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The Silent Killer: Improving the Understanding of Chagas Disease

Chagas Disease

The protozoan parasite Trypanosoma cruzi was first described by Carlos Chagas after isolation of the organism from the blood of a Brazilian patient in 1909 (Garcia et al., 2015). An estimated 7.5 to 10 million persons are infected with Chagas disease worldwide (Hotez et al., 2008; Hotez et al., 2014). In the United States, the disease is anecdotally referred to as a “silent killer” with a 30% chance of those infected to develop a potentially fatal cardiac disease. According to Cantey et al. (2012), Chagas disease is emerging as a significant public health concern in the United States. Given the proximity of Texas to Latin America, cases imported from highly endemic areas in Latin America would likely occur in Texas. Recent communication from the Centers for Disease Control and Prevention that the bite of blood-sucking triatomine bugs in the subfamily Triatominae also termed “kissing bugs” that transfers the parasites to humans have now been found in 28 states, including California and Pennsylvania. Garcia et al. (2015) argued that despite the numerous publications related to Chagas disease in the southern US and northern regions of Mexico, very little is known about the disease burden from imported and locally acquired T. cruzi infection.There is concern that Chagas disease might be undiagnosed in the US as a result of documented low physician awareness (Stimpert & Montgomery, 2010). While the zoonotic nature of Chagas’ life cycle implies unfeasible eradication; entomological surveillance is and will remain crucial to containing Chagas disease transmission (Tarleton et al., 2007).

While it is considered safe to breastfeed even if the mother has Chagas disease (Centers for disease control and prevention, 2013); people can also become infected through blood transfusion, congenital transmission (from a pregnant woman to her baby), organ transplantation, accidental laboratory exposure and consumption of uncooked food contaminated with feces from infected bugs. If the mother has cracked nipples or blood in the breast milk, it is warranted to pump and discard the milk until the bleeding resolves and the nipples heal  (Centers for disease control and prevention, 2013). The enduring challenge of household reinfestation by locally native vectors as stated by Abad-Franch et al. (2011), horizontal strategies works better when the community takes on a protagonist role. Encouraging vector notification by residents and other simple forms of participation can substantially enhance the effectiveness of surveillance (Abad-Franch et al., 2011). Therefore, control programs in concert with community-based approaches as a strategic asset from inception that requires a timely, professional response to every notification, benefiting from a strengthened focus on community empowerment. According to Schofield (1978), when bug population density is low, vector detection failures are unavoidable. Decision-making will be dependent upon the accurate estimation of infestation rates (World Health Organization, 2002), and imperfect detection can seriously misguide Chagas disease control management program. Continued attentiveness from governmental and health organizations are warranted, as this disease continue to be a globalized public health issue. Improved diagnostic tools, expanded surveillance and increased research funding will be required in maintaining existing effective public health strategies and in preventing the spread of the disease to new areas and populations (Bonney, 2014). To improve outbreak control, and improve Chagas disease response, it is essential to discuss the gaps in the scientific knowledge of the disease. Moreover,  crucial in improving the morbidity in the state of Texas and neighboring states is the recommendation of the needed steps to enhance the understanding of T. cruzi.

References

Abad-Franch, F., Vega, M. C., Rolón, M. S., Santos, W. S., & de Arias, A. R. (2011). Community participation in Chagas disease vector surveillance: systematic review. PLoS Negl Trop Dis, 5(6), e1207.

Bonney, K. M. (2014). Chagas disease in the 21st century: a public health success or an emerging threat?. Parasite, 21, 11.

Cantey, P. T., Stramer, S. L., Townsend, R. L., Kamel, H., Ofafa, K., Todd, C. W., … & Hall, C. (2012). The United States Trypanosoma cruzi Infection Study: evidence for vector‐borne transmission of the parasite that causes Chagas disease among United States blood donors. Transfusion, 52(9), 1922-1930.

