Exposure and Health Effects of Air Pollution - Coursework Example

Air Pollution Introduction Air pollution is associated with adverse health effects. These health effects have been linked to both particulate and gaseous components of air pollution, and to both acute and chronic exposure. To monitor and improve the air quality environmental agencies have been conducting comprehensive air-pollution monitoring and modeling over the last decades. Although these monitoring have helped to identify the potential unhealthy levels of air quality at specific areas, and the air quality in general has been improved for the past few years, air quality in some areas (such as Houston) fails to meet the Clean Air Act goal (Heidi et al., 2 - 20). More importantly, there were very few public agencies and academic institutions tracking environmental health effects caused by air pollution on a regional scale. This lack of regional-scale environmental health monitoring and studies has raised the concern and awareness of both regional municipal administrations and the general public in recent years. A fundamental assessment of air pollution and related adverse health effects is needed. Exposure and Health Effects of Air Pollution Air pollution is a complex mixture of particles and gases that can vary in composition depending on geographic location, season, and time of day. In urban settings it consists primarily of particulate matter derived from motor vehicle and industrial emissions, primary gaseous pollutants such as sulphur dioxide, carbon monoxide, and the secondary pollutants nitrogen dioxide and ozone (Pope, III and Dockery 709 - 710). Respirable particles are generally classified by aerodynamic diameter and fall into three main modes: a nucleation mode (smaller than 0.1 μm); an accumulation mode (between 0.1 μm and 1 μm); and a coarse mode (larger than 1 μm) (Pope, III and Dockery 709 - 742). Current regulations of particulate matter set limits for the allowable mass of particles per cubic meter below a certain aerodynamic diameter. Hence, a limit for PM10 refers to particulate matter with aerodynamic diameters less than 10 μm, The larger particles account for the greatest proportion of ambient particle mass; however, fine and ultra fine particles are present in much higher numbers and present a greater total surface area per unit of mass to carry reactive co-pollutants and interact with cellular targets. Particle size will determine the probability of deposition in different regions of the airways and may impact on clearance dynamics and physiologic responses. Compared to larger particles, fine and ultra fine particles are more likely to deposit in the gas-exchange regions of the lungs, and may not be as readily phagocytosed as larger particles. In addition to size, the inherent toxicity of particles may relate to their composition, with metals in particular being associated with toxicity (Pope, III and Dockery 709 - 742). For air pollution exposure studies, the most prevalent air pollutants are ozone (O3), particulate matter (PM), nitrogen oxide (NOx), and the usual diseases under study have included respiratory and cardiovascular disorders. PMIO can increase susceptibility to respiratory infectious diseases and exacerbate asthma and chronic obstructive pulmonary diseases (COPD) (Stephania et al. 810 - 817). PM and Ozone are also associated with cough, premature death, bronchitis, and decline in lung function. Ozone promotes asthma and causes respiratory illness, especially among children (At a Glance 1-4, Stephania et al. 810 - 817). Although immunological, developmental, and reproductive effects are also mentioned in some papers, such studies are not as common as those examining respiratory or cardiovascular effects (At a Glance 1 - 4, Stephania et al. 810 - 817). Initial epidemiologic studies focused on health effects in the days following periods of severe air pollution. Episodes of extremely high air pollution such as the Meuse Valley Fog of 1930 and the London Fog of 1952 were associated with substantial increases in cardiopulmonary morbidity and mortality, and subsequent regulatory controls were implemented primarily to reduce or eliminate the occurrence of such episodes (cited in Pope, III and Dockery 709 - 742). It was not until the early 1990s that studies began to emerge showing apparent health effects at substantially lower levels commonly experienced in urban settings. In a cohort study that followed over 8000 adults in six American cities for a period of 14-16 years (referred to as the Harvard Six Cities