Background and objectives: Smoking is associated with a lower health-related quality of life (HRQOL). However, there is little information about the association between HRQOL in relation to race, income, and smoking status. The present study aimed to assess the association between HRQOL and smoking status for those of different races and income levels. Materials and Methods: This study applied a cross-sectional design using data from the 2017 patient survey of the Louisiana Tobacco Control Initiative. We obtained 1108 responses from patients at eight Louisiana public hospitals. The EuroQol (EQ-5D) US index score assessed HRQOL. Smoking status was classified into four groups: never smoked, former smoker, current smoker with a quit attempt, and current smoker without a quit attempt. Multivariate linear regression analyses were used to estimate the HRQOL for black or African Americans and whites. Results: The patients were predominantly black or African American (58.9%) with lower-income (71.2%). Bivariate analyses showed that there were differences in income levels between black or African Americans and whites (p = 0.006). Moreover, black or African Americans (median = 0.80) had a higher mean of HRQOL than whites (median = 0.76). Among lower-income black or African Americans, current smokers with a quit attempt had a lower HRQOL than current smokers (coefficient = −0.12; p < 0.01). Conclusions: Racial and income disparities were evident with regards to HRQOL, with lower-income black or African Americans who were current smokers with a quit attempt having a lower HRQOL. Intervention programs for smoking cessation should target lower-income black or African American smokers who have a prior quit attempt and provide effective cessation services to help them quit smoking and improve their HRQOL.

Excessive alcohol intake is a well-known modifiable risk factor for many cancers. It is still unclear whether genetic variants or single nucleotide polymorphisms (SNPs) can modify alcohol intake’s impact on prostate cancer (PCa) aggressiveness. The objective is to test the alcohol–SNP interactions of the 7501 SNPs in the four pathways (angiogenesis, mitochondria, miRNA, and androgen metabolism-related pathways) associated with PCa aggressiveness. We evaluated the impacts of three excessive alcohol intake behaviors in 3306 PCa patients with European ancestry from the PCa Consortium. We tested the alcohol–SNP interactions using logistic models with the discovery-validation study design. All three excessive alcohol intake behaviors were not significantly associated with PCa aggressiveness. However, the interactions of excessive alcohol intake and three SNPs (rs13107662 [CAMK2D, p = 6.2 × 10⁻⁶], rs9907521 [PRKCA,p = 7.1 × 10⁻⁵], and rs11925452 [ROBO1, p = 8.2 × 10⁻⁴]) were significantly associated with PCa aggressiveness. These alcohol–SNP interactions revealed contrasting effects of excessive alcohol intake on PCa aggressiveness according to the genotypes in the identified SNPs. We identified PCa patients with the rs13107662 (CAMK2D) AA genotype, the rs11925452 (ROBO1) AA genotype, and the rs9907521 (PRKCA) AG genotype were more vulnerable to excessive alcohol intake for developing aggressive PCa. Our findings support that the impact of excessive alcohol intake on PCa aggressiveness was varied by the selected genetic profiles.