Effects of airborne particulate matter on respiratory morbidity in asthmatic children

Background

The effects of airborne particulate matter (PM) are a major human health concern. In this panel study, we evaluated the acute effects of exposure to PM on peak expiratory flow (PEF) and wheezing in children.

Methods

Daily PEF and wheezing were examined in 19 asthmatic children who were hospitalized in a suburban city in Japan for approximately 5 months. The concentrations of PM less than 2.5 µm in diameter (PM_2.5) were monitored at a monitoring station proximal to the hospital. Moreover, PM_2.5 concentrations inside and outside the hospital were measured using the dust monitor with a laser diode (PM_2.5(LD)). The changes in PEF and wheezing associated with PM concentration were analyzed.

Results

The changes in PEF in the morning and evening were significantly associated with increases in the average concentration of indoor PM_2.5(LD) 24 h prior to measurement (-2.86 L/min [95%CI: -4.12, -1.61] and -3.59 L/min [95%CI: -4.99, -2.20] respectively, for 10-µg/m³ increases). The change in PEF was also significantly associated with outdoor PM_2.5(LD) concentrations, but the changes were smaller than those observed for indoor PM_2.5(LD). Changes in PEF and concentration of stationary-site PM_2.5 were not associated. The prevalence of wheezing in the morning and evening were also significantly associated with indoor PM_2.5(LD) concentrations (odds ratios = 1.014 [95%CI: 1.006, 1.023] and 1.025 [95%CI: 1.013, 1.038] respectively, for 10-µg/m³ increases). Wheezing in the evening was significantly associated with outdoor PM_2.5(LD) concentration. The effects of indoor and outdoor PM_2.5(LD) remained significant even after adjusting for ambient nitrogen dioxide concentrations.

Conclusion

Indoor and outdoor PM_2.5(LD) concentrations were associated with PEF and wheezing among asthmatic children. Indoor PM_2.5(LD) had a more marked effect than outdoor PM_2.5(LD) or stationary-site PM_2.5.Key words: Particulate Matter, Asthma, Peak Expiratory Flow Rate, Respiratory Sounds     

Associations between PM2.5 and Heart Rate Variability Are Modified by Particle Composition and Beta-Blocker Use in Patients with Coronary Heart Disease

Background

It has been hypothesized that ambient particulate air pollution is able to modify the autonomic nervous control of the heart, measured as heart rate variability (HRV). Previously we reported heterogeneous associations between particulate matter with aerodynamic diameter < 2.5 μm (PM_2.5) and HRV across three study centers.

Objectives

We evaluated whether exposure misclassification, effect modification by medication, or differences in particle composition could explain the inconsistencies.

Methods

Subjects with coronary heart disease visited clinics biweekly in Amsterdam, the Netherlands; Erfurt, Germany; and Helsinki, Finland for 6–8 months. The standard deviation (SD) of NN intervals on an electrocardiogram (ECG; SDNN) and high frequency (HF) power of HRV was measured with ambulatory ECG during paced breathing. Outdoor levels of PM_2.5 were measured at a central site. In Amsterdam and Helsinki, indoor and personal PM_2.5 were measured during the 24 hr preceding the clinic visit. PM_2.5 was apportioned between sources using principal component analyses. We analyzed associations of indoor/personal PM_2.5, elements of PM_2.5, and source-specific PM_2.5 with HRV using linear regression.

Results

Indoor and personal PM_2.5 were not associated with HRV. Increased outdoor PM_2.5 was associated with decreased SDNN and HF at lags of 2 and 3 days only among persons not using beta-blocker medication. Traffic-related PM_2.5 was associated with decreased SDNN, and long-range transported PM_2.5 with decreased SDNN and HF, most strongly among persons not using beta blockers. Indicators for PM_2.5 from traffic and long-range transport were also associated with decreased HRV.

Conclusions

Our results suggest that differences in the composition of particles, beta-blocker use, and obesity of study subjects may explain some inconsistencies among previous studies on HRV.     

