Related Articles

Background

Particulate air pollution has been consistently linked to increased risk of arterial cardiovascular disease. Few data on air pollution exposure and risk of venous thrombosis are available. We investigated whether living near major traffic roads increases the risk of deep vein thrombosis (DVT), using distance from roads as a proxy for traffic exposure.

Methods and Results

Between 1995-2005, we examined 663 patients with DVT of the lower limbs and 859 age-matched controls from cities with population>15,000 inhabitants in Lombardia Region, Italy. We assessed distance from residential addresses to the nearest major traffic road using geographic information system methodology. The risk of DVT was estimated from logistic regression models adjusting for multiple clinical and environmental covariates.

The risk of DVT was increased (Odds Ratio [OR]=1.33; 95% CI 1.03-1.71; p=0.03 in age-adjusted models; OR=1.47; 95%CI 1.10-1.96; p=0.008 in models adjusted for multiple covariates) for subjects living near a major traffic road (3 meters, 10th centile of the distance distribution) compared to those living farther away (reference distance of 245 meters, 90th centile). The increase in DVT risk was approximately linear over the observed distance range (from 718 to 0 meters), and was not modified after adjusting for background levels of particulate matter (OR=1.47; 95%CI 1.11-1.96; p=0.008 for 10th vs. 90th distance centile in models adjusting for area levels of particulate matter <10 μm in aerodynamic diameter [PM10] in the year before diagnosis).

Conclusions

Living near major traffic roads is associated with increased risk of DVT.

Summary

Background

Two recent case-control studies in Italy reported that long-term exposure to particulate air pollution or living near major traffic roads was associated with an increased risk of deep vein thrombosis (DVT). No prospective evidence exists about long-term traffic-related air pollution and incident venous thromboembolism (VTE).

Objectives

To examine the association between long-term traffic exposure and incident VTE in a population-based prospective cohort study.

Methods

We studied 13,143 middle-aged men and women in the Atherosclerosis Risk in Communities Study without history of DVT or pulmonary embolus (PE) at baseline examination (1987-1989). Geographical Information System (GIS)-mapped traffic density and distance to major roads in the four study communities served as measures of traffic exposure. We examined the association between traffic exposure and incident VTE using proportional hazards regression models.

Results

405 subjects developed VTE through 2005. Traffic density was not significantly associated with VTE. Relative to those in the lowest quartile of traffic density, the adjusted hazard ratios across increasing quartiles were 1.18 (95%CI 0.88-1.57), 0.99 (95%CI 0.74-1.34) and 1.14 (95%CI 0.86-1.51) (p for trend across quartiles = 0.64). For residents living within 150 meters of major roads compared to subjects living further away, the adjusted hazard ratio was 1.16 (95%CI 0.95-1.42, p=0.14).

Conclusions

This first prospective study in the general population does not support an association between air pollution exposure or traffic proximity and risk of DVT. More data may be needed to clarify whether traffic or air pollution influences the risk of VTE.

Background

Evidence links exposure to ambient air pollution during pregnancy, particularly gaseous pollutants and particulate matter, to an increased risk of adverse reproductive outcomes but the results for birth defects have been inconsistent.

Methods

We compared estimated exposure to ambient air pollutants during early pregnancy among mothers of children with oral cleft defects (cases) to that among mothers of controls, adjusting for available risk factors from birth certificates. We obtained ambient air pollutant data from air monitoring sites in New Jersey for carbon monoxide (CO), nitrogen dioxide (NO2), ozone (O3), sulfur dioxide (SO2), particulate matter less than 10 µm in aerodynamic diameter (PM10) and particulate matter less than 2.5 µm in aerodynamic diameter (PM2.5). We used values from the nearest monitor (within 40 km of the residence at birth) for controls, cleft lip with or without cleft palate (CLP) and cleft palate only (CPO).

Results

Based on logistic regression analyses for each contaminant and all contaminants together, there were no consistent elevated associations between selected air pollutants and cleft malformations. Quartile of CO concentration showed a consistent protective association with CPO (p<.01). For other contaminants, confidence intervals (95%) of the odds ratios for some quartiles excluded one. CLP showed limited evidence of an association with increasing SO2 exposure while CPO showed weak associations with increasing O3 exposure.

Conclusion

There was little consistent evidence associating cleft malformations with maternal exposure to ambient air pollutants. Evaluating particular pollutants or disease subgroups would require more detailed measurement of exposure and classification of cleft defects.

Background

Mild hyperhomocysteinemia is independently associated with an increased risk of cardiovascular disease. Air pollution exposure induces short-term inflammatory changes that may determine hyperhomocysteinemia, particularly in the presence of a preexisting proinflammatory status such as that found in cigarette smokers.

Objective

We examined the relation of air pollution levels with fasting and postmethionine-load total homocysteine (tHcy) in 1,213 normal subjects from Lombardia, Italy.

