Pediatric Annals

CME Article 

Origins of Outcome Disparities in Pediatric Respiratory Disease

Kimberly Danieli Watts, MD, MS; Michael S. Schechter, MD, MPH

Abstract

Respiratory diseases account for a significant portion of morbidity and mortality in pediatric medicine, but this burden is not evenly distributed across the population. In asthma and cystic fibrosis, low socioeconomic status (SES) and minority status have been associated with worse outcomes.1–3 Understanding the origins of these disparities may allow the development of interventions that will improve outcomes and reduce health inequality.

Abstract

Respiratory diseases account for a significant portion of morbidity and mortality in pediatric medicine, but this burden is not evenly distributed across the population. In asthma and cystic fibrosis, low socioeconomic status (SES) and minority status have been associated with worse outcomes.1–3 Understanding the origins of these disparities may allow the development of interventions that will improve outcomes and reduce health inequality.

Kimberly Danieli Watts, MD, MS, is Instructor, Pediatrics, Northwestern University Feinberg School of Medicine; and Attending, Pulmonary Medicine, Children’s Memorial Hospital, Chicago, IL. Michael S. Schechter, MD, MPH, is Associate Professor with Department of Pediatrics Children’s Healthcare of Atlanta, Division of Pulmonary, Allergy/Immunology, Cystic Fibrosis and Sleep, Emory University School of Medicine, Department of Environmental Health, Rollins School of Public Health.

Dr. Watts and Dr. Schechter have disclosed no relevant financial relationships.

Address correspondence to: Kimberly Danieli Watts, MD, MS, 2300 Children’s Plaza, Box #43, Chicago, IL 60614; fax: 773-880-6300; or e-mail: kwatts@childrensmemorial.org.

Respiratory diseases account for a significant portion of morbidity and mortality in pediatric medicine, but this burden is not evenly distributed across the population. In asthma and cystic fibrosis, low socioeconomic status (SES) and minority status have been associated with worse outcomes.1–3 Understanding the origins of these disparities may allow the development of interventions that will improve outcomes and reduce health inequality.

Disparities in health outcomes are not unique to pediatrics or to respiratory medicine. Research has shown that many facets of health care are affected by SES, such as immunization rates, emergency room use, and the incidence of cancer and obesity.4,5 Low SES is often the most influential risk factor for poor health outcomes in acute or chronic disease. SES is made up of a number of factors and has no single ideal measure.

Different components affect health in different ways (eg, family income affects financial resources; maternal education influences disease self-management abilities). However, information on these characteristics may not be available in secondary data sources, leading to the use of proxy measures, such as insurance status and median income by ZIP code. It is important to recognize that these gross proxy measures may overlook the key underlying factors that cause worse outcomes.

A comprehensive approach to examining health disparities requires an appreciation and understanding of how environmental factors interact with molecular and genetic factors. Environmental influences include not only the physical environment in which a patient lives (ie, built environment), but also factors beyond their physical health, such as family income, cultural influences, access, literacy, and community. Less studied but emerging explanations for disparate health outcomes are the molecular influences, including genetic variability, inflammatory profiles, and genetic predispositions. Recognition that outcome disparities are multifactorial and the interplay of these factors is crucial to finding strategies for reduction.

This article reviews health disparities literature for two important respiratory diseases in pediatrics: asthma and cystic fibrosis. Asthma is a heterogeneous multifactorial genetic disease with no single etiology and multiple factors affecting outcomes. Cystic fibrosis is a classic Mendelian disease not caused by a single gene defect but by a range of outcomes largely independent of that specific gene defect exist. A review of these diseases can help pediatricians to understand which factors affect outcomes, to study those in a given population, and to set a framework for further interventional studies.

Asthma

Defining the Disparity

According to the most recent summary health statistics for children in the US, more than 10 million US children 17 years and younger have ever been diagnosed with asthma, and 7.1 million children are asthmatic. Non-Hispanic black children are more likely to have been diagnosed with asthma (22%) compared with Hispanic children (13%) or non-Hispanic white children (12%).

Children living in poverty are more likely to have been diagnosed with asthma (18%) or to still have asthma (14%) than children in families who were not poor (13% and 8%).1 Childhood asthma has long-term effects on general health status, including increased rate of obesity and more missed days of work/school as an adult.6 Therefore, minimizing disparities and improving outcomes can leave lasting effects from both a medical and economic perspective.