Personal exposures to traffic-related air pollution and acute respiratory health among Bronx schoolchildren with asthma

Background

Previous studies have reported relationships between adverse respiratory health outcomes and residential proximity to traffic pollution, but have not shown this at a personal exposure level.

Objective

We compared, among inner-city children with asthma, the associations of adverse asthma outcome incidences with increased personal exposure to particulate matter mass ≤ 2.5 μm in aerodynamic diameter (PM_2.5) air pollution versus the diesel-related carbonaceous fraction of PM_2.5.

Methods

Daily 24-hr personal samples of PM_2.5, including the elemental carbon (EC) fraction, were collected for 40 fifth-grade children with asthma at four South Bronx schools (10 children per school) during approximately 1 month each. Spirometry and symptom scores were recorded several times daily during weekdays.

Results

We found elevated same-day relative risks of wheeze [1.45; 95% confidence interval (CI), 1.03–2.04)], shortness of breath (1.41; 95% CI, 1.01–1.99), and total symptoms (1.30; 95% CI, 1.04–1.62) with an increase in personal EC, but not with personal PM_2.5 mass. We found increased risk of cough, wheeze, and total symptoms with increased 1-day lag and 2-day average personal and school-site EC. We found no significant associations with school-site PM_2.5 mass or sulfur. The EC effect estimate was robust to addition of gaseous pollutants.

Conclusion

Adverse health associations were strongest with personal measures of EC exposure, suggesting that the diesel “soot” fraction of PM_2.5 is most responsible for pollution-related asthma exacerbations among children living near roadways. Studies that rely on exposure to PM mass may underestimate PM health impacts.     

Ambient air pollution and birth weight in full-term infants in Atlanta, 1994-2004

Background

An emerging body of evidence suggests that ambient levels of air pollution during pregnancy are associated with fetal growth.

Objectives

We examined relationships between birth weight and temporal variation in ambient levels of carbon monoxide, nitrogen dioxide (NO₂), sulfur dioxide (SO₂), ozone, particulate matter ≤ 10 μm in diameter (PM₁₀), ≤ 2.5 μm (PM_2.5), 2.5 to 10 μm (PM_2.5–10), and PM_2.5 chemical component measurements for 406,627 full-term births occurring between 1994 and 2004 in five central counties of metropolitan Atlanta.

Methods

We assessed relationships between birth weight and pollutant concentrations during each infant’s first month of gestation and third trimester, as well as in each month of pregnancy using distributed lag models. We also conducted capture-area analyses limited to mothers residing within 4 miles (6.4 km) of each air quality monitoring station.

Results

In the five-county analysis, ambient levels of NO₂, SO₂, PM_2.5 elemental carbon, and PM_2.5 water-soluble metals during the third trimester were significantly associated with small reductions in birth weight (−4 to −16 g per interquartile range increase in pollutant concentrations). Third-trimester estimates were generally higher in Hispanic and non-Hispanic black infants relative to non-Hispanic white infants. Distributed lag models were also suggestive of associations between air pollutant concentrations in late pregnancy and reduced birth weight. The capture-area analyses provided little support for the associations observed in the five-county analysis.

Conclusions

Results provide some support for an effect of ambient air pollution in late pregnancy on birth weight in full-term infants.     

Survival analysis of long-term exposure to different sizes of airborne particulate matter and risk of infant mortality using a birth cohort in Seoul, Korea

Background

Several studies suggest that airborne particulate matter (PM) is associated with infant mortality; however, most focused on short-term exposure to larger particles.

Objectives

We evaluated associations between long-term exposure to different sizes of particles [total suspended particles (TSP), PM ≤ 10 μm in aerodynamic diameter (PM₁₀), ≤ 10–2.5 μm (PM_10–2.5), and ≤ 2.5 μm (PM_2.5)] and infant mortality in a cohort in Seoul, Korea, 2004–2007.

Methods

The study includes 359,459 births with 225 deaths. We applied extended Cox proportional hazards modeling with time-dependent covariates to three mortality categories: all causes, respiratory, and sudden infant death syndrome (SIDS). We calculated exposures from birth to death (or end of eligibility for outcome at 1 year of age) and pregnancy (gestation and each trimester) and treated exposures as time-dependent variables for subjects’ exposure for each pollutant. We adjusted by sex, gestational length, season of birth, maternal age and educational level, and heat index. Each cause of death and exposure time frame was analyzed separately.

