Biomedical subjects

Robert G Hamilton

Publications and source records attributed to Robert G Hamilton.

42 records · Page 3Linked to original sources

PubMed2002

Dust-mite allergen removal from feathers by commercial processing.

BACKGROUND: Individuals with allergies or asthma have had a long-standing bias against the use of chicken, goose, and duck feather pillows, comforters, quilts, and mattresses. OBJECTIVE: We show that raw, unprocessed feathers contain dust-mite allergen that is removed by washing, and that feather pillows, whether covered or not, do not internally accumulate dust-mite allergen when used in mite-infested bedrooms over a 3-month period. METHODS: Feathers obtained from six companies as unprocessed feathers (n = 8 batches) and processed feathers (n = 16 batches) were analyzed for dust-mite (Der p 1 and Der f 1) using monoclonal antibody-based immunoenzyametric assays with appropriate internal controls. Five pairs of new feather pillows (one covered and one uncovered) were placed in five bedrooms with known dust-mite contamination for 90 days. The pillows were then assayed for mite content. RESULTS: Dust-mite allergen was detected in 7 of 8 unprocessed feather samples; combined Der p 1 and Der f 1 mean = 524 ng/g, range 152 to 1,850 ng/g, whereas all 17 manufacturer-processed feather samples contained no detectable dust-mite. Although 4 of 5 bedrooms contained significant dust-mite allergen (>2,000 ng or Der p 1 and f 1, range 2,500 to 10,300 ng/g), none of the 90-day feather pillows became contaminated by dust-mite allergen even in the absence of a pillow cover. CONCLUSIONS: Feathers washed using industrial methods do not contain detectable dust-mite allergen. Pillows manufactured with processed feathers, whether encased in a dust cover or not, do not become contaminated by dust-mite allergen after 90 days of use in environments containing significant dust-mite allergen contamination.

Animals↗

PubMed2002

Natural rubber latex allergy after 12 years: recommendations and perspectives.

Natural rubber latex (NRL) allergy is a "new" illness whose prevalence reached epidemic proportions in highly exposed populations during the last decade. In children with spina bifida and in patients exposed to NRL during radiologic procedures, institution of prophylactic safety measures has had demonstrable effects in preventing allergic reactions. The risk of NRL allergy appears to be largely linked to occupational exposure, and NRL-associated occupational asthma is due almost solely to powdered latex glove use. Prevalence of NRL-allergic sensitization in the general population is quite low; several studies of young adults demonstrate rates of positive skin test results that are less than 1%. After occupational exposure, rates of sensitization and NRL-induced asthma rise dramatically in individuals using powdered NRL gloves but not in individuals using powder-free gloves. Airborne NRL is dependent on the use of powdered NRL gloves; conversion to non-NRL or nonpowdered NRL substitutes results in predictable rapid disappearance of detectable levels of aeroallergen. For these reasons, adoption of the following institutional policies designed to prevent new cases of NRL allergy and maximize safety is recommended: (1) NRL gloves should be used only as mandated by accepted Standard Precautions; (2) only nonpowdered, nonsterile NRL gloves should be used; and (3) nonpowdered, sterile NRL gloves are preferred for use. Low-protein powdered, sterile gloves may be used, but only in conjunction with an ongoing assessment for development of allergic reactions.

Asthma↗

PubMed2002

Inhaled latex allergen (Hev b 1).

BACKGROUND: IgE-mediated responses to natural rubber latex allergens have become a major health problem among recognized risk groups. OBJECTIVE: The purpose of this investigation was to measure the amounts of Hevea brasiliensis latex allergen (Hev b 1) inhaled and deposited on surfaces when latex or vinyl gloves were worn and compare the results with the conventional measures (breathing zone samplers) of occupational exposure. METHODS: Hev b 1 exposure was measured by nasal sampling and breathing zone sampling. Latex allergen exposure was generated by having each subject don a pair of powdered latex examination gloves and continuing his or her normal daily activity for 30 minutes. By means of adhesive tape, surface dust samples were collected from the surfaces of gloves, the subject's hands, and work areas. Sampling was performed with subjects wearing no gloves, subjects wearing powdered vinyl gloves, subjects wearing powdered latex gloves, and nearby colleagues wearing latex gloves. All samples were assayed through use of the HALOgen assay (Inhalix, Sydney, Australia) with a Hev b 1-specific mAb. Particles transporting latex allergen were identified by a surrounding immunostain halo, and these were quantified and reported as total numbers of particles inhaled, airborne, or found on surface areas evaluated. RESULTS: Study subjects inhaled 26 times more allergen when powdered latex gloves were worn than under the "no glove" and powdered vinyl glove conditions. During the same period, Hev b 1 particle levels measured in the ambient air through use of the breathing zone sampler increased by 24-fold. The median numbers of particles carrying Hev b 1 allergen per square centimeter on the surface of the hands after the wearing of latex and vinyl gloves were 1964 and 5, respectively. Latex allergen was physically associated both with cornstarch granules and with larger dust particles having a darker, more irregular appearance. CONCLUSION: In a laboratory where gloves are worn for protection, the use of latex gloves resulted in a 26-fold increase in inhaled latex allergen over background levels measured while vinyl gloves were worn as controls. Low levels of latex exposure also occurred when vinyl gloves or no gloves were worn; the reasons for this are under investigation.