Methods

We obtained hourly concentrations of particulate matter < 10 μm in aerodynamic diameter (PM10) and gaseous pollutants (carbon monoxide, nitrogen dioxide, sulfur dioxide, ozone) from 53 monitoring sites covering the study area. We applied generalized additive models to compute standardized regression coefficients controlled for age, sex, body mass index, smoking, alcohol, hormone use, temperature, day of the year, and long-term trends.

Results

The estimated difference in tHcy associated with an interquartile increase in average PM10 concentrations in the 24 hr before the study was nonsignificant [0.4%; 95% confidence interval (CI), −2.4 to 3.3 for fasting; and 1.1%, 95% CI, −1.5 to 3.7 for postmethionine-load tHcy]. In smokers, 24-hr PM10 levels were associated with 6.3% (95% CI, 1.3 to 11.6; p < 0.05) and 4.9% (95% CI, 0.5 to 9.6; p < 0.05) increases in fasting and postmethionine-load tHcy, respectively, but no association was seen in nonsmokers (p-interaction = 0.005 for fasting and 0.039 for postmethionine-load tHcy). Average 24-hr O3 concentrations were associated with significant differences in fasting tHcy (6.7%; 95% CI, 0.9 to 12.8; p < 0.05), but no consistent associations were found when postmethionine-load tHcy and/or 7-day average O3 concentrations were considered.

Conclusions

Air particles may interact with cigarette smoking and increase plasma homocysteine in healthy subjects.

Background: Exposure to traffic-related air pollution is a risk factor for cardiovascular events, probably involving mechanisms of inflammation and coagulation. Little is known about effects of the short exposures encountered while participating in traffic.

Objectives: The objective of the study was to examine effects of exposure of commuters to air pollution on cardiovascular biomarkers.

Methods: Thirty-four healthy adult volunteers commuted for 2 hr by bus, car, or bicycle during the morning rush hour. During the commute, exposure to particle number, particulate matter (PM) ≤ 2.5 µm in aerodynamic diameter (PM2.5), PM ≤ 10 µm in diameter (PM10), and soot was measured. We estimated inhaled doses based on heart rate monitoring. Shortly before exposure and 6 hr after exposure, blood samples were taken and analyzed for CC16 (Clara cell protein 16), blood cell count, coagulation markers, and inflammation markers. Between June 2007 and June 2008, 352 pre- and postexposure blood samples were collected on 47 test days. We used mixed models to analyze the associations between exposure and changes in health parameters.

Results: We observed no consistent associations between the air pollution exposures and doses and the various biomarkers that we investigated.

Conclusions: Air pollution exposure during commuting was not consistently associated with acute changes in inflammation markers, blood cell counts, or blood coagulation markers.

Background

The relationship between ambient air pollution exposure and mortality of cardiovascular and cerebrovascular diseases in human is controversial, and there is little information about how exposures to ambient air pollution contribution to the mortality of cardiovascular and cerebrovascular diseases among Chinese. The aim of the present study was to examine whether exposure to ambient-air pollution increases the risk for cardiovascular and cerebrovascular disease.

Methodology/Principal Findings

We conducted a retrospective cohort study among humans to examine the association between compound-air pollutants [particulate matter <10 µm in aerodynamic diameter (PM10), sulfur dioxide (SO2) and nitrogen dioxide (NO2)] and mortality in Shenyang, China, using 12 years of data (1998–2009). Also, stratified analysis by sex, age, education, and income was conducted for cardiovascular and cerebrovascular mortality. The results showed that an increase of 10 µg/m3 in a year average concentration of PM10 corresponds to 55% increase in the risk of a death cardiovascular disease (hazard ratio [HR], 1.55; 95% confidence interval [CI], 1.51 to 1.60) and 49% increase in cerebrovascular disease (HR, 1.49; 95% CI, 1.45 to 1.53), respectively. The corresponding figures of adjusted HR (95%CI) for a 10 µg/m3 increase in NO2 was 2.46 (2.31 to 2.63) for cardiovascular mortality and 2.44 (2.27 to 2.62) for cerebrovascular mortality, respectively. The effects of air pollution were more evident in female that in male, and nonsmokers and residents with BMI<18.5 were more vulnerable to outdoor air pollution.

Conclusion/Significance

Long-term exposure to ambient air pollution is associated with the death of cardiovascular and cerebrovascular diseases among Chinese populations.

