Inner city homes had higher levels of particulate matter, NO2, and O3 than found in suburban homes, and a different pattern of allergen in settled dust. Our findings document the differences in inner city Baltimore and suburban homes of children with asthma, with respect to type of home, location, state of repair, moisture, carpeting, and cigarette smoke exposure. Airborne mouse allergen levels and bedroom dust levels of mouse and cockroach allergen were higher in the inner city, whereas dust mite, dog and cat allergen levels were higher in suburban homes.
Our finding that particulate levels in inner city Baltimore homes were more than twice as high as those in suburban homes may be compared to earlier reports. In urban homes, some of which contained smokers, Pellizzari and colleagues20
reported median PM10
levels of 28 μg/m3
in Indianapolis and 23 μg/m3
in Toronto; PM2.5
levels were 18 and 15 μg/m3
, respectively. Liu and colleagues measured indoor particulate levels in 19 nonsmoking homes of 6- to 13-year-old children with asthma living in Seattle and found geometric mean PM10
levels of 16.8
levels of 7.9
Williams and colleagues22
reported levels of PM10
) and PM2.5
) in homes in a retirement center; they commented that these unusually low levels were probably related to decreased cooking and other activities in the retirement site that they studied. There are few inner city comparators. Using laser nephelometry that approximated PM2.5
levels, Wallace and colleagues9
examined 292 inner city homes in eight U.S. cities and found geometric mean levels of 17.2
, substantially lower than our levels. Using methods similar to the ones used in the present study, Keeler and colleagues23
found arithmetic mean PM10
levels of 52.2 μg/m3
levels of 34.4 μg/m3
in inner city Detroit. Thus, using various methodologies, earlier studies found similar levels to those we report in suburban homes, but variable levels in inner city homes.
It was tempting to explain the higher PM levels in inner city homes by the large proportion of these homes containing a smoker (67%). Environmental tobacco smoke is the major contributor to indoor PM. Wallace and colleagues9
reported that PM2.5
levels were 37 μg/m3
higher in homes with at least one smoker. Keeler and colleagues23
reported a PM increase in homes with a cigarette smoker comparable to our results (33%), and found that these differences were similar in winter, when windows were closed, and in summer. In our study, inner city homes with at least one smoker had PM10
levels of 53 μg/m3
compared to 34 μg/m3
in nonsmoking homes. At the same time, when we compared PM levels in homes in the suburbs and inner city in which smoking was not reported, PM levels remained significantly higher in the inner city homes, so other urban sources of airborne particles, such as traffic, may be contributing.9
Other home characteristics associated with particulate levels in bivariate analysis and linear regression included the presence of a cat or dog and a gas stove. Although the multivariate model was likely more valid, there was no good explanation for an association of higher particulate levels with cat or dog ownership or the presence of a gas stove. Although frying and burning during cooking are important contributors to indoor particulate levels9
, both gas and electric stoves have been associated with elevated particulate levels.9,24
In the suburban homes, the range of O3
levels was small. In both the city and suburban homes, air monitoring was conducted in more than one season and included data collected during the warmer seasons, when ambient O3
levels are expected to be higher. Although O3
levels are expected to be higher in urban areas than in neighboring regions25
exposure in suburban areas is becoming an increasing concern,26
and our study showed remarkably low levels of O3
in the suburbs. The lower O3
levels in the suburban homes may reflect a greater distance from arterial streets or windows being left closed on days of high ambient O3
levels, compared with the inner city homes.
In this study, the suburban homes of children with asthma contained a lower percentage of smokers than that of the general Maryland population reported in the Maryland Tobacco Statistics.27
In that survey, the percentages of households with minor children and an adult who smoked cigarettes were 49.6% in Baltimore City, 35.1% in Baltimore County, 31.8% in Anne Arundel County, and 27.1% in Howard County. In our study, a higher percentage of homes had a smoker in the inner city (67%), than had been reported in the earlier survey of Baltimore city as a whole. This increase may explain the higher airborne particulate levels found in this study, compared with the levels in other studies, where inner city homes were not specifically selected. The lower percentage of smokers in the suburban homes of this study (5%) compared to all homes with a child in counties surrounding Baltimore (27–35%) may reflect a volunteer bias or changes in practice as a result of participation in a previous asthma trial.
Although standards specific for home indoor air quality have not been established, we found that inner city children were exposed to home pollutant levels in excess of the Environmental Protection Agency’s National Ambient Air Quality Standards.28
We found that 53% of the inner city children studied were exposed to PM2.5
levels that exceeded the 24-hour PM2.5
standard (35 μg/m3
), whereas none of the suburban homes reached this level. Eighty-five percent of inner city homes and 22% of suburban homes had PM2.5
levels higher than the annual standard (15 μg/m3
). Fourteen percent of inner city homes had NO2
levels above the EPA recommended limit (53 ppb). No suburban home had NO2
levels greater than the EPA standard.
We found that 31% of inner city homes had evidence of water damage, compared to only one suburban home, and 32% of inner city homes had evidence of mildew. By comparison, census data for the entire United States describe exterior leaks found in 11% of urban homes and 12% of suburban homes. Excess residential moisture has been shown to affect asthma symptoms, so these differences are likely to be significant health risks. A survey of nearly 6,000 Russian children in nine cities reported water damage and mold in 10% of living areas in the past 12 months. Compared to homes without water damage and molds, the odds ratios (OR) of current asthma-like symptoms were 1.77 (95% CI 1.36–2.03) for water damage and 1.98 (1.53–2.55) for presence of molds.29
In a survey of nearly 15,000 Canadian children in 30 cities, molds were reported in 32% of homes, flooding in 24%, and moisture in 14%. Compared to homes without mold, the OR for cough with mold at one site in a home was 1.61 (95% CI 1.36–1.89) and the OR for cough with mold at two sites in a home was 2.26 (1.80–2.83). Similar effects were seen for wheeze, dyspnea, and a diagnosis of asthma.10
In a case-control study of Dutch children with asthma, home dampness was shown to be strongly associated with sensitization to dust mites or mold, in combination with respiratory symptoms.30
More inner city homes had signs of mouse and cockroach infestations, and higher measured dust Bla g 1 and Mus m 1 allergen levels were seen in inner city homes with signs of infestation. Although previous studies have detected Bla g 1 in the kitchens of suburban homes with no history or signs of cockroach infestation31
, we did not detect Bla g 1 in the child’s bedroom of suburban homes. Cat ownership was not significantly different between inner city and suburban homes, and we speculated that the higher bedroom dust allergen levels of Fel d 1 in the suburbs might reflect urban residents keeping cats outdoors.
The strength of this study is that we used the same questionnaires and techniques to compare home characteristics and air pollutants in inner city and suburban homes. The format for the questionnaires and home inspection checklists of the suburban comparison group was dictated by those used for the inner city group. In addition, participation in the suburban group was restricted to children with a positive skin test to an indoor allergen. However, within the limitations of the study design, the inner city and suburban groups were a representative sample of the large numbers of children with doctor-diagnosed asthma from which they were selected.
This study had several weaknesses that affected its interpretation. A small number of homes were studied in the suburban setting. In addition, the suburban homes were selected from allergic children with asthma who had recently completed a clinical trial that selected participants based on allergic asthma and had tested an intervention intended to modify families’ allergen reduction strategies. However, the inner city participants included both allergic and non-allergic children with asthma. It is entirely possible that suburban homes had been modified by the intervention in ways that would have decreased environmental conditions that we have examined. Given the differences that we describe here, it will be important to confirm these findings.