Among inner-city children, most of whom were African American, we found that PM concentrations measured indoors were significantly associated with asthma symptoms and rescue medication use. In our cohort, indoor fine and coarse PM concentrations were associated with increases in respiratory symptoms that were clinically significant in terms of their magnitude. For example, a 10-μg/m3 increase in PM2.5–10 concentration was associated with an 8% increased incidence in days of symptoms severe enough to slow a child’s activity.
Our findings are consistent with what is known about the effects of indoor PM on childhood asthma and provide new evidence of a detrimental health effect of indoor coarse PM. In a previous study, Delfino et al. (2004)
investigated PM exposures among 19 school-age children with asthma living in California and found that forced expiratory volume in 1 sec was inversely associated with personal, indoor, and ambient PM2.5
. They found stronger associations with indoor than with ambient PM concentrations among these children but did not evaluate the effects of PM on symptoms or medication use. Studies of school-age children in Seattle, Washington, have shown that indoor PM2.5
exposure was associated with decreased pulmonary function in a subgroup of 11 children not taking inhaled corticosteroids, but these studies did not include indoor measurements of PM2.5–10
(Koenig et al. 2005
; Trenga et al. 2006
). Thus, the present study, which includes a much larger sample size compared with previous studies, adds to the growing evidence that indoor PM exposure adversely affects asthma health and provides for the first time evidence that exposure to the indoor coarse (PM2.5–10
) fraction is harmful for children with asthma, especially those of preschool age.
Our findings demonstrate that both indoor coarse and fine PM distinctly affect respiratory health. There are physiologic reasons that can explain why PM of these different size fractions can contribute separately to asthma morbidity. In vitro
studies have shown that coarse PM preferentially induces inflammatory mediators in bronchial epithelial cells and alveolar macrophages compared with fine PM and that bacterial and endotoxin components of coarse PM may play a key role in this process (Becker et al. 2003
). Although fine PM may be capable of reaching the alveoli, regions responsible for gas exchange, the deposition of coarse PM in conducting airways and subsequent bronchial hyperreactivity may be driving the symptomatic response measured in these preschool children. Although analyzing the composition of the PM and investigating the mechanism by which PM exacerbates asthma are beyond the scope of the present investigation, fine and coarse PM are known to have different sources, compositions, and deposition patterns in the respiratory tract, all of which may contribute to the differential health effects reported in our study. Understanding the components of indoor PM and the mechanism by which PM exacerbates asthma will be an important focus of future studies.
The strong relationship between indoor and ambient fine PM exposure and exercise-related symptoms was striking. Previous investigators have suggested that exercise may play a role in asthma by modifying the effect of environmental stimuli and pollutants. In a study of asthmatic children, McConnell et al. (2003)
found that nitrogen dioxide was associated with bronchitic symptoms only among children participating in team sports. The authors hypothesized that the increased minute ventilation may in part explain why the effect of NO2
was modified by exercise. Our findings of increased exercise symptoms in response to fine PM exposure may be attributable to increased minute ventilation and an increased dose of fine PM in the distal airways and the pulmonary circulation that is more potent in eliciting exercise-related symptoms than the doses of coarse PM that deposit in the more proximal airways.
The study population is a key strength of our study design. We were able to enroll a study population of predominantly African-American, inner-city children who spent a substantial portion of time in their homes. Our results may provide insight about a potentially important contributor to the high burden of asthma in this population. African Americans are more likely than whites to live in geographic regions with poor outdoor air quality. For example, in 2002, 71% of African Americans lived in counties that violated federal air pollution standards, compared with 58% of the white population (American Lung Association 2005
). Suboptimal indoor environments may contribute additional risk beyond that of the poor outdoor air quality. In Baltimore, a previous study has demonstrated that among children with asthma, those living in the inner city had in-home PM concentrations that were two to three times greater than did those in the local suburbs (Simons et al. 2007
). Compared with what is considered acceptable quality for outdoor air, the children in the present study lived in homes with relatively elevated PM concentrations. For example, 85% of children lived in homes that would fail to meet the NAAQS annual standard for acceptable ambient air quality and 55% lived in homes that would fail to meet the more stringent 24-hr standard (U.S. EPA 1997
). We have demonstrated that PM concentrations in the indoor air are associated with additional asthma morbidity after controlling for the effects of ambient PM measured simultaneously. Thus, indoor PM exposure may be an important contributor to the disproportionate burden of disease among African Americans living in inner cities.