The link between air pollution exposure and adverse birth outcomes is of public health concern due to the relationship between poor pregnancy outcomes and the onset of childhood and adult diseases. As personal exposure measurements are difficult and expensive to obtain, proximate measures of air pollution exposure are traditionally used. We explored how different air pollution exposure metrics affect birthweight regression models. We examined the effect of maternal exposure to ambient levels of particulate matter <10, <2.5 μm in aerodynamic diameter (PM10, PM2.5) on birthweight among infants in North Carolina. We linked maternal residence to the closest monitor during pregnancy for 2000–2002 (n=350,754). County-level averages of air pollution concentrations were estimated for the entire pregnancy and each trimester. For a finer spatially resolved metric, we calculated exposure averages for women living within 20, 10, and 5 km of a monitor. Multiple linear regression was used to determine the association between exposure and birthweight, adjusting for standard covariates. In the county level model, an interquartile increase in PM10 and PM2.5 during the entire gestational period reduced birthweight by 5.3 g (95% CI: 3.3 – 7.4) and 4.6 g (95% CI: 2.3 – 6.8), respectively. This model also showed a reduction in birthweight for PM10 (7.1 g, 95% CI: 1.0–13.2) and PM2.5 (10.4 g, 95% CI: 6.4 – 14.4) during the third trimester. Proximity models for 20, 10, and 5 km distances showed similar results to the county level models. County level models assume that exposure is spatially homogeneous over a larger surface area than proximity models. Sensitivity analysis demonstrated that at varying spatial resolutions, there is still a stable and negative association between air pollution and birthweight, despite North Carolina’s consistent attainment of federal air quality standards.

Background: Exposure to ambient fine particulate matter air pollution (PM2.5; < 2.5 µm in aerodynamic diameter) induces endothelial dysfunction and increases the risk for cardiovascular disease. Endothelial progenitor cells (EPCs) contribute to postnatal endothelial repair and regeneration. In humans and mice, EPC levels are decreased upon exposure to elevated levels of PM2.5.

Objective: We examined the mechanism by which PM2.5 exposure suppresses circulating levels of EPCs.

Methods: Mice were exposed to HEPA-filtered air or concentrated ambient fine particulate matter (CAP, 30–100 µg/m3) from downtown Louisville (Kentucky) air, and progenitor cells from peripheral blood or bone marrow were analyzed by flow cytometry or by culture ex vivo.

Results: Exposure of the mice to CAP (6 hr/day) for 4–30 days progressively decreased circulating levels of EPCs positive for both Flk-1 and Sca-1 (Flk-1+/Sca-1+) without affecting stem cells positive for Sca-1 alone (Sca-1+). After 9 days of exposure, a 7-day exposure-free period led to complete recovery of the circulating levels of Flk-1+/Sca-1+ cells. CAP exposure decreased circulating levels of EPCs independent of apoptosis while simultaneously increasing Flk-1+/Sca-1+ cells in the bone marrow. We observed no change in tissue deposition of these cells. CAP exposure suppressed vascular endothelial growth factor (VEGF)-induced Akt and endothelial nitric oxide synthase (eNOS) phosphorylation in the aorta, and it prevented VEGF/AMD3100-induced mobilization of Flk-1+/Sca-1+ cells into the peripheral blood. Treatment with stem cell factor/AMD3100 led to a greater increase in circulating Flk-1+/Sca-1+ cells in CAP-exposed mice than in mice breathing filtered air.

Conclusion: Exposure to PM2.5 increases EPC levels in the bone marrow by preventing their mobilization to the peripheral blood via inhibition of signaling events triggered by VEGF-receptor stimulation that are upstream of c-kit activation. Suppression of EPC mobilization by PM2.5 could induce deficits in vascular repair or regeneration.

Background

Over the past decade there has been mounting evidence that ambient air pollution during pregnancy influences fetal growth.

Objectives

This study was designed to examine possible associations between fetal ultrasonic measurements collected from 15,623 scans (13–26 weeks gestation) and ambient air pollution during early pregnancy.

Methods

We calculated mothers’ average monthly exposures over the first 4 months of pregnancy for the following pollutants: particulate matter < 10 μm aerodynamic diameter (PM10), ozone, nitrogen dioxide, and sulfur dioxide. We examined associations with fetal femur length (FL), biparietal diameter (BPD), head circumference (HC), and abdominal circumference (AC). Final analyses included scans from only those women within 2 km of an air pollution monitoring site. We controlled for long-term trend, season, temperature, gestation, mother’s age, socioeconomic status, and fetal sex.

Results

A reduction in fetal AC was associated with O3 during days 31–60 [−1.42 mm; 95% confidence interval (CI), −2.74 to −0.09], SO2 during days 61–90 (−1.67 mm; 95% CI, −2.94 to −0.40), and PM10 during days 91–120 (−0.78 mm; 95% CI, −1.49 to −0.08). Other results showed a reduction in BPD (−0.68 mm; 95% CI, −1.09 to −0.27) associated with SO2 during days 0–30, a reduction in HC (−1.02 mm; 95% CI, −1.78 to −0.26) associated with PM10 during days 91–120, and a reduction in FL associated with PM10 during days 0–30 (−0.28 mm; 95% CI, −0.48 to −0.08) and 91–120 (−0.23; 95% CI, −0.42 to −0.04).

