The cigarette smoke has more than 8700 harmful substances related to the occurrence of the most varied diseases. Among them, a relevant substance is the hydroquinone (HQ), generated upon the biotransformation of inhaled benzene. In vitro and in vivo analyses have demonstrated that HQ can suppress both innate and adaptive immune responses. However, no study has approached the effect of the HQ exposure on the vaccination-induced response. Thus, would the exposure to the cigarette smoke or HQ influence the B-cell and antibody responses elicited by immunizations with antiviral vaccines? We observed a "tendency" to lower titers of IgG total and IgG1 anti-EDIII in mice daily exposed to 2,500 ppm of HQ for 8 weeks and vaccinated. Histological analyses revealed a smaller number of follicles and a significant reduction in their area in the HQ group in comparison to their counterparts. In order to understand the effect of the HQ on the humoral response, we performed an analysis of public transcriptome data derived from human blood samples. We observed that the HQ up-regulates the expression of genes related to B cell activation as well as the migration and chemotaxis of neutrophils and other leukocytes. Considering that N2 neutrophils have the ability to help the B cell response, we have hypothesized that the HQ exposure may trigger an immunocompensatory effect, increasing the humoral response.