Centers for disease control and prevention. (2013). Parasites-American Trypanosomiasis (also known as Chagas Disease). Retrieved 21 July, 2016, from http://www.cdc.gov/parasites/chagas/gen_info/detailed.html

Garcia, M. N., Woc-Colburn, L., Aguilar, D., Hotez, P. J., & Murray, K. O. (2015). Historical perspectives on the epidemiology of human chagas disease in Texas and recommendations for enhanced understanding of clinical chagas disease in the Southern United States. PLOS Negl Trop Dis, 9(11), e0003981.

Hotez, P. J., Bottazzi, M. E., Franco-Paredes, C., Ault, S. K., & Periago, M. R. (2008). The neglected tropical diseases of Latin America and the Caribbean: a review of disease burden and distribution and a roadmap for control and elimination. PLoS Negl Trop Dis, 2(9), e300.

Hotez, P. J., Alvarado, M., Basáñez, M. G., Bolliger, I., Bourne, R., Boussinesq, M., … & Carabin, H. (2014). The global burden of disease study 2010: interpretation and implications for the neglected tropical diseases. PLoS Negl Trop Dis, 8(7), e2865.

Schofield, C. J. (1978). A comparison of sampling techniques for domestic populations of Triatominae. Transactions of the Royal Society of Tropical Medicine and Hygiene, 72(5), 449-455.

Stimpert, K. K., & Montgomery, S. P. (2010). Physician awareness of Chagas disease, USA. Emerging infectious diseases, 16(5), 871.

Tarleton, R. L., Reithinger, R., Urbina, J. A., Kitron, U., & Gürtler, R. E. (2007). The challenges of Chagas disease—Grim outlook or glimmer of hope?. PLoS Med, 4(12), e332.

World Health Organization. (2002). Control of Chagas disease: second report of the WHO expert committee.

A Promise to a Dying Brother

When I was inducted into the Honor Society in winter 2013, I thought that being on top of my batch will be enough to get me through my journey as a Public Health Ph.D. candidate. Recruiting a dissertation chair is the most challenging so far, especially getting a response from them. What if I do not get a dissertation chair who will be a good match with my dissertation topic? Can I submit my premise and finish my dissertation to another university? A night before my youngest brother passed away; I was on the phone with him. He told me that he is too tired, and I responded that it is okay to let go. He asked me to promise him to go back to school and take on a graduate degree to make a difference. “Promise me that at some point to be involved in a research project that could make a difference to individuals diagnosed with pancreatic cancer.” He passed away in 2007, a few weeks before his 40th birthday, and three months before his only daughter’s first birthday.