Results

We found a relationship between gestational exposures to PM and infant mortality from all causes or respiratory causes for normal-birth-weight infants. For total mortality (all causes), risks were 1.44 (95% confidence interval, 1.06–1.97), 1.65 (1.18–2.31), 1.53 (1.22–1.90), and 1.19 (0.83–1.70) per interquartile range increase in TSP, PM₁₀, PM_2.5, and PM_10–2.5, respectively; for respiratory mortality, risks were 3.78 (1.18–12.13), 6.20 (1.50–25.66), 3.15 (1.26–7.85), and 2.86 (0.76–10.85). For SIDS, risks were 0.92 (0.33–2.58), 1.15 (0.38–3.48), 1.42 (0.71–2.87), and 0.57 (0.16–1.96), respectively.

Conclusions

Our findings provide supportive evidence of an association of long-term exposure to PM air pollution with infant mortality.     

Are Particulate Matter Exposures Associated with Risk of Type 2 Diabetes?

Background

Although studies have found that diabetes mellitus (DM) modifies the impact of exposures from air pollution on cardiovascular outcomes, information is limited regarding DM as an air pollution-associated outcome.

Objectives

Using two prospective cohorts, the Nurses’ Health Study (NHS) and the Health Professionals Follow-Up Study (HPFS), we investigated the relationship of incident type 2 DM with exposures to particulate matter (PM) <2.5 μm (PM_2.5), PM <10 μm (PM₁₀), and PM between 2.5 and 10 μm in aerodynamic diameter (PM_10–2.5) in the previous 12 months and the distance to roadways.

Methods

Cases were reported and confirmed through biennial and supplemental questionnaires of diagnosis and treatment information. During follow-up from 1989 to 2002, questionnaires provided information on time-varying covariates and updated addresses. Addresses were geocoded and used to assign air pollution exposures from spatiotemporal statistical models.

Results

Among participants living in metropolitan areas of the northeastern and midwestern United States, there were 3,784 incident cases of DM in the NHS, and 688 cases in the HPFS. Pooled results from random effects meta-analysis of cohort-specific models adjusted for body mass index and other known risk factors produced hazard ratios (HRs) for incident DM with interquartile range (IQR) increases in average PM during the 12 months before diagnosis of 1.03 [95% confidence interval (CI), 0.96–1.10] for PM_2.5, 1.04 (95% CI, 0.99–1.09) for PM₁₀, and 1.04 (95% CI, 0.99–1.09) for PM_10–2.5. Among women, the fully adjusted HR for living < 50 m versus ≥ 200 m from a roadway was 1.14 (95% CI, 1.03–1.27).

Conclusions

Overall, results did not provide strong evidence of an association between exposure to PM in the previous 12 months and incident DM; however, an association with distance to road (a proxy marker of exposure to traffic-related pollution) was shown among women.     

Ambient PM2.5 exposure up-regulates the expression of costimulatory receptors on circulating monocytes in diabetic individuals

Background

Exposure of humans to air pollutants such as ozone and particulate matter (PM) may result in airway and systemic inflammation and altered immune function. One putative mechanism may be through modification of cell-surface costimulatory molecules.

Objectives

We examined whether changes in expression of costimulatory molecules on circulating cells are associated with ambient levels of fine PM [aerodynamic diameter ≤ 2.5 μm (PM_2.5)] in a susceptible population of diabetic individuals.

Methods

Twenty subjects were studied for 4 consecutive days. Daily measurements of PM_2.5 and meteorologic data were acquired on the rooftop of the exam site. Circulating cell-surface markers that mediate innate immune and inflammatory responses were assessed by flow cytometry on each day. Sensitivity analysis was conducted on glutathione S-transferase M1 (GSTM1) genotype, body mass index, and glycosylated hemoglobin A1c (HbA1c) levels to determine their role as effect modifiers. Data were analyzed using random effects models adjusting for season, weekday, and meteorology.

