Bisphenol A (BPA) is a phenol derivative and widely used in the manufacture of polycarbonate plastics and epoxy resins. It is one of the largest industrial products in the world. The extensive use of BPA makes it more easily exposed to the general population. BPA is believed to be a typical estrogen-like endocrine disruptor that can induce multiple toxic effects on the human body. High-dose BPA exerts its endocrine-disrupting effects mainly by antagonizing estrogen receptors (ERs); environmentally-relevant low-dose BPA cannot compete with estrogen for binding to ERs, and induces biological effects in a non-genomic manner mainly through the membrane receptor-mediated signaling pathways. However, it is still unclear which membrane receptor mediates the low-dose effect of BPA and the related molecular mechanisms. Based on this, our laboratory has done a series of work in these areas in recent years. We have found that membrane G protein-coupled receptor 30 and integrin αvβ3 and their mediated signaling pathways mediate the effects of environmentally-relevant low-dose BPA on the induction of male germ cells proliferation and the transcription of thyroid hormone genes, respectively. An in-depth understanding of the molecular mechanism of environmentally-relevant low-dose BPA will contribute to a more objective and realistic evaluation and prediction of the potential effects of environmental exposure on human health and then perform targeted prevention and interventions. Likewise, it will also provide a theoretical basis and technical support for evaluating the health effects of endocrine disruptors in other similar structural estrogen-like environments. This article combines our research work in recent years, reviews the current progress in the molecular mechanism of environmental low-dose BPA exposure on human health, existing problems, and some future research.