Amanda J. Wheeler

Acute Effects of Air Pollution on Pulmonary Function, Airway Inflammation, and Oxidative Stress in Asthmatic Children

Background Air pollution is associated with respiratory symptoms, lung function decrements, and hospitalizations. However, there is little information about the influence of air pollution on lung injury. Objective In this study we investigated acute effects of air pollution on pulmonary function and airway oxidative stress and inflammation in asthmatic children. Methods We studied 182 children with asthma, 9–14 years of age, for 4 weeks. Daily ambient concentrations of sulfur dioxide, nitrogen dioxide, ozone, and particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5) were monitored from two stations. Once a week we measured spirometry and fractional exhaled nitric oxide (FeNO), and determined thiobarbituric acid reactive substances (TBARS) and 8-isoprostane—two oxidative stress markers—and interleukin-6 (IL-6) in breath condensate. We tested associations using mixed-effects regression models, adjusting for confounding variables. Results Interquartile-range increases in 3-day average SO2 (5.4 ppb), NO2 (6.8 ppb), and PM2.5 (5.4 μg/m3) were associated with decreases in forced expiratory flow between 25% and 75% of forced vital capacity, with changes being −3.1% [95% confidence interval (CI), −5.8 to −0.3], −2.8% (95% CI, −4.8 to −0.8), and −3.0% (95% CI, −4.7 to −1.2), respectively. SO2, NO2, and PM2.5 were associated with increases in TBARS, with changes being 36.2% (95% CI, 15.7 to 57.2), 21.8% (95% CI, 8.2 to 36.0), and 24.8% (95% CI, 10.8 to 39.4), respectively. Risk estimates appear to be larger in children not taking corticosteroids than in children taking corticosteroids. O3 (5.3 ppb) was not associated with health end points. FeNO, 8-isoprostane, and IL-6 were not associated with air pollutants. Conclusion Air pollution may increase airway oxidative stress and decrease small airway function of asthmatic children. Inhaled corticosteroids may reduce oxidative stress and improve airway function.

The Inflammatory Bowel Diseases and Ambient Air Pollution: A Novel Association

OBJECTIVES:The inflammatory bowel diseases (IBDs) emerged after industrialization. We studied whether ambient air pollution levels were associated with the incidence of IBD.METHODS:The health improvement network (THIN) database in the United Kingdom was used to identify incident cases of Crohns disease (n=367) or ulcerative colitis (n=591), and age- and sex-matched controls. Conditional logistic regression analyses assessed whether IBD patients were more likely to live in areas of higher ambient concentrations of nitrogen dioxide (NO2), sulfur dioxide (SO2), and particulate matter <10μm (PM10), as determined by using quintiles of concentrations, after adjusting for smoking, socioeconomic status, non-steroidal anti-inflammatory drugs (NSAIDs), and appendectomy. Stratified analyses investigated effects by age.RESULTS:Overall, NO2, SO2, and PM10 were not associated with the risk of IBD. However, individuals ≤23 years were more likely to be diagnosed with Crohns disease if they lived in regions with NO2 concentrations within the upper three quintiles (odds ratio (OR)=2.31; 95% confidence interval (CI)=1.25–4.28), after adjusting for confounders. Among these Crohns disease patients, the adjusted OR increased linearly across quintile levels for NO2 (P=0.02). Crohns disease patients aged 44–57 years were less likely to live in regions of higher NO2 (OR=0.56; 95% CI=0.33–0.95) and PM10 (OR=0.48; 95% CI=0.29–0.80). Ulcerative colitis patients ≤25 years (OR=2.00; 95% CI=1.08–3.72) were more likely to live in regions of higher SO2; however, a dose–response effect was not observed.CONCLUSIONS:On the whole, air pollution exposure was not associated with the incidence of IBD. However, residential exposures to SO2 and NO2 may increase the risk of early-onset ulcerative colitis and Crohns disease, respectively. Future studies are needed to explore the age-specific effects of air pollution exposure on IBD risk.