Results

We found significantly increased monocyte expression (mean fluorescent intensity) of CD80, CD40, CD86, HLA-DR, and CD23 per 10-μg/m³ increase in PM_2.5 at 2- to 4-day lag times after exposure. These findings were significantly higher in obese individuals, in individuals with HbA1c > 7%, and in participants who were GSTM1 null.

Conclusions

Exposure to PM_2.5 can enhance antigen-presenting cell phenotypes on circulating cells, which may have consequences in the development of allergic or autoimmune diseases. These effects are amplified in diabetic individuals with characteristics that are associated with insulin resistance or with oxidative stress.     

Ozone and other air pollutants and the risk of oral clefts

Background

Air pollution influences the development of oral clefts in animals. There are few epidemiologic data on the relation of prenatal air pollution exposure and the risk of oral clefts.

Objectives

Our goal in this study was to assess the relations between exposure to ambient air pollution and the risk of cleft lip with or without cleft palate (CL/P).

Methods

We conducted a population-based case–control study of all 653 cases of CL/P and a random sample of 6,530 control subjects from 721,289 Taiwanese newborns in 2001–2003. We used geographic information systems to form exposure parameters for sulfur dioxide, nitrogen oxides, ozone, carbon monoxide, and particulate matter with an aerodynamic diameter ≤ 10 μm (PM₁₀) during the first 3 months of pregnancy using inverse distance weighting method. We present the effect estimates as odds ratios (ORs) per 10-ppb change for SO₂, NO_x, and O₃, 100-ppb change for CO, and 10-μg/m³ change for PM₁₀.

Results

The risk of CL/P was increased in relation to O₃ levels in the first gestational month [adjusted OR = 1.20; 95% confidence interval (CI), 1.02–1.39] and second gestational month (adjusted OR = 1.25; 95% CI, 1.03–1.52) in the range from 16.7 ppb to 45.1 ppb, but was not related to CO, NO_x, SO₂, or PM₁₀.

Conclusions

The study provides new evidence that exposure to outdoor air O₃ during the first and second month of pregnancy may increase the risk of CL/P. Similar levels of O₃ are encountered globally by large numbers of pregnant women.     

Long-term exposure to airborne particles and arterial stiffness: the Multi-Ethnic Study of Atherosclerosis (MESA)

Background

Increased arterial stiffness could represent an intermediate subclinical outcome in the mechanistic pathway underlying associations between average long-term pollution exposure and cardiovascular events.

Objective

We hypothesized that 20 years of exposure to particulate matter (PM) ≤ 2.5 and 10 μm in aerodynamic diameter (PM_2.5 and PM₁₀, respectively) would be positively associated with arterial stiffness in 3,996 participants from the Multi-Ethnic Study of Atherosclerosis (MESA) who were seen at six U.S. study sites.

Methods

We assigned pollution exposure during two decades preceding a clinical exam (2000–2002) using observed PM₁₀ from monitors nearest participants’ residences and PM₁₀ and PM_2.5 imputed from a space-time model. We examined three log-transformed arterial stiffness outcome measures: Young’s modulus (YM) from carotid artery ultrasound and large (C₁) and small (C₂) artery vessel compliance from the radial artery pulse wave. All associations are expressed per 10 μg/m³ increment in PM and were adjusted for weather, age, sex, race, glucose, triglycerides, diabetes, waist:hip ratio, seated mean arterial pressure, smoking status, pack-years, cigarettes per day, environmental tobacco smoke, and physical activity. C₁ and C₂ models were further adjusted for heart rate, weight, and height.

Results

Long-term average particle exposure was not associated with greater arterial stiffness measured by YM, C₁, or C₂, and the few associations observed were not robust across metrics and adjustment schemes.

Conclusions

Long-term particle mass exposure did not appear to be associated with greater arterial stiffness in this study sample.     

The Effect of Ambient Air Pollution on Sperm Quality

Background

Research has suggested an association with ambient air pollution and sperm quality.

