doi:10.1378/chest.07-1906
(Chest. 2007; 132:782S-788)
© 2007 American College of Chest Physicians
The Environment and Asthma in US Inner Cities*
Peyton A. Eggleston, MD
* From Johns Hopkins University, School of Medicine, Department of Pediatrics, Baltimore, MD.
Correspondence to: Peyton A. Eggleston, MD, The Johns Hopkins University, Department of Pediatrics, School of Medicine/CMCSC 1102, Baltimore, MD 21287-3923; e-mail: pegglest{at}jhmi.edu
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Abstract
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Poor, minority children living in US inner cities have increased rates of asthma morbidity and mortality. Factors that contribute to these increased rates are varied and complex, with current evidence suggesting that the environment is an important causative factor. Respiratory morbidity is often the result of allergens and air pollutants. Additionally, for children living in urban environments, underlying societal susceptibility factors specific to the inner city serve to increase asthma morbidity. Even though ambient pollutants have been declining in US cities, asthma morbidity and mortality rates have been increasing. Indoor pollutants are closely linked to increased asthma prevalence and morbidity. While the understanding of environmental influences is still relatively limited, we can say that indoor exposures are more important than ambient pollutants, and we know that bioaerosols containing allergenic proteins are especially important. Additionally, certain particulate aerosols and ozone cause inflammation individually and may act synergistically to enhance the acute and chronic IgE-mediated inflammation. The purpose of this article is to review the data relating exposure to environmental pollutants and airborne allergens, and the relationship of this exposure to asthma prevalence and morbidity in order to inform plans for public health programs to reduce an asthma burden.
Key Words: asthma • environment • inner cities
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Introduction
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The reasons for increased asthma morbidity and mortality rates among poor, minority children living in US inner cities are obviously complex and must include many factors that have nothing to do with the environment. At the same time, current evidence suggests that environmental exposure is at least one of the most important the causative factors. In addition, environmental exposures may be a risk factor that is more amenable to successful public health measures than are other factors such as social or psychosocial problems. Perhaps, like clean water supply and immunizations, we can introduce concrete measures that will have broad impact on health through an organized societal effort. The purpose of this article is to review the data relating exposure to environmental pollutants and airborne allergens and the relationship of this exposure to asthma prevalence and morbidity in order to inform plans for public health programs to reduce an asthma burden.
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Background
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In approaching our understanding of the importance of environmental exposure, the model shown in Figure 1
is a useful guide. In this model, environmental exposure to allergens and air pollutants such as particulate matter (PM), environmental tobacco smoke (ETS), and ozone affect a susceptible host, resulting in airway inflammation and obstruction that leads to respiratory morbidity. Underlying and influencing each step of this process are societal susceptibility factors (eg, psychosocial stress, high smoking rates, inappropriate medication use, inadequate resources, and poor access to quality health care) that are specific to the inner city and serve to increase asthma morbidity.
Another critical factor that influences host susceptibility to environmental stimuli is the genetic background of the person exposed. As seen in Figure 1, both environmental allergen exposure and pollution can increase asthma morbidity. Environmental allergen exposure induces inflammation through two steps. A person with the appropriate genetic susceptibility has a specific IgE antibody to the allergenic protein following repeated or prolonged exposure. We currently believe that polymorphisms of a number of genes coding for critical regulatory proteins are responsible for the genetic susceptibility to sensitization to environmental allergens seen in asthmatic patients.1 Besides those variations in genes influencing immune response, other factors that influence inflammation or airway hyperresponsiveness are also important.2 Once sensitized, the asthmatic patient is susceptible to acute asthma in response to very small exposures of airborne allergens.3 Pollutants, both ozone4 and PM,56 have been shown to be associated with direct effects on the asthmatic airway and with indirect synergistic effects on allergic sensitization and inflammation. Underlying these processes are important social or psychosocial factors that increase susceptibility in poor inner-city residents. Other influences include impaired access to good medical care for acute or chronic treatment of asthma, inappropriate overuse of ß-adrenergic agents,7 and emotional stress, depression, and anxiety.89
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Environmental Pollutants and Asthma
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It has been suggested that urban pollution might contribute to increased asthma morbidity in the inner city. However, most ambient pollutants have declining steadily in US cities10 at the same time that asthma morbidity and mortality rates have increased. This does not exclude the importance of indoor pollutants, but much less published data are available regarding indoor pollutants.
