Thanks. I have been thinking about topical antihistamines a lot lately, and I think this paragraph summarizes where I think they exert their mechanism of action pretty well:
Skin keratinocytes respond to antigens or trigger inflammation in response to repeated, exposure to pollution, UV damage, reactive oxygen species [26], nitric oxide [27], prostaglandins and histamine [28] leading to progressive inflammation. As mentioned earlier, Kalkan, Seçkin et al. [11], proposed that the ROS forms covalent bond with endogenous proteins in the cells, changing their immune signature and making them behave as new antigens, becoming targets of immunity, inflammation and autoimmune reactions. All these processes, lead to accumulation and release of intracellular cytokines. IL-1alpha, IL-1beta, which are shown to inhibit hair elongation in hair follicle cultures in vitro [29,30]. The same effect is also supported by cytokines and chemokine, monocyte chemo attractant protein-1 (MCP-1), [31], which has been identified to be active in hair follicles and sebaceous glands in androgenetic alopecia. Surrounding fibroblasts too can respond to these pro inflammatory stimuli [32].
Antihistamines like cetirizine should block a lot of those pathways.