Quality of indoor residential air and health

About 90% of our time is spent indoors where we are exposed to chemical and biological contaminants and possibly to carcinogens. These agents may influence the risk of developing nonspecific respiratory and neurologic symptoms, allergies, asthma and lung cancer. We review the sources, health effects and control strategies for several of these agents. There are conflicting data about indoor allergens. Early exposure may increase or may decrease the risk of future sensitization. Reports of indoor moulds or dampness or both are consistently associated with increased respiratory symptoms but causality has not been established. After cigarette smoking, exposure to environmental tobacco smoke and radon are the most common causes of lung cancer. Homeowners can improve the air quality in their homes, often with relatively simple measures, which should provide health benefits.

The Relationship between Ambient Air Pollution and Heart Rate Variability Differs for Individuals with Heart and Pulmonary Disease

Associations between concentrations of ambient fine particles [particulate matter < 2.5 μ m aerodynamic diameter (PM2.5)] and heart rate variability (HRV) have differed by study population. We examined the effects of ambient pollution on HRV for 18 individuals with chronic obstructive pulmonary disease (COPD) and 12 individuals with recent myocardial infarction (MI) living in Atlanta, Georgia. HRV, baseline pulmonary function, and medication data were collected for each participant on 7 days in fall 1999 and/or spring 2000. Hourly ambient pollution concentrations were obtained from monitoring sites in Atlanta. The association between ambient pollution and HRV was examined using linear mixed-effect models. Ambient pollution had opposing effects on HRV in our COPD and MI participants, resulting in no significant effect of ambient pollution on HRV in the entire population for 1-, 4-, or 24-hr moving averages. For individuals with COPD, interquartile range (IQR) increases in 4-hr ambient PM2.5 (11.65 μ g/m3) and nitrogen dioxide (11.97 ppb) were associated with 8.3% [95% confidence interval (CI), 1.7–15.3%] and 7.7% (95% CI, 0.1–15.9%) increase in the SD of normal R-R intervals (SDNN), respectively. For individuals with MI, IQR increases in 4-hr PM2.5 (8.54 μ g/m3) and NO2 (9.25 ppb) were associated with a nonsignificant 2.9% (95% CI, –7.8 to 2.3) and significant 12.1 (95% CI, –19.5 to –4.0) decrease in SDNN. Beta-blocker and bronchodilator intake and baseline forced expiratory volume in 1 sec modified the PM–SDNN association significantly, with effects consistent with those by disease group. Results indicate heterogeneity in the autonomic response to air pollution due to differences in baseline health, with significant associations for ambient NO2 suggesting an important role for traffic-related pollution.

Effects of indoor, outdoor, and personal exposure to particulate air pollution on cardiovascular physiology and systemic mediators in seniors.

Objective: To investigate the associations between exposure to particulate air pollution and changes in cardiovascular function and plasma mediators in seniors. Methods: We monitored daily indoor and outdoor black carbon and particulate matter ≤2.5 &mgr;m (pm2.5) and personal pm2.5 repeatedly for 28 nonsmoking seniors. We then measured their blood pressure, heart rate, and brachial artery function, and determined plasma mediators of inflammation, vascular function, and oxidative stress. We tested associations using mixed-effects models. Results: Increases in black carbon and pm2.5 were associated with increases in blood pressure, heart rate, endothelin-1, vascular endothelial growth factor, and oxidative stress marker thiobarbituric acid reactive substances, and a decrease in brachial artery diameter (P < 0.05). Conclusion: Daily exposure to particulate pollution, likely traffic-related, may result in adverse effects on cardiovascular function and blood mediators that modulate vascular system in seniors.

