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The Environmental Risk Factors Associated with Asthma - Term Paper Example

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The author states that there is increasing evidence of environmental causes of asthma of which inhaled allergens and pollutants have a substantial role in provoking an attack of asthma. Identifying specific environmental risk factors helps to design strategies to reduce the incidence of asthma. …
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The Environmental Risk Factors Associated with Asthma
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Current thinking on the environmental risk factors associated with asthma Introduction Asthma Asthma is a chronic lung disease that inflames and reversibly narrows the bronchi making breathing difficult. The rapidly increasing prevalence of Asthma in the developed world has resulted in considerable attention on its disposition and risk factors. Though the precise reasons for the higher incidence of asthma are unknown the effects of environmental pollution on the development and exacerbation of asthma have been major topics of discussion and debate on the national and international front. With the large number of studies conducted there is increasing evidence of environmental causes of asthma of which inhaled agents such as allergens and pollutants seem to have a substantial role in provoking an attack of asthma. Identifying specific environmental risk factors helps to design and develop strategies to reduce the incidence of asthma and reduce asthma-related health complications. Environmental Risk Factors Environmental risk factors of asthma include those originating from both the indoor and outdoor environment. A large body of data shows that the outdoor environment acts as an inciting factor for asthma (Gilmour et al, 2006) whereas the indoor environment which accounts for the bulk of most persons’ exposure time plays a major role in exacerbating the disease. However indoor environment is strongly linked to the increase in asthma prevalence as a person’s indoor exposure such as those in home, workplace and school contributes largely to his/her total exposure (Klepeis et al, 2001). Both indoor and outdoor environment includes exposure to particulate matter, tobacco smoke, Nitrogen Dioxide, Ozone and allergens. However the sources of exposure for each of these factors differ in indoor and outdoor environment and are hence considered separately in the essay. Indoor Environment Risk factors Studies have recognized the indoor environment to be a major source of exposure to pollutants and allergens that exacerbate asthma. Total indoor air pollution is a mixture of pollutants that originate from indoor sources as well as those migrating from outdoors. However those originating indoors contribute much to the contamination of air indoors (Diette et al, 2008). Indoor pollutant sources relevant to asthma as listed in the table are dealt separately in the following section. Particulate Matter Particulate matter is the most common air pollutant that affects people’s health. It consists of solid particles and liquid droplets originating from a number of sources. One of the major indoor sources of particulate matter is tobacco smoke (Wallace et al, 2003). Wood heaters, cooking exhausts, stoves burning wood and cleaning activities are also sources of particulate matter in the indoor environment (McCormack, 2008). Particulate matter is generally characterized into bigger and smaller particles according to size. Bigger particles are between 2.5 and 10 micrometers in diameter and are caller PM10 and smaller particles are less than 2.5 micrometers and are caller PM2.5. The particles enter the respiratory system along with air during inhaling and the smaller particles are capable of reaching the alveoli and the bigger particles stick to the sides of the narrow airways. Studies in children with asthma have shown a decrease in lung functioning and an increase in respiratory complications with higher concentration of indoor particulate matter. Studies have also found particulate matter originating indoors to be of more concern as it is more potent in decreasing lung function when compared to those originating from outdoor environment. Tobacco smoke exposure is also arguably one of the most important indoor air pollutants and contributes significantly to air-borne particulate matter. Involuntarily inhaled tobacco smoke is linked to an exacerbation of asthma in both children and adults. A study by Tarlo (2003) shows that the irritant substances in tobacco smoke may incite chronic inflammation in the respiratory airways