Conclusion

We found strong effects of ambient air pollution on ultrasound measures. Future research, including more individually detailed data, is needed to confirm our results.

We examined the association of infant bronchiolitis with acute exposure to ambient air pollutants.

Design

We employed a time-stratified case–crossover method and based the exposure windows on a priori, biologically based hypotheses.

Participants

We evaluated effects in 19,901 infants in the South Coast Air Basin of California in 1995–2000 with a hospital discharge record for bronchiolitis in the first year of life (International Classification of Diseases, 9th Revision, CM466.1).

Evaluations/Measurements

Study subjects’ ZIP code was linked to ambient air pollution monitors to derive exposures. We estimated the risk of bronchiolitis hospitalization associated with increases in wintertime ambient air pollutants using conditional logistic regression.

Results

We observed no increased risk after acute exposure to particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5), carbon monoxide, or nitrogen dioxide. PM2.5 exposure models suggested a 26–41% increased risk in the most premature infants born at gestational ages between 25 and 29 weeks; however, these findings were based on very small numbers.

Conclusions

We found little support for a link between acute increases in ambient air pollution and infant bronchiolitis except modestly increased risk for PM2.5 exposure among infants born very prematurely. In these infants, the periods of viral acquisition and incubation concurred with the time of increased risk.

Relevance to Professional Practice

We present novel data for the infant period and the key respiratory disease of infancy, bronchiolitis. Incompletely explained trends in rising bronchiolitis hospitalization rates and increasing number of infants born prematurely underscore the importance of evaluating the impact of ambient air pollution in this age group in other populations and studies.

The association of air pollution with the prevalence of chronic lower respiratory tract symptoms among children with a history of asthma or related symptoms was examined in a cross-sectional study. Parents of a total of 3,676 fourth, seventh, and tenth graders from classrooms in 12 communities in Southern California completed questionnaires that characterized the children's histories of respiratory illness and associated risk factors. The prevalences of bronchitis, chronic phlegm, and chronic cough were investigated among children with a history of asthma, wheeze without diagnosed asthma, and neither wheeze nor asthma. Average ambient annual exposure to ozone, particulate matter (PM(10) and PM(2.5); [less than/equal to] 10 microm and < 2.5 microm in aerodynamic diameter, respectively), acid vapor, and nitrogen dioxide (NO(2)) was estimated from monitoring stations in each community. Positive associations between air pollution and bronchitis and phlegm were observed only among children with asthma. As PM(10) increased across communities, there was a corresponding increase in the risk per interquartile range of bronchitis [odds ratio (OR) 1.4/19 microg/m(3); 95% confidence interval (CI), 1.1-1.8). Increased prevalence of phlegm was significantly associated with increasing exposure to all ambient pollutants except ozone. The strongest association was for NO(2), based on relative risk per interquartile range in the 12 communities (OR 2.7/24 ppb; CI, 1.4-5.3). The results suggest that children with a prior diagnosis of asthma are more likely to develop persistent lower respiratory tract symptoms when exposed to air pollution in Southern California.

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Objective: To investigate the association between ambient concentrations of air pollutants and respiratory and cardiovascular mortalities in Hong Kong.

Methods: Retrospective ecological study. A Poisson regression of concentrations of daily air pollutants on daily mortalities for respiratory and cardiovascular diseases in Hong Kong from 1995 to the end of 1998 was performed using the air pollution and health: the European approach (APHEA) protocol. The effects of time trend, seasonal variations, temperature, and humidity were adjusted. Autocorrelation and overdispersion were corrected. Daily concentrations of nitrogen dioxide (NO2), sulphur dioxide (SO2), ozone (O3), and particulate matter <10 µm in aerodynamic diameter (PM10) were averaged from eight monitoring stations in Hong Kong. Relative risks (RRs) of respiratory and cardiovascular mortalities (per 10 µg/m3 increase in air pollutant concentration) were calculated.

Results: Significant associations were found between mortalities for all respiratory diseases and ischaemic heart diseases (IHD) and the concentrations of all pollutants when analysed singly. The RRs for all respiratory mortalities (for a 10 µg/m3 increase in the concentration of a pollutant) ranged from 1.008 (for PM10) to 1.015 (for SO2) and were higher for chronic obstructive pulmonary diseases (COPD) with all pollutants except SO2, ranging from 1.017 (for PM10) to 1.034 (for O3). RRs for IHD ranged from 1.009 (for O3) to 1.028 (for SO2). In a multipollutant model, O3 and SO2 were significantly associated with all respiratory mortalities, whereas NO2 was associated with mortality from IHD. No interactions were detected between any of the pollutants or with the winter season. A dose-response effect was evident for all air pollutants. Harvesting was not found in the short term.

