Changes in Lung Function and Airway Inflammation Among Asthmatic Children Residing in a Woodsmoke-Impacted Urban Area
Faculty of Health Sciences, Simon Fraser University, Burnaby, British Columbia, Canada. Inhalation Toxicology
(Impact Factor: 2.26).
03/2008; 20(4):423-33. DOI: 10.1080/08958370801903826
Fine particulate matter (PM(2.5)) is associated with respiratory effects, and asthmatic children are especially sensitive. Preliminary evidence suggests that combustion-derived particles play an important role. Our objective was to evaluate effect estimates from different PM(2.5) exposure metrics in relation to airway inflammation and lung function among children residing in woodsmoke-impacted areas of Seattle. Nineteen children (ages 6-13 yr) with asthma were monitored during the heating season. We measured 24-h outdoor and personal concentrations of PM(2.5) and light-absorbing carbon (LAC). Levoglucosan (LG), a marker of woodsmoke, was also measured outdoors. We partitioned PM(2.5) exposure into its ambient-generated (E(ag)) and nonambient (E(na)) components. These exposure metrics were evaluated in relation to daily changes in exhaled nitric oxide (FE(NO)), a marker of airway inflammation, and four lung function measures: midexpiratory flow (MEF), peak expiratory flow (PEF), forced expiratory volume in the first second (FEV(1)), and forced vital capacity (FVC). E(ag), but not E(na), was correlated with combustion markers. Significant associations with respiratory health were seen only among participants not using inhaled corticosteroids. Increases in FE(NO) were associated with personal PM(2.5), personal LAC, and E(ag) but not with ambient PM(2.5) or its combustion markers. In contrast, MEF and PEF decrements were associated with ambient PM(2.5), its combustion markers, and E(ag), but not with personal PM(2.5) or personal LAC. FEV(1) was associated only with ambient LG. Our results suggest that lung function may be especially sensitive to the combustion-generated component of ambient PM(2.5), whereas airway inflammation may be more closely related to some other constituent of the ambient PM(2.5) mixture.
Available from: Patricia Fabian
- "Studies were excluded for a variety of reasons, including a lack of focus on short-term changes in lung function due to short-term changes in air pollution. We eliminated 12 of these studies given issues such as the use of FEV1 rather than FEV1% as the outcome measure without sufficient data to allow for conversion [45,46,50,53-55,57-59], season-specific characterization , or missing quantification of values necessary for our study [47,51]. For the remaining five studies, two [43,44] were panel studies in Los Angeles, two [49,60] were studies of the same panel of children in Windsor, Ontario, and one  was based on children within the Inner City Asthma Study. "
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In the United States, asthma is the most common chronic disease of childhood across all socioeconomic classes and is the most frequent cause of hospitalization among children. Asthma exacerbations have been associated with exposure to residential indoor environmental stressors such as allergens and air pollutants as well as numerous additional factors. Simulation modeling is a valuable tool that can be used to evaluate interventions for complex multifactorial diseases such as asthma but in spite of its flexibility and applicability, modeling applications in either environmental exposures or asthma have been limited to date.
We designed a discrete event simulation model to study the effect of environmental factors on asthma exacerbations in school-age children living in low-income multi-family housing. Model outcomes include asthma symptoms, medication use, hospitalizations, and emergency room visits. Environmental factors were linked to percent predicted forced expiratory volume in 1 second (FEV1%), which in turn was linked to risk equations for each outcome. Exposures affecting FEV1% included indoor and outdoor sources of NO2 and PM2.5, cockroach allergen, and dampness as a proxy for mold.
Model design parameters and equations are described in detail. We evaluated the model by simulating 50,000 children over 10 years and showed that pollutant concentrations and health outcome rates are comparable to values reported in the literature. In an application example, we simulated what would happen if the kitchen and bathroom exhaust fans were improved for the entire cohort, and showed reductions in pollutant concentrations and healthcare utilization rates.