Among indoor pollutants, ETS is most closely linked with increased asthma prevalence and morbidity.51112 In a general population survey smoking exposure is similar among whites, African Americans, and Hispanics in the United States as reported in the Six City Study,11 cigarette consumption greater than one pack a day was reported by 29.9% of white mothers and 16.8% of African-American mothers. The same study11 reported smoking by 2.4% of 14-year-old white boys, 11.7% of white girls, 4.1% of black boys, and 6.7% of black girls. These data represent the total population and do not separate ethnic groups by income. Although no direct comparisons between middle-class and inner-city populations are available, a study10 in an urban emergency department may provide data for inner-city populations: > 50% of children had at least one smoker in their homes, and > 38% had elevated urinary cotinine compatible with heavy exposure to ETS. Similar findings were found in eight urban medical centers in the National Cooperative Inner City Asthma Study (NCICAS)13: 59% of the families included at least one smoker, 39% of the primary caretakers smoked, and urinary cotinine levels were elevated (> 30 mg/g of creatinine) in 48% of the children. These data suggest that exposure to ETS in the home is more common in US inner cities than in the general population, but it is not known how important this is as a cause of increased morbidity.
Another indoor pollutant considered in relation to asthma is nitrogen dioxide. Nitrogen dioxide is an industrial pollutant that is generated as a byproduct of combustion and is considered to be an important component of urban smog. It is generated in homes by gas stoves and space heaters, but indoor concentrations are rarely elevated to levels that are considered health risks. Indoor nitrogen dioxide was measured in the NCICAS and was as high as 480 parts per billion (ppb), with 24% of families exposed to levels 
40 ppb.13 These excessive levels were thought to relate to the gas stoves used by 89% of families and the fact that 24% of kitchens did not have functioning windows. To put this in context, the Environmental Protection Agency air standards consider annual average levels of 50 ppb to constitute a risk factor for acute and chronic lung disease. Computer modeling of data from the Six Cities Study demonstrated that levels > 30 ppb would result in annual exposures of > 50 ppb.14 Thus, inner-city homes frequently contain levels of an important pollutant in excess of Environmental Protection Agency environmental standards, and could be expected to contribute to asthma morbidity.
Ozone and PM have also been associated with exacerbations of asthma. Symptoms and medication use have been associated with ambient levels of both pollutants in reports from Mexico City,15 southern New Jersey,16 and Atlanta, GA.17 In a panel study of asthmatic patients, Delfino et al18 showed a close correlation between daily symptoms and exposure to ozone, particulates, and fungal spores. In addition, exposure to ozone4 and residual oil combustion products (diesel exhaust)619 increases airway response to allergens in experimental airway challenges. While it is not clear that inner-city residents are exposed to unusual concentrations of these pollutants, ozone equilibrates rapidly between indoor and outdoor air, and this pollutant is clearly related to urban rather that suburban areas. In addition, particulates are much higher in indoor air from homes with smokers and higher ETS.20 In the absence of data from inner-city homes, we can only speculate that ozone and PM pollutants interact with indoor allergen exposures to increase asthma morbidity.
Exposure to indoor allergens has recently been suggested to be a source of respiratory morbidity. Between 70% and 90% of children and young adults with asthma have one or more positive skin test results to aeroallergen,1321 and the frequency is similar in asthmatic patients in urban clinics.222324 The pattern of specific allergen sensitivity differs from that in the general population, with a higher frequency of sensitivity to cockroach and molds and less frequent sensitivity to cats and dogs and house dust mites. In the NCICAS, at least one positive skin test result was seen in 77% of children, and 47% has three or more positive test results. The most common positive skin test finding was alternaria (38%), followed by cockroach (36%) and house dust mite (35%). Allergies to rat (19%) and mouse (15%) were almost as common as allergies to cat (24%) and dog (16%). Most children were sensitive to several allergens. The distinct pattern of skin test reactivity is mirrored by the pattern of allergen exposure found in inner-city homes. Cockroach allergen was detectable in 89% of bedroom samples, while mite and cat were found in only 49% and 86%, respectively.313 Later reports2526 demonstrated increased exposure to rodent allergens. Indoor fungal exposure has been studied infrequently, but a report27 suggested that contamination is common in urban homes. Therefore, it appears that exposure to fungal and cockroach allergens is characteristic of inner-city homes, leading to more frequent sensitization to these allergens than to house dust mite and animal dander.
A strong association was found in the NCICAS3 between chronic morbidity from asthma and the combination of sensitization and exposure. The rate of hospitalization in this group was almost three times higher (0.37 hospitalizations per child per year) and unscheduled visits are almost twice as frequent (2.56 visits per child per year) in these children compared to those who were either not sensitized or not exposed, adjusted for gender, family history, and smoking exposure.