Conclusions: Mortality risks were detected at current ambient concentrations of air pollutants. The associations with the particulates and some gaseous pollutants when analysed singly were consistent with many reported in temperate countries. PM10 was not associated with respiratory or cardiovascular mortalities in multipollutant analyses.

We examined respiratory health effects of long-term exposure to ambient air pollution in 7,621 schoolchildren residing in eight districts of four Chinese cities. The four cities exhibited wide between-city and within-city gradients in ambient levels of four size fractions of particulate matter [less than or equal to 2.5 micro m in aerodynamic diameter (PM(2.5)), between 2.5 and 10 micro m (PM(10-2.5)), less than or equal to 10 micro m (PM(10)), and total suspended particulates (TSP)] and two gaseous pollutants (SO(2) and NO(x)). Informed consent and written responses to questionnaires about children's personal, residential, and family information, as well as their health histories and status, were obtained with the help of the parents and the school personnel. We used a two-stage regression approach in data analyses. In the first-stage logistic regressions, we obtained logits of district-specific prevalence of wheeze, asthma, bronchitis, hospitalization for respiratory diseases, persistent cough, and persistent phlegm, adjusted for covariates representing personal, household, and family parameters. Some of these covariates were found to be risk factors of children's respiratory health, including being younger in the study group, being male, having been breast-fed, sharing bedrooms, sharing beds, room being smoky during cooking, eye irritation during cooking, parental smoking, and a history of parental asthma. In several of the second-stage variance-weighted linear regressions, we examined associations between district-specific adjusted prevalence rates and district-specific ambient levels of each pollutant. We found positive associations between morbidity prevalence and outdoor levels of PM of all size fractions, but the association appeared to be stronger for coarse particles (PM(10-2.5)). The results also present some evidence that ambient levels of NO(x) and SO(2) were positively associated with children's respiratory symptoms, but the evidence for these two gaseous pollutants appeared to be weaker than that for the PM.

Background

New approaches to link health surveillance data with environmental and population exposure information are needed to examine the health benefits of risk management decisions.

Objective

We examined the feasibility of conducting a local assessment of the public health impacts of cumulative air pollution reduction activities from federal, state, local, and voluntary actions in the City of New Haven, Connecticut (USA).

Methods

Using a hybrid modeling approach that combines regional and local-scale air quality data, we estimated ambient concentrations for multiple air pollutants [e.g., PM2.5 (particulate matter ≤ 2.5 μm in aerodynamic diameter), NOx (nitrogen oxides)] for baseline year 2001 and projected emissions for 2010, 2020, and 2030. We assessed the feasibility of detecting health improvements in relation to reductions in air pollution for 26 different pollutant–health outcome linkages using both sample size and exploratory epidemiological simulations to further inform decision-making needs.

Results

Model projections suggested decreases (~ 10–60%) in pollutant concentrations, mainly attributable to decreases in pollutants from local sources between 2001 and 2010. Models indicated considerable spatial variability in the concentrations of most pollutants. Sample size analyses supported the feasibility of identifying linkages between reductions in NOx and improvements in all-cause mortality, prevalence of asthma in children and adults, and cardiovascular and respiratory hospitalizations.

Conclusion

Substantial reductions in air pollution (e.g., ~ 60% for NOx) are needed to detect health impacts of environmental actions using traditional epidemiological study designs in small communities like New Haven. In contrast, exploratory epidemiological simulations suggest that it may be possible to demonstrate the health impacts of PM reductions by predicting intraurban pollution gradients within New Haven using coupled models.

Background

Preterm delivery and preeclampsia are common adverse pregnancy outcomes that have been inconsistently associated with ambient air pollutant exposures.

Objectives

We aimed to prospectively examine relations between exposures to ambient carbon monoxide (CO) and fine particulate matter [≤ 2.5 μm in aerodynamic diameter (PM2.5)] and risks of preeclampsia and preterm delivery.

Methods

We used data from 3,509 western Washington women who delivered infants between 1996 and 2006. We predicted ambient CO and PM2.5 exposures using regression models based on regional air pollutant monitoring data. Models contained predictor terms for year, month, weather, and land use characteristics. We evaluated several exposure windows, including prepregnancy, early pregnancy, the first two trimesters, the last month, and the last 3 months of pregnancy. Outcomes were identified using abstracted maternal medical record data. Covariate information was obtained from maternal interviews.

Results

Predicted periconceptional CO exposure was significantly associated with preeclampsia after adjustment for maternal characteristics and season of conception [adjusted odds ratio (OR) per 0.1 ppm = 1.07; 95% confidence interval (CI), 1.02–1.13]. However, further adjustment for year of conception essentially nullified the association (adjusted OR = 0.98; 95% CI, 0.91–1.06). Associations between PM2.5 and preeclampsia were nonsignificant and weaker than associations estimated for CO, and neither air pollutant was strongly associated with preterm delivery. Patterns were similar across all exposure windows.