Objectives

We investigated the effect of exposure to ozone (O₃) and particulate matter < 2.5 μm in aerodynamic diameter (PM_2.5) on sperm quality.

Methods

We reexamined a previous cohort study of water disinfection by-products to evaluate sperm quality in 228 presumed fertile men with different air pollution profiles. Outcomes included sperm concentration, total sperm per ejaculate (count), and morphology, as well as DNA integrity and chromatin maturity. Exposures to O₃ and PM_2.5 were evaluated for the 90–day period before sampling. We used multivariable linear regression, which included different levels of adjustment (i.e., without and with season and temperature) to assess the relationship between exposure to air pollutants during key periods of sperm development and adverse sperm outcomes.

Results

Sperm concentration and count were not associated with exposure to PM_2.5, but there was evidence of an association (but not statistically significant) with O₃ concentration and decreased sperm concentration and count. Additionally, a significant increase in the percentage of sperm cells with cytoplasmic drop [β = 2.64; 95% confidence interval (CI), 0.21–5.06] and abnormal head (β = 0.47; 95% CI, 0.03–0.92) was associated with PM_2.5 concentration in the base model. However, these associations, along with all other sperm outcomes, were not significantly associated with either pollutant after controlling for season and temperature. Overall, although we found both protective and adverse effects, there was generally no consistent pattern of increased abnormal sperm quality with elevated exposure to O₃ or PM_2.5.

Conclusions

Exposures to O₃ or PM_2.5 at levels below the current National Ambient Air Quality Standards were not associated with statistically significant decrements in sperm outcomes in this cohort of fertile men. However, some results suggested effects on sperm concentration, count, and morphology.     

Exploration of the rapid effects of personal fine particulate matter exposure on arterial hemodynamics and vascular function during the same day

Background

Levels of fine particulate matter [≤ 2.5 μm in aerodynamic diameter (PM_2.5)] are associated with alterations in arterial hemodynamics and vascular function. However, the characteristics of the same-day exposure–response relationships remain unclear.

Objectives

We aimed to explore the effects of personal PM_2.5 exposures within the preceding 24 hr on blood pressure (BP), heart rate (HR), brachial artery diameter (BAD), endothelial function [flow-mediated dilatation (FMD)], and nitroglycerin-mediated dilatation (NMD).

Methods

Fifty-one nonsmoking subjects had up to 5 consecutive days of 24-hr personal PM_2.5 monitoring and daily cardiovascular (CV) measurements during summer and/or winter periods. The associations between integrated hour-long total personal PM_2.5 exposure (TPE) levels (continuous nephelometry among compliant subjects with low secondhand tobacco smoke exposures; n = 30) with the CV outcomes were assessed over a 24-hr period by linear mixed models.

Results

We observed the strongest associations (and smallest estimation errors) between HR and TPE recorded 1–10 hr before CV measurements. The associations were not pronounced for the other time lags (11–24 hr). The associations between TPE and FMD or BAD did not show as clear a temporal pattern. However, we found some suggestion of a negative association with FMD and a positive association with BAD related to TPE just before measurement (0–2 hr).

Conclusions

Brief elevations in ambient TPE levels encountered during routine daily activity were associated with small increases in HR and trends toward conduit arterial vasodilatation and endothelial dysfunction within a few hours of exposure. These responses could reflect acute PM_2.5-induced autonomic imbalance and may factor in the associated rapid increase in CV risk among susceptible individuals.     

Distributed lag analyses of daily hospital admissions and source-apportioned fine particle air pollution

Background

Past time-series studies of the health effects of fine particulate matter [aerodynamic diameter ≤ 2.5 μm (PM_2.5)] have used chemically nonspecific PM_2.5 mass. However, PM_2.5 is known to vary in chemical composition with source, and health impacts may vary accordingly.

Objective

We tested the association between source-specific daily PM_2.5 mass and hospital admissions in a time-series investigation that considered both single-lag and distributed-lag models.

