Quantification of surface defects on chemically protective gloves following their use in agriculture.

Chemically protective gloves are one of the most widely used barriers against hand exposure to pesticide contamination available to workers in primary industry. Polyvinyl chloride and nitrile butadiene rubber gloves were collected from four typical agricultural enterprises in Tasmania. Surface images of new and used gloves, up to 1000 x magnification, were obtained from an environmental scanning electron microscope and were used to classify defects, such as cracks, crazes, cavities, convexities, smooth areas and slumps. Some defects, e.g. cracks, were related to the working life of the gloves, whereas others, e.g. slumps, were associated with the manufacturing process. After viewing, the gloves were analysed by X-ray energy-dispersive spectroscopy. Phosphorus and sulfur peaks were indicative of pesticide retention. Rinsates from the interior of used polyvinyl chloride gloves were analysed by gas chromatography and mass spectrometry. Pesticide traces were found suggesting inadequate protection against dermal exposure. It is concluded that these gloves were unable to withstand the rigours of agricultural work because of the nature of the surface defects and they were contaminated with pesticides, outside and inside. Thus, their management needs improvement.

Laboratory simulation of splashes and spills of organophosphate insecticides on chemically protective gloves used in agriculture.

Agricultural workers rely on chemically protective gloves for protection from dermal exposure to insecticides. In Australia the most widely used gloves are manufactured from polyvinyl chloride or nitrile butadiene rubber. During insecticide application splashes and spills frequently occur on the external surfaces of gloves which may compromise the integrity of the membrane. Interaction of two organophosphate insecticides, chlorpyrifos (Lorsban 500 EC(R)) and diazinon (Jetdip(R)), with glove surfaces was investigated in laboratory conditions. The external surface of gloves was treated with concentrated insecticides for one minute and diluted and concentrated insecticides for 24, 36 and 48 hours and later examined by environmental scanning electron microscopy. Two classes of defects, cavities and convexities, were evident in the polyvinyl chloride gloves following all treatments, whereas cracking was significant in the nitrile butadiene rubber gloves after 24 hours. In addition, X-ray energy-dispersive microanalysis was used to evaluate chemical changes on the glove surfaces. Phosphorus and sulfur were useful indicators for organophosphate retention over specific time frames. Results corroborated the need for more robust chemically protective gloves to be developed for routine agricultural use.

Effect of myeloma IgE injections on passive and active cutaneous anaphylaxis in rats.

The ability of injected rat IgE myeloma protein IR162 to inhibit passive and active cutaneous anaphylaxis in Lewis rats was investigated. IgE injected i.p. 24 hr before the sensitization with IgE anti-ovalbumin (OVA) completely inhibited both IgE- and IgG2a-induced passive cutaneous anaphylactic (PCA) reactions at a dose (2.5 mg/100 g body weight) that resulted in peak serum concentrations of 150 micrograms IgE IR162/ml. Peak IgE IR162 serum concentrations of 20 to 60 micrograms/ml inhibited the PCA reaction in approximately 50% of the rats. Intracutaneous injection of a mixture of myeloma IgE and anti-OVA IgE in a ratio of 100:1 or more also inhibited the PCA reaction. In contrast, the PCA reaction was not inhibited by seven daily doses of IgE beginning 24 hr after passive sensitization. Likewise, the cutaneous anaphylactic reaction elicited in rats 14 days after immunization with OVA and Bordetella pertussis was not prevented by daily injections of myeloma IgE despite a 1000- to 3000-fold excess of the myeloma IgE to anti-OVA IgE serum concentration. The data demonstrate that parenteral administration of myeloma IgE inhibits the PCA reaction only when given before passive sensitization and does not prevent cutaneous anaphylaxis in actively immunized rats. Because myeloma IgE failed to inhibit anaphylactic reactions in actively immunized rats, it is questionable whether administering human IgE-derived synthetic peptides or recombinant DNA-produced IgE fragments will be able to prevent allergic diseases by blocking the IgE Fc receptors on mast cells.