective

    We investigated the effect of prenatal exposure to traffic-related air pollution via geographic information system (GIS) models on birth weight in 570 newborns from the INMA (Environment and Childhood) Sabadell cohort.

    Methods

    We estimated pregnancy and trimester-specific exposures to nitrogen dioxide and aromatic hydrocarbons [benzene, toluene, ethylbenzene, m/p-xylene, and o-xylene (BTEX)] by using temporally adjusted land-use regression (LUR) models. We built models for NO2 and BTEX using four and three 1-week measurement campaigns, respectively, at 57 locations. We assessed the relationship between prenatal air pollution exposure and birth weight with linear regression models. We performed sensitivity analyses considering time spent at home and time spent in nonresidential outdoor environments during pregnancy.

    Results

    In the overall cohort, neither NO2 nor BTEX exposure was significantly associated with birth weight in any of the exposure periods. When considering only women who spent < 2 hr/day in nonresidential outdoor environments, the estimated reductions in birth weight associated with an interquartile range increase in BTEX exposure levels were 77 g [95% confidence interval (CI), 7–146 g] and 102 g (95% CI, 28–176 g) for exposures during the whole pregnancy and the second trimester, respectively. The effects of NO2 exposure were less clear in this subset.

    Conclusions

    The association of BTEX with reduced birth weight underscores the negative role of vehicle exhaust pollutants in reproductive health. Time–activity patterns during pregnancy complement GIS-based models in exposure assessment.

  • article

    Association between Local Traffic-Generated Air Pollution and Preeclampsia and Preterm Delivery in the South Coast Air Basin of California

    Abstract

    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.

  • article

    Limitations of Remotely Sensed Aerosol as a Spatial Proxy for Fine Particulate Matter

    Abstract

    Background

    Recent research highlights the promise of remotely sensed aerosol optical depth (AOD) as a proxy for ground-level particulate matter with aerodynamic diameter ≤ 2.5 μm (PM2.5). Particular interest lies in estimating spatial heterogeneity using AOD, with important application to estimating pollution exposure for public health purposes. Given the correlations reported between AOD and PM2.5, it is tempting to interpret the spatial patterns in AOD as reflecting patterns in PM2.5.

    Objectives

    We evaluated the degree to which AOD can help predict long-term average PM2.5 concentrations for use in chronic health studies.

    Methods

    We calculated correlations of AOD and PM2.5 at various temporal aggregations in the eastern United States in 2004 and used statistical models to assess the relationship between AOD and PM2.5 and the potential for improving predictions of PM2.5 in a subregion, the mid-Atlantic.

    Results

    We found only limited spatial associations of AOD from three satellite retrievals with daily and yearly PM2.5. The statistical modeling shows that monthly average AOD poorly reflects spatial patterns in PM2.5 because of systematic, spatially correlated discrepancies between AOD and PM2.5. Furthermore, when we included AOD as a predictor of monthly PM2.5 in a statistical prediction model, AOD provided little additional information in a model that already accounts for land use, emission sources, meteorology, and regional variability.

    Conclusions

    These results suggest caution in using spatial variation in currently available AOD to stand in for spatial variation in ground-level PM2.5 in epidemiologic analyses and indicate that when PM2.5 monitoring is available, careful statistical modeling outperforms the use of AOD.

  • article

    Modification of the Interleukin-6 Response to Air Pollution by Interleukin-6 and Fibrinogen Polymorphisms

    Abstract

    Background

    Evidence suggests that cardiovascular effects of air pollution are mediated by inflammation and that air pollution can induce genetic expression of the interleukin-6 gene (IL6).

    Objectives

    We investigated whether IL6 and fibrinogen gene variants can affect plasma IL-6 responses to air pollution in patients with cardiovascular disease.

    Methods

    We repeatedly determined plasma IL-6 in 955 myocardial infarction survivors from six European cities (n = 5,539). We conducted city-specific analyses using additive mixed models adjusting for patient characteristics, time trend, and weather to assess the impact of air pollutants on plasma IL-6. We pooled city-specific estimates using meta-analysis methodology. We selected three IL6 single-nucleotide polymorphisms (SNPs) and one SNP each from the fibrinogen α-chain gene (FGA) and β-chain gene (FGB) for gene–environment analyses.