Methods

Daily PM_2.5 speciation measurements collected in midtown Manhattan were analyzed via positive matrix factorization source apportionment. Daily and distributed-lag generalized linear models of Medicare respiratory and cardiovascular hospital admissions during 2001–2002 considered PM_2.5 mass and PM_2.5 from five sources: transported sulfate, residual oil, traffic, steel metal works, and soil.

Results

Source-related PM_2.5 (specifically steel and traffic) was significantly associated with hospital admissions but not with total PM_2.5 mass. Steel metal works–related PM_2.5 was associated with respiratory admissions for multiple-lag days, especially during the cleanup efforts at the World Trade Center. Traffic-related PM_2.5 was consistently associated with same-day cardiovascular admissions across disease-specific subcategories. PM_2.5 constituents associated with each source (e.g., elemental carbon with traffic) were likewise associated with admissions in a consistent manner. Mean effects of distributed-lag models were significantly greater than were maximum single-day effect models for both steel- and traffic-related PM_2.5.

Conclusions

Past analyses that have considered only PM_2.5 mass or only maximum single-day lag effects have likely underestimated PM_2.5 health effects by not considering source-specific and distributed-lag effects. Differing lag structures and disease specificity observed for steel-related versus traffic-related PM_2.5 raise the possibility of distinct mechanistic pathways of health effects for particles of differing chemical composition.     

Ambient carbon monoxide and fine particulate matter in relation to preeclampsia and preterm delivery in western Washington State

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 (PM_2.5)] 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 PM_2.5 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 PM_2.5 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.     

Modifying Effect of Age on the Association between Ambient Ozone and Nighttime Primary Care Visits Due to Asthma Attack

Background

We examined the association between short-term exposure to outdoor air pollution and nighttime primary care visits due to asthma attack. We also investigated the modifying effects of age on this association.

Methods

A case–crossover study was conducted at a primary care clinic in metropolitan Tokyo. The subjects were 308 children aged 0–14 years and 95 adolescents and adults aged 15–64 years. All subjects made visits to the clinic for an asthma attack at between 7 PM and 12 AM. Data on hourly concentrations of particulate matter with a 50% cut-off aerodynamic diameter ≤2.5 µm (PM_2.5), ozone, and nitrogen dioxide (NO₂) were obtained. A conditional logistic regression model was used to estimate odds ratios (ORs) of primary care visits per unit increment of each air pollutant.

Results

Among children, the ORs in warmer months per 10 ppb increment of the 24-hour mean concentration of ozone were 1.16 (95% confidential interval [CI], 1.00–1.33) adjusted for temperature, and 1.29 (95% CI, 1.08–1.55) adjusted for PM_2.5, NO₂, and temperature. With respect to modification of the association by age, the ORs for 24-hour mean concentration of ozone—after adjustment for PM_2.5, NO₂ and temperature in warmer months—in children aged 0–1 years, 2–5 years, and 6–14 years were 1.06 (95% CI, 0.63–1.78), 1.37 (95% CI, 1.05–1.71), and 1.25 (95% CI, 0.87–1.82), respectively. There was no association between ozone and primary care visits among adults.

Conclusions

An association was found between ozone and nighttime primary care visits for asthma attack in warmer months; the association was greater among preschool children.Key words: air pollution, asthma, ozone, particulate matter, preschool children     

Long-term exposure to traffic-related air pollution and the risk of coronary heart disease hospitalization and mortality

Background

Epidemiologic studies have demonstrated that exposure to road traffic is associated with adverse cardiovascular outcomes.

Objectives

We aimed to identify specific traffic-related air pollutants that are associated with the risk of coronary heart disease (CHD) morbidity and mortality to support evidence-based environmental policy making.

Methods

This population-based cohort study included a 5-year exposure period and a 4-year follow-up period. All residents 45–85 years of age who resided in Metropolitan Vancouver during the exposure period and without known CHD at baseline were included in this study (n = 452,735). Individual exposures to traffic-related air pollutants including black carbon, fine particles [aerodynamic diameter ≤ 2.5 μm (PM_2.5)], nitrogen dioxide (NO₂), and nitric oxide were estimated at residences of the subjects using land-use regression models and integrating changes in residences during the exposure period. CHD hospitalizations and deaths during the follow-up period were identified from provincial hospitalization and death registration records.

