Particles originating from bacteria, fungi (including mold spores, mildew, yeast), pollen, dust mites, and viruses can induce immune responses that trigger allergies and asthma. Carpeting is believed to act as a "sink" where bioparticulates are trapped via adhesive interactions and then are released by foot traffic or cleaning. This scenario can result in an accumulation of contaminants at higher levels than would be found outdoors or in a carpet-less environment. Numerous organizations (school districts, hospitals) have taken steps to remove carpeting, even though this hypothesis remains unproven. While statistical studies exist both in support and denial of the accumulation hypothesis, there is little fundamental understanding of the microscopic-level interactions between carpet and bioparticles. A fundamental understanding of particle affinities with polymers utilized in carpet would help to develop accurate models and address real problems in a rational and productive manner. In addition, a solution to the bioparticulate accumulation problem would have a profound impact on US health, resulting in significant economic savings. More than 20 million people suffer from asthma in the U.S., with children being the most vulnerable. In 2000 there were 9.3 million physician office visits and 1.8 million emergency room visits due to asthma alone, resulting in an estimated $9.4 billion in medical costs and $4.6 billion in lost productivity annually. In this thesis, two measurement techniques were developed to quantify the adhesive interactions between biological particulates and polymeric carpeting materials. Atomic force microscopy (AFM) was used to measure the adhesive interactions of relevant biological particulates (in this case the E. coli bacteria and A. artemisiifolia ragweed pollen grains) with Nylon-6 and Nylon-6,6, polyamide-12 and polystyrene. The adhesion force measurements were modeled using several adhesion theories. We found that the Hamaker models were sufficient for explaining the data, indicating the prominence of van der Waals forces in controlling bioparticle interactions with polyamides. In addition, the geometry of the pollen played a significant role: adhesion forces were approximately a multiple of the number of contact points the grain has with the surface. Forces for E. coli and polyamides were about the same magnitude as polyamide-polyamide surface self-interactions.