    Results

    We found the most consistent modifications for variants in IL6 rs2069832 and FBG rs1800790 after exposure to carbon monoxide (CO; 24-hr average; p-values for interaction, 0.034 and 0.019, respectively). Nitrogen dioxide effects were consistently modified, but p-values for interaction were larger (0.09 and 0.19, respectively). The strongest effects were seen 6–11 hr after exposure, when, for example, the overall effect of a 2.2% increase in IL-6 per 0.64 mg/m CO was modified to a 10% (95% confidence interval, 4.6–16%) increase in IL-6 (p-value for interaction = 0.002) for minor homozygotes of FGB rs1800790.

    Conclusions

    The effect of gaseous traffic-related air pollution on inflammation may be stronger in genetic subpopulations with ischemic heart disease. This information could offer an opportunity to identify postinfarction patients who would benefit more than others from a cleaner environment and antiinflammatory treatment.

  • article

    Decreased PM10 Exposure Attenuates Age-Related Lung Function Decline: Genetic Variants in p53, p21, and CCND1 Modify This Effect

    Abstract

    Background

    Decreasing exposure to airborne particulates was previously associated with reduced age-related decline in lung function. However, whether the benefit from improved air quality depends on genetic background is not known. Recent evidence points to the involvement of the genes p53 and p21 and of the cell cycle control gene cyclin D1 (CCND1) in the response of bronchial cells to air pollution.

    Objective

    We determined in 4,326 participants of the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA) whether four single-nucleotide polymorphisms in three genes [CCND1 (rs9344 [P242P], rs667515), p53 (rs1042522 [R72P]), and p21 (rs1801270 [S31R])] modified the previously observed attenuation of the decline in the forced expiratory flow between 25% and 75% of the forced vital capacity (FEF25–75) associated with improved air quality.

    Methods

    Subjects of the prospective population-based SAPALDIA cohort were assessed in 1991 and 2002 by spirometry, questionnaires, and biological sample collection for genotyping. We assigned spatially resolved concentrations of particulate matter with aerodynamic diameter ≤ 10 μm (PM10) to each participant’s residential history 12 months before the baseline and follow-up assessments.

    Results

    The effect of diminishing PM10 exposure on FEF25–75 decline appeared to be modified by p53 R72P, CCND1 P242P, and CCND1 rs667515. For example, a 10-μg/m decline in aver-age PM10 exposure over an 11-year period attenuated the average annual decline in FEF25–75 by 21.33 mL/year (95% confidence interval, 10.57–32.08) among participants homozygous for the CCND1 (P242P) GG genotype, by 13.72 mL/year (5.38–22.06) among GA genotypes, and by 6.00 mL/year (−4.54 to 16.54) among AA genotypes.

    Conclusions

    Our results suggest that cell cycle control genes may modify the degree to which improved air quality may benefit respiratory function in adults.

  • article

    Effects of Ambient Air Pollution on Hemostasis and Inflammation

    Abstract

    Background

    Air pollution has consistently been associated with increased morbidity and mortality due to respiratory and cardiovascular disease. Underlying biological mechanisms are not entirely clear, and hemostasis and inflammation are suggested to be involved.

    Objectives

    Our aim was to study the association of the variation in local concentrations of airborne particulate matter (PM) with aerodynamic diameter < 10 μm, carbon monoxide, nitrogen monoxide, nitrogen dioxide, and ozone with platelet aggregation, thrombin generation, fibrinogen, and C-reactive protein (CRP) levels in healthy individuals.

    Methods

    From 40 healthy volunteers, we collected 13 consecutive blood samples within a 1-year period and measured light-transmittance platelet aggregometry, thrombin generation, fibrinogen, and CRP. We performed regression analysis using generalized additive models to study the association between the hemostatic and inflammatory variables, and local environmental concentrations of air pollutants for time lags within 24 hr before blood sampling or 24–96 hr before blood sampling.

    Results

    In general, air pollutants were associated with platelet aggregation [average, +8% per interquartile range (IQR), p < 0.01] and thrombin generation (average, +1% per IQR, p < 0.05). Platelet aggregation was not affected by in vitro incubation of plasma with PM. We observed no relationship between any of the air pollutants and fibrinogen or CRP levels.

    Conclusions

    Air pollution increased platelet aggregation as well as coagulation activity but had no clear effect on systemic inflammation. These prothrombotic effects may partly explain the relationship between air pollution and the risk of ischemic cardiovascular disease.