Validation of continuous particle monitors for personal, indoor, and outdoor exposures

Continuous monitors can be used to supplement traditional filter-based methods of determining personal exposure to air pollutants. They have the advantages of being able to identify nearby sources and detect temporal changes on a time scale of a few minutes. The Windsor Ontario Exposure Assessment Study (WOEAS) adopted an approach of using multiple continuous monitors to measure indoor, outdoor (near-residential) and personal exposures to PM2.5, ultrafine particles and black carbon. About 48 adults and households were sampled for five consecutive 24-h periods in summer and winter 2005, and another 48 asthmatic children for five consecutive 24-h periods in summer and winter 2006. This article addresses the laboratory and field validation of these continuous monitors. A companion article (Wheeler et al., 2010) provides similar analyses for the 24-h integrated methods, as well as providing an overview of the objectives and study design. The four continuous monitors were the DustTrak (Model 8520, TSI, St. Paul, MN, USA) and personal DataRAM (pDR) (ThermoScientific, Waltham, MA, USA) for PM2.5; the P-Trak (Model 8525, TSI) for ultrafine particles; and the Aethalometer (AE-42, Magee Scientific, Berkeley, CA, USA) for black carbon (BC). All monitors were tested in multiple co-location studies involving as many as 16 monitors of a given type to determine their limits of detection as well as bias and precision. The effect of concentration and electronic drift on bias and precision were determined from both the collocated studies and the full field study. The effect of rapid changes in environmental conditions on switching an instrument from indoor to outdoor sampling was also studied. The use of multiple instruments for outdoor sampling was valuable in identifying occasional poor performance by one instrument and in better determining local contributions to the spatial variation of particulate pollution. Both the DustTrak and pDR were shown to be in reasonable agreement (R2 of 90 and 70%, respectively) with the gravimetric PM2.5 method. Both instruments had limits of detection of about 5 μg/m3. The DustTrak and pDR had multiplicative biases of about 2.5 and 1.6, respectively, compared with the gravimetric samplers. However, their average bias-corrected precisions were <10%, indicating that a proper correction for bias would bring them into very good agreement with standard methods. Although no standard methods exist to establish the bias of the Aethalometer and P-Trak, the precision was within 20% for the Aethalometer and within 10% for the P-Trak. These findings suggest that all four instruments can supply useful information in environmental studies.

Further interpretation of the acute effect of nitrogen dioxide observed in Canadian time-series studies.

In this paper, the pooled NO2 association with nonaccidental mortality is examined across 10 cities in Canada in single- and two-pollutant time-series models. The results reaffirm that NO2 has the strongest association with mortality, particularly in the warm season. Although attributing such effects to NO2 cannot be ruled out, it is plausible that NO2 is acting as an indicator for some other exposure affecting the population. This could include PM2.5, as has been suggested from some personal exposure data, but it could also be indicating a more specific type of PM2.5, such as traffic-related particles, given that in cities the main source of NO2 is motor vehicle exhaust. NO2 could also be acting as a surrogate for other pollutant(s) originating from motor vehicles or high-temperature combustion, such as volatile organic compounds (VOCs) or polycyclic aromatic hydrocarbons. Another possibility is other oxidized nitrogen species (“NOz”) or photochemically produced pollutants that can co-vary with NO2, especially during urban stagnation events. Data to test these different possibilities across several Canadian cities are examined. The focus is on correlations in time or space between NO2 and other pollutants that are more strongly linked to vehicle emissions. The results support the hypothesis that NO2 is a better indicator than PM2.5 of a range of other toxic pollutants. This includes VOCs, aldehydes, NOz and particle-bound organics in motor vehicle exhaust. Thus, overall, the strong effect of NO2 in Canadian cities could be a result of it being the best indicator, among the pollutants monitored, of fresh combustion (likely motor vehicles) as well as photochemically processed urban air.

Long-term exposure to traffic-related air pollution and cardiovascular mortality.