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Impact of Changing Environmental Exposures
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The finding of a strong association between cockroach allergen exposure and asthma in the inner city has important public health implications. If it can be shown that disease can be improved by changing environmental exposures, this would support programs to improve housing conditions in the inner city. In addition, if it is possible to provide practical measures for avoiding exposure to pollutants such as ETS, particles, ozone, or nitrogen dioxide to allergens, we may change the current epidemiology of asthma.
We currently have practical measures to reduce exposure to cockroach, rodents, and house dust mite.2829 A report30 from the Inner-city Asthma Study suggest that these measures, in combination with high-efficiency particulate air filtration and home-based education, are capable of reducing daily symptoms if not emergency department use and hospitalizations.
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Exposure Assessment and the Study of Childhood Asthma
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The goal of the exposure assessment as a part of an epidemiologic study is to estimate and properly classify exposure with respect to environmental agents suspected of causing asthma. This can be achieved through an approach of direct and/or indirect assessment.3132 A direct assessment entails monitoring the individual using samplers that can be attached or worn by the individual. The advantage of the assessment is that it provides the single best measurement of individual exposure.33 The disadvantage of personal monitoring is that it can be costly and it presents a burden to the subject that can adversely affect response rate. Indirect assessment relies on measurements in one or more microenvironments combined with time/activity data in a model that weights the microenvironmental concentration by the time the individual spent in that microenvironment. This approach has been successfully employed in a number of air pollution studies.343536 The major advantage to this approach is that the subject is not required to carry a personal monitor. This advantage comes at the cost of decreased accuracy of the exposure estimate. Because it includes indoor air where children spend most of their time, it is believed that the approach will capture most of the variability of individual exposures.
The home is the single most important environment for assessing exposure because people spend most of their time there, there are large and unique indoor sources (eg, cooking, animals, mites, smoking, dust resuspension), and ventilation with outdoor air is limited. A report37 on human activity patterns shows that school-age children spend most of their time indoors at home (68%); school is the next important microenvironment, occupying on average 15% of their time. Central site ambient monitoring by itself has been shown to provide a very poor surrogate for individual exposure for most air pollutants.3839 This is particularly true for the pollutants of greatest concern for asthma, include bioaerosols, airborne particles, nitrogen dioxide, ozone, and ETS.
Particle exposure is especially complex because of large spatial and temporal variability in air concentrations, numerous and varied sources, and an observed phenomena of an increasing concentration gradient in the immediate proximity of the individual ("personal cloud").36 In addition, particles are highly variable in shape, size, density, and chemistry. Airborne particles are formed through mechanical and combustion processes for which there are myriad sources, both indoors and outdoors.40 There is consistent and convincing evidence that smoking is the single largest indoor source of fine particles in homes with smokers.36 Smoking adds 25 to 45 µg/m3 to indoor airborne PM up to 2.5 µm in diameter, with 1 to 2 µg/m3 coming from each cigarette when averaged over a 24-h period. Source strength for smoking is estimated as 12.7 ± 0.8 mg per cigarette (± SE).41 Cooking is the second-largest identifiable indoor source, contributing 10 to 20 µg/m3. The Particle Total Exposure Assessment Methodological Study42 in Riverside, CA, showed that across all homes (smoking and nonsmoking), on average 76% of the measured indoor airborne PM up to 10 µm in diameter were from outdoor sources.
Numerous particle exposure studies3637 have been summarized to show that central site ambient measurements provide a poor surrogate for an individual’s actual exposure, explaining only 0 to 25% of the variation in personal measurements. Outdoor air is an especially poor surrogate in cross-sectional evaluations where exposure variability is primarily driven by interpersonal differences. In contrast, in longitudinal studies4143 in which the influence of intrapersonal variability is lessened, outdoor central site measurements appear to provide a better surrogate. If the variation in outdoor PM is not predictive of the variations in personal exposures, then use of outdoor central site measurements will tend to misclassify exposures resulting in an attenuation in the exposure/response relationship.
In contrast to airborne particles, the determinants of exposure to nitrogen dioxide and ozone are less complex because these pollutants are specific chemicals with well-characterized physical and chemical properties. A major outdoor source for nitrogen oxides is the automobile.37 Indoor sources including kerosene heaters, gas stoves, and their impact on indoor air concentrations have been well characterized. A number of different studies253539 have shown that much of the variability in nitrogen dioxide personal exposure can be explained by indirect assessment with indoor and outdoor measurements in a time-weighted model. A similar situation exists for ozone that is formed outdoors as a secondary pollutant. Since there are no indoor residential sources, the exposure variability is driven by outdoor concentration gradients and building factors (eg, air exchange, air conditioning) affecting the decay of ozone. Liu et al38 reported an indoor/outdoor ratio of 0.45 ± 0.23 and an R2 of 0.72 for a microenvironmental model relying on home indoor and outdoor, work place, and central site measurements in a study conducted in State College, PA.