Conclusions

Because both CO concentrations and preeclampsia incidence declined during the study period, secular changes in another preeclampsia risk factor may explain the association observed here. We saw little evidence of other associations with preeclampsia or preterm delivery in this setting.

Background: Few studies have examined the acute health effects of air pollution exposures experienced while cycling in traffic.

Objectives: We conducted a crossover study to examine the relationship between traffic pollution and acute changes in heart rate variability. We also collected spirometry and exhaled nitric oxide measures.

Methods: Forty-two healthy adults cycled for 1 hr on high- and low-traffic routes as well as indoors. Health measures were collected before cycling and 1–4 hr after the start of cycling. Ultrafine particles (UFPs; ≤ 0.1 μm in aerodynamic diameter), particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5), black carbon, and volatile organic compounds were measured along each cycling route, and ambient nitrogen dioxide (NO2) and ozone (O3) levels were recorded from a fixed-site monitor. Mixed-effects models were used to estimate associations between air pollutants and changes in health outcome measures relative to precycling baseline values.

Results: An interquartile range increase in UFP levels (18,200/cm3) was associated with a significant decrease in high-frequency power 4 hr after the start of cycling [β = –224 msec2; 95% confidence interval (CI), –386 to –63 msec2]. Ambient NO2 levels were inversely associated with the standard deviation of normal-to-normal (NN) intervals (β = –10 msec; 95% CI, –20 to –0.34 msec) and positively associated with the ratio of low-frequency to high-frequency power (β = 1.4; 95% CI, 0.35 to 2.5) 2 hr after the start of cycling. We also observed significant inverse associations between ambient O3 levels and the root mean square of successive differences in adjacent NN intervals 3 hr after the start of cycling.

Conclusions: Short-term exposures to traffic pollution may contribute to altered autonomic modulation of the heart in the hours immediately after cycling.

The mechanisms by which exposure to particulate matter increases the risk of cardiovascular events are not known. Recent human and animal data suggest that particulate matter may induce alterations in hemostatic factors. In this study we determined the mechanisms by which particulate matter might accelerate thrombosis. We found that mice treated with a dose of well characterized particulate matter of less than 10 μM in diameter exhibited a shortened bleeding time, decreased prothrombin and partial thromboplastin times (decreased plasma clotting times), increased levels of fibrinogen, and increased activity of factor II, VIII, and X. This prothrombotic tendency was associated with increased generation of intravascular thrombin, an acceleration of arterial thrombosis, and an increase in bronchoalveolar fluid concentration of the prothrombotic cytokine IL-6. Knockout mice lacking IL-6 were protected against particulate matter–induced intravascular thrombin formation and the acceleration of arterial thrombosis. Depletion of macrophages by the intratracheal administration of liposomal clodronate attenuated particulate matter–induced IL-6 production and the resultant prothrombotic tendency. Our findings suggest that exposure to particulate matter triggers IL-6 production by alveolar macrophages, resulting in reduced clotting times, intravascular thrombin formation, and accelerated arterial thrombosis. These results provide a potential mechanism linking ambient particulate matter exposure and thrombotic events.

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.

Particulate air pollution is known to be associated with cardiovascular disease. The relation of particulate air pollution with cerebrovascular disease (CVD) has not been extensively studied, particularly in relation to different subtypes of stroke. A time-series study was conducted to evaluate the association between daily air pollution and acute stroke unit hospitalizations in Mantua, Italy. We analyzed 781 CVD consecutive patients living in Mantua county admitted between 2006–08. Data on stroke types, demographic variables, risk factors were available from the Lombardia Stroke Registry. Daily mean value of particulate matter with a diameter <10 µm (PM10), carbon monoxide, nitric oxide, nitrogen dioxide, sulphur dioxide, benzene and ozone were used in the analysis. The association between CVD, ischemic strokes subtypes and pollutants was investigated with a case-crossover design, using conditional logistic regression analysis, adjusting for temperature, humidity, barometric pressure and holidays. Among the 781 subjects admitted 75.7% had ischemic stroke, 11.7% haemorrhagic stroke 12.6% transient ischemic attack. In men admission for stroke was associated with PM10 [odds ratio (OR) 1.01, 95%; confidence interval (CI) 1.00–1.02; P<0.05]. According to the clinical classification, lacunar anterior circulation syndrome stroke type was related to PM10 level registered on the day of admission for both genders (OR: 1.01, 95%; CI: 1.00–1.02; P<0.05) while for total anterior circulation syndrome stroke only in men (OR: 1.04, 95%; CI 1.01–1.07; P<0.05).

In conclusion, our study confirms that air pollution peaks may contribute to increase the risk of hospitalization for stroke and particulate matter seems to be a significant risk factor, especially for lacunar stroke.