Focusing on the impact of cigarette smoking as a factor that promotes pancreatic cancer rather than initiates it will amplify the importance of behavioral change, and enhance the quality of life. The outcome of pancreatic cancer remains dismal, even with treatment combinations of surgery, radiotherapy and chemotherapy with an estimated annual economic burden of $4.9 billion annually (Pandol, Apte, Wilson, Gukovskaya, and Edderkaoui, 2012). Advances in patient management and understanding the biology of pancreatic cancer has taken substantial progress over the years. Herman, Schulick, Hruban and Goggins (2011) found that screening first-degree relatives of individuals with family members affected by pancreatic cancer can identify non-invasive precursors of the disease. In this 2011 study shows the gradual rise in the incidence and number of deaths caused by pancreatic tumors, even with the decline in incidence and mortality of other common cancers. Furthermore, Vincent et al. found that despite developments in detection and management of pancreatic cancer, only about 4% of patients will live five years after diagnosis. Moreover, Vincent et al. (2011) found that present surgical resectioning offers the only chance of cure and improve the survival rate for those with malignant disease localized to the pancreas. Statistical analysis in 2012 study shows 80–85% of patients with advanced unresectable disease responds poorly to most chemotherapeutic agents. Therefore, it is warranted to have continued understanding of the biological mechanisms contributory to the development and progression of pancreatic tumors. On the other hand, Klein et al. (2004) emphasized the significance of quantification of the risk of individuals with a family history of pancreatic cancer as a rational basis for cancer risk screening and counseling. In a prospective registry-based approach of this 2004 study, the risk of these individuals showed an increased risk of developing the disease. Klein et al. (2004) performed standardized incidence ratios and compared the number of incident pancreatic cancers observed with those expected using Surveillance, Epidemiology and End Results (SEER) rates. It was quantified in this registry-based study the pancreatic cancer risk in kindreds with a family member who was diagnosed with the disease, supporting the hypothesis of increased risk in association with family history. While Blackford et al. (2009) failed to identify the signature tobacco-related mutation in cigarette smokers that could have strong implication to the development of pancreatic cancer; this 2009 study found the nonspecific DNA damage caused by tobacco carcinogens. Furthermore, the combined causality of non-tobacco-related mutagenic risk factors such as inherited predisposition to cancer may share mutagenic properties with the tobacco mutagens active in pancreatic tissues (Ding et al., 2008; Prokopczyk et al., 2002). The types and patterns of these mutations provide insight into the mechanisms by which cigarette smoking causes pancreatic cancer (Blackford et al., 2009). Porta et al. (2009) and Blackford et al. (2009) suggested that smoking enhances the risk for pancreatic cancer through mechanisms other than genetic mutation. The development of pancreatic cancer may have a non-significant association to pipe smoking and smokeless tobacco use, but in a large collaborative pooled analysis of non-cigarette tobacco use in 11 studies within the International Pancreatic Cancer Case-Control Consortium (PanC4) found that cigar smoking is associated with an excess risk of the disease (Bertuccio et al., 2011). Cigarette smoking was found to be an established risk factors— both exposure to environmental tobacco smoke (ETS), and active cigarette smoking (Vrieling et al., 2010). Over 40,000 individuals are diagnosed with pancreatic cancer, and less than 5% of patients diagnosed has a survival rate of five years. The component of the smoke of cigarettes that produced in the body as a metabolite of nicotine and the most abundant carcinogens in tobacco smoke is 4-(methyl nitrosamine)-1-(3-pyridyl)-1-butanone (NNK). Vary widely in nicotine content and carcinogenic nicotine metabolites, cigarettes, cigars, and other tobacco products—nicotine reaches the lungs and is quickly absorbed into the bloodstream during smoking. A cigar containing as many as 20 grams of tobacco can have nicotine between 5.9 and 335.2 mg per gram of tobacco (Henningfield, Fant, Radzius, & Frost, 1999). Prokopczyk et al. (2002) noted that the nicotine levels in pancreatic juice in smokers is seven times higher than non-smokers. Blackford et al. (2009) concluded that smokers diagnosed with pancreatic carcinomas harbors more mutations than the non-smoker, therefore, doubles the risk, accounting for 20 to 25% of pancreatic cancers.

Pandol et al. (2012) stated that the pro-carcinogenic effects of smoking on the pancreas are inadequately studied, confirming that tobacco smoking is the strongest avoidable risk and the major environmental factor for pancreatic cancer. Pandol et al. provided valuable insights into the pathogenesis of pancreatic cancer, particularly in the initiation and progression of the disease. Determining the mechanisms underlying the effect of smoking compounds on fibrosis and inflammation will improve our limited knowledge of pancreatic biology. Pancreatic cancer can be classified as genetic, environmental, or both; as well as a disease caused by inherited DNA mutation or mutation by chance. While advances in Genomics gives the promise to early pancreatic cancer detection through better understanding of pancreatic biology, it is paramount to embrace the significance of lifestyle habits that can be modified to evidence-based healthier concepts that translates to reduced cancer risk. Applying lessons learned from the outcome of my proposed study, and existing body of knowledge will prevent the emergence of pancreatic cancer, reduce cancer risk and advance population health. Early behavioral change and interventions will improve the survival rate and quality of life during the time course of pancreatic cancer progression.

References

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Bertuccio, P., La Vecchia, C., Silverman, D. T., Petersen, G. M., Bracci, P. M., Negri, E., … & Boffetta, P. (2011). Cigar and pipe smoking, smokeless tobacco use and pancreatic cancer: an analysis from the International Pancreatic Cancer Case-Control Consortium (PanC4). Annals of Oncology, mdq613.

Blackford, A., Parmigiani, G., Kensler, T. W., Wolfgang, C., Jones, S., Zhang, X., … & Hruban, R. H. (2009). Genetic mutations associated with cigarette smoking in pancreatic cancer. Cancer research69(8), 3681-3688.

