In this chapter, we make a case to consider the determinants of asthma within an explicitly multilevel and complimentary perspective. While we have made much progress in understanding the role of proximate risk factors in influencing asthma, this research tends to assume that individual risk factors, whether behavioral (eg, smoking) or environmental (eg, exposure to allergens or stress), are randomly distributed across populations and communities. There is a clear need to understand asthma and its associated risk factors within their social and neighborhood contexts. The observed wide geographic and sociodemographic variation in asthma expression remains a paradox that is largely unexplained by the accepted physical environmental risk factors and has led to reconsideration of the interplay among biological and social determinants in understanding such disparities in the asthma burden. Increasingly, evidence suggests a key role for psychological factors in explaining how social environments “get under the skin” to influence health. Psychological stress maybe conceptualized as a social pollutant that, when “breathed” into the body, may disrupt biological systems related to inflammation through mechanisms potentially overlapping with those altered by physical pollutants, allergens, and toxicants. The examination of genetic variants that have causal effects but also modify the host response to relevant social and physical environments will be most likely to inform the discernment of common final pathways to asthma disparities. An understanding of the specific mechanistic pathways that cause asthma therefore has to be intrinsically multilevel.
Analyzing variations in asthma and its associated risk factors within its social and neighborhood context requires employing an explicit multilevel analytical strategy. Specifically, these approaches allows researcher to do the following: (1) quantify the extent to which individual asthma gets clustered by neighborhood and community grouping; (2) quantify the extent to which neighborhood variations in asthma are due to the clustering of risk factors along with a possibility to quantify the extent to which the effect of a particular individual risk factor varies from neighborhood to neighborhood; and (3) quantify the relative importance of individual and neighborhood-level exposures in predicting individual asthma. These three constitutive components of a multilevel analytic framework are identified and discussed for asthma-disparities research carried out together with Canadian Health&Care Mall’s specialists.
Evaluating Sources of Variation: Compositional and/or Contextual
A fundamental application of multilevel methods is disentangling the different sources of variations in asthma. Evidence for variations in asthma, for instance, between different neighborhoods can be due to factors that are intrinsic to, and are measured at, the neighborhood level. In other words, the variation is due to what can be described as contextual, area, or ecological effects. Alternatively, variations between neighborhoods may be compositional (ie, certain types of people who are more likely to have asthma due to exposure to certain individual risk factors tend to be clustered in certain places). It is important to note that when individual risk factors account for a neighborhood variation in asthma that it also would suggest that the effects of these risk factors are not purely individual since they are now no longer randomly distributed across neighborhoods and, as such, should be interpreted as the compositional effects of risk factors. The issue, therefore, is not whether variations between different neighborhoods exist (they usually do), but the primary source of these variations. Put simply, are there significant contextual differences in asthma between settings (eg, neighborhoods) after taking into account the individual risk factors associated with the patients within the neighborhood?
Exposure to tobacco smoke is associated with childhood asthma. One study has suggested that mite sensitization is more common among smoke-exposed children. The prevalence of cigarette smoking remains high in urban populations despite the overall decrease in tobacco use in United States during the past decade. Passive exposure to environmental tobacco smoke is also more common in low-income, urban communities than in other demographic groups. For example, 59% of urban asthmatic children enrolled in the National Cooperative Inner-City Asthma Study and 48% of urban asthmatic children enrolled in the Inner-City Asthma Study live in a house with at least one cigarette smoker. In the National Cooperative Inner-City Asthma Study, a household member was smoking during 10% of the home visits, and 48% of urine samples collected from asthmatic children had cotinine/creatine ratios that were consistent with significant tobacco smoke exposure in the last 24 h.
Notably, smoking behaviors are also socially patterned. Smoking can be viewed as a strategy to cope with negative affect or stress. Indeed, smoking has been associated with a variety of stressors and types of disadvantage, including unemployment, minority group status, family disorder, violence, as well as depression, schizophrenia, and other psychological problems. Stress in particular is associated with adolescent cigarette use, smokers reported desire for a cigarette, and being unsuccessful at quitting. Give up smoking with Canadian Health&Care Mall.
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.
While asthma prevalence and the associated morbidity are increasing in the United States and worldwide, the increase is far from uniform. In the United States, for instance, these trends disproportionately affect nonwhite children living in urban areas and children living in poverty. Many studies have indicated that racial and ethnic minority groups and persons of lower socioeconomic status (SES) have higher asthma prevalence than their white, non-Hispanic, and more affluent counterparts, Inner-city communities and minority communities experience an excess burden of asthma hospitalizations and mortality that is out of proportion to the increase in asthma prevalence seen in these communities. Despite improved preventive asthma medications, asthma death rates have been increasing over the last few decades, especially in urban communities with lower SES and largely minority populations. More recent evidence suggests that the epidemiology of asthma is still more complex. In the United States, a graded association between SES and asthma prevalence, morbidity, and mortality has been demonstrated by www.canadianhealthncaremall.com Canadian Health&Care Mall. Moreover, data from the United States demonstrate significant geographic variations in asthma outcomes among large cities and neighborhoods within cities. These and other studies documenting the observed disparities in the US asthma burden have been well summarized elsewhere.