Avoidance of harmful environmental exposures is a key component of national and international guideline recommendations for management of asthma (Global Initiative for Asthma 2006
; National Heart, Lung, and Blood Institute 2007
). Guidelines identify PM as a pollutant of concern, but specific recommendations are limited and focus mostly on avoiding exposure to elevated outdoor concentrations. This approach may imply that the indoor environment confers an advantage of lower exposure. However, our results demonstrate that the indoor environment may be less favorable in some circumstances. Although some previous studies have found indoor PM concentrations that are similar to or lower than outdoor concentrations (Koenig et al. 2005
; Turpin et al. 2007
), our findings are consistent with previous studies that have demonstrated indoor PM concentrations that greatly exceed outdoor concentrations (Breysse et al. 2005
; Keeler et al. 2002
; Wallace 1996
; Wallace et al. 2003
). Current recommendations for improving home indoor air quality focus mostly on avoidance of indoor environmental tobacco smoke. However, there are other important modifiable sources of indoor PM, including common cleaning and cooking activities (McCormack et al. 2008
; Wallace et al. 2003
). In urban environments especially, penetration of outdoor air, which contains traffic-related PM, into the indoors may also be an important contributor to the composition of the indoor air (Turpin et al. 2007
). In the present study, the homes were all in the inner city, and most were close to the road, making exposure to traffic-related urban dust a likely contributing factor to the composition of PM in most homes. Thus, our results are most generalizable to populations of children who live in urban settings. Although our study cannot determine which sources of indoor PM are responsible for exacerbating asthma symptoms, previous studies have shown that PM concentrations can be lowered indoors (Eggleston et al. 2005
). Such studies have shown that a multifaceted indoor environmental control approach can reduce asthma morbidity, but the independent effect of PM reduction has not yet been determined (Eggleston et al. 2005
; Morgan et al. 2004
). Intervention studies to assess the impact of improving indoor air quality on asthma symptoms and which PM reduction methods are most beneficial will be critical to provide data to inform guidelines and policy initiatives.
A limitation of this study is the potential for measurement error. Although the study area was relatively homogeneous, and all homes were within 2 miles of the central monitoring site, we took estimates of outdoor PM exposure from a central monitoring site rather than outdoor monitoring at the individual home. This approach could have resulted in nondifferential measurement error and may have contributed to the lack of a significant health effect of ambient PM exposure on non-exercise-related symptoms. The methods of sampling indoor, and ambient air differed and although we did not conduct side-by-side comparisons, systematic differences of up to 17% have been previously reported (Williams et al. 2000
). We obtained the PM2.5–10
concentrations by subtracting PM 2.5
concentrations from PM10
, making the PM2.5–10
measurement subject to greater error than either individual measurement. We determined that the precision of the indoor PM2.5
measures, determined by collocated samplers, were ±7% and ±6%, respectively, resulting in an expected error in PM2.5–10
of 9%, which is consistent with the precision described previously (Chen et al. 2007
; Vanderpool et al. 2004
; Williams et al. 2000
). Importantly, we conducted environmental monitoring in the same manner for all study participants and did not differ it based on asthma status. Thus, nondifferential measurement error would be expected to bias our results toward the null and would not be responsible for the observed association between indoor PM concentrations and asthma symptoms in this study.
In the present longitudinal study, fine and coarse PM concentrations measured indoors were associated with increased asthma morbidity, including more frequent respiratory symptoms and rescue medication use, among inner-city minority children. Although the present study cannot delineate which sources of PM measured indoors were responsible for the observed health effects, these findings suggest that improving air quality in the indoor environment with a strategy that reduces PM concentration may improve asthma health. These findings do not negate the importance of optimizing outdoor air quality, because outdoor PM concentrations are linked to adverse health effects, especially among those with underlying pulmonary disease, and outdoor air is an important determinant of the composition of indoor air. Instead, improving indoor air quality and lowering indoor PM concentrations may provide an additional means of improving asthma health, especially among children living in inner cities.