The Relationship Between Air Pollution And Asthma Amongst City Dwellers


City dwellers have continually suffered disproportionate asthma morbidity regardless of the efforts put in place in the United States to significantly reduce asthma mortality and morbidity. Despite recent studies indicating that many factor are attributed to this phenomenon, city air pollution and indoor environment has been considered the strong contributor to hindrance to asthma control(Middleton, Yiallouros, Nicolaou, Kleanthous, Pipis, Maria, Demokritou, & Koutrakis, 2010). Studies have shown that inner-city dwellers are among the population that have risk of asthma prevalence. This is attributed to air quality and closed environment where fresh air and ventilation is limited to most of the residences. Public health has recognized that city dwellers are exposed to air pollution that elevate asthma prevalence among the residences especially to those residences dwelling and working in overcrowded areas with little ventilation.

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Studies have indicated that air pollution in city environment include dust, smoke from motor vehicles and other allergens such as cockroaches, mice, pets and rats. These allergens triggers chronic and acute symptoms in patients with asthma. Air pollution is a mixture of complex pollutant originating from outdoor air and indoor pollutants generated by activities taking place in the surrounding environment(Middleton, et al., 2010). Empirical evidence in the past studies indicated that most studies have focused on the outdoor air pollutions rather than indoor pollutants. Air pollution is attributed to the increased respiratory symptoms, airway reactivity as well as reducing lung functions. City dwellers are exposed to air pollutions such as asthma morbidity, secondhand cigarette smoke, particulate matter, ozone and nitrogen oxide.

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Particulate matter

            These consists of liquid and solid particulate matter suspended in the air. Activities that increases the emission of particulate matter into the environment in city environment include cooking such as frying food and using stove, cleaning the house through sweeping and dusting the room(Public Health Information Team, 2012). Also, smoking the cigarettes has proved to be the main distributor of indoor particulate matters. Outdoor and indoor air pollution investigations have indicated that increased exhaled nitric oxide thus stimulating airway inflammation. This means that patients with asthma symptoms are exposed to more allergens in this environment. Studies have shown that children are the most affect group in the environment.

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Nitrogen dioxide

In city dwelling environment, the most common sources of nitrogen dioxide include common ambient air pollutant such as high temperature combustions. Indoor and outdoor sources include fireplaces, furnace, space heaters and gas stoves. Studies indicated that nitrogen dioxide elevated asthma symptoms in patients with asthma especially children because it decreases airflow in the airways(Matsui, Hansel, McCormack, Rusher, Breysse, & Diette, 2008). Further studies indicated that continuous exposure to nitrogen dioxide is attributed to wheezing and chest tightness especially those individuals living in multifamily housing units which is common in the urban setting. Also, housing setting is common to people categorized under lower socioeconomic status. In addition, nitrogen dioxide air pollution is concentrated in the urban center because of the use of gas stove.

Secondhand smoke

Secondhand smoke is describe as involuntarily inhaled cigarette smoke composed of gases and particles created through the combustion of additives, paper and tobacco. Studies have indicated that secondhand smoke air pollution exposure is attributed to wheeze illness among the patients with asthma(Matsui, et al., 2008). Parents who regularly smoke cigarettes in presences of their children exposes them to increased symptoms of asthma. Also, exhaust fumes from fuel combustion in urban setting increases the complication of asthma symptoms amongst asthma patients.

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