Bosetti, C., Lucenteforte, E., Silverman, D. T., Petersen, G., Bracci, P. M., Ji, B. T., … & La Vecchia, C. (2012). Cigarette smoking and pancreatic cancer: an analysis from the International Pancreatic Cancer Case-Control Consortium (Panc4). Annals of oncology23(7), 1880-1888.

Bouvier, A. M., David, M., Jooste, V., Chauvenet, M., Lepage, C., & Faivre, J. (2010). Rising incidence of pancreatic cancer in France. Pancreas39(8), 1243-1246.

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Chowdhury, P., Doi, R., Tangoku, A., & Rayford, P. L. (1995). Structural and functional changes of rat exocrine pancreas exposed to nicotine. International journal of pancreatology, 18(3), 257-264.

Colby, S. M., Clark, M. A., Rogers, M. L., Ramsey, S., Graham, A. L., Boergers, J., … & Abrams, D. B. (2012). Development and reliability of the lifetime interview on smoking trajectories. Nicotine & Tobacco Research14(3), 290-298.

Colditz, G. A., Wolin, K. Y., & Gehlert, S. (2012). Applying what we know to accelerate cancer prevention. Science translational medicine4(127), 127rv4-127rv4.

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Ding, L., Getz, G., Wheeler, D. A., Mardis, E. R., McLellan, M. D., Cibulskis, K., … & Sawyer, C. S. (2008). Somatic mutations affect key pathways in lung adenocarcinoma. Nature, 455(7216), 1069-1075. Chicago.

Edderkaoui, M., Park, C., Lee, I., Nitsche, C., Gerloff, A., Grippo, P. J., … & Gukovskaya, A. S. (2011, November). Novel model of pancreatic neoplastic lesions induced by smoking compound NNK. In Pancreas (Vol. 40, No. 8, pp. 1321-1321). 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA: LIPPINCOTT WILLIAMS & WILKINS.

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Gould, G. S., Watt, K., Cadet-James, Y., & Clough, A. R. (2015). Using the risk behaviour diagnosis scale to understand Australian Aboriginal smoking—a cross-sectional validation survey in regional New South Wales. Preventive Medicine Reports2, 4-9.

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Henningfield, J. E., Fant, R. V., Radzius, A., & Frost, S. (1999). Nicotine concentration, smoke pH and whole tobacco aqueous pH of some cigar brands and types popular in the United States. Nicotine & Tobacco Research1(2), 163-168.

Hoffmann, D., Hoffmann, I., & El-Bayoumy, K. (2001). The less harmful cigarette: a controversial issue. A tribute to Ernst L. Wynder. Chemical research in toxicology14(7), 767-790.

Hruban, R. H., Iacobuzio-Donahue, C., Wilentz, R. E., Goggins, M., & Kern, S. E. (2000). Molecular pathology of pancreatic cancer. Cancer journal (Sudbury, Mass.)7(4), 251-258.

Institute for Health Metrics and Evaluation. (2015). US County Profile: Dallas County, Texas. 2301 Fifth Ave., Suite 600 Seattle, WA 98121 USA.

Jiao, L., Mitrou, P. N., Reedy, J., Graubard, B. I., Hollenbeck, A. R., Schatzkin, A., & Stolzenberg-Solomon, R. (2009). A combined healthy lifestyle score and risk of pancreatic cancer in a large cohort study. Archives of internal medicine, 169(8), 764-770.

Kadam, P., & Bhalerao, S. (2010). Sample size calculation. International journal of Ayurveda research1(1), 55.

Kirby, A., Gebski, V., & Keech, A. C. (2002). Determining the sample size in a clinical trial. Medical journal of Australia177(5), 256-257.

Klein, A. P., Brune, K. A., Petersen, G. M., Goggins, M., Tersmette, A. C., Offerhaus, G. J. A., … & Hruban, R. H. (2004). Prospective risk of pancreatic cancer in familial pancreatic cancer kindreds. Cancer Research, 64(7), 2634-2638. Chicago

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Labilles, U. (2015). Reevaluating the Impact of Cigarette Smoking on Pancreatic Cancer (Unpublished, Advanced Quantitative Reasoning and Analysis (RSCH – 8250H – 3), 2015 Summer Qtr. Wk11Assgn3LabillesU) Walden University, Minneapolis.