We describe the design and evaluation of a discrete event simulation model of pediatric asthma for children living in low-income multi-family housing. Our model simulates the effect of environmental factors (combustion pollutants and allergens), medication compliance, seasonality, and medical history on asthma outcomes (symptom-days, medication use, hospitalizations, and emergency room visits). The model can be used to evaluate building interventions and green building construction practices on pollutant concentrations, energy savings, and asthma healthcare utilization costs, and demonstrates the value of a simulation approach for studying complex diseases such as asthma.
Available from: Jorma Mäki-Paakkanen
- "Thus, the genotoxic and cytotoxic responses to the particles emitted from the most inefficient combustion phase in SS were clearly enhanced when the emission factor was taken into account. These kinds of poor wood combustion appliances may be responsible for very high local PM levels (Boman et al., 2003; Allen et al., 2008). It has been shown recently that particles collected from wood smoke emissions in ambient air induce similar oxidative and genotoxic responses in vitro as pure wood combustion particles (Danielsen et al., 2011). "
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ABSTRACT: Particulate matter (PM) has been identified as a major environmental pollutant causing severe health problems. Large amounts of the harmful particulate matter (PM) are emitted from residential wood combustion, but the toxicological properties of wood combustion particles are poorly known.
To investigate chemical and consequent toxicological characteristics of PM(1) emitted from different phases of batch combustion in four heating appliances.
Mouse RAW264.7 macrophages and human BEAS-2B bronchial epithelial cells were exposed for 24 h to different doses (15-300 µg/mL) of wood combustion particles. After the exposure, cytotoxicity, genotoxicity, production of the inflammatory mediators (TNF-α and MIP-2) and effects on the cell cycle were assessed. Furthermore, the detected toxicological responses were compared with the chemical composition of PM(1) samples including PAHs, metals and ions.
All the wood combustion samples exerted high cytotoxicity, but only moderate inflammatory activity. The particles emitted from the inefficient phase of batch combustion in the sauna stove (SS) induced the most extensive cytotoxic and genotoxic responses in mammalian cells. Polycyclic aromatic hydrocarbons (PAHs) and other organic compounds in PM(1) samples might have contributed to these effects. Instead, water-soluble metals seemed to participate in the cytotoxic responses triggered by the particles from more efficient batch combustion in the masonry heaters. Overall, the toxicological responses were decreased when the combustion phase was more efficient.
Efficiency of batch combustion plays a significant role in the harmfulness of PM even under incomplete wood combustion processes.
Available from: Jakob Hjort Bønløkke
- "Researchers’ hypothesise that increased mortality can be associated with the particle levels in urban air [4-7]. Several studies have reported that especially the fine and ultrafine particles have an adverse effect on airways; and that children and asthmatics, among other vulnerable groups, may be at greater risk for developing adverse health effects of air pollutants . "
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ABSTRACT: There is growing evidence that particulate air pollution derived from wood stoves causes acute inflammation in the respiratory system, increases the incidence of asthma and other allergic diseases, and increases respiratory morbidity and mortality. The objective of this study was to evaluate acute respiratory effects from short-term wood smoke exposure in humans. Twenty non-smoking atopic volunteers with normal lung function and without bronchial responsiveness were monitored during three different experimental exposure sessions, aiming at particle concentrations of about 200 μg/m(3), 400 μg/m(3), and clean air as control exposure. A balanced cross-over design was used and participants were randomly allocated to exposure orders. Particles were generated in a wood-burning facility and added to a full-scale climate chamber where the participants were exposed for 3 hours under controlled environmental conditions. Health effects were evaluated in relation to: peak expiratory flow (PEF), forced expiratory volume in the first second (FEV1), and forced vital capacity (FVC). Furthermore, the effects were assessed in relation to changes in nasal patency and from markers of airway inflammation: fractional exhaled nitric oxide (FENO), exhaled breath condensate (EBC) and nasal lavage (NAL) samples were collected before, and at various intervals after exposure.
No statistically significant effect of wood smoke exposure was found for lung function, for FENO, for NAL or for the nasal patency. Limited signs of airway inflammation were found in EBC.
In conclusion, short term exposure with wood smoke at a concentration normally found in a residential area with a high density of burning wood stoves causes only mild inflammatory response.
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