that could lead to a kind of irritant-induced asthma. Clinical trials and studies have shown that management of particulate matter by the use of air filters and increased ventilation can improve asthma health. However avoidance of second-hand exposure of tobacco smoke is the best way to improve asthma outcomes which requires education and encouragement to quit smoking in indoor spaces especially in work places and homes. Nitrogen Dioxide Indoor sources of Nitrogen Dioxide include fireplaces and furnaces, gas stoves and heaters which have been linked to respiratory complications. Studies on children with asthma have shown association of Nitrogen dioxide with asthma morbidity (Belanger, 2006). Some of the respiratory symptoms that were shown with an increase in indoor Nitrogen dioxide concentration were daytime and night-time asthma attacks, wheezing, breathlessness and chest tightness (Smith, 2000). Exposure to Nitrogen dioxide has also shown impairment in innate immunity resulting in reduced host resistance to respiratory viruses and bacteria (Jakab, 1987). Reducing mean indoor Nitrogen dioxide concentration by modification of the sources and proper ventilation are general control strategies suggested by studies. Ozone Indoor ozone levels are considerably lower than outdoor ozone levels and are a cause of concern only in higher temperatures wherein the levels of ozone increases due to penetration from outside. However studies on outdoor ozone levels have found significant association with asthma morbidity (Mortimer, 2002). Therefore indoor ozone sources such as ozone generating air cleaners and photocopying machines in schools and offices is best avoided by patients with asthma. Allergens An allergen is an antigen capable of stimulating an immunoglobin E response or type-I hypersensitivity reaction in atopic individuals. Allergens cause asthma symptoms in sensitized patients. Indoor allergens are associated with perennial symptoms as they are generally present throughout the year. Some of the common indoor allergens include dust mite, cockroach, rodent, furred pet and mould allergens. Dust Mite allergens Dust Mite allergens belong to the class arachnid that thrive well in warm and humid regions. They infest upholstered furnishings, carpets and bedding and feed on human skin scales (Arlian, 2001). In sensitized patients dust mites exacerbate asthma showing severe symptoms including poor lung functions and greater requirement for medications. However a prospective study also shows evidence to dust mites inducing asthma according to which infants exposed to higher levels of dust mite allergens are more likely to develop asthma later in childhood when compared to those not exposed to such higher levels (Sporik, 1990). Dust mite allergen reduction will therefore reduce asthma symptoms in sensitized patients as well as prevent development in children. Control measures include allergen proof furnishings and treatments to kill and denature the allergens. Field studies however have not shown much improvement though lab studies gave positive results to the treatments. Cockroach and Rodent allergens Pest infestation has strong association with asthma morbidity in sensitized patients. Studies have shown that exposure to cockroach allergens in the first three months of life results in wheezing and asthma (Santos, 1999). An integrated pest management approach that combines professional application of insecticides and rigorous household cleaning can bring about sustained decrease in cockroach allergen levels. Rodents are common in poorly maintained houses and urban multi-family dwellings. Rodents excrete urinary allergens that get carried on small airborne particles. Though the significance of rodent allergens in the pathogenesis of asthma had been long known in occupational settings such as in the laboratory, recent studies have highlighted their role in home environment (Matsui, 2006). Mouse and rat are the most common source of rodent allergens. However with an increase in rodent pets hamsters and rabbits can also cause allergen exposure in an indoor setting. Like in the case of cockroach abatement integrated pest management is the best approach to reduce rodent allergens. A combination of mouse and rat extermination, cleaning, proper food remains disposal and sealing of holes and cracks in indoor spaces can control re-infestation of rodents. Furred pet allergens Furred pet allergens are one of the most common indoor allergens with a large number of children sensitized to cat or dog allergens. The sources of allergens in pets include protein in the saliva, dander or urine. Furred pet allergens are passively transferred from one