Cause of Disparities Access to Care and Health Services

The burden of asthma can be measured by many variables, including level of control, quality of life, severity of illness, and hospitalization rates. In a recent study examining the effects of socioeconomic factors on level of control in a community-based pediatric cohort, Medicaid insurance was an independent predictor of poor control. In this cohort, having another sibling with asthma and also maternal work outside the home were also associated with poorer outcomes. Lack of consistent use of asthma guidelines occurs more often in low-income communities and leads to increased symptoms and worse control.7

Asthmatic black and Hispanic children use emergency departments and are hospitalized more often than white children.5 Those with lower income use the emergency department or urgent-care facilities as the primary means of obtaining medical attention for a child’s asthma symptoms more often.

A recent study by Flores et al. further shows that race/ethnicity is an independent risk factor for the use of urgent care, even after adjusting for insurance, symptom severity, and socioeconomic factors. This use of an urgent-care model for asthma underscores the lack of medical home and necessary follow-up for low SES patients. Lack of an asthma care specialist and an asthma action care plan have been associated with higher rates of acute asthma exacerbation.8

Access to treatment, however, includes more than access to a medical professional. A patient or family’s ability to obtain prescribed treatment is an important component of self-management. This financial burden may cause low-income families to choose between medications and other basic living needs, leading to possible gaps in medical management. Access to health care services may also be limited in obtaining appropriate testing and diagnostics in a timely manner. Assessment and testing for allergic triggers and the use of environmental control practices occur less often in low- and middle-income households and in minority children.9

Self-Management and Literacy

Poor perception of asthma symptoms increases morbidity and mortality in asthma. A study of the association between ethnicity and perception in asthma was performed using home peak flow and spirometry measures. Latino children were less accurate than non-Latino children in estimating their pulmonary function.10

Increasing asthma knowledge and addressing literacy gaps are important factors in reducing health disparities in asthma. Low literacy among parents of asthmatic children is associated with more severe asthma in the children and increased use of rescue medication.11 The ability to understand and interpret information is directly affected by the communication between patient and health care provider. Poor provider–patient communication has been shown to contribute to health care disparities in minority populations with asthma.12 By providing interventions aimed at increasing literacy and education for asthma, the additional benefit of increasing reading level and self-efficacy in inner-city children has been demonstrated.13

Environmental Exposures

Indoor and outdoor environments influence asthma outcomes. Lower SES households are at risk for an increased rate of exposure to indoor and outdoor allergens that can trigger asthma. Exposure to air pollution is associated with increased severity of asthma in children.

Studies show that “pockets” of asthma, or small geographic areas with very high asthma rates, can be identified in urban areas. Within these areas of high risk, locally generated air pollution influences asthma severity and hospitalization encounters.14 Children who live in census tracts facing intersections with major highways or railroads also have an increased risk of asthma.15 The school environment also plays an important role in childhood exposures. Schools and homes with higher rates of water leaks, mold, and pest infestations, especially cockroaches, have higher than average asthma rates.16

Having at-risk communities gain understanding of air quality, use the Air Quality Index, and advocate for improved conditions are important targets for improving outcomes.

Stress

Environmental influences are not limited to outdoor exposures and indoor allergens. Exposure to violence, crime, and chronic psychosocial stressors also influence asthma prevalence and outcomes.17–19 Interparental conflict and lifetime exposure to violence were found to be associated with decreased lung function in an innercity cohort of children independent of socioeconomic status, tobacco smoke exposure, and birth weight.20 Comprehensive asthma management programs in the patient’s community or in familiar settings can promote wellness and include structured programs focusing on asthma controller therapy, asthma-specific education, and periodic assessment of asthma control.21

Genetic Factors

An understanding of health disparities in asthma is expanded by investigation into the interaction between environmental and molecular factors. Genome-wide transcriptional profiles have demonstrated an over-expression of genes regulating the inflammatory process in children from low socioeconomic backgrounds.22 This finding is supported by a study that found increased production of inflammatory cytokines and eosinophils in lower SES children.23 Similar influences on inflammatory state have been found in the perinatal period. Higher cord blood IgE levels are associated with lower SES. Higher prenatal stress has also been associated with increased IL-8, TNF-alpha, and IL-13 levels.19 Further study is needed into the pathway between heightened inflammatory state and SES.

