Retention of allergic potential of parthenium following composting
Parthenium hysterophorus is known to cause allergic contact dermatitis (1). Changing clinical patterns of the dermatitis are reported (2, 3). Recently, the role of type I (immediate) and type III (Arthus phenomenon) has been postulated (4, 5). This weed, a native of tropical America, is wide spread in grasslands, fruit tree orchards, and arable land in neutral and acid soils. This weed interferes with the growth of other plants (allelopathic potential) resulting from the release of phytotoxic substances such as ferulic, caffeic, vanillic, chlorogenic, p-hydroxybenzoic acids, parthenin, ambrosin, and coronopilin, which inhibit the germination and growth of several crop plants (6). Because it has no economic value, efforts have been made to use parthenium as a green leaf manure, as a biopesticide, as a compost for agricultural purposes, and as an additive with cattle manure in biogas production (7). Compost obtained from parthenium can be used for agricultural purposes and as manure. This is likely to get widely dispersed, get airborne, and aggravate parthenium dermatitis if the allergenicity is retained. Parthenium compost was obtained from the Department of Agronomy, Tamil Nadu Agricultural University, Coimbatore. Compost made by 2 methods, anaerobic and aerobic, was collected. The composting procedure was carried out for 90 days for each of themethods. Samples were obtained on D45 and D90. The 2 methods of composting are described below.
Changing clinical patterns of Parthenium dermatitis
We ha've seen 30 new patients with allergic contact dermatitis from Partllrniumltystervplwrus between Octoher 1993 and July 1996. All were men from :?lS to 76 years of age. with duration of dermatitis from 6 months ro 14 years. 9 had dermatitis in a photo-pattern, of whom 4 had lesions only in sun-exposed areas. '"hile 5 also had minimal involvement of flexural and shaded areas. The remaining 11 had features of airborne contat.:t dermatitis. Irrespective of clinical pattern. the majority complained of photosensitivity. Of the 9 with predominant photodistribution of lesions. 2 had no pht.lll)Scnsitivity. with I showing features of actinic n:liculoid (I).
Etiopathogenesis of atopic dermatitis--an overview.
Atopic eczema/dermatitis syndrome is a term that covers different subtypes of atopic dermatitis. The "intrinsic" type of atopic dermatitis is non-IgE-associated, and the "extrinsic" type is IgE-associated atopic eczema/dermatitis syndrome. In the etiopathogenesis of atopic dermatitis there are well known interactions among genetic, environmental, skin barrier, immune factors, and stress. Genetic factors determine the expression of atopic dermatitis as pure or mixed with concomitant respiratory or intestinal allergy, depending on genetic susceptibility. Immunologic abnormalities of type I and type IV reactions have been described in patients with atopic dermatitis. Immunologic triggers are aeroallergens, food allergens, microbial products, autoallergens and contact allergens. Immune reactions determine many features of atopic dermatitis. These immune reactions also include cell mediated or delayed hypersensitivity. The currently accepted model proposes a predominant Th2 cytokine milieu in the initiating stages of acute atopic dermatitis lesions, and a mixed Th1 and Th2 pattern in chronic lesions. A two-phase model includes Th2 initiation with attraction of macrophages and eosinophils, which in turn produce interleukin 12 that is the activator of Th1 type response. Atopic dermatitis skin contains an increased number of IgE-bearing Langerhans cells which bind allergens via the high-affinity IgE receptor (FcepsilonRI). Langerhans cells play an important role in cutaneous allergen presentation to Th2 cells via major histocompatibility molecules. Eosinophilia and IgE production are influenced by type 2 cytokines. Degranulation of eosinophils occurs in the dermis with the release of toxic proteins such as major basic protein and could account for much of the inflammation. Mast cells are increased in number and produce mediators other than histamine that induce pruritus and may have an effect on interferon gamma expression. Mast cells produce a number of proinflammatory cytokines. There is an elevated production of prostaglandin E2 by peripheral monocytes. Prostaglandin E2 has at least two potential roles in the initiation of atopic dermatitis. Firstly, it reduces interferon-gamma production by T helper cells, thereby favoring the initial, dominant Th2 immune response; and secondly, it directly enhances IgE production by B lymphocytes with an increased secretion of interleukin 4, interleukin 5 and interleukin 13. Many lesions of atopic dermatitis result from scratching, thus it is tempting to speculate that immune perturbations in genetically predisposed individuals provoke the release of local pruritogens and keratinocyte-derived cytokines, which then further exacerbate the previously described immune response.