Results

An interquartile range elevation in the average concentration of black carbon (0.94 × 10⁻⁵/m filter absorbance, equivalent to approximately 0.8 μg/m³ elemental carbon) was associated with a 3% increase in CHD hospitalization (95% confidence interval, 1–5%) and a 6% increase in CHD mortality (3–9%) after adjusting for age, sex, preexisting comorbidity, neighborhood socioeconomic status, and copollutants (PM_2.5 and NO₂). There were clear linear exposure–response relationships between black carbon and coronary events.

Conclusions

Long-term exposure to traffic-related fine particulate air pollution, indicated by black carbon, may partly explain the observed associations between exposure to road traffic and adverse cardiovascular outcomes.     

Ambient particulate air pollution and cardiac arrhythmia in a panel of older adults in Steubenville, Ohio

Objectives

Ambient particulate air pollution has been associated with increased risk of cardiovascular morbidity and mortality. Pathways by which particles may act involve autonomic nervous system dysfunction or inflammation, which can affect cardiac rate and rhythm. The importance of these pathways may vary by particle component or source. In an eastern US location with significant regional pollution, the authors examined the association of air pollution and odds of cardiac arrhythmia in older adults.

Methods

Thirty two non‐smoking older adults were evaluated on a weekly basis for 24 weeks during the summer and autumn of 2000 with a standardised 30 minute protocol that included continuous electrocardiogram measurements. A central ambient monitoring station provided daily concentrations of fine particles (PM_2.5, sulfate, elemental carbon) and gases. Sulfate was used as a marker of regional pollution. The authors used logistic mixed effects regression to examine the odds of having any supraventricular ectopy (SVE) or ventricular ectopy (VE) in association with increases in air pollution for moving average pollutant concentrations up to 10 days before the health assessment.

Results

Participant specific mean counts of arrhythmia over the protocol varied between 0.1–363 for SVE and 0–350 for VE. The authors observed odds ratios for having SVE over the length of the protocol of 1.42 (95% CI 0.99 to 2.04), 1.70 (95% CI 1.12 to 2.57), and 1.78 (95% CI 0.95 to 3.35) for 10.0 μg/m³, 4.2 μg/m³, and 14.9 ppb increases in five day moving average PM_2.5, sulfate, and ozone concentrations respectively. The other pollutants, including elemental carbon, showed no effect on arrhythmia. Participants reporting cardiovascular conditions (for example, previous myocardial infarction or hypertension) were the most susceptible to pollution induced SVE. The authors found no association of pollution with VE.

Conclusion

Increased levels of ambient sulfate and ozone may increase the risk of supraventricular arrhythmia in the elderly.     

Ambient particulate matter air pollution and venous thromboembolism in the Women's Health Initiative Hormone Therapy trials

Background

The putative effects of postmenopausal hormone therapy on the association between particulate matter (PM) air pollution and venous thromboembolism (VTE) have not been assessed in a randomized trial of hormone therapy, despite its widespread use among postmenopausal women.

Objective

In this study, we examined whether hormone therapy modifies the association of PM with VTE risk.

Methods

Postmenopausal women 50–79 years of age (n = 26,450) who did not have a history of VTE and who were not taking anticoagulants were enrolled in the Women’s Health Initiative Hormone Therapy trials at 40 geographically diverse U.S. clinical centers. The women were randomized to treatment with estrogen versus placebo (E trial) or to estrogen plus progestin versus placebo (E + P trial). We used age-stratified Cox proportional hazard models to examine the association between time to incident, centrally adjudicated VTE, and daily mean PM concentrations spatially interpolated at geocoded addresses of the participants and averaged over 1, 7, 30, and 365 days.