In the US and throughout the world, poverty and low SES disproportionately affect minority populations. In addition, polymorphisms in the human genome cluster with race and ethnicity and are associated with asthma risk. Asthma susceptibility has been linked to genes involved in the inflammatory cascade, and certain variants associated with increased risk of asthma have been found in the Latino population.24 For blacks, single nucleotide polymorphisms (SNP) at the IL-4 locus, as well as in the gene encoding for the sphingosine-1-phosphate receptor, are associated with susceptibility to asthma.25,26 Susceptibility to asthma can also be altered by environmental interactions. For example, a polymorphism in the TGF-beta-1 gene is associated with an increased risk of asthma when the subject is exposed to maternal smoking in utero or to traffic-related emissions.27

Outcomes in asthma are also affected by response to treatment. Genetic studies have been performed that show altered response to medications based on ethnicity and race. In patients of Puerto Rican descent, a specific SNP in an enzyme that regulates endogenous bronchodilator response also increases the risk of asthma and yields a lower exogenous bronchodilator response. This lack of response was further altered when genetic variants in beta-2-adrenergic receptor were present in a mixed Mexican and Puerto Rican cohort.28

When examining the IL-6 and IL-6 receptor genes, a gene–gene interaction was noted, resulting in a higher drug response to albuterol in the Hispanic population but a lower response in the black cohort.29 In black children, a combination of four SNP within three potential asthma loci was associated with a 70% predictive value for lack of response to therapy.30

When considering genetic influences of health disparities, it is important to understand that no single polymorphism is likely to explain differential outcomes. The polygenetic nature of asthma makes understanding the origins of disparity particularly challenging. Understanding the interplay between environmental risk factors and molecular differences is imperative to developing interventions to address why certain populations suffer disproportionately from disease.

Cystic Fibrosis

Defining the Disparity

Cystic fibrosis (CF) is a monogenic autosomal recessive disease caused by defects in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Although CF affects far fewer patients than asthma, there is substantial morbidity and mortality associated with the disease. Low SES in CF is associated with worse lung function and an increased annual risk of death, even when other markers of disease severity are taken into account.31

Although the severity of CF is partially correlated with the severity of the CFTR defect, there is marked variability in health outcomes of CF patients with the same CFTR mutation. These differences have been attributed to environmental and genetic variability. As US population demographics change, and with the advent of prenatal maternal screening and newborn screening for CF, the number of Hispanic and black patients with CF will increase. Given the increased rate of poverty in these populations, it is important to understand the interaction of SES, as well as genetic variation.

Cause of the Disparities: Access to Care and Health Services

Care for CF in the US often starts in the newborn period. In CF newborn screening, there is potential for public health disparity. Although CF is universally screened for across the US, newborn protocols differ by state. Choice of diagnostic protocol takes into account the population it serves, as well as logistics and cost.

Depending on the methodology chosen, false negatives can disproportionately affect the minority population. When genetic evaluations of the newborn include a preselected panel of mutations, ethnic and racial minorities with less common mutations may be missed on the initial screen.32 Although processes are in place to minimize false negatives, attention to equity from a public health perspective is important in policy construction.

Treatment complexity and burden is considerable in CF. Although clinic visits are similar for Medicaid and privately insured patients with CF, those who are insured by Medicaid have a significant higher adjusted rate of death, lower lung function, and worse nutritional status. In diseases, such as asthma, access to quality care is a key component in health outcome disparities.

In contrast, it is estimated that more than 85% of CF patients are seen at Cystic Fibrosis Foundation-accredited CF care centers. SES does not seem to reduce access, at least as measured by number of outpatient clinic visits.3 Understanding health outcome disparities in CF requires looking beyond simple access to appropriate health care providers.

Access to a CF center does not necessarily translate into access for health care needs. Even among those patients who attend clinic regularly, the treatment burden of CF can be cost-prohibitive. Cost of prescriptions and significant copays can cause financial strain and breaks in medication administration.

Because nutritional status is so closely linked to outcomes in CF, food availability affects health status. Food scarcity is a concern in low socioeconomic communities and may contribute to why social disadvantage predicts poorer growth outcomes in CF.31

In a recent study by Schechter et al., three indictors of SES (median household income by ZIP code, maternal educational attainment, and state insurance coverage), were evaluated as predictors of health care use and chronic therapy prescription patterns. Disease severity inversely correlated with each marker of SES. However, results differed depending on the indicator used when assessing therapy. Two of three indicators of low SES were associated with increased use of IV antibiotics to treat pulmonary exacerbations, even when adjusting for disease severity. Moreover, in the Medicaid population, more outpatient prescriptions for antibiotics were given, leading to greater therapeutic intervention in the population.33 Because access seems to be unimpaired in those with low SES, understanding how care gets translated from clinic to home is an important target for future studies.

