Occupational lung disease is occupational asthma Essay Example

Occupational lung disease is occupational asthma Essay Example Occupational lung disease is occupational asthma Essay Occupational lung disease is occupational asthma Essay MOLECULAR MECHANISMS BY WHICH CHEMICALS CAN CAUSE OCCUPATIONAL ASTHMA Introduction Occupational asthma can be defined as a disease characterized by airflow restriction and/or airway hyper reactivity due to causes and conditions attributable to a peculiar occupational environment and non to stimuli encountered outside the workplace ( Bernstein et al. , 1993 ) . In most industrialised states, the most common occupational lung disease is occupational asthma and it was reported by Mantyjarvi et al. , 1992 that close to 200 agents are known to bring on occupational asthma. Chemical-induced occupational asthma is chiefly determined by the degree and manner of exposure to such chemicals. The mechanisms by which chemicals causes occupational asthma are non to the full understood and it is possible for common tracts to be shared. Some of the postulated mechanisms by which chemicals cause occupational asthma include immunological and non-immunological mechanisms. The immunological mechanism is non to the full clear but it can happen either through Ig E ( IgE ) dependant mech anism or non-IgE dependent mechanism. It was besides established from surveies that occupational asthma can be caused by more than one mechanism. Other postulated mechanisms include familial mechanism, pharmacological mechanism, neurogenic and airway redness ( Mapp et al. , 1994 ) . Compounds that cause occupational asthma can be classified into high molecular and low molecular weight compounds. Largely, low molecular weight compounds ( MW lt ; 1000KDa ) causes occupational asthma because they act every bit haptens as a consequence of adhering to bearer proteins and they besides contain chemically reactive groups ( Bernstein J.A 1996 ) . In contrast, bulk of high molecular weight compounds are either protein or carbonhydrate compounds unlike low molecular weight compounds that are largely chemicals. In this essay, much accent will be on the low molecular weight compounds because bulk of them are chemicals. Low molecular weight chemicals Some low molecular weight chemicals ( MW lt ; 1000 KDa ) are known as inducers of occupational asthma and are either IgE dependant or nons of low molecular chemicals that are IgE dependent include metals such as Ni, Cr and Pt, acerb anhydrides and pharmaceutical merchandises. Metallic elements Exposures to metals at work topographic point are known to do occupational asthma. Largely, when metallic compounds are inhaled, it can ensue in metal smoke febrility, bronchitis and chemical pneumonitis. Inhalation of metallic compounds at chronic degree consequences in chronic bronchitis, pneumonoconiosis and emphysema. Exposure to metals can happen at different occupational degree such as metallurgical industries, metal excavation, soldering and welding industries. Categorically, metals doing occupational asthma can be classified as ( 1 ) difficult metals, e.g. Co ( 2 ) passage metals, e.g. Zn, Cr, Ni ( 3 ) cherished metals e.g. Pd and Pt. Chromium exposure to chromium salts are known to bring on occupational asthma. Contact dermatitis consequences when worlds are exposed to chromium salts in workplace such as cement and pigment production, tanning and electroplating. Occupational asthma as a consequence of Cr is noted and observed by a history of contact dermatitis ( Chang-Yeung et al. , 1994 ) . Besides, nickel-induced asthma may be enhanced by cell-mediated hypersensitivity. Nickel worlds are exposed to nickel at workplace such as smelting and refinement procedure, excavation, milling and electroplating industries. In open workers, nickel doing asthma is rare unlike Cr which causes contact dermatitis. It was reported that nickel-induced asthma consequences when workers are exposed to nickel sulfate ( Malo et al. , 1982 ) . In some instances, specific IgE antibodies to nickel-human serum albumen conjugate have been reported ( Malo et al. , 1982 ) . Furthermore, nickel induced asthma can be enhanced by cell-mediated hypersensitivity as a consequence of transformed lymph cell found in patients with nickel-induced asthma ( Kusaka et al. , 1991 ) . Zinc different illustrations of zinc-induced asthma are common following exposure to exhausts of Zn oxide. Workers exposed to zinc in steel fabrication and insect powder industries, welding of galvanized Fe and exhausts of Zn oxide are known to hold occupational asthma. Metal fume febrility with cough and breath shortness are reported symptoms of fume zinc oxide exposure. Platinum exposure to platinum salts are widely known to bring on asthma. Workers exposed to platinum in chemical industries, excavation and refinement procedures are reported to hold occupational asthma. The most widely known Pt salt which causes occupational asthma is the halide salts. Platinum salts were found in