As discussed in the previous section, when allergens are introduced to the intrauterine environment, a fetus can become sensitized. Maternal toxicant exposure has the potential to affect the sensitization process in various ways. Whereas in utero sensitization usually provides neonates with healthy immune responses, hyperresponsiveness can also occur. Moreover, environmental toxicants concom-itantly encountered during in utero sensitization have the potential to deviate normal physiologic processes to pathological outcomes, including asthma. These processes potentially include: isotype switching by fetal B cells; functional maturation of fetal APCs, B cells, and T cells; expression of adhesion molecules on inflammatory cells, thus affecting migration to the airways; a change in the cytokine secretion profiles of T cell subsets; epigenetic changes affecting fetal programming; and modulation of biochemical signal transduction pathways and transcription factors in any of the cells involved in asthmatic inflammation and pathogenesis. The following section reviews what little is known regarding the development of asthma from maternal-fetal exposures to allergens, environmental toxicants, and tobacco smoke.
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If you suffer with asthma, you will no doubt be familiar with the uncomfortable sensations as your bronchial tubes begin to narrow and your muscles around them start to tighten. A sticky mucus known as phlegm begins to produce and increase within your bronchial tubes and you begin to wheeze, cough and struggle to breathe.