Results

During the follow-up period (mean, 7.7 years), 508 participants (2.0%) had VTEs at a rate of 2.6 events per 1,000 person-years. Unadjusted and covariate-adjusted VTE risk was not associated with concentrations of PM < 2.5 μm (PM_2.5) or < 10 μm (PM₁₀)] in aerodynamic diameter and PM × active treatment interactions were not statistically significant (p > 0.05) regardless of PM averaging period, either before or after combining data from both trials [e.g., combined trial-adjusted hazard ratios (95% confidence intervals) per 10 μg/m³ increase in annual mean PM_2.5 and PM₁₀, were 0.93 (0.54–1.60) and 1.05 (0.72–1.53), respectively]. Findings were insensitive to alternative exposure metrics, outcome definitions, time scales, analytic methods, and censoring dates.

Conclusions

In contrast to prior research, our findings provide little evidence of an association between short-term or long-term PM exposure and VTE, or clinically important modification by randomized exposure to exogenous estrogens among postmenopausal women.     

An Estimate of the Global Burden of Anthropogenic Ozone and Fine Particulate Matter on Premature Human Mortality Using Atmospheric Modeling

Background

Ground-level concentrations of ozone (O₃) and fine particulate matter [≤ 2.5 μm in aerodynamic diameter (PM_2.5)] have increased since preindustrial times in urban and rural regions and are associated with cardiovascular and respiratory mortality.

Objectives

We estimated the global burden of mortality due to O₃ and PM_2.5 from anthropogenic emissions using global atmospheric chemical transport model simulations of preindustrial and present-day (2000) concentrations to derive exposure estimates.

Methods

Attributable mortalities were estimated using health impact functions based on long-term relative risk estimates for O₃ and PM_2.5 from the epidemiology literature. Using simulated concentrations rather than previous methods based on measurements allows the inclusion of rural areas where measurements are often unavailable and avoids making assumptions for background air pollution.

Results

Anthropogenic O₃ was associated with an estimated 0.7 ± 0.3 million respiratory mortalities (6.3 ± 3.0 million years of life lost) annually. Anthropogenic PM_2.5 was associated with 3.5 ± 0.9 million cardiopulmonary and 220,000 ± 80,000 lung cancer mortalities (30 ± 7.6 million years of life lost) annually. Mortality estimates were reduced approximately 30% when we assumed low-concentration thresholds of 33.3 ppb for O₃ and 5.8 μg/m³ for PM_2.5. These estimates were sensitive to concentration thresholds and concentration–mortality relationships, often by > 50%.

Conclusions

Anthropogenic O₃ and PM_2.5 contribute substantially to global premature mortality. PM_2.5 mortality estimates are about 50% higher than previous measurement-based estimates based on common assumptions, mainly because of methodologic differences. Specifically, we included rural populations, suggesting higher estimates; however, the coarse resolution of the global atmospheric model may underestimate urban PM_2.5 exposures.     

Chronic bronchitis and urban air pollution in an international study

Objectives

The chronic effects of urban air pollution are not well known. The authors'' aim was to investigate the association between the prevalence and new onset of chronic bronchitis and urban air pollution.

Methods

Subjects from the general population randomly selected for the European Community Respiratory Health Survey (ECRHS I) during 1991–93 in 21 centres in 10 countries were followed up from the years 2000 to 2002 (n = 3232 males and 3592 females; average response rate = 65.3%). PM_2.5 and elements, with the same equipment at centre level, and home outdoor NO₂ in 1634 individuals were measured. Hierarchical models were used.

Results

The prevalence and new onset of chronic phlegm during follow up were 6.9% and 4.5%, respectively, 5.3% in males and 3.5% in females. Smoking, rhinitis, poor education, and low social class were associated with (prevalence and new onset of) chronic phlegm in both genders, and occupational exposures in males and traffic intensity (adjusted odds ratio for constant traffic, OR = 1.86; 95% CI 1.24 to 2.77) as well as home outdoor NO₂ (OR > 50 μg/m³v < 20μg³  =  2.71; 95% CI 1.03 to 7.16) among females. PM_2.5 and S content at centre level did not show any association with prevalence or new onset of chronic phlegm. Similar results were obtained with chronic productive cough.

Conclusion

Individual markers of traffic at household level such as reported intensity and outdoor NO₂ were risk factors for chronic bronchitis among females.