To evaluate the relative importance of various measures of particulate and gaseous air pollution as predictors of daily mortality in Inchon, South Korea, the association between total daily mortality and air pollution was investigated for a 20-month period (January 1995 through August 1996). Poisson regression was used to regress daily death counts on each air pollutant, controlling for time trends, season, and meteorologic influences such as temperature and relative humidity. Regression coefficients of a 5-day moving average of particulate matter less than or = to 10 microm in aerodynamic diameter (PM(10)) on total mortality were positively significant when considered separately and simultaneously with other pollutants in the model. PM(10) remained significant when the models were confined to cardiovascular or respiratory mortality. Sulfur dioxide (SO(2)) and carbon monoxide (CO) were significantly related to respiratory mortality in the single-pollutant model. Ozone exposure was not statistically significant with regard to mortality in the above models, and graphic analysis showed that the relationship was nonlinear. A combined index of PM(10), nitrogen dioxide, SO(2), and CO seemed to better explain the exposure-response relationship with total mortality than an individual air pollutant. Pollutants should be considered together in the risk assessment of air pollution, as opposed to measuring the risk of individual pollutants.

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We extended our previous analyses of term low birth weight (LBW) and preterm birth to 1994–2000, a period of declining air pollution levels in the South Coast Air Basin. We speculated that the effects we observed previously for carbon monoxide, particulate matter < 10 μm in aero-dynamic diameter (PM10), and traffic density were attributable to toxins sorbed to primary exhaust particles. Focusing on CO, PM10, and particulate matter < 2.5 μm in aerodynamic diameter (PM2.5), we examined whether varying residential distances from monitoring stations affected risk estimates, because effect attenuation may result from local pollutant heterogeneity inadequately captured by ambient stations. We geocoded home locations, calculated the distance to the nearest air monitors, estimated exposure levels by pregnancy period, and performed logistic regression analyses for subjects living within 1–4 mi of a station. For women residing within a 1-mi distance, we observed a 27% increase in risk for high (≥ 75th percentile) first-trimester CO exposures and preterm birth and a 36% increase for high third-trimester pregnancy CO exposures and term LBW. For particles, we observed similar size effects during early and late pregnancy for both term LBW and preterm birth. In contrast, smaller or no effects were observed beyond a 1-mi distance of a residence from a station. Associations between CO and PM10 averaged over the whole pregnancy and term LBW were generally smaller than effects for early and late pregnancy. These new results for 1994–2000 generally confirm our previous observations for the period 1989–1993, again linking CO and particle exposures to term LBW and preterm birth. In addition, they confirm our suspicions about having to address local heterogeneity for these pollutants in Los Angeles.

During the winters of 1986-1987 through 1991-1992, rainfall throughout much of Northern California was subnormal, resulting in intermittent accumulation of air pollution, much of which was attributable to residential wood combustion (RWC). This investigation examined whether there was a relationship between ambient air pollution in Santa Clara County, California and emergency room visits for asthma during the winters of 1988-1989 through 1991-1992. Emergency room (ER) records from three acute-care hospitals were abstracted to compile daily visits for asthma and a control diagnosis (gastroenteritis) for 3-month periods during each winter. Air monitoring data included daily coefficient of haze (COH) and every-other-day particulate matter with aerodynamic diameter equal to or less than 10 microns (PM10, 24-hr average), as well as hourly nitrogen dioxide and ozone concentrations. Daily COH measurements were used to predict values for missing days of PM10 to develop a complete PM10 time series. Daily data were also obtained for temperature, precipitation, and relative humidity. In time-series analyses using Poisson regression, consistent relationships were found between ER visits for asthma and PM10. Same-day nitrogen dioxide concentrations were also associated with asthma ER visits, while ozone was not. Because there was a significant interaction between PM10 and minimum temperature in this data set, estimates of relative risks (RRs) for PM10-associated asthma ER visits were temperature-dependent. A 60 micrograms/m3 change in PM10 (2-day lag) corresponded to RRs of 1.43 (95% CI = 1.18-1.69) at 20 degrees F, representing the low end of the temperature distribution, 1.27 (95% CI = 1.13-1.42) at 30 degrees F, and 1.11 (95% CI = 1.03-1.19) at 41 degrees F, the mean of the observed minimum temperature. ER visits for gastroenteritis were not significantly associated with any pollutant variable. Several sensitivity analyses, including the use of robust regressions and of nonparametric methods for fitting time trends and temperature effects in the data, supported these findings. These results demonstrate an association between ambient wintertime PM10 and exacerbations of asthma in an area where one of the principal sources of PM10 is RWC.

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Background

Acute exposure to ambient air pollution has been associated with acute changes in cardiac outcomes, often within hours of exposure.

Objectives

We examined the effects of air pollutants on heart-rate–corrected QT interval (QTc), an electrocardiographic marker of ventricular repolarization, and whether these associations were modified by participant characteristics and genetic polymorphisms related to oxidative stress.