  • article

    Self-Reported Truck Traffic on the Street of Residence and Symptoms of Asthma and Allergic Disease: A Global Relationship in ISAAC Phase 3

    Abstract

    Background

    Associations between traffic pollution on the street of residence and a range of respiratory and allergic outcomes in children have been reported in developed countries, but little is known about such associations in developing countries.

    Methods

    The third phase of the International Study of Asthma and Allergies in Childhood (ISAAC) was carried out in 13- to 14-year-old and 6- to 7-year-old children across the world. A question about frequency of truck traffic on the street of residence was included in an additional questionnaire. We investigated the association between self-reported truck traffic on the street of residence and symptoms of asthma, rhinoconjunctivitis, and eczema with logistic regression. Adjustments were made for sex, region of the world, language, gross national income, and 10 other subject-specific covariates.

    Results

    Frequency of truck traffic on the street of residence was positively associated with the prevalence of symptoms of asthma, rhinoconjunctivitis, and eczema with an exposure–response relationship. Odds ratios (95% confidence intervals) for “current wheeze” and “almost the whole day” versus “never” truck traffic were 1.35 (1.23–1.49) for 13- to 14-year-olds and 1.35 (1.22–1.48) for 6- to 7-year-olds.

    Conclusions

    Higher exposure to self-reported truck traffic on the street of residence is associated with increased reports of symptoms of asthma, rhinitis, and eczema in many locations in the world. These findings require further investigation in view of increasing exposure of the world’s children to traffic.

  • article

    Exposure to Traffic Pollution and Increased Risk of Rheumatoid Arthritis

    Abstract

    Background

    Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease that affects approximately 1% of the adult population, and to date, genetic factors explain < 50% of the risk. Particulate air pollution, especially of traffic origin, has been linked to systemic inflammation in many studies.

    Objectives

    We examined the association of distance to road, a marker of traffic pollution exposure, and incidence of RA in a prospective cohort study.

    Methods

    We studied 90,297 U.S. women in the Nurses’ Health Study. We used a geographic information system to determine distance to road at the residence in 2000 as a measure of traffic exposure. Using Cox proportional hazard models, we examined the association of distance to road and incident RA (1976–2004) with adjustment for a large number of potential confounders.

    Results

    In models adjusted for age, calendar year, race, cigarette smoking, parity, lactation, menopausal status and hormone use, oral contraceptive use, body mass index, physical activity, and census-tract-level median income and house value, we observed an elevated risk of RA [hazard ratio (HR) = 1.31; 95% confidence interval (CI), 0.98–1.74] in women living within 50 m of a road, compared with those women living 200 m or farther away. We also observed this association in analyses among nonsmokers (HR = 1.62; 95% CI, 1.04–2.52), nonsmokers with rheumatoid factor (RF)-negative RA (HR = 1.77; 95% CI, 0.93–3.38), and nonsmokers with RF-positive RA (HR = 1.51; 95% CI, 0.82–2.77). We saw no elevations in risk in women living 50–200 m from the road.

    Conclusions

    The observed association between exposure to traffic pollution and RA suggests that pollution from traffic in adulthood may be a newly identified environmental risk factor for RA.

  • article

    Baseline Repeated Measures from Controlled Human Exposure Studies: Associations between Ambient Air Pollution Exposure and the Systemic Inflammatory Biomarkers IL-6 and Fibrinogen

    Abstract

    Introduction

    Systemic inflammation may be one of the mechanisms mediating the association between ambient air pollution and cardiovascular morbidity and mortality. Interleukin-6 (IL-6) and fibrinogen are biomarkers of systemic inflammation that are independent risk factors for cardiovascular disease.

    Objective

    We investigated the association between ambient air pollution and systemic inflammation using baseline measurements of IL-6 and fibrinogen from controlled human exposure studies.

    Methods

    In this retrospective analysis we used repeated-measures data in 45 nonsmoking subjects. Hourly and daily moving averages were calculated for ozone, nitrogen dioxide, sulfur dioxide, and particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5). Linear mixed-model regression determined the effects of the pollutants on systemic IL-6 and fibrinogen. Effect modification by season was considered.

    Results

    We observed a positive association between IL-6 and O3 [0.31 SD per O3 interquartile range (IQR); 95% confidence interval (CI), 0.08–0.54] and between IL-6 and SO2 (0.25 SD per SO2 IQR; 95% CI, 0.06–0.43). We observed the strongest effects using 4-day moving averages. Responses to pollutants varied by season and tended to be higher in the summer, particularly for O3 and PM2.5. Fibrinogen was not associated with pollution.