environment to another as they are found in settings outside home such as in schools and other public buildings. They easily stick to surfaces and clothing as they are carried by small air borne particles. The high prevalence of patience with pet sensitization results in a large risk of allergen induced asthma-symptoms like wheezing. Studies have shown a reduction in medication intake among pet sensitized adults who chose to remove pets from homes (Shirai, 2005). These evidences highlight the importance of pet removal in the well-being of patients with furred pet allergies. Mould allergens Indoor dampness is a major cause of mould growth and studies have shown association with asthma and exposure to indoor mould growth. A study showed evidence to risk of asthma related to the presence of mould and its odour but not to damp stains and water damage (Jakkola, 2002). Interventions that reduce moisture and humidity such as air conditioning, increased ventilation and dehumidification can check mould growth to an extent. Prevention and elimination of water leakage can also help prevent mould growth and thereby control asthma. Occupational Asthma Occupational asthma refers to asthmatic conditions caused by factors present in the workplace environment (Bernstein, 1999). Two of the main agents that have been implicated as risk factors are high molecular weight compounds that include animal protein, flour or natural rubber latex and low molecular weight compounds such as metals, organic chemicals, certain medication, wood dust (Chistiani) which is considered sensitizers. Bakers, milers and farm workers are susceptible to allergy and asthma from grains and flours. Grain handling operations have reportedly caused asthma outbreaks in people exposed to winds carrying grain dust (Christiani, 1996). Once sensitized to these materials exposure to even very small amounts of it can exacerbate asthma. Another less common form of occupational asthma is irritant induced asthma which occurs after exposure to high inhaled concentrations of workplace irritants accidentally. System first begin within 24 hours after accidental exposure to irritants in the case of irritant induced occupational asthma whereas sensitizer induced occupational asthma shows symptoms during the working period and are worse at work or after work and lessen during weekends and holidays (Tarlo, 2003). Outdoor Environment Risk Factors Ambient air pollution is a major risk factor associated with onset and exacerbation of asthma. Some of the major pollutants that affect asthma include particulate matter, gaseous pollutants such as sulphur dioxide and Nitrogen dioxide. Ozone and pollen allergens also contribute to the morbidity of the disease. Outdoor particulate Matter Exposure to particulate matter in the outdoor environment is associated with higher mortality (Samet, 2000). Ambient particulate matter is seen to exacerbate asthma, decline lung function and show chronic symptoms in patients according to studies (Platts- Mills, 1986). Nitrogen Dioxide Automobile exhaust, local industries and power plants are major sources of ambient Nitrogen dioxide in the environment. A number of studies have shown the association of increased Nitrogen dioxide concentration with increased symptoms of asthma and its exacerbation (Nitschke, 1999). Diesel exhaust contribute much to the incidence of asthma as it is a mixture of chemicals that include Nitrogen dioxide, Sulphur dioxide, elemental carbon, carbon monoxide, polycyclic aromatic hydrocarbons, nitric oxide, acid aerosols and volatile organic compounds. Studies also suggest that some of the components of the diesel exhaust can cause responses that are asthma related (Walker, 2003). Sulphur Dioxide Sulphur Dioxide is an ambient air pollutant which is formed by sulphur coal or oil combustion. The major source of the gaseous pollutant in the environment is coal power stations and metal smelting. Sulphur dioxide is believed to cause respiratory tract irritation and exacerbation of respiratory diseases including asthma. Experimental studies in exercising adults with asthma suggest a decrease in lung function (Roger, 1985). Ozone Ozone is a reactive gas formed by a reaction of sunlight on mixtures of hydrocarbons and Nitrogen dioxide. Industries and power plants as well as vehicular traffic contribute to harmful concentration of ozone in the ambient environment. A number of adverse health effects of ozone including its various alterations in the respiratory system have caught enormous toxicological interest. Some of the respiratory complications associated with ozone include airway inflammation and hyper responsiveness (Bayram, 2001), reduced lung