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Tobacco smoking and alcohol use disorder (AUD) are highly prevalent among individuals receiving medication for opioid use disorder (MOUD) treatment, yet their combined impact on treatment outcomes remains underexplored. This study investigates the differences in clinical profiles and treatment outcomes based on smoking and AUD status among individuals initiating MOUD.
This secondary analysis utilized data from a multi-site randomized clinical trial (CTN-0027) evaluating the hepatotoxicity during 24 weeks of buprenorphine or methadone treatment. Participants were categorized into four groups based on baseline smoking and AUD status: Non-AUD/Non-smoker, Smoker Only, AUD Only, and AUD+Smoker. Clinical profiles and treatment outcomes were compared across groups.
Among 973 participants (68.6% male, 70.5% White, mean age 37.5 years), 50% were Smoker Only, 16% AUD+Smoker, 8% AUD Only, and 27% Non-AUD/Non-smoker. Smoking prevalence was high (66%), while AUD prevalence was lower (24%). AUD+Smoker and AUD Only groups had significantly higher rates of additional substance use disorders (p < .01). However, treatment outcomes—measured by urinalysis results, retention, and completion—did not differ significantly across groups.
Smoking and AUD status were not associated with poorer MOUD outcomes, but the high prevalence of smoking, and the clustering of additional substance use disorders among individuals with AUD suggest the need for integrated care. These findings support inclusion of adjunctive behavioral and public health interventions within MOUD programs.
This study uniquely examines the joint impact of smoking and AUD on MOUD outcomes, offering insight into clinical complexity not previously explored in combination.
Chronic tobacco smoking contributes to oral health problems, such as periodontitis and tooth decay, which can result from smoking-altered oral microbiomes. The impact of chronic tobacco smoking on the oral microbiome remains not fully understood.
This was a cross-sectional study comparing the oral salivary microbiomes of 20 chronic tobacco smokers and 23 nonsmoking controls, all of whom were Chinese males, using microbial 16S rRNA sequencing. The duration of smoking, age, and information on gingivitis were collected and analyzed using the nonparametric Mann–Whitney test and a regression model.
The most increased and decreased oral microbiomes in smokers versus controls were the genera Streptococcus and Neisseria, respectively. After adjusting for age, gingivitis, smoking duration, and FDR, only the abundance of the Pectinatus genus and Streptococcus australis species was significantly increased in smokers compared to controls.
This study reveals that long-term oral tobacco smoking is associated with the enrichment of some proinflammatory microbiomes, such as S. australis.
Our study suggests that maintaining good oral hygiene, using oral probiotics that reduce proinflammatory microbiomes, or treating oral diseases may help prevent the pathogenesis of tobacco-enriched commensal pathobionts.
Background and objectives: Numerous genome-wide association studies suggest that rs1051730 is significantly associated with nicotine dependence and further lung cancer in Caucasian. Since rs1051730 is a synonymous variant at CHRNA3 (cholinergic receptor nicotinic alpha 3 subunit), it might be hypothesized that the causal variant might be other SNP(s) in strong linkage disequilibrium (LD).
Methods: LD analysis and functional genomics work, including chromosome conformation capture (3C), luciferase assay, and chromatin immunoprecipitation (ChIP), were performed.
Results: Allele-specific expression indicates an overexpression of C allele than T at rs1051730 in lung tissues, thus verifying the hypothesis. Through LD analysis for 1000 genomes project data, 17 genetic variants are identified in strong LD with rs1051730. 3C indicates that two restrictive segments, chr15:78845145-78852557 and chr15:78867861-78872762, display high interaction efficiency with CHRNA3 promoter and contain two SNPs in core haplotype, rs72740964 and rs2036527, respectively. Luciferase assay suggests that only rs2036527 can alter enhancer activity. Further 3C indicates that CHRNA5 (cholinergic receptor nicotinic alpha 5 subunit) is an additional target of the enhancer containing rs2036527, which is verified by expression quantitative trait locus analysis. By ChIP, the related transcription factor, FOXA2 (forkhead box A2), is identified and their interaction is evaluated.
Discussion and conclusions: rs2036527 is the cis-regulatory variant for CHRNA3 and CHRNA5, which can further influence nicotine dependence.
Scientific significance: This is the first report to indicate that rs2036527 genotype might be a better marker to predict the probability of developing nicotine dependence and that FOXA2, CHRNA5, and CHRNA3 might be treatment targets for nicotine dependence.
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