Ethnicity/Race

Ethnicity and race also play an important part in health disparities of CF. A recent study using patient-reported outcomes as measured by a health-related quality-of-life survey found that lower SES was associated with lower health-related quality-of-life scores in CF.

After controlling for disease severity and SES, black and Hispanic patients reported worse emotional and social functioning.34 Hispanic ethnicity has also been found to be an independent risk factor for a steeper rate of decline in lung function and increased mortality in CF.2,35 Latino CF patients are diagnosed earlier and have lower lung function, earlier acquisition of Pseudomonas aeruginosa, and more liver complications when compared with the non-Hispanic CF population.36 These findings suggest a possible genetic component for worse outcomes in the Hispanic CF community, although the effect of cultural differences regarding disease perception and self-management is another plausible explanation.

Environmental Exposures

Poor air quality tends to be clustered around low socioeconomic areas. In CF, exposure to particulate air pollution is associated with an increased risk of pulmonary exacerbation and a decline in lung function.37 Exposure to secondhand smoke also has adverse affects on lung function in CF, with increased rates of smoking reported in low SES patients.38 As with asthma, addressing environmental risk factors is an important component to reduce disparities.

Genetic Factors

There are several ongoing studies investigating the potential role of modifier genes in affecting CF disease outcomes.39 If a certain pattern of genetic variation is found to be associated with clinical risk factors, it is possible, as in asthma, that these cluster in genetically similar populations. As with asthma, gene–environment interaction affects CF lung disease. In CF, the negative effects of second-hand smoke are amplified when a specific polymorphism in transforming growth factor beta is present.38 Further studies of genetic and gene–environment causes of disparities in CF are needed to understand these relationships better.

As strides are made in developing new therapies for CF, including therapies targeted directly to the CFTR defect, representing the underserved in studies and in clinical trials becomes increasingly important. In a study of participation in clinical trials among CF patients, patients with public insurance and those who were non-white were less likely to participate in research.40 The generalizability of any study and the efficacy of new drugs require that a representative population is established in the cohort. Encouraging and educating our most medically vulnerable patients is critical to having them represented as the science moves forward.

Conclusions

Understanding the origins of health disparities in asthma and CF requires a broad view of environmental and molecular influences on outcomes. As these factors are identified, it is important to move past identification and focus on interventions that can change outcomes for patients. Identifying that a patient is at higher risk because of lower SES or a high-risk genotype does not, by itself, help the patient. Tools for education, community involvement, literacy, and environmental safety need to be developed, tested, and disseminated. The basic science of health disparities, including gene-environment interactions, must move forward in a coordinated fashion with these efforts. Moving disparity research forward requires not only using information from the community to fuel research, but rather taking that research, whether it be bench or clinical, back to the community in a meaningful way.