study), researchers found a 26% difference in the mortality rate between the most and least polluted cities, of which cardiovascular disease accounted for the largest category of excess deaths. Another study that used data collected on over 500000 adults (as part ofthe American Cancer Society (ACS) Cancer Prevention II project) found that a 10 μg/m3 increase in annual PM2.5 was associated with a 4 % increase in cardiopulmonary mortality. These studies, among others (cited in Pope, III and Dockery 709 - 742), indicate that long-term exposure to air pollution at ambient levels increases the risk of mortality. Short-term effects of air pollution exposure have also been detected. Analysis of pollutant levels and mortality in eight Canadian cities revealed an association between gaseous and particulate pollutants and fluctuations in daily mortality rates (Burnett et al., cited in Pope, III and Dockery 709 - 742). In a study involving 50 million people in the 20 largest cities in the United States from 1987 to 1994, daily variations of PM10, and to a lesser extent ozone, were associated with increased mortality due to cardiovascular and respiratory disease (Samet et al., cited in Pope, III and Dockery 709 - 742). Numerous other studies have reported similar effects of acute and chronic exposure (for example, reviewed by Pope, III and Dockery 709 - 742), substantiating the notion that air pollution causes increased morbidity and mortality. Although the relative risk for respiratory effects is often higher, cardiovascular morbidity and mortality associated with air pollution is greater due to the larger population at risk. Indeed, a recent epidemiologic study found that air pollution is associated with twice as many deaths from cardiovascular disease compared to cancer and respiratory disease (Pope, III and Dockery 709 - 742). Particulate matter has been the pollutant most commonly associated with cardiovascular effects. Analysis of time series data by the United Kingdom Department of Health produced an estimate that a 10 μg/m3 reduction in PM10 would result in a 0.8 % reduction in cardiovascular admissions (Anderson et al., cited in Pope, III and Dockery 709 - 742). This argument has been substantiated by population studies in which levels of a major pollutant have been reduced. For example, a ban on coal sales that reduced the concentration of black smoke by 35.6 μg/m3 was associated with a 10.3% decrease in cardiovascular mortality in Dublin, Ireland (Clancy et aI., cited in Pope, III and Dockery 709 - 742). A recent evaluation of the Harvard Six Cities cohort that extended the period of analysis for an additional eight years found that reductions of particulate matter levels over this period were associated with reduced risk of mortality (Laden et al. 667-672). Confounders of Air Pollution For confounders, the exposure to ozone critically affects infants, children, and persons with asthma, elderly, those who have adverse pre-conditions, or are smokers (Birnbaum and Jung 814- 822; Stephania et al. 810- 817). Confounders, however, are not restricted to age, gender, pre-condition, and life styles. In recent years, many organizations and studies have related the gradients of health effects caused by air pollution to population of low socio-economic status (SES) such as low-income population or racial minority. Research of this kind is labeled health disparity studies. A comprehensive discussion about theory and methodology of this inclusive view was written by ONeill et al. In the primer, they pointed out that race/ethnicity and SES have been shown to have different effects on health and thus the distinction between race/ethnicity and SES are important in research design (Soto-Martinez and Sly, 173-186; Birnbaum and Jung 814 - 822). Population at risk The most common theory of health disparity, especially related to air pollution, is environmental risk exposure, which attributes the health disparity between racial or SES underprivileged groups and middle class white population to the disproportionate exposure to the environmental pollution carried by the racial or SES underprivileged population (Evans and Kantrowitz 2002). Several large-scaled cohort studies demonstrated that there were increasing risks of chronic exposure to air pollution and higher mortalities among lower educational attainment population (cited in Pope, III and Dockery 709 - 742). Another health disparity theory is related to susceptibility (ONeill et at cited in Pope, III and Dockery 709 - 742). Susceptibility is determined by the SES related