Background: Findings from previous cohort studies suggest a positive association between traffic-related air pollution and cardiovascular mortality. However, few studies have assessed intraurban variation in traffic-related pollution or evaluated cardiovascular effects at lower levels of pollution that are typically seen in Canadian cities. Methods: We conducted a cohort study of traffic-related air pollution and cardiovascular mortality among adults who lived in three cities in Ontario, Canada. Study members of the cohort were a random sample from the federal family income tax database, comprising 205,440 adults age 35–85 years, who lived in Toronto, Hamilton, or Windsor between 1982 and 1986. Follow-up ended on 31 December 2004. Mortality from cardiovascular and cerebrovascular diseases was ascertained using the Canadian Mortality Database. We estimated time-dependent concentrations of ambient nitrogen dioxide (NO2) from land-use regression models and assigned exposures to residences of subjects. Rate ratios (RRs) were estimated from Cox proportional hazard model adjusted for individual risk factors and selected contextual covariables. We adjusted indirectly for smoking and obesity. Results: The spatial distributions of NO2 did not change appreciably over the follow-up period. Cumulative exposure to NO2 was associated with a 12% increase in mortality from cardiovascular disease for each increase of 5 parts per billion of NO2 (95% confidence interval [CI] = 7%–17%) and a 15% increase (8%–21%) in mortality from ischemic heart disease. Risks of cardiovascular mortality were also increased with shorter term exposures, but the RRs were somewhat smaller. No association was found for cerebrovascular mortality (RR = 0.99 [95% CI = 0.91–1.08]). Conclusion: Traffic-related air pollution at relatively low concentrations in Ontario was associated with increased mortality from cardiovascular disease.

The influence of living near roadways on spirometry and exhaled nitric oxide in elementary schoolchildren.

Background Living near major roadways has been associated with an increase in respiratory symptoms, but little is known about how this relates to airway inflammation. Objective We assessed the effects of living near local residential roadways based on objective indicators of ventilatory function and airway inflammation. Methods We estimated ambient air pollution, resolved to the level of the child’s neighborhood, using a land-use regression model for children 9–11 years of age. We also summed the length of roadways found within a 200-m radius of each child’s neighborhood. We had measurements of both air pollution exposure and spirometry for 2,328 children, and also had measurements of exhaled nitric oxide (eNO) for 1,613 of these children. Results Each kilometer of local roadway within a 200-m radius of the home was associated with a 6.8% increase in eNO (p = 0.045). Each kilometer of any type of roadway (local, major, highway) was also associated with an increase in eNO of 10.1% (p = 0.002). Each microgram per cubic meter increase in PM2.5 was associated with a 3.9% increase in eNO (p = 0.058) and 0.70% decrease in forced vital capacity (FVC) expressed as a percentage of predicted (p = 0.39). Associations between roadway density and both forced expired volume in 1 sec and FVC were negative but not statistically significant at p < 0.05. Conclusion Traffic from local neighborhood roadways may cause airway inflammation as indicated by eNO. This may be a more sensitive indicator of adverse air pollution effects than traditional measures of ventilatory function.

Characterisation of Particulate Matter Sampled during a Study of Children's Personal Exposure to Airborne Particulate Matter in a UK Urban Environment

The personal exposure of children aged 9 – 11 years to particulate matter (PM10 and PM2.5) was carried out between January and September 1997 in the London Borough of Barnet. Personal sampling along with home, garden and classroom microenvironmental monitoring was completed for all ten children. Each child was monitored for five days during winter, spring and summer. All children completed daily time activity diaries to provide information on any potential activities that could influence their exposure to particulate matter. Each evening a household activity questionnaire was also completed by the parents. Personal Environmental Monitors were used to sample personal exposure to PM10 and PM2.5. Harvard Impactors were used for the microenvironmental sampling of both size fractions. The childrens mean personal exposure concentrations for PM10 during winter, spring and summer were 72, 54 and 35 µg/m3 respectively and for PM2.5 22, 17 and 18 µg/m3 respectively. In order to determine the potential sources of particulate matter, analysis of the Teflon filters has been undertaken. The physical characteristics of the particles have been identified using Scanning Electron Microscopy. The relationships between personal exposure concentrations and the different microenvironments will be discussed.