- Seymour BWP,
- Pinkerton KE,
- Friebertshauser KE,
- Coffman RL,
- Gershwin LJ
Secondhand smoke, also known as environmental tobacco smoke (ETS), has been implicated as a contributing factor to asthma, allergy and elevated immunoglobulin E (IgE) levels. In all asthmatic and allergic children, the T-Helper cells designated as T helper-2 (Th2) are increased. These specific T-cells are responsible for the cytokines that drive the allergic and asthmatic responses (eg, IL-4, IL-5, IL-13). In this study mice sensitized to egg protein develop allergy and elevated Th-2 cells and then are exposed to ETS (at levels found in homes of smokers) or ambient air.
Balb/c mice were immunized to egg protein using standardized techniques. Once sensitized the study mice were exposed to sidestream cigarette smoke from a smoking machine for 6 hours/day 5 days/week for 47 days. Control mice were only exposed to ambient air. IgE was measured serially. Lung cytokines were measured. Mice without egg protein sensitization exposed to ambient air and ETS were also included.
Serum IgE was significantly highest in the egg-sensitized, ETS-exposed mice and was sustained for the entire protocol. The nonsensitized, ETS-exposed mice had no change in IgE levels. The egg-sensitized, ambient air mice developed elevated IgE, which was not sustained. IL-4, the Th-2 cytokine partially responsible for regulating IgE, was found to be significantly highest in the mice egg-sensitized and ETS-exposed.
Serum IgE, a well recognized marker for atopy, and the cytokine that regulates IgE production, IL-4, were increased in mice sensitized to egg protein and then exposed to ETS.
In this study ETS provided potentiation to the production of IgE in mice sensitized to egg. This would suggest that children with allergic rhinitis and asthma might produce more IL-4 and make more IgE when they are exposed to ETS. As if it wasn't bad enough without the smoke exposure!