intrinsic and some extrinsic confounders. Among the confounders, indoor air condition, poor access to nutrition and health care, lifestyle choices such as smoking, and psychosomatic factors cause the air pollution health disparity consequences. Application of GIS Geographical Information Science (GI Science) has been used increasingly to map and explore environment and health issues due to its great potential to help understand the spatial and temporal relationship among pollution, health, and socio­economic variables. Most researchers in environmental and health areas adopted GIS (Geographical Information System) as an advanced exploratory data analysis tool (Aguilera et al. 1322). On the other hand, GI Scientists have called attention to an interdisciplinary advancement from scholars of both physical and social sciences to advance the theories of analysis in spatial statistics, geostatistics, spatial econometrics, time-space modeling, geo-computation algorithms, and visualization. GI science and geostatistics can be used to explore the spatial pattern of disease and ozone, and then to employ spatial statistics to investigate the relationship between the spatial patterns of disease and ozone, and between disease and SES variables. Conclusion Ozone and PM10 are major contributor to photochemical smog, which is the major risk factor for respiratory and cardiovascular diseases. Individuals exposed to unhealthy ozone and particulate matter levels may be subject to cardiovascular and respiratory diseases such as asthma attack, neurophilic inflammation, and chronic obstructive pulmonary disease (COPD). Previous studies have indicated that long-term exposure to air pollution at ambient levels increases the risk of mortality. Furthermore, literature reviewed in this paper also identified that most of those whose health condition is affected by low quality air levels are from low-income or minority groups. These discoveries contribute to the etiological factors, temporal association, and the confounded factors, i.e. SES, of the health effects of ozone. Place, time, and populations are three crucial elements that are concerned by general public as well as policy makers when dealing with public health prevention and environmental policy. In order to fully understand the health effect caused by air pollution, a regional ecological study focusing on the spatial association among air quality levels, health effects, and SES is needed. Work Cited "At a Glance." Environmental Health Perspectives  118.9 (2010): A374, , 4 pgs. ProQuest Health and Medical Complete, ProQuest. Web.  26 Oct. 2011. Aguilera, Inmaculada, Guxens, Mònica Garcia-Esteban, Raquel., Teresa Corbella, Mark J. Nieuwenhuijsen, Carles M. Foradada, and Jordi Sunyer. “Association between GIS-Based Exposure to Urban Air Pollution during Pregnancy and Birth Weight in the INMA Sabadell Cohort.” Environ Health Perspect. 2009 August; 117(8): 1322–1327. Birnbaum, L., and P. Jung. "From Endocrine Disruptors To Nanomaterials: Advancing Our Understanding Of Environmental Health To Protect Public Health. " Health Affairs  30.5 (2011): 814-822.  Heidi L. Bethel, et al. (2008). A Closer Look at Air Pollution in Houston: Identifying Priority Health Risks A summary of the Report of the Mayor’s Task Force on the Health Effects of Air Pollution, Mayor’s Task Force. EPA Internship Program. Kristin A. Miller, David S. Siscovick, Lianne Sheppard, Kristen Shepherd, Jeffrey H. Sullivan, Garnet L. Anderson, and Joel D. Kaufman, “Long-Term Exposure to Air Pollution and Incidence of Cardiovascular Events in Women.” N Engl J Med 2007; 356:447-458 Laden, F.; Schwartz, J.; Speizer, F.E.; “Dockery D.W. Reduction in Fine Particulate Air Pollution and Mortality: Extended Follow-Up of the Harvard Six Cities Study.” Am. J. Respir. Crit. Care Med. 2006, 173, 667-672. Pope III, C.A. and Dockery D.W. “Health Effects of Fine Particulate Air Pollution: Lines that Connect.” J. Air Waste Manage. Assoc. 56 (2006): 709 – 742. Soto-Martinez, M., and P. Sly. "Review Series: What goes around, comes around: childhood influences on later lung health?: Relationship between environmental exposures in children and adult lung disease: The case for outdoor exposures. Chronic Respiratory Disease  7.3 (2010): 173-186.  Stephania A Cormier, Slawo Lomnicki, Wayne Backes, and Barry Dellinger. "Origin and Health Impacts of Emissions of Toxic By-Products and Fine Particles from Combustion and Thermal Treatment of Hazardous Wastes and Materials" Environmental Health Perspectives  114.6 (2006): 810-817.  Read More