    Conclusions

    This study demonstrates a significant association between ambient pollutant levels and baseline levels of systemic IL-6. These findings have potential implications for controlled human exposure studies. Future research should consider whether ambient pollution exposure before chamber exposure modifies IL-6 response.

  • article

    Chronic Fine and Coarse Particulate Exposure, Mortality, and Coronary Heart Disease in the Nurses’ Health Study

    Abstract

    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/m 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.

  • article

    Traffic-Related Air Pollution, Oxidative Stress Genes, and Asthma (ECHRS)

    Abstract

    Background

    Traffic-related air pollution is related with asthma, and this association may be modified by genetic factors.

    Objectives

    We investigated the role of genetic polymorphisms potentially modifying the association between home outdoor levels of modeled nitrogen dioxide and asthma.

    Methods

    Adults from 13 cities of the second European Community Respiratory Health Survey (ECRHS II) were included (n = 2,920), for whom both DNA and outdoor NO2 estimates were available. Home addresses were geocoded and linked to modeled outdoor NO2 estimates, as a marker of local traffic-related pollution. We examined asthma prevalence and evaluated polymorphisms in genes involved in oxidative stress pathways [gluthatione S-transferases M1 (GSTM1), T1 (GSTT1), and P1 (GSTP1) and NAD(P)H:quinine oxidoreductase (NQO1)], inflammatory response [tumor necrosis factor α (TNFA)], immunologic response [Toll-like receptor 4 (TLR4)], and airway reactivity [adrenergic receptor β2 (ADRB2)].

    Results

    The association between modeled NO2 and asthma prevalence was significant for carriers of the most common genotypes of NQO1 rs2917666 [odds ratio (OR) = 1.54; 95% confidence interval (CI), 1.10–2.24], TNFA rs2844484 (OR = 2.02; 95% CI, 1.30–3.27). For new-onset asthma, the effect of NO2 was significant for the most common genotype of NQO1 rs2917666 (OR = 1.52; 95% CI, 1.09–2.16). A significant interaction was found between NQO1 rs2917666 and NO2 for asthma prevalence (p = 0.02) and new-onset asthma (p = 0.04).

    Conclusions

    Genetic polymorphisms in the NQO1 gene are related to asthma susceptibility among persons exposed to local traffic-related air pollution. This points to the importance of antioxidant pathways in the protection against the effects of air pollution on asthma.

  • article

    Air Pollution, Aeroallergens, and Emergency Room Visits for Acute Respiratory Diseases and Gastroenteric Disorders among Young Children in Six Italian Cities

    Abstract

    Background

    Past studies reported evidence of associations between air pollution and respiratory symptoms and morbidity for children. Few studies examined associations between air pollution and emergency room (ER) visits for wheezing, and even fewer for gastroenteric illness. We conducted a multicity analysis of the relationship between air pollution and ER visits for wheezing and gastroenteric disorder in children 0–2 years of age.

    Methods

    We obtained ER visit records for wheezing and gastroenteric disorder from six Italian cities. A city-specific case–crossover analysis was applied to estimate effects of particulate matter (PM), nitrogen dioxide, sulfur dioxide, ozone, and carbon monoxide, adjusting for immediate and delayed effects of temperature. Lagged effects of air pollutants up to 6 prior days were examined. The city-specific results were combined using a random-effect meta-analysis.

    Results

    CO and SO2 were most strongly associated with wheezing, with a 2.7% increase [95% confidence interval (CI), 0.5–4.9] for a 1.04-μg/m increase in 7-day average CO and a 3.4% (95% CI, 1.5–5.3) increase for an 8.0-μg/m increase in SO2. Positive associations were also found for PM with aerodynamic diameter ≤ 10 μg and NO2. We found a significant association between the 3-day moving average CO and gastroenteric disorders [3.8% increase (95% CI, 1.0–6.8)]. When data were stratified by season, the associations were stronger in summer for wheezing and in winter for gastroenteric disorders.

    Conclusion

    Air pollution is associated with triggering of wheezing and gastroenteric disorders in children 0–2 years of age; more work is needed to understand the mechanisms to help prevent wheezing in children.