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Dallas’ Renaissance Plan: A Response to the Second Wave of Environmental Justice

Dallas is the seventh largest city in the United States with a population exceeding 1.1 million citizens in the year 2000. Dallas is the fourth largest park system in the United States. The second wave of the environmental justice movement is a concept concerned with urban design, public health, and availability of outdoor physical activities. The upgrade to the 21,526 acres of parkland will amplify the quality of and access to outdoor recreation. The Dallas Park and Recreation Department’s “Renaissance Plan” is a response to  the increased demand of the citizens for new and expanded park facilities, recreation programs, open space areas, and unique recreational amenities. Physical activity is one of the health indicators for Healthy People 2010, and responding to these demands is a step forward of meeting its goals.  Dallas’ wide spectrum of park facilities will provide physical activities that will have positive health outcome to Dallas residents including the low-income population of the Dallas County and contiguous counties. Recognition of environmental exposure affecting economically and politically disadvantaged members of the community gave birth to the first wave of environmental justice movement. In addition to health problems related to environmental exposures, environmental justice (EJ) also cover disparities in physical activity, dietary habits, and obesity among different populations. Disparities on the access of public facilities and resources for physical activity (PA) is an EJ issue that has a negative impact on health among low-income and racial/ethnic minorities (Labilles, 2013). The 2007 cross-sectional study of Taylor et al. suggest an association between disproportionate low access to parks and recreation services (PRS) and other activity-friendly environments in low-income and racial/ethnic minority communities.  The prevalence of lower levels of PA and higher rates of obesity was observed in the minority population, which is a direct outcome of the prevalence of lower levels of PA. These differences violate the fair treatment principle necessary for environmental justice.

The treatment of health conditions associated with physical inactivity such as obesity poses an economic cost of at least $117 billion each year. Physical inactivity contributes to many physical and mental health problems.  The reported 200,000-deaths per year in the US is attributed to physical inactivity, and data from surveillance system indicate that people from some racial/ethnic minority groups experience disproportionately higher rates of chronic diseases associated with physical inactivity. Taylor, Poston, Jones & Kraft (2006) findings, provided preliminary evidence for the hypothesis that socioeconomic status disparities in overweight and obesity are related to differences in environmental characteristics. However, most of the studies had encountered epidemiologic “black box” problem, making it impossible to determine which characteristics of the environment (e.g., density of food service outlets or physical activity resources) may be most important (Labilles, 2013). Ellaway et al. found that body-mass index (BMI), waist circumference, and prevalence of obesity, and greater obesity risk is associated with low area or neighborhood socio-economic status.

References

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Labilles, U. (2013). Environment Matters: The Disproportionate Burden of Environmental Challenges. PUBH 8115-1 Environmental Health Spring Qtr. Minneapolis: Walden University.

Taylor, W., Floyd, M., Whitt-Glover, M. & Brooks, J. (2007).  Environmental Justice: A Framework for Collaboration between the Public Health and Parks and Recreation Fields to Study Disparities in Physical Activity. Journal of Physical Activity & Health, 4, supp 1, s50-s63.

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A Summer Phenomenon

For 26 days in 2011, every place in Texas showed higher concentrations of lung-damaging ozone than allowed by federal air-quality standards, especially in Dallas. The federal standard set in 2008 is 75 parts per billion. The spike in ozone which is particularly a summer phenomenon is exacerbated by trucks carrying drilling materials that emit nitrogen oxides, and natural gas escaping from pipelines or storage tanks that emit volatile organic compounds, or VOCs. Known ozone “precursors” such as nitrogen oxides and VOCs can react with each other to form ozone when aided by sunlight. The most difficult environmental issue North Central Texas face today is air quality. Dallas Forth Worth (DFW) region meets the standard for five of six criteria air pollutants defined by the EPA. The six pollutants are carbon monoxide, lead, nitrogen dioxides, ozone, particulate matter, and sulfur dioxide. The only air pollutant for which DFW do not meet the National Ambient Air Quality Standard is the ozone. In hot summers, combination of nitrogen dioxides and VOCs and concentrations of traffic and industry, Dallas is an ideal incubator for the creation of ground-level ozone.

