What About Air Pollution?
Special Climate of Colorado
What is Air Pollution?
What Are the Health Effects of Air Pollution?
Are Certain Populations More at Risk?
What About Cigarette Smoke (Active) and Its Adverse Health Effects?
What About Cigarette Smoke (Passive) and Its Adverse Health Effects?
What About Particulate Matter Its Adverse Health Effects?
What About Ozone and Its Adverse Health Effects?
What About Nitrogen Dioxide and Its Adverse Health Effects?
References
Special Climate of Colorado
Colorado's semi arid climate and average of 300 days of sunshine per year leads to:
- high natural dust concentrations in the inhalable (15 mm) and respirable (2.5 mm) particle size ranges,
- rapid photochemical transformations of primary pollution gases, and
- less wet deposition and cleansing of the atmosphere by rain and snow.
Moreover, because ventilation is increased at high altitudes, residents of Colorado may inhale an increased amount of air pollution. Denver sits in a river basin that is bordered on the west by the Continental Divide and on the north and south by lower mountain ranges. Due to its geography, the city experiences frequent temperature inversions. Temperature inversions occur when warm air forms a cap above cool, stable air. In Denver, these inversions trap pollutants nearer the ground, approximately level with skyscrapers. Therefore, during these frequent wintertime thermal inversions, the metropolitan area encounters elevated pollution concentrations and human exposures near the ground.
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What is air pollution?
Air pollution is a concentration of substances in excess of our ecological system's natural capacity to recycle waste.
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What are the health effects of air pollution?
Common adverse health effects of air pollution are increased irritation of the respiratory tract, chronic cough, chest tightness, decreased pulmonary function, and increased vulnerability to allergens and other immune system challenges. Individual air pollutants, such as particulate matter, are characteristically associated with various specific adverse health effects.
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Are certain populations more at risk?
Researchers are especially concerned about the adverse health effects of certain subpopulations. In particular, many studies are being conducted to determine the extent of air pollution's effect on preadolescent children, the elderly, asthmatics, and persons with chronic obstructive pulmonary disease (COPD).
The effects of air pollution experienced by the elderly are of interest since elder adults may already suffer diminished pulmonary function as a result of degenerative changes in the lungs.
Similarly, children are at greater risk for declining health following exposure to air pollution because their airways are narrower than those of adults. Moreover, children have significantly greater needs for oxygen relative to their size, breathing more rapidly and inhaling more pollutant per pound of body weight than do adults. Finally, children engage more frequently in outdoor activities, where exposure to most air pollutants is greatest and ventilation rates significantly increased over resting rates.
Due to their already compromised respiratory function, individuals with pre-existing respiratory conditions may be more vulnerable to adverse health effects as a result of air pollution than healthy individuals. Asthma is generally characterized by reversible airway obstruction, airway inflammation, and increased airway responsiveness or tendency of the airways to constrict upon exposure to irritants or viral infections. An immunologically mediated inflammatory disease of the airways, asthma is typically distinguished from chronic obstructive pulmonary disease by the reversibility of airway obstruction.
Second only to asthma as being the most common chronic lower respiratory disease, COPD may be either predominantly emphysemic or chronic bronchitic. Persons with emphysemic COPD have reduced single breath diffusing capacity for carbon monoxide while persons with chronic bronchitic COPD have near normal single breath diffusing capacity for carbon monoxide. The hallmark of COPD is the slowing of expiratory airflow measured by spirometric testing, with a persistently low FEV1 (forced expiratory volume or the volume of air a subject can forcibly exhale in the first second following maximal inhalation).
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What about active cigarette smoke?
Smoking a cigarette produces three types of tobacco smoke: mainstream smoke, exhaled mainstream smoke, and sidestream smoke. A smoker directly inhales mainstream smoke through a burning cigarette. Exhaled mainstream smoke is that smoke breathed out by the smoker from his/her lungs. Exhaled mainstream smoke and sidestream smoke—the smoke that drifts from the end of the lit cigarette—is often referred to as environmental tobacco smoke (ETS). Passive smoking, the act of inhaling ETS, will be covered in the section to follow: Passive Cigarette Smoke.
What are the adverse health effects of cigarette smoke?
Cigarette smoke causes air passages to close up, making breathing more difficult. Cigarette smoking is the major cause of chronic obstructive pulmonary disease (COPD) and lung cancer. Inhalation of cigarette smoke decreases the lungs' ability to defend against infection because irritating gases and particles from cigarette smoke slow down the cilia, one of the lungs'
clearance mechanisms. Cigarette smoke causes chronic inflammation in the lungs, leading to chronic bronchitis. It also leads to the destruction of lung tissue that occurs in emphysema by changing the enzyme balance of the lungs.
Moreover, smoking is a significant cause of cardiovascular disease. Nicotine, the addictive component of tobacco, increases heart rate and blood pressure. Smokers experience a threefold to fourfold increase in risk for myocardial infarction, cardiac arrest, and stroke.
What is the mechanism of cigarette’s harmful effects?