Methods

We studied repeated measurements of QTc on 580 men from the Veterans Affairs Normative Aging Study (NAS) using mixed-effects models with random intercepts. We fitted a quadratic constrained distributed lag model to estimate the cumulative effect on QTc of ambient air pollutants including fine particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5), ozone (O3), black carbon (BC), nitrogen dioxide (NO2), carbon monoxide (CO), and sulfur dioxide (SO2) concentrations during the 10 hr before the visit. We genotyped polymorphisms related to oxidative stress and analyzed pollution–susceptibility score interactions using the genetic susceptibility score (GSS) method.

Results

Ambient traffic pollutant concentrations were related to longer QTc. An interquartile range (IQR) change in BC cumulative during the 10 hr before the visit was associated with increased QTc [1.89 msec change; 95% confidence interval (CI), −0.16 to 3.93]. We found a similar association with QTc for an IQR change in 1-hr BC that occurred 4 hr before the visit (2.54 msec change; 95% CI, 0.28–4.80). We found increased QTc for IQR changes in NO2 and CO, but the change was statistically insignificant. In contrast, we found no association between QTc and PM2.5, SO2, and O3. The association between QTc and BC was stronger among participants who were obese, who had diabetes, who were nonsmokers, or who had higher GSSs.

Conclusions

Traffic-related pollutants may increase QTc among persons with diabetes, persons who are obese, and nonsmoking elderly individuals; the number of genetic variants related to oxidative stress increases this effect.

Rationale: Population-based studies have demonstrated associations between ambient air pollution exposures and mortality, but few have been able to adjust for occupational exposures. Additionally, two studies have observed higher risks in individuals with occupational dust, gas, or fume exposure.

Objectives: We examined the association of ambient residential exposure to particulate matter less than 10 μm in diameter (PM10), particulate matter less than 2.5 μm in diameter (PM2.5), NO2, SO2, and mortality in 53,814 men in the U.S. trucking industry.

Methods: Exposures for PM10, NO2, and SO2 at each residential address were assigned using models combining spatial smoothing and geographic covariates. PM2.5 exposures in 2000 were assigned from the nearest available monitor. Single and multipollutant Cox proportional hazard models were used to examine the association of an interquartile range (IQR) change (6 μg/m3 for PM10, 4 μg/m3 for PM2.5, 4ppb for SO2, and 8ppb for NO2) and the risk of all-cause and cause-specific mortality.

Measurements and Main Results: An IQR change in ambient residential exposures to PM10 was associated with a 4.3% (95% confidence interval [CI], 1.1–7.7%) increased risk of all-cause mortality. The increase for an IQR change in SO2 was 6.9% (95% CI, 2.3–11.6%), for NO2 was 8.2% (95% CI, 4.5–12.1%), and for PM2.5 was 3.9% (95% CI, 1.0–6.9%). Elevated associations with cause-specific mortality (lung cancer, cardiovascular and respiratory disease) were observed for PM2.5, SO2, and NO2, but not PM10. None of the pollutants were confounded by occupational exposures. In multipollutant models, overall, the associations were attenuated, most strongly for PM10. In sensitivity analyses excluding long-haul drivers, who spend days away from home, larger hazard ratios were observed.

Conclusions: In this population of men, residential ambient air pollution exposures were associated with mortality.

Previous studies have explored the association between air pollution levels and adverse birth outcomes such as lower birth weight. Existing literature suggests an association, although results across studies are not consistent. Additional research is needed to confirm the effect, investigate the exposure window of importance, and distinguish which pollutants cause harm.

We assessed the association between ambient pollutant concentrations and term birth weight for 1,548,904 births in TX from 1998 to 2004. Assignment of prenatal exposure to air pollutants was based on maternal county of residence at the time of delivery. Pollutants examined included particulate matter with aerodynamic diameter ≤10 and ≤2.5 μm (PM10 and PM2.5), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3). We applied a linear model with birth weight as a continuous variable. The model was adjusted for known risk factors and region. We assessed pollutant effects by trimester to identify biological exposure window of concern, and explored interaction due to race/ethnicity.

An interquartile increase in ambient pollutant concentrations of SO2 and O3 was associated with a 4.99-g (95% confidence interval [CI], 1.87–8.11) and 2.72-g (95% CI, 1.11–4.33) decrease in birth weight, respectively. Lower birth weight was associated with exposure to O3 in the first and second trimester, whereas results were not significant for other pollutants by trimester. A positive association was exhibited for PM2.5 in the first trimester. Effects estimates for PM10 and PM2.5 were inconsistent across race/ethnic groups.

Current ambient air pollution levels may be increasing the risk of lower birth weight for some pollutants. These risks may be increased for certain racial/ethnic groups. Additional research including consideration of improved methodology is needed to investigate these findings. Future studies should examine the influence of residual confounding.