Abstract CN11-02: Models of the pathways between socioeconomic status and health

Although there have been striking socioeconomic gradients in smoking prevalence, cessation, and disease burden for decades, these disparities have become even more pronounced over time. Individuals with lower education, income, and occupational status are both more likely to smoke and less likely to quit. Unfortunately, relatively few studies have delineated the specific pathways and mechanisms that link SES with smoking‐related outcomes. Gaining a greater understanding of the pathways through which SES influences smoking cessation may help to identify treatment and policy targets, improve current cessation interventions, and ultimately reduce the burden of smoking‐related disease in low SES populations. Several major conceptual models have been proposed that identify key mechanisms linking SES to health behavior (e.g., Adler and Ostrove, 1999; Gallo and Matthews, 2003). These models hypothesize that socioeconomically disadvantaged individuals tend to be less healthy than more advantaged individuals due to higher exposure to stress; lower access to physical and environmental resources; greater environmental constraints; fewer interpersonal, affective, and cognitive resources; and poorer health behavior. Although the models diverge on some hypothesized pathways, they are very similar overall. Social cognitive models of substance abuse also identify key mechanisms that may link SES to smoking cessation. For example, affect, craving, and agency are mediating variables that link distal risk factors to cessation. Importantly, these models hypothesize reciprocal relationships among these factors. For example, increased negative affect is thought to increase craving and decrease agency just as decreased agency is posited to increase craving and worsen affect. The purpose of the current study was to develop and test a conceptual model of the pathways linking SES to cessation by integrating current conceptual models and findings from previous research. Hypothesized mechanisms included neighborhood disadvantage (e.g., problems, low social capital), social support, stress/negative effect, craving, and agency. The primary outcome was abstinence at 4‐weeks postcessation. Constructs assessing SES, neighborhood disadvantage, and social support were assessed precessation, with stress/negative effect, craving, and agency measured on the quit date. The conceptual model included reciprocal relationships between negative affect/stress, agency, and craving, and was evaluated using a latent variable modeling approach in a diverse sample of 424 smokers seeking treatment (139 Whites; 144 African Americans; 141 Latinos). Finally, a multiple group structural modeling analysis was conducted to determine if the final model was a good fit across racial/ethnic groups. Most of the individual links among constructs in the conceptual model are supported by previous research. As hypothesized, SES had significant direct and indirect effects on cessation. Specifically, neighborhood disadvantage, social support, stress/negative effect, craving, and agency mediate the relation between SES and smoking cessation. Importantly, the multiple group analysis indicated few differences in model pathways across racial/ethnic groups. Additional analyses examined other hypothesized mechanisms linking SES to cessation. These analyses demonstrated that current financial strain, living in an environment characterized by close proximity to a tobacco outlet, and low subjective social status all decrease the likelihood of cessation over and above the effects of SES. Although many of the hypothesized relationships in the proposed model were supported, others were not. For instance, a number of previous studies have found significant direct paths between SES and negative affect/stress. However, only indirect pathways between these two variables were significant in the current study. This finding is consistent with the Gallo and Matthews model, which suggests that low SES tends to increase negative affect and negative health outcomes by increasing the likelihood of negative experiences (e.g., via neighborhood disadvantage), and decreasing reserve capacity (e.g., social support). Previous research has shown that social support and neighborhood characteristics can directly impact self‐efficacy for completing specific behaviors. However, the hypothesized direct impacts of social support and neighborhood disadvantage on agency were nonsignificant in the current study. Instead, these paths were mediated by negative affect/stress. The hypothesized direct pathways from negative affect/stress and craving to cessation were not significant. However, negative affect/stress and craving indirectly decreased the chance of cessation by reducing agency. This finding builds upon several previous studies that have demonstrated that heightened negative affect and craving may result in decreased agency. Additionally, this finding is congruent with results from a previous study conducted by the investigators, showing that postcessation agency mediated the relationship between pre‐cessation depression and smoking cessation. Results of the current study suggest that agency may be a final common pathway linking negative affect/stress and craving to smoking cessation. Although reciprocal relationships between quit date measures of agency, craving, and negative affect/stress were hypothesized in the original model, only unidirectional relationships were found in the final model. As expected, quit date craving tended to increase negative affect/stress and decrease agency. Unexpectedly, the path from negative affect/stress to craving was not significant. Future research might use ecological momentary assessment techniques to gain a better understanding of how negative affect/stress, craving, and agency interact on a moment to moment basis to influence smoking cessation. The current model took the timing of assessments into account by utilizing a prospective design that incorporated both precessation and quit date predictors of abstinence assessed four weeks postcessation. Also, multiple indicators of SES were used to create a SES latent variable, which may have provided a more complete picture of socioeconomic context. Additionally, the use of structural equation modeling techniques allowed us to concurrently examine complex mediational relationships among latent variables. Finally, the sample was made up of nearly identical numbers of White, African American, and Latino smokers, which allowed us to test the model across several racial/ethnic groups. Several limitations temper our conclusions and should be addressed in future research. First, overrepresentation of the lower end of the SES spectrum may have resulted in underestimation of the direct and indirect effects of SES on smoking cessation. Second, both negative affect and stress manifest variables were used to form a single latent variable. This was done because these measures were highly correlated and we believed that the items were an acceptable gauge of current psychological distress. However, future research in this area may benefit from parsing the effects of stress and negative effect. Additionally, inclusion of subjective (e.g., perceived stress) and objective measures (e.g., biological markers of stress, number of current stressors) of both acute and chronic stress may result in more powerful smoking cessation models. Finally, although our model adequately fit the data, it is possible that other models may have been an equivalent or better fit for the data. Validation across multiple samples is needed to provide additional support for the validity of this model. An improved understanding of the relationship between SES and smoking cessation is important for the development of treatments that specifically target underserved populations. Our findings demonstrate the complex relationship between SES and cessation and highlight potential targets for future public policy changes and smoking cessation interventions. Specifically, public policies that have a positive impact on SES variables (e.g., employment, education, insurance, income) and that reduce the high level of tobacco exposure often seen in low SES neighborhoods are likely to enhance smoking cessation. At the neighborhood level, community based interventions focused on reducing neighborhood problems (e.g., crime, litter) and increasing social capital may result in reductions in smoking. At the individual level, it may be particularly important to address negative affect/stress and agency among underserved populations given that these variables appear to function as key mediators in the pathways between SES, neighborhood disadvantage, social support, craving, and smoking cessation. The present study provides one of the first models illuminating the specific mechanisms that link SES and smoking cessation. Policy, community, and individual‐level interventions that target low SES smokers and address the specific pathways identified in the current model could potentially attenuate the impact of SES on smoking cessation. Citation Information: Cancer Prev Res 2010;3(1 Suppl):CN11-02.