ETS exposure can be effectively monitored by measuring cotinine in urine44 or nicotine air concentrations. Urine cotinine has been shown to be a stable and effective biomarker for classifying children from homes with and without smokers.44 Henderson et al45 showed that urinary cotinine levels were not affected by collection time of day, and over a 1-month period sequential urine levels were highly correlated (r > 0.88).
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Interactions of Pollutants and Allergens
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With the recent understanding of the importance of CD4 T cells in the pathogenesis of asthma, much attention has been paid to the potential role of particulates in augmenting or initiating responses that may lead to activation of CD4 T cells. Although few controlled human or animal studies have examined the effects of real-world PM exposure on allergen-driven airway responses, studies using diesel exhaust particulates (DEP) or residual oil fly ash (ROFA) have shown enhancement of allergic responses in susceptible individuals. For example, Diaz-Sanchez and colleagues46 have shown that nasal challenge of human asthmatics with DEP markedly enhanced their IgE responses to ragweed challenge and skewed cytokine production to one of a T-helper type 2 cell pattern. Similarly, studies4647 in several animal models have confirmed these findings using a variety of sources of PM (ie, ROFA, fly ash, and DEP). For example, Takano et al47 demonstrated that exposure to DEP enhances allergen-driven airway hyperresponsiveness and eosinophilic inflammation in mice sensitized with allergen. In this model, T-helper type 2 cytokine production in DEP-exposed animals was elevated over and above that seen with allergen exposure alone. Gavett et al48 found similar results in mice exposed to ROFA, and Walters et al49 found that ambient particulates from inner-city sources can induce inflammation as primary exposure or when introduced during allergen sensitization. These studies suggest that PM may exacerbate asthma by enhancing production of T-helper type 2 cytokines in allergic individuals.
The mechanism(s) by which PM induce pulmonary inflammation and alters immune responses to allergens are currently unknown. Perhaps the simplest explanation is that PM serves as carriers to transport allergens into the respiratory tract. However, studies50 in which allergens have been delivered by nonpulmonary routes show that the effects of PM on allergic responses are not solely due to their potential to serve as a carrier for allergens. However, exposure to PM or its components has been shown to have a number of effects on macrophages and B cells that may augment their responsiveness to allergen exposure. Specifically, DEP has been shown to induce expression of the co-stimulatory molecule CD80 in both human lavage cells and in the human macrophage cell line (THP-1).5152 CD80 binds with high affinity to its co-receptor CD28 on T cells and results in co-stimulation of T cells. Thus, it is conceivable that PM could alter the response of the host to ubiquitous allergens by enhancing activation of T cells by providing required co-stimulatory signals. A potential explanation for DEPs effects on IgE production may be through its documented ability to directly enhance IgE production in normal human tonsillar B cells and peripheral blood B lymphocytes.51 The results of these studies suggest that perhaps the IgE-enhancing effects of DEP may result from direct effects on B lymphocytes.
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Conclusion
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Asthma is a classic example of a disease caused by gene/environment interaction. The need to understand this interaction has been intensified by our recognition that asthma is becoming increasingly common and severe in industrialized countries. Our understanding of the environmental influences is still in its infancy, but we can say that indoor exposures are more important than ambient pollutants and that bioaerosols containing allergenic proteins are especially important. We understand that certain particulate aerosols and ozone, known to cause inflammation individually, may act synergistically to enhance the acute and chronic IgE-mediated inflammation. As a consequence, environmental exposure assessment undertaken in epidemiologic studies must measure a variety of agents simultaneously if we are to understand the reality of environmental exposure. Finally, we understand that environment to be studied must include not only important airborne pollutants and allergens but the psychosocial milieu in which the asthmatic patient lives. New genetic methods help us to dissect the genetic basis of the increased susceptibility in asthma of inflammation caused by either IgE-mediated mechanisms and those with no immunologic basis. Once identified in animal studies, individual genes can be confirmed in human populations and susceptible alleles sought so that preventive strategies can be focused on susceptible individuals.
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Footnotes
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Abbreviations: DEP = diesel exhaust particulates; ETS = environmental tobacco smoke; NCICAS = National Cooperative Inner City Asthma Study; PM = particulate matter; ppb = parts per billion; ROFA = residual oil fly ash
The author has no conflict of interest to disclose.
Received for publication December 20, 2006.
Accepted for publication August 2, 2007.
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Eliminating Asthma Disparities Through Multistakeholder Partnerships
Chest,
November 1, 2007;
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1422 - 1424.
[Full Text]
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Abstract
Introduction