function, increased rescue medication and exacerbation of asthma (Gent, 2003). A greater asthmatic response also may be caused by the interaction of allergens with ozone exposure among people with allergic asthma (Peden, 1995). Outdoor allergens Mould and pollen are the major allergens seen in the outdoor environment. Mould allergens are seen in humid and damp environment as dealt in the indoor environment. Pollen allergens cause asthma exacerbations and are produced seasonally. Depending upon the regions tree pollens are common in spring, grass pollen in summer and weed pollen in fall with slight variations and sensitized patients show an increase in symptoms of asthma during the relevant season. Interaction of Environmental Factors Studies have shown that exposure to a mixture of irritants and allergens can at times promote the induction of asthma. Some of the environmental conditions such as humidity and temperature may alter the composition of aeroallergens. For example the antigen in pollen may be altered by humidity, Nitrogen dioxide and sulphate exposure. Interaction of pollen with the ambient particulate matter might alter the exposure characteristics and possible biological response to it (Taylor, 2002). Climatic changes might also cause an increase in the abundance of aeroallergens such as pollens which may contribute to greater incidence and severity of allergic diseases (Gilmour, 2006). Gene-environmental factor interactions Recent studies have shown environment factors and genes interact to cause asthmatic conditions. Mouse animal model studies have implicated tumour necrosis factor-α (TNF) and toll-like receptor 4 (TLR4) in ozone response susceptibility to asthma (Savov, 2004). Research has also suggested the roles of specific oxidative stress related genes like GSTM1 (Romieu, 2006) and TNF (Yang, 2005) in pulmonary impairment due to ozone and environmental tobacco smoke. Conclusion The complex issue of increasing asthma worldwide has been attributed to a large number of risk factors. However there has not yet been a consensus on the relative importance of these factors. The substantial evidence of broad spectrum environmental risk factors of asthma from recent and ongoing studies will contribute much to the overall management of asthma through environmental control practices and patients’ awareness and education, much needs to be learned about a lot of other dimensions of the same issue including interaction between an environmental challenge and its asthmatic response. More population, climatic and toxicological studies linking exposure to various agents are necessary to better understand and quantify the association of environmental risk factors and the development and exacerbation of asthma. References Arlian, L.G., 2001. Dust mites: update on their allergens and control. Current Allergy and Asthma Reports, 1(6), pp.581–586. Bayram, H., Sapsford, R.J., Abdelaziz, M.M., Khair, O.A., 2001. Effect of ozone and nitrogen dioxide on the release of proinflammatory mediators from bronchial epithelial cells of nonatopic nonasthmatic subjects and atopic asthmatic patients in vitro. Journal of Allergy and Clinical Immunology, 107(2), pp.287–294. Belanger, K., Gent, J.F., Triche, E.W., Bracken, M.B., Leaderer, B.P., 2006. Association of indoor nitrogen dioxide exposure with respiratory symptoms in children with asthma. American Journal of Respiratory Critical Care Medicine, 173 (3), pp.297–303. Bernstein I.L., Chan-Yeung M., Malo, J.L., Bernstein, D.I. , 1999.Definition and classification of asthma. In: Asthma in the workplace. 2nd ed. N Y: Marcel Dekker Inc.pp. 1-4. Nitschke, M., Smith, B.J., Pilotto, L.S., Pisaniello, D.,Abramson, M.J., Ruffin, R.E.1999. Respiratory health effects of nitrogen dioxide exposure and current guidelines. International Journal of Environmental Health Research, 9, pp.39–53. Diette G.B., McCormack M.C., Hansel N. N., Breysse P. N., Matsui E.C., 2008. Environmental issues in managing asthma. Respiratory Care, 53(5), pp. 602–617. Gent, J.F., Triche, E.W., Holford, T.R., Belanger, K., Bracken, M.B., Beckett, W.S., et al., 2003 Association of lowlevel ozone and fine particles with respiratory symptoms in children with asthma. Journal of the American Medical Association, 290 (14), pp.1859–1867. Gilmour, M. I., Jaakkola, M.S., London, S.J., Nel, A.E., Rogers, C.A., 2006. How exposure to environmental tobacco smoke, outdoor air pollutants, and increased pollen burdens influences the incidence of asthma. Environmental Health Perspectives, 114, pp.627–633. Jakab, G.J., 1987. Modulation of pulmonary defense mechanisms by acute exposures to nitrogen dioxide. Environmental Reserach , 