Paper Outline
Long-term Effects of Harmful Substances on the Respiratory System
Lung cancer and smoking
Smoking triggers asthma
Quit smoking
Motor vehicle emissions and respiratory diseases
COPD, upper respiratory tract infections, respiratory failure, asthma
Use of non-fossil fuels to prevent automotive pollution
Asbestos as an occupational hazard
Causes asbestosis, lung cancer and pleural abnormalities
Asbestos should be banned
Long-term Effects of Harmful Substances on the Respiratory System
Introduction
The respiratory system is prone to harm that may result from hazardous substances that may be contained in the air. These harmful substances may come naturally from the environment, out of a polluted environment, due to risky lifestyles as well as in the form of occupational hazards. Exposure to hazardous substances such as asbestos, smoke (from tobacco or marijuana) and automotive exhaust may result into severe long-term effects on the respiratory system. Some of the long term effects include lung cancer, tuberculosis, respiratory failure, asthma and asbestosis.
Lifestyle, Environmental and Occupational Hazards
According to the National Cancer Institute (2010), smoking predisposes individuals to lung cancer which leads to many deaths. For instance, 90% of deaths resulting from lung cancer in the United States are due to smoking. This is regardless of whether one is exposed to direct or passive smoke. The smoke may be from cigarettes or from marijuana. In addition to increased risk of developing lung cancer, exposure to smoke increases the risk of developing cancer of the mouth cancer of the pharynx, cancer of the larynx as well as cancer of the throat. The National Cancer Institute (2010) also cites that smoking increases the risk of developing chronic obstructive lung disease which is mainly characterized by emphysema and bronchitis. The risk of developing these respiratory conditions increases is proportion to severity of exposure to smoke. The Cancer Research UK (2009) mentions that “smoking is the single biggest cause of cancer in the world” (para 1) and the survival rates of lung cancer are very low. Smoke from tobacco is also known to trigger asthma as irritant substances from smoke occupy the epithelium of the airways. Good enough, lung cancer emanating from exposure to smoke can be prevented by quitting smoking and avoiding exposure to passive smoke.
Exposure to emissions from motor vehicles puts one to the risk of developing a variety of respiratory conditions including asthma, upper respiratory tract infection and chronic obstructive pulmonary disease (COPD). Exposure to particulate matter from motor vehicle emissions is common among urban dwellers especially persons who are in streets that are busy with motor vehicles. Buckeridge et al. (2002) have confirmed that exposure to particulate matter (PM2.5) increases the risk of hospitalization from COPD, upper respiratory tract infection and asthma. This is according to a study conducted in a busy urban area in Southeast Toronto. The risk of developing the respiratory conditions is higher in busy urban streets because the concentration of PM2.5 is up to 30 times higher compared to background concentrations. Other than particulate matter, vehicle emissions can also be in form of benzene, nitrogen dioxide, lead and sulphur dioxide. Benzene has the capacity to cause respiratory failure, nitrogen dioxide fumes usually leads to pulmonary edema as well as pneumonia whereas sulfur dioxide causes damage to upper respiratory tract due to irritation. Aromatic hydrocarbons from vehicle exhaust lead to occupational asthma as they increase hypersensitivity in the respiratory system (Weiss, 1978).
Respiratory conditions arising due to exposure to automotive exhausts can be reduced by cutting down the vehicle emissions. This is achievable through the use of vehicles that do not depend on fossil fuels. In addition, use of non-pollutant means of transport such as bicycles can go a long way in reducing automotive exhausts while interfering with transport minimally.
Among the most hazardous occupational substances that severely affects the respiratory system is asbestos. The main source of occupational exposure to asbestos is asbestos cement thus workers in such cement mines have an increased risk of developing asbestos-related respiratory conditions. When asbestos fibers are inhaled, there is increased risk of developing parenchymal asbestosis, lung cancer, pleural thickening, mesothelioma, bronchial asthma, pulmonary tuberculosis and allergic rhinitis among other common respiratory diseases (ASTDR, 2007).
Parenchymal asbestosis usually presents at approximately 20 to 40 years after exposure to asbestos fibbers but it may develop earlier if exposures were high. Respiratory failure may occur as a result of severe asbestosis and the ultimate end is death. Some pleural abnormalities are also known to result to exposure to asbestos. For instance, pleural plaques appear 20 to 30 years after exposure, pleural effusions occur after about 10 years and diffuse pleural thickening appear after about 15 years. Rounded atelectasis is also common although it depends on levels of occupational exposure. Lung carcinoma occurs after about 20 to 30 years whereas pleural mesothelioma appears between 10 and 57 years after exposure (ASTDR, 2007). A complete ban on the use of asbestos should be enacted by governments to prevent its hazards and options such as fire bricks should substitute asbestos.
Conclusion
The respiratory system is prone to various diseases due to exposure to occupational, environmental and lifestyle-related hazards. Smoking increases the risk of lung cancer and cancer of the pharynx among others as well as triggering asthma. Automotive exhausts cause upper respiratory tract infections and COPD among other diseases whereas asbestos fibers cause lung carcinoma and asbestosis among other pleural abnormalities. The risk of lung cancer due to smoking can be minimized by quitting smoking, automotive exhausts can be reduced through use of non-fossil fuels while asbestos should be banned to prevent the adverse respiratory system effects thereof.
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