  • article

    A Framework for Examining Social Stress and Susceptibility to Air Pollution in Respiratory Health

    Abstract

    Objective

    There is growing interest in disentangling the health effects of spatially clustered social and physical environmental exposures and in exploring potential synergies among them, with particular attention directed to the combined effects of psychosocial stress and air pollution. Both exposures may be elevated in lower-income urban communities, and it has been hypothesized that stress, which can influence immune function and susceptibility, may potentiate the effects of air pollution in respiratory disease onset and exacerbation. In this paper, we attempt to synthesize the relevant research from social and environmental epidemiology, toxicology, immunology, and exposure assessment to provide a useful framework for environmental health researchers aiming to investigate the health effects of environmental pollution in combination with social or psychological factors.

    Data synthesis

    We review the existing epidemiologic and toxicologic evidence on synergistic effects of stress and pollution, and then describe the physiologic effects of stress and key issues related to measuring and evaluating stress as it relates to physical environmental exposures and susceptibility. Finally, we identify some of the major methodologic challenges ahead as we work toward disentangling the health effects of clustered social and physical exposures and accurately describing the interplay among these exposures.

    Conclusions

    There is still tremendous work to be done toward understanding the combined and potentially synergistic health effects of stress and pollution. As this research proceeds, we recommend careful attention to the relative temporalities of stress and pollution exposures, to nonlinearities in their independent and combined effects, to physiologic pathways not elucidated by epidemiologic methods, and to the relative spatial distributions of social and physical exposures at multiple geographic scales.

  • article

    Central Neuroplasticity and Decreased Heart Rate Variability after Particulate Matter Exposure in Mice

    Abstract

    Background

    Epidemiologic studies show that exposure to fine particulate matter [aerodynamic diameter ≤ 2.5 μm (PM2.5)] increases the total daily cardiovascular mortality. Impaired cardiac autonomic function, which manifests as reduced heart rate variability (HRV), may be one of the underlying causes. However, the cellular mechanism(s) by which PM2.5 exposure induces decreased HRV is not known.

    Objectives

    We tested the hypothesis that exposure to PM2.5 impairs HRV by decreasing the excitability of the cardiac vagal neurons in the nucleus ambiguus. We also detemined the effect of iron on PM-exposure–induced decrease in HRV.

    Methods

    We measured 24-hr HRV in time domains from electrocardiogram telemetry recordings obtained in conscious, freely moving mice after 3 days of exposure to PM2.5 in the form of soot only or iron-soot. In parallel studies, we determined the intrinsic properties of identified cardiac vagal neurons, retrogradely labeled with a fluorescent dye applied to the sinoatrial node.

    Results

    Soot-only exposure decreased short-term HRV (root mean square of successive difference). With the addition of iron, all HRV parameters were significantly reduced. In nonexposed mice, vagal blockade significantly reduced all HRV parameters, suggesting that HRV is, in part, under vagal regulation in mice. Iron-soot exposure had no significant effect on resting membrane potential but decreased spiking responses of the identified cardiac vagal neurons to depolarizations (p < 0.05). The decreased spiking response was accompanied with a higher minimal depolarizing current required to evoke spikes and a lower peak discharge frequency.

    Conclusions

    The data suggest that PM-induced neuroplasticity of cardiac vagal neurons may be one mechanism contributing to the cardiovascular consequences associated with PM2.5 exposure seen in humans.

  • article

    Association of Heart Rate Variability in Taxi Drivers with Marked Changes in Particulate Air Pollution in Beijing in 2008

    Abstract

    Background

    Heart rate variability (HRV), a marker of cardiac autonomic function, has been associated with particulate matter (PM) air pollution, especially in older patients and those with cardiovascular diseases. However, the effect of PM exposure on cardiac autonomic function in young, healthy adults has received less attention.

    Objectives

    We evaluated the relationship between exposure to traffic-related PM with an aerodynamic diameter ≤ 2.5 μm (PM2.5) and HRV in a highly exposed panel of taxi drivers.

    Methods

    Continuous measurements of personal exposure to PM2.5 and ambulatory electrocardiogram monitoring were conducted on 11 young healthy taxi drivers for a 12-hr work shift during their work time (0900–2100 hr) before, during, and after the Beijing 2008 Olympic Games. Mixed-effects regression models were used to estimate associations between PM2.5 exposure and percent changes in 5-min HRV indices after combining data from the three time periods and controlling for potentially confounding variables.

