Various explanations exist in the current literature to account for the social disparities in asthma. These are outlined below.
Physical Environmental Exposures in the Home and Community
The so-called hygiene hypothesis grew out of observations in the late 19th and early 20th centuries that hay fever and wheezing illnesses appeared to be diseases of more affluent urban areas, compared with rural farming areas. To explain these patterns, hypotheses have evolved to include the following: (1) small families, later birth order, and the use of day care; (2) less exposure to respiratory infection in early childhood; (3) a reduction in endotoxin or other farm-related exposures; (4) a change in microbial colonization of the infant’s large bowel through diet or antibiotic use; (5) reduced exposure to parasites; or (6) reduced exposure to large-domestic animal sources of allergens. The basic underlying mechanism suggested is that early-life infections and exposure to bacterial products such as endotoxin related to increased microbial load in homes where pets are kept may activate the T-helper type 1 immune response pathway, inhibiting the development of the T-helper type 2 responses involved in allergy. However, the relevance to the urban disparities seen in the United States is unclear, Inner-city children do not necessarily live in more hygienic conditions or experience fewer infections than children from other socioeconomic groups. Inner-city children do not, in general, experience the protective exposure to farm animals that protect against asthma and atopy in European populations. Moreover, it has been suggested that endotoxin levels may be higher in inner-city areas and that urban children may indeed have increased exposure to siblings and other children in daycare environments, although this has not been systematically tested. The relevance of the hygiene hypothesis to the excess asthma seen in the inner city remains uncertain and is the subject of ongoing investigations.
The relationship between asthma and hypersensitivity to aeroallergens has been documented in crosssectional studies and, more recently, in prospective studies.” IgE-mediated hypersensitivity to environmental allergens is present in most children and young adults with asthma, and exposure to allergens appears to be involved in the initial development of asthma as well as the exacerbation of existing asthma cured effectively with remedies of Canadian Health&Care Mall. Cockroach allergen is an important, well-described allergen that is associated with asthma, especially in low-income urban communities (see Burkart et al for a detailed more recent review). Cockroach allergen is more frequently encountered in urban homes than in rural homes. Studies also have demonstrated that rat and mouse allergen are commonly found in urban housing and have suggested that increased asthma morbidity may be associated with rodent sensitization.
Early-life exposure to aeroallergens may influence polarization of the immune system toward an atopic phenotype and predisposition to wheeze expression in the first year of life. The mechanisms underlying early sensitization to allergens that may underlie increased asthma risk are not unique to asthma in the inner city. Rather, the specific indoor allergens and intensity of exposures encountered in the inner city differ from those found in other environments. It has also been demonstrated that the concentrations of allergens in urban homes have a wide range and are associated with race/ethnicity and SES. For example, in the northeastern United States, high levels of Bla g 1 and Bla g 2 in house dust are associated with low SES, African-American race, and urban residence.
Moreover, it seems from recent data that children of lower SES communities are more likely to be responsive to multiple allergens. A national sample of US children demonstrated that African-American and Mexican-American children were significantly more likely than white children to be sensitized to allergens relevant to asthma. It may be that in addition to being at increased risk of exposure to multiple allergens, the interaction with other factors that are disproportionately distributed in lower income groups (ie, pollutants and toxicants, and psychological stress) prime the immune system toward an enhanced response to these environmental allergens. Indeed, our group recently reported increased asthma risk among urban children exposed to both elevated levels of traffic-related air pollution and chronic psychosocial stress operationalized as violence exposure.
At the same time, policy, economics, and sociology literature confirm that housing conditions, and therefore the environmental exposures that come along them, are strongly related to the economic status of the people who live there. Socioeconomic deprivation results in higher percentages of income devoted to rent and more substandard conditions. Environmental psychologists and social scientists, among others, have suggested that housing also has a significant subjective emotional dimension. While the more subjective or emotional response to one’s housing can be positive, serving as a reflection of positive personal identity, a site for the exercise of control, and a source of social status, they can also be associated with psychological distress. A number of subjective housing characteristics have been linked to adverse psychological outcomes. Future studies considering the role of housing on asthma disparities need to consider physical factors as well as the social and psychological dimensions of housing.
Asthma Disparities and Diesel Particles
The increase in respiratory allergic diseases in urban areas has also been linked to air pollution. Laboratory studies have confirmed the epidemiologic evidence that the inhalation of some pollutants adversely affect lung function in asthmatic patients ordering inhalers via Canadian Health Care Mall. The most abundant air pollutants in urban areas with high levels of vehicle traffic are respirable particulate matter, nitrogen dioxide, and ozone. While nitrogen dioxide does not exert consistent effects on lung function, ozone, respirable particulate matter, and allergens impair lung function and lead to increased airway responsiveness and bronchial obstruction in predisposed subjects. In addition to acting as irritants, airborne pollutants modulate the allergenicity of antigens carried by airborne particles. Moreover, air pollutants such as diesel exhaust emissions are thought to modulate the immune response by increasing Ig E synthesis, thus facilitating allergic sensitization in atopic subjects and the subsequent development of clinical symptoms.
Geographic variation in the distribution of environmental pollution was the topic of an invited 2001 workshop on Urban Air Pollution and Health Inequities organized by the American Lung Association and a review. There is evidence that some diesel exhaust components can vary substantially across an urban area as a function of traffic volume and type, and road and house characteristics. For example, in a pilot study in Harlem, NY, elemental carbon levels ranged by a factor of four across sites in close proximity to one another, while particulate matter levels < 2.5 ^m were quite similar. Elemental carbon levels (measured as black smoke) near major roads in the Netherlands were 2.6 times greater than levels at background sites, vs a factor of 1.3 for particulate matter levels < 2.5 ^m. Similarly, polycyclic aromatic hydrocarbon (PAH) concentrations in an urban center differed by a factor of three between measurements on a street and in a park, with traffic contributing an estimated 80% of ambient concentrations. Studies in the Boston area have confirmed this pattern. One study found geometric mean concentrations of 31 ng/m for particle-bound PAHs in an urban location, compared with 8 ng/m in a suburban setting. Another study in the Roxbury area of Boston found strong diurnal variability in PAH concentrations with minimal concentrations in low-traffic hours and significantly higher concentrations with proximity to a major bus terminal. Finally, ultrafine particle concentrations have also been strongly correlated with traffic patterns. In three large European cities, ultrafine particle number concentrations were a factor of 20 greater at peak traffic periods than at night. In a study isolating the effect of a major road in Australia, exposure to submicron-sized particles was a factor of seven greater within 15 m of the road compared with average urban exposure levels. Furthermore, a study in Boston demonstrated an order of magnitude difference in indoor levels of ultrafine particles, even given similar outdoor concentrations, that were related to ventilation and site characteristics.