Administration, Inhalation↗

PubMed2002

Clinical and laboratory-based methods in the diagnosis of natural rubber latex allergy.

The accurate diagnosis of hypersensitivity to natural rubber latex is the initial step in the effective management of individuals with latex allergy and in ensuring the quality of epidemiologic studies. The diagnostic algorithm used in the evaluation of an individual with suspected latex allergy begins with a comprehensive clinical history during which risk factors (atopy, food allergies, hand dermatitis) and temporal relationships between symptoms and natural rubber product exposure are identified. If type IV hypersensitivity is suspected because of the delayed nature (hours to days) and confinement of symptoms to the skin-latex product contact areas, patch testing can be conducted to confirm the presence of activated T cells with specificity for rubber chemicals. If type I hypersensitivity is suspected because of ocular, upper and lower airway, and/or systemic symptoms that have rapid onset (minutes) after a definable latex exposure, a confirmatory skin or blood test for IgE antibody may be conducted to verify a state of sensitization within the individual. The definitive diagnosis would then be made only after consideration of the individual's clinical history and confirmatory in vivo and/or in vitro laboratory test results. If discordance remains between highly convincing latex-associated symptoms as identified in the history and repetitively negative confirmatory IgE antibody test results, then one of several types of in vivo provocation tests may be performed for adjudication. This overview examines the current state of the art in both in vivo and in vitro diagnostic methods for latex-specific IgE antibody detection in skin and blood. The performance, advantages, and limitations of each diagnostic method are compared.

Algorithms↗

PubMed2002

Diagnosis of Hymenoptera venom sensitivity.

PURPOSE OF REVIEW: The objective of this review is to highlight recent advances in the preparation, documentation and performance of reagents and methods used in the diagnosis of Hymenoptera-venom-induced immediate-type hypersensitivity. RECENT FINDINGS: The following potent allergens have been reported: (1) a low-molecular-weight honey-bee allergen (Api m 6) has been described; (2) venom allergens in the North American species of bumble-bee (Bombus pennsylvanicus) have been more fully characterized, with the focus on phospholipase A2; (3) the vespid venom Ves v 5 allergen has been structurally mapped to identify immunoglobulin-E-binding epitopes; (4) the possible role of carbohydrate antigen epitopes as a cause of cross-reactivity among honey-bee and vespid venom proteins has been reported; and (5) the venom of Pachycondyla chinensis, an ant found commonly in the Far East, has been described. The most significant reports during this period have focused on the less-than-ideal performance of the intradermal venom skin-test reagents. The issue of the patient that is positive for venom allergy history but negative for an intradermal venom skin test is raised, and it is suggested that there is a need for caution and the use of serology as a supplementary diagnostic test. SUMMARY: The important issue this year is the reminder that intradermal skin tests may be negative in venom-allergic patients, possibly because of changes in the potency of the extracts. The clinical history should drive the diagnosis of insect-sting allergy. When negative confirmatory venom skin-test or serology results are considered to be inconsistent with a positive history, they should be repeated.

Allergens↗

PubMed2002

Eotaxin-2 alters eosinophil integrin function via mitogen-activated protein kinases.

Adhesion molecules and chemokines contribute to selective eosinophil recruitment in allergic inflammation. In this study, we examined the effects of eotaxin-2, a CCR3-specific chemokine, on integrin-mediated eosinophil adhesion to vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), or both using a parallel plate flow system. Tissue culture plates were coated with various combinations of VCAM-1, ICAM-1, and/or eotaxin-2. Human eosinophils were infused at physiologic shear stress (0.5 dyn/cm(2)) for 10 min, and the numbers of attached eosinophils were monitored using video microscopy. Cells accumulated efficiently on VCAM-1 and even better on surfaces co-coated with VCAM-1 and ICAM-1, but poorly on surfaces coated with ICAM-1 or bovine serum albumin alone. When eotaxin-2 was co-immobilized with adhesion proteins, fewer cells adhered to VCAM-1 and more adhered to ICAM-1, whereas levels of attachment to VCAM-1 plus ICAM-1 showed no net change. However, experiments with adhesion molecule blocking monoclonal antibody showed that the contribution of ICAM-1-mediated adhesion was always greater if eotaxin-2 was present. Pretreatment of cells with a CCR3-blocking mAb, or PD98059, a MAP-kinase inhibitor, prevented the eotaxin-2-induced changes in eosinophil attachment. These data suggest that eotaxin-2, acting via MAP kinases, may facilitate eosinophil recruitment at sites of allergic inflammation by shifting their adhesion molecule usage away from VCAM-1-dominated to ICAM-1-dominated pathways.

Chemokine CCL24↗