allergic workers with a positive tegument trial and the wireless allergosorbent trial processs are used to observe specific IgE antibodies ( Pepys et al. , 1972 ; Biagini et al. , 1985 ) . Acid anhydrides Acid anhydrides used in epoxy and alkyd rosins such as hexahydrophthalic, trimellitic, phthalic and tetrachlorophthalic anhydrides consequences in hypersensitivity reactions in open workers. They tend to adhere with endogenous proteins to organize conjugates with antibodies and besides act as haptens with the antibodies observing the haptens ( Zeiss et al. , 1993 ) . They can besides unite with self-proteins to bring forth new, carrier-dependent antigenic determiners with antibody uniting sites being directed against a conformational alteration in self-proteins ( Zeiss et al. , 1993 ) . Trimellitic anhydride when trimellitic anhydride are coupled with proteins, new determiners are induced which are antigenic in nature. This is really similar to when trimellitic anhydride induces specific IgE, IgM, IgG and IgA antibodies against hapten. Lung diseases such as asthma, pneumonic disease-anaemia syndrome, and coryza are caused as a consequence of high degree of exposure to trimellitic anhydride. Tetrachlorophthalate anhydride ( TCPA ) high exposure to TCPA at workplace has been reported to bring on occupational asthma. Workers exposed to TCPA-conjugate showed a high addition in specific IgE antibodies in a study carried out by Chang-Yeung et al. , 1994. The degree of exposure to TCPA is really of import as workers removed from exposure showed a lessening in IgE antibodies degree ( Chang-Yeung et al. , 1994 ) . It was besides reported by Chang-Yeung et Al that airway hyper reactivity was absent but several types of hypersensitivity reactions were induced. Non-IgE dependant chemicals The molecular mechanisms for low molecular weight chemicals which are nons of chemicals which are non-IgE dependent includes ; Diisocyanates Diisocyanates are chemicals which have N, C and O group. These groups are attached to a extremist and react with compounds such as polyglycols to organize polyurethane. They are extensively used in industries and are known as inducers of occupational asthma. They are low molecular weight compounds synthesised when there is a reaction between their hydrochlorides or aminoalkanes with phosgene. Pre-polymers of diisocyanates such as methylbenzene diisocyanate ( TDI ) , methyldiphenyl diisocyanate ( MDI ) and hexamethylene diisocyanate ( HDI ) are known to do occupational asthma. Chang-Yeung et Al ( 1994 ) reported that the most common cause of occupational asthma in many industrialised states is toluene diisocyanate. Furthermore, hypersensitivity reactions which are cell-mediated have been observed in open workers. Although the mechanisms of TDI-induced asthma is non to the full understood but it was reported that they show belongingss which are similar to that of ?- adrenergic encircle ment. Furthermore, MDI is besides an inducer of occupational asthma. Exposed workers seem to hold specific IgE and IgG antibodies which indicate sensitisation instead than a disease. The mechanism by which MDI induced occupational asthma is non to the full clear. HDI are extensively used in aircraft and car spray pigments and are more volatile than TDI. The mechanism by which HDI induced asthma is non clearly understood but instances of HDI exposure have been reported in literatures ( Bohner C.B. et al. , 1941 ) . Besides, intracellular glutathione lack can be induced by diisocyanates which in bends lead to the activation of mitogen-activated protein kinase. The degrees of intracellular peroxide additions in workers exposed to diisocyanates and adhesion molecule in monocytic cell lines are expressed ( Elms J et al. , 2001 ) . Plicatic acid ( PA ) Plicatic acids are low molecular weight chemicals which are present in forests and are known to do ruddy cedar asthma ( Harris MG et al. , 1977 ) . The molecular weight of plicatic acid is 440 K Da. Allergen is formed when there is a junction between plicatic acid and human serum albumen. Patients with ruddy cedar asthma have been reported to involved in histamine release but recent surveies indicates that specific IgE antibodies are non responsible for the histamine release. Further surveies are required as the mechanism by which PA-induced asthma is non to the full understood. Amines Amines are widely used in primary and secondary fabrication industries such as cosmetics, hair dye, gum elastic and pelt industries ( Wernfors M et al. , 1986 ) . Quarternary, third and secondary aminoalkanes either aromatic or aliphatic are known as inducers of occupational asthma. The molecular mechanism by which asthma are induced by aminoalkanes still remain ill-defined. Formaldehyde Formaldehyde is a chemical that induce occupational asthma through non-immunological mechanisms. In lower concentrations, they serve as sensitiser and at high concentrations, they are thorns. 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