BACKGROUND: Antimicrobial resistance (AMR) and smoking of tobacco products are two of the most important threats to global human health. Both are associated with millions of deaths every year. Surprisingly, the immediate interactions between these two threats remain poorly understood.

OBJECTIVES: We aimed to elucidate the effect of toxic compounds from cigarette smoke, ashes, and filters on the spread of antibiotic resistance genes in human lung and environmental microbiomes.

METHODS: Conjugation experiments using donor and recipient strain pairs of either Pseudomonas putida or Escherichia coli and AMR-encoding plasmids were conducted under exposure to different concentrations of cigarette smoke condensate in lung sputum medium, as well as cigarette ash and filter leachate in environmental media. We further measured reactive oxygen species (ROS) production of the donor strain under exposure to the cigarette-derived compounds to explore whether stress experienced by the bacteria could be one of the underlying mechanisms of change in plasmid transfer frequencies. Furthermore, used cigarette filters were submerged in a wastewater stream for several weeks, and the colonizing communities were analyzed using high-throughput sequencing and high-throughput quantitative polymerase chain reaction and compared with communities colonizing unused control filters.

RESULTS: Exposure to cigarette smoke condensate at relevant concentrations resulted in > 2 -fold higher transfer rates of a multidrug-resistance-encoding plasmid in artificial lung sputum medium. This was associated with higher ROS production as part of the bacterial stress response when exposed to cigarette-derived toxicants. Similar results were obtained for cigarette ash leachate in an environmental medium. Further, used cigarette filters were colonized by different microbial communities compared with unused filters. Those communities were significantly enriched with potential human pathogens and AMR.

DISCUSSION: The results of this study suggest that cigarette-derived compounds can indeed promote the spread of AMR within simulated human lung and environmental conditions. This study highlights that the consumption of cigarettes has not only direct but may also have indirect adverse effects on human health by promoting AMR. https://doi.org/10.1289/EHP14704.