Tobacco use exposes smokers to polycyclic aromatic hydrocarbons and heterocyclic amines, compounds that can interfere with the process of cellular replication. The resulting genetic damage and mutations are generally irreversible after several cycles of cell replication. Smoking may also alter the rate of metabolism of hormones and vitamins, making smokers more susceptible to cancer.
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What about passive cigarette smoke (secondhand smoke)?
Of the 4,000 chemicals in secondhand smoke (environmental tobacco smoke) 200 are known poisons and 43 are carcinogens.
What are the adverse health effects of secondhand smoke?
In addition to irritating the eyes, nose, throat and lungs and producing chest discomfort, secondhand smoke causes 3,000 lung cancer deaths per year in persons who do not smoke. Secondhand smoke is also associated with 37,000 heart disease deaths per year.
Exposure to parental smoking is associated with an increased incidence of acute lower respiratory illnesses observed during a child's first two years of life. Similarly, children with asthma exposed to parental smoking experience exacerbations of their disease and adults exposed to ETS at home or in the workplace have a 40-60% increase in risk for asthma.
What’s the mechanism of cigarette smoke related adverse health effects?
Environmental tobacco smoke (ETS) causes coronary heart disease by changing low-density lipoprotein to oxidized low-density lipoprotein. Cigarette smoke has also been shown to increase platelet aggregation and cause endothelial cell damage. The effects of ETS on cardiovascular and platelet function, as well as plaque formation, demonstrate most reliably the relationship between ETS and coronary heart disease.
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What about particulate matter?
Particulate matter is a complex and variable mixture whose sources include motor vehicle emissions, factory and utility smokestacks, residential wood burning, construction activity, mining, agricultural tilling, open burning, wind-blown dust, and fire. Combustion of fossil fuels contributes not only particulate matter to the atmosphere, but also gaseous sulfur oxides and nitrogen oxides which readily undergo chemical reactions to form secondary pollutants, such as photochemical oxidants.
What are the adverse health effects of particulate matter?
Several studies have shown a conclusive relationship between respiratory disease and suspended particulate pollution, including increased prevalence of chronic cough, chest illness, bronchitis, hospital admissions for various respiratory conditions, and decrements in lung function.
Fine particulate matter (particles with diameters <10 mm) is of great concern because of the relative ease with which these particles are inhaled into the lungs. These particulates often contain acid sulfates and trace metals and sometimes elude the respiratory system's defense mechanisms. Within the 10 mm diameter range, larger particles tend to deposit in the tracheobronchial region and smaller ones in the alveolar region, where they may remain for long periods due to the slow mucociliary clearance system of the alveoli.
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What about ozone?
A common air pollutant and major component of smog, ozone is formed by ambient photochemical processes between nitrogen oxides and volatile organic compounds. Common sources of precursor pollutants include automobiles, power plants, fireplaces and barbecues.
What are the adverse health effects of ozone?
Ozone can lower resistance to infection, facilitate sensitization and airway responses to airborne allergens, and act synergistically with airborne acidity to damage deep lung tissue. Additionally, ozone is known to cause such symptoms as chest tightness, painful breathing, cough and shortness of breath, and reversible changes in measures of lung function in sensitive individuals. Some researchers have shown that ozone causes a transient decrease in one such measure, FEV1. Moreover, the existence of cellular and biochemical markers of inflammation and cell injury in airway fluids provides additional evidence of inhaled ozone's affect on individuals.
Asthmatics may be especially sensitive to ozone because two characteristics of asthma, namely airway inflammation and increased nonspecific airway responsiveness, are also common reactions to ozone inhalation. Without affecting baseline pulmonary function, low ozone concentrations found in large urban areas can increase an asthmatic's bronchial responsiveness to allergens. Furthermore, short-term ozone exposure has been proven to sensitize asthmatic adolescents to sub-threshold concentrations of sulfur dioxide, meaning that concentrations of sulfur dioxide which previously were not shown to cause any significant change in pulmonary function were proven to cause significant change in pulmonary function when inhaled after exposure to ozone.
Despite concurrent occurrence of ozone and sulfur dioxide in the atmosphere, researchers believe that sequential exposure to ozone and sulfur dioxide is a realistic situation because peak concentrations of sulfur dioxide occur during minima of ozone concentrations; air pollution components preferentially bond ozone molecules, leaving sulfur dioxide molecules free in the atmosphere.
What is the mechanism of ozone’s harmful effects?
Upon inhalation, ozone reacts with surface mucus and airway epithelium. The result is the appearance of inflammatory cells in the airways, mainly polymorphonuclear leukocytes (a subgroup of white blood cells). Inflammatory cell recruitment also involves the activation of immune cells and airway epithelial cells. Once activated, these cells produce and release cytokines that further stimulate the growth and activation of inflammatory cells. Moreover, significant changes in pulmonary function as a consequence of concurrent sulfur dioxide and ozone exposure may result because airway epithelial permeability increases after ozone exposure.
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What about nitrogen dioxide?