42(1), pp.215–228. Klepeis, N.E., Nelson, W.C., Ott, W.R., Robinson, J.P., Tsang, A.M., Switzer, P., et al., 2001.The National Human Activity Pattern Survey (NHAPS): a resource for assessing exposure to environmental pollutants. Journal of Exposure Analysis and Environmental Epidemiology, 11(3), pp.231–252. Matsui, E.C., Eggleston, P.A., Buckley, T.J., Krishnan, J.A., Breysse, P.N., Rand, C.S., Diette, G.B.,2006. Household mouse allergen exposure and asthma morbidity in inner-city pre-school children. Annals of Allergy Asthma and Immunology, 97(4), pp.514–520. McCormack, M.C., Breysse, P.N., Hansel, N.N., Matsui, E.C., Tonorezos, E.S., Curtin-Brosnan, J., et al., 2008. Common household activities are associated with elevated particulate matter concentrations in bedrooms of inner-city Baltimore pre-school children. Environmental Research, 106(2), pp.148–155. Mortimer, K.M., Neas, L.M., Dockery, D.W., Redline, S., Tager, I.B., 2002. The effect of air pollution on inner-city children with asthma. European Respiratory Journal, 19(4), pp.699–705. Peden, D.B., Setzer, R.W., Devlin, R.B., 1995.Ozone exposure has both a priming effect on allergen-induced responses and an intrinsic inflammatory action in the nasal airways of perennially allergic asthmatics. American Journal of Respiratory and Critical Care Medicine, 151(5), pp.1336–1345. Platts-Mills, T.A., Heymann, P.W., Longbottom, J.L., Wilkins, S.R., 1986. Airborne allergens associated with asthma: particle sizes carrying dust mite and rat allergens measured with a cascade impactor. Journal of Allergy and Clinical Immunology, 77(6), pp.850–857. Roger, L.J., Kehrl, H.R., Hazucha, M., Horstman, D.H., 1985. Bronchoconstriction in asthmatics exposed to sulphur dioxide during repeated exercise. Journal of Applied Physiology 59(3), pp.784–791. Samet, J.M., Dominici, F., Curriero, F.C., Coursac, I., Zeger, S.L., 2000. Fine particulate air pollution and mortality in 20 US cities, 1987-1994. New England Journal of Medicine ,343(24), pp.1742–1749. Walker, B.,Stokes L. D.,Warren R.Environmental Factors associated with Asthma. J Natl Med Assoc. 2003; 95:152-166. Santos, A., Chapman, M., Aalberse, R., Vailes, L., Ferriani, V., Oliver, C.,Rizzo, M., Naspitz, C., Arruda L. 1999. Cockroach allergens and asthma in Brazil: Identification of tropomyosin as a major allergen with potential cross-reactivity with mite and shrimp allergens. Journal of Allergy and Clinical Immunology, 104, pp. 329-37. Shirai, T., Matsui, T., Suzuki, K., Chida, K., 2005. Effect of pet removal on pet allergic asthma. Chest, 127 (5), pp.1565–1571. Smith, B.J., Nitschke, M., Pilotto, L.S., Ruggin. R.E., Pisaniello, D.L., Willson, K.J., 2000 Health effects of daily indoor nitrogen dioxide exposure in people with asthma. European Respiratory Journal, 6(5):879–885. Savov, J.D., Whitehead, G.S., Wang, J., Liao, G., Usuka, J., Peltz, G., Foster, W.M., Schwartz, D.A. 2004 Ozone-induced acute pulmonary injury in inbred mouse strains. American Journal of Respiratory Cell and Molecular Biology, 31: 69–77 Romieu, I., Ramirez-Aguilar, M., Sienra-Monge, J.J., Moreno-Macias, H., del Rio-Navarro, B.E., David, G., Marzec, J., Hernandez-Avila , M., London S. 2006 GSTM1 and GSTP1 and respiratory health in asthmatic children exposed to ozone. European Respiratory Journal 28:953–959. Yang, I.A., Holz, O., Jorres, R.A., Magnussen, H., Barton, S.J., Rodriguez, S., Cakebread, J.A., Holloway, J.W., Holgate, S.T., 2005 Association of tumor necrosis factor-alpha polymorphisms and ozone-induced change in lung function. American Journal of Respiratory and Critical Care Medicine 171:171–176. Sporik, R., Holgate, S.T., Platts-Mills, T.A., Cogswell, J.J., 1990. Exposure to house-dust mite allergen (Der p I) and the development of asthma in childhood. A prospective study. The New England Journal of Medicine ,323(8), pp.502–507. Tarlo, S.M.,2003.Workplace irritant exposures: do they produce true occupational asthma? Annals of Allergy Asthma and Immunology, 90(suppl 2), pp.19–23. Tarlo, S.M., Liss, G.M., 2003. Occupational asthma: an approach to diagnosis and management. Canadian Medical Association Journal, 168(7), pp.867- 871 Taylor, P.E., Flanagan, R.C., Valenta, R., Glovsky, M.M., 2002. Release of allergens as respirable aerosol: a link between grass pollen and asthma. Journal of Allergy and Clinical Immunology, 109, pp.51-56. Wallace, L.A., Mitchell, H., O’Connor G.T., Neas, L., Lippmann, M., Kattan M., Koenig, J., et al., 2003. Particle concentrations in inner-city homes of children with asthma: the effect of smoking, cooking, and outdoor pollution. Environmental Health Perspectives, 111(9), pp.1265–1272. Read More
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