Particulate matter is a principal component of indoor air pollution in homes. PM originates from a variety of human-made and natural sources. Natural sources include pollen, spores, bacteria, plant and animal debris, and suspended crustal materials. Human-made sources consist of industrial emissions and combustion by-products from incinerators, motor vehicles, and power plants. Indoor sources include cigarette smoking, cooking, wood and other biomass burning in stoves and fireplaces, cleaning activities that re-suspend dust particles (e.g., sweeping), and penetration of outdoor particles into the indoor environment (11
). Indoor PM differs from outdoor PM in source, composition, and concentration (11
). As a result, the health effects of indoor PM cannot be readily extrapolated from studies of outdoor air pollution. presents the time-dependent PM concentrations determined using a light scattering nephelometer (MIE pDR 1000; ThermoElectron, Franklin, MA) measured simultaneously inside a home, immediately outside the home, and at a central monitoring site. In this instance, PM measured inside the home is clearly higher and more variable than outside either at the home or a central monitoring site, demonstrating the importance and complexity of addressing the health effects of indoor airborne particles.
Comparison of particulate matter (PM) concentrations simultaneously measured indoors, immediately outdoors, and at a central monitoring site.
There are relatively few studies of indoor PM and asthma. Studies of school-age children in Seattle found that indoor PM2.5
exposure was associated with decreased pulmonary function in a subgroup of 10 children not using inhaled corticosteroids (17
). In this study, Koenig and coworkers (17
) also found that PM2.5
originating from indoor sources was more potent in decreasing lung function than was outdoor-derived PM. A California study of 19 predominantly white children found significant decrements in lung function (FEV1
) associated with indoor PM. While this study found associations between ambient PM and lung function, they found stronger associations for indoor than outdoor central site PM concentrations (18
A longitudinal study of 150 inner city preschool children with asthma, conducted as a part of the Johns Hopkins Center for Childhood Asthma (Baltimore Indoor Environment Study of Asthma in Kids [BIESAK] Study) investigated the impact of indoor fine (PM2.5) and coarse PM (PM2.5–10) on asthma morbidity (). The mean indoor PM2.5 concentration in the BIESAK study was roughly twice as high as the indoor coarse PM fraction (PM2.5–10) concentration, 40.3 ± 35.4 μg/m3 and 17.4 ± 21.1 μg/m3, respectively. The in-home PM2.5 and PM2.5–10 concentrations were significantly higher than the respective average ambient measurements made over the same time period, 12.4 ± 6.2 μg/m3 and 10.3 ± 21.0 ().
Distributions of indoor PM in the child's bedroom.
Significant determinants of indoor PM concentrations included smoking, sweeping, and stove use (19
), activities that are modifiable and provide opportunities for exposure reduction. Smoking has been consistently described as a major source of indoor particulates over the last several decades, with more than 30% of all U.S. children exposed to secondhand smoke (20
). Our results suggest that smoking continues to be a significant contributor to PM exposure in the inner city. The difference in PM2.5
between smoking and nonsmoking households of 26 μg/m3
is similar to the range of 25 to 45 μg/m3
that has been previously reported (11
Indoor coarse PM concentrations were associated with substantial increases in asthma symptoms (). For example, for every 10-μg/m3 increase in indoor PM2.5–10 concentration, there was a 6% increase in the number of days of cough, wheeze, or chest tightness, after adjusting for age, race, sex, socioeconomic status, season, indoor fine PM, and ambient fine and coarse PM concentrations. In adjusted models, higher indoor coarse PM concentration was also significantly associated with increased incidence of symptoms severe enough to slow a child's activity, wheezing that limited speaking ability, nocturnal symptoms, and rescue medication use. Outdoor coarse PM was not associated with increased asthma symptoms or rescue medication use.
Figure 3. Indoor PM concentrations, asthma symptoms, and rescue medication use: multivariate models (coarse module adjusted for age, sex, race, parent education level, season, indoor fine PM, ambient fine PM, ambient coarse PM; fine module adjusted for age, sex, (more ...)
Fine PM was also positively associated with respiratory symptoms and with rescue medication use (). For example, for every 10-μg/m3 increase in PM2.5 measured indoors, there was a 7% increase in days of wheezing severe enough to limit speech and a 4% increase in days on which rescue medication was needed, after adjustment for potential confounders. Both indoor and ambient fine PM concentrations were also associated with exercise-related respiratory symptoms. In multivariate models adjusting for participant characteristics that were potential confounders as well as for simultaneous indoor and ambient coarse PM, for every 10-μg/m3 increase in indoor and ambient PM2.5, there was a 7% and a 26% (data on ambient PM not shown in ) increase in days of exercise-related symptoms, respectively. In contrast, neither indoor nor ambient coarse PM concentrations were associated with exercise-related symptoms.
These findings demonstrate that both indoor coarse and fine PM distinctly affect respiratory health in children with asthma. There are physiologic reasons that can explain why PM of these different size fractions can contribute separately to asthma morbidity. Although fine PM may be capable of reaching the alveoli, the regions responsible for gas exchange, the deposition of coarse PM in upper airways and subsequent bronchial hyperreactivity may be responsible for the symptomatic response measured in these preschool children.
The strong relationship between indoor and ambient fine PM exposure and exercise-related symptoms was striking in this study. Previous investigators have indicated that exercise may play a role in asthma by modifying the effect of environmental stimuli and pollutants (18
). 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. The increased fine PM doses in the distal airways may be more potent in eliciting exercise-related symptoms than the doses of coarse PM that deposit in the more proximal airways.