Nitrogen dioxide is one of the more common nitrogen oxides, as nitric oxide is progressively oxidized to nitrogen dioxide in air. Nitrogen dioxide is less reactive than ozone and, because of its low solubility, penetrates to the lung periphery where greater than 60% is deposited. Indoor sources of the pollutant include unvented gas stoves and water heaters, space heaters, and cigarette smoke. The main outdoor sources are emissions from cars and other internal-combustion engines. Less common sources include missile fuels, explosives, and grain fermentation.
What are the adverse health effects of nitrogen dioxide?
Common symptoms following nitrogen dioxide exposure are lung, nose or throat irritation, cough, and an increased susceptibility to respiratory infections. Exposure to nitrogen dioxide is also known to result in increased airway resistance and impairment of normal gas exchange between the blood and lungs in otherwise healthy individuals.
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References
American Lung Association, "Common Lung Hazards," When You Can't Breathe, Nothing Else Matters, 1998.
Anonymous, American Academy of Pediatrics Committee on Environmental Health, "Ambient Air Pollution: Respiratory Hazards to Children," Pediatrics, June 1993, 91 (6):1210-1212.
Anonymous, "Populations at Risk from Particulate Air-Pollution," Morbidity and Mortality Weekly Report, April 29, 1994, 43 (16):290-293.
Balmes, J.R., R.M. Aris, L.L. Chen, C. Scannell, I.B. Tager, W. Finkbeiner, D. Christian, T. Kelly, P.Q. Hearne, R. Ferrando, and B. Welch, "Effects of Ozone on Pulmonary Function and Airway Inflammation in Normal and Potentially Sensitive Human Subjects," Health Effects Institute Research Report, 1997, 78 (1):1-3.
Bauer, U., D. Berg, M. A. Kohn, R.A. Meriwether, R.A. Nickle, "Acute Effects of Nitrogen
Dioxide After Accidental Release," Public Health Reports, 1998, 113:62-70.
Colorado Department of Public Health and Environment, "1996 Colorado Air Quality Data Report," 1996, p. 40.
Committee of the Environmental and Occupational Health Assembly of the American Thoracic Society, "Health Effects of Outdoor Air Pollution," American Journal of Respiratory and Critical Care Medicine, 1996, 153:3-50.
Coultas, D., "Passive Smoking and Risk of Adult Asthma and COPD: An Update," Thorax, 1998, 53:381-387.
Fuhlbrigge, A., S. Weiss, "Domestic Gas Appliances and Lung Disease," Thorax, 1997, 52:S58-62.
Health Effects Institute Research Report, Commentary, 1998, 82 (1):19-20.
Health Effects Institute Research Report, Commentary, 1997, 78 (1):81-84.
Koenig, J.Q., D. S. Covert, Q. S. Hanley, G. Van Belle, and W.E. Pierson, "Prior Exposure to Ozone Potentiates Subsequent Response to Sulfur Dioxide in Adolescent Asthmatic Subjects," American Review of Respiratory Disease, 1990, 141:377-380.
Koren, H.S., "Environmental Risk Factors in Atopic Asthma," International Archive of Allergy and Immunology, 1997, 113:65-68.
Kritz, H., P. Schmid, H. Sinzinger, "Passive Smoking and Cardiovascular Risk," Archives of Internal Medicine, 1995, 155: 1942-1948.
Molfino, N.A., S.C. Wright, I. Katz, S. Tarlo, F. Silverman, P.A. McClean, J.P. Szalai, M. Raizenne, A.S. Slutsky, and N. Zamel, "Effect of Low Concentrations of Ozone on Inhaled Allergen Responses in Asthmatic Subjects," Lancet, 1991, 338:199-203.
Pope, C. Arden III, "Respiratory Hospital Admissions Associated with PM10 Pollution in Utah, Salt Lake, and Cache Valleys," Archives of Environmental Health, 1991, 46:90-97.
Skaar, K.L., J.Y. Tsoh, J.B. McClure, P.M. Cinciripini, K. Friedman, D.W. Wetter, and E.R. Gritz, "An Overview of Research. (Smoking Cessation, Part 1)," Behavioral Medicine, 1997, 23:5-13.
Strachan, P. and D.G. Cook, "Parental Smoking and Childhood Asthma: Longitudinal and Case-Control Studies," Thorax, 1998, 53:204-212.
United States Environmental Protection Agency, "Review of the National Ambient Air Quality Standard for Nitrogen Dioxide," Assessment of Scientific and Technical Information, 1982, EPA-450/5-82-002.
Utell, M. J., and J. M. Samet, "Particulate Air Pollution and Health: New Evidence of an Old Problem,"
Victorian Smoking and Health Program, "Chapter 4: The Health Effects of Passive Smoking," Tobacco in Australia: Facts and Issues, 1995.
[Editorial; Comment], American Review of Respiratory Disease, June 1993, 147 (6 Pt. 1):1334-1335.
http://www.ozemail.com.au/~lynnrowe/Pulmonary/index.html
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