Discussion

Under the Clean Air Act, ozone pollution has long been regulated because of its tremendous hazards to the public. Under the Clean Air Act, ozone poses tremendous hazards to the public health and the environment. High ozone levels lead to respiratory distress and disorders; decreased lung function; increases in the emergency room visits and sick days. To address the serious problem of ozone, the Clean Air Act provides a multi-step process for ensuring that all areas of the country achieve acceptable ozone levels. EPA establish nationwide air quality standards for ozone (called National Ambient Air Quality Standards), which are required to be strong enough to protect public health with an adequate margin of safety. The next step, EPA designate areas of the country that meet the standards, and those who do not. The last step, requiring states to submit plans for achieving and maintaining compliance with EPA’s ozone standards — with especially strict requirements for areas that currently do not meet the standards. The U.S. Environmental Protection Agency (EPA) updated its ozone air quality standards in March 2008. The EPA towards the end of 2012 promised the DFW residents for stronger protections against the harmful public health and environmental impacts of ground-level ozone. The agency announced on January 7, 2012 about its determination that Wise County, Texas contributes to high ozone levels in nearby Dallas-Fort Worth. This action required polluters in Wise County  to do their fair share to reduce ozone levels in Dallas-Fort Worth. Wise County was included in the DFW ozone designation due in large part to the emissions of nitrogen oxides, and volatile organic compounds from a recent boom in oil and gas production in the area. According to the Technical Support Document (TSD), the final area designations in the Dallas-Fort Worth (DFW) area for the 2008 ozone national ambient air quality standards are based on several factors and indicators. The population density and degree of urbanization were analyzed. TSD stated: EPA evaluated the population and vehicle use characteristics and trends of the area as indicators of the probable location and magnitude of non-point source emissions. These include ozone precursor emissions from on-road and off-road vehicles and engines, consumer products, residential fuel combustion, and consumer services. Areas of dense population or commercial development are an indicator of area source and mobile source NO2 and VOC emissions that may contribute to ozone formation that contributes to nonattainment in the area. Rapid growth in population or vehicle miles traveled (VMT) in a county on the urban perimeter signifies increasing integration with the core urban area and indicates that it may be appropriate to include such perimeter area(s) as part of the nonattainment area.

Conclusion

It is very important to recognize the effect of ozone to a population, especially adults and children who are already had chronic respiratory diseases such as asthma. Exposure may compromise the ability of the body to fight respiratory infections. Bell et al. (2004) a multisite time-series study of 95 large US urban communities throughout a 14-year period  found that widespread pollutant such as ozone adversely affects public health.

References

Area Designations for the 2008 Ozone National Ambient Air … (n.d.). Retrieved from http://www.epa.gov/airquality/ozonepollution/designations/2008standards/documents/R6_DFW_TSD_Final.pdf

Bell, M., McDermott, A., Zeger, S., Samet, J. & Dominici, F. (2004). Ozone and Short-term Mortality in 95 US Urban Communities, 1987-2000. JAMA;292(19):2372-2378. doi:10.1001/jama.292.19.2372.

Dallas Fort-Worth Breathes Easier Following EPA’s Decision … (n.d.). Retrieved from http://blogs.edf.org/energyexchange/2013/01/16/dallas-fort-worth-breathes-easier-following-epas-decision-on-wise-county-ozone-petitions/

Green Dallas…building a greener city! (n.d.). Retrieved from http://www.greendallas.net/air_quality.html

Labilles, U. (2013). Obstacles of Disease Surveillance Interoperability: A Challenge to Public Health. (Unpublished,  PUBH-8115-1/HUMN-8115-1-Soc Behave Cultural Fact in Public Health. 2013 Spring Qtr. WK7Disc) Walden University, Minneapolis.