    Results

    Personal exposures of taxi drivers to PM2.5 changed markedly across the three time periods. The standard deviation of normal-to-normal (SDNN) intervals decreased by 2.2% [95% confidence interval (CI), −3.8% to −0.6%] with an interquartile range (IQR; 69.5 μg/m) increase in the 30-min PM2.5 moving average, whereas the low-frequency and high-frequency powers decreased by 4.2% (95% CI, −9.0% to 0.8%) and 6.2% (95% CI, −10.7% to −1.5%), respectively, in association with an IQR increase in the 2-hr PM2.5 moving average.

    Conclusions

    Marked changes in traffic-related PM2.5 exposure were associated with altered cardiac autonomic function in young healthy adults.

  • article

    Short-Term Effects of PM10 and NO2 on Respiratory Health among Children with Asthma or Asthma-like Symptoms: A Systematic Review and Meta-Analysis

    Abstract

    Objective

    Our goal was to quantify the short-term effects of particulate matter with aerodynamic diameter ≤ 10 μm (PM10) and nitrogen dioxide (NO2) on respiratory health of asthmatic children from published panel studies, and to investigate the influence of study and population characteristics as effect modifiers.

    Data extraction

    After a systematic literature review, we extracted quantitative estimates of the association of PM10 and/or NO2 with respiratory symptoms and peak expiratory flow (PEF). Combined effect estimates for an increase of 10 μg/m were calculated by random effects meta-analysis for all studies and for different strata defined by study characteristics. The effect of publication bias was investigated with Egger’s and Begg’s tests and “trim-and-fill” analyses.

    Data synthesis

    We identified 36 studies; 14 were part of the European Pollution Effects on Asthmatic Children in Europe (PEACE) study. Adverse associations of PM10 with asthma symptoms were statistically significant [odds ratio (OR) = 1.028; 95% confidence interval (CI), 1.006–1.051]. There were also associations, although not statistically significant, of PM10 with cough (OR = 1.012; 95% CI, 0.997–1.026) and on PEF (decrease of −0.082 L/min; 95% CI, −0.214 to 0.050). NO2 had statistically significant associations with asthma symptoms in the overall analysis considering all possible lags (OR = 1.031; 95% CI, 1.001–1.062), but not when we evaluated only the 0–1 lag. We found no publication bias, although it appeared when excluding the PEACE studies. When we applied the trim-and-fill method to the data set without the PEACE studies, the results were similar to the overall estimates from all studies. There was an indication for stronger PM10 associations for studies conducted in summer, outside of Europe, with longer lags, and in locations with higher NO2 concentrations.

    Conclusions

    We found clear evidence of effects of PM10 on the occurrence of asthma symptom episodes, and to a lesser extent on cough and PEF. The results for NO2 are more difficult to interpret because they depend on the lag times examined. There was an indication of effect modification by several study conditions.

  • article

    Malondialdehyde–Deoxyguanosine Adducts among Workers of a Thai Industrial Estate and Nearby Residents

    Abstract

    Background

    Humans living near industrial point emissions can experience high levels of exposures to air pollutants. Map Ta Phut Industrial Estate in Thailand is the location of the largest steel, oil refinery, and petrochemical factory complexes in Southeast Asia. Air pollution is an important source of oxidative stress and reactive oxygen species, which interact with DNA and lipids, leading to oxidative damage and lipid peroxidation, respectively.

    Objective

    We measured the levels of malondialdehyde–deoxyguanosine (dG) adducts, a biomarker of oxidative stress and lipid peroxidation, in petrochemical workers, nearby residents, and subjects living in a control district without proximity to industrial sources.

    Design

    We conducted a cross-sectional study to compare the prevalence of malondialdehyde-dG adducts in groups of subjects experiencing various degrees of air pollution.

    Results

    The multivariate regression analysis shows that the adduct levels were associated with occupational and environmental exposures to air pollution. The highest adduct level was observed in the steel factory workers. In addition, the formation of DNA damage tended to be associated with tobacco smoking, but without reaching statistical significance. A nonsignificant increase in DNA adducts was observed after 4–6 years of employment among the petrochemical complexes.

    Conclusions

    Air pollution emitted from the Map Ta Phut Industrial Estate complexes was associated with increased adduct levels in petrochemical workers and nearby residents. Considering the mutagenic potential of DNA lesions in the carcinogenic process, we recommend measures aimed at reducing the levels of air pollution.