References

  1. Bloom B, Cohen RA, Freeman G. Summary health statistics for U.S. children: National Health Interview Survey, 2008. Vital Health Stat 10. 2009;(244):1–81.
  2. O’Connor GT, Quinton HB, Kahn R, et al. Northern New England Cystic Fibrosis Consortium. Case-mix adjustment for evaluation of mortality in cystic fibrosis. Pediatr Pulmonol. 2002;33(2):99–105. doi:10.1002/ppul.10042 [CrossRef]
  3. Schechter MS, Shelton BJ, Margolis PA, Fitzsimmons SC. The association of socioeconomic status with outcomes in cystic fibrosis patients in the United States. Am J Respir Crit Care Med. 2001;163(6):1331–1337.
  4. Chin MH, Alexander-Young M, Burnet DL. Health care quality-improvement approaches to reducing child health disparities. Pediatrics. 2009Nov;124Suppl 3:S224–S236. doi:10.1542/peds.2009-1100K [CrossRef]
  5. Stingone JA, Claudio L. Disparities in the use of urgent health care services among asthmatic children. Ann Allergy Asthma Immunol. 2006;97(2):244–250. doi:10.1016/S1081-1206(10)60021-X [CrossRef]
  6. Fletcher JM, Green JC, Neidell MJ. Long-term effects of childhood asthma on adult health. J Health Econ. 2010;29(3):377–387. doi:10.1016/j.jhealeco.2010.03.007 [CrossRef]
  7. Bloomberg GR, Banister C, Sterkel R, et al. Socioeconomic, family, and pediatric practice factors that affect level of asthma control. Pediatrics. 2009;123(3):829–835. doi:10.1542/peds.2008-0504 [CrossRef]
  8. Flores G, Snowden-Bridon C, Torres S, et al. Urban minority children with asthma: substantial morbidity, compromised quality and access to specialists, and the importance of poverty and specialty care. J Asthma. 2009;46(4):392–398. doi:10.1080/02770900802712971 [CrossRef]
  9. Stingone JA, Claudio L. Disparities in allergy testing and health outcomes among urban children with asthma. J Allergy Clin Immunol. 2008Oct;122(4):748–753. doi:10.1016/j.jaci.2008.08.001 [CrossRef]
  10. Fritz GK, McQuaid EL, Kopel SJ, et al. Ethnic differences in perception of lung function: a factor in pediatric asthma disparities?Am J Respir Crit Care Med. 2010;182(1):12–18. doi:10.1164/rccm.200906-0836OC [CrossRef]
  11. DeWalt DA, Dilling MH, Rosenthal MS, Pignone MP. Low parental literacy is associated with worse asthma care measures in children. Ambul Pediatr. 2007;7(1):25–31. doi:10.1016/j.ambp.2006.10.001 [CrossRef]
  12. Diette GB, Rand C. The contributing role of health-care communication to health disparities for minority patients with asthma. Chest. 2007;132(5 Suppl):802S–809S. doi:10.1378/chest.07-1909 [CrossRef]
  13. Robinson LD Jr, Calmes DP, Bazargan M. The impact of literacy enhancement on asthma-related outcomes among underserved children. J Natl Med Assoc. 2008;100(8):892–896.
  14. Delfino RJ, Chang J, Wu J, et al. Repeated hospital encounters for asthma in children and exposure to traffic-related air pollution near the home. Ann Allergy Asthma Immunol. 2009;102(2):138–144. doi:10.1016/S1081-1206(10)60244-X [CrossRef]
  15. Juhn YJ, Qin R, Urm S, Katusic S, Vargas-Chanes D. The influence of neighborhood environment on the incidence of childhood asthma: a propensity score approach. J Allergy Clin Immunol. 2010;125(4):838–843.e2. doi:10.1016/j.jaci.2009.12.998 [CrossRef]
  16. Graham T, Zotter J, Camacho M. Who’s sick at school: linking poor school conditions and health disparities for Boston’s children. New Solut. 2009;19(3):355–364.
  17. Gupta RS, Zhang X, Springston EE, et al. The association between community crime and childhood asthma prevalence in Chicago. Ann Allergy Asthma Immunol. 2010;104(4):299–306. doi:10.1016/j.anai.2009.11.047 [CrossRef]
  18. Quinn K, Kaufman JS, Siddiqi A, Yeatts KB. Parent perceptions of neighborhood stressors are associated with general health and child respiratory health among low-income, urban families. J Asthma. 2010;47(3):281–289. doi:10.3109/02770901003605324 [CrossRef]
  19. Wright RJ, Visness CM, Calatroni A, et al. Prenatal maternal stress and cord blood innate and adaptive cytokine responses in an inner-city cohort. Am J Respir Crit Care Med. 2010;182(1):25–33. doi:10.1164/rccm.200904-0637OC [CrossRef]
  20. Suglia SF, Ryan L, Laden F, Dockery DW, Wright RJ. Violence exposure, a chronic psychosocial stressor, and childhood lung function. Psychosom Med. 2008;70(2):160–169. doi:10.1097/PSY.0b013e318160687c [CrossRef]
  21. Clement LT, Jones CA, Cole J. Health disparities in the United States: childhood asthma. Am J Med Sci. 2008;335(4):260–265. doi:10.1097/MAJ.0b013e318169031c [CrossRef]
  22. Chen E, Miller GE, Walker HA, Arevalo JM, Sung CY, Cole SW. Genome-wide transcriptional profiling linked to social class in asthma. Thorax. 2009;64(1):38–43. doi:10.1136/thx.2007.095091 [CrossRef]
  23. Chen E, Hanson MD, Paterson LQ, Griffin MJ, Walker HA, Miller GE. Socioeconomic status and inflammatory processes in childhood asthma: the role of psychological stress. J Allergy Clin Immunol. 2006;117(5):1014–1020. doi:10.1016/j.jaci.2006.01.036 [CrossRef]
  24. Via M, De Giacomo A, Corvol H, et al. Genetics of Asthma in Latino Americans (GALA) Study. The role of LTA4H and ALOX5AP genes in the risk for asthma in Latinos. Clin Exp Allergy. 2010;40(4):582–589.
  25. Haller G, Torgerson DG, Ober C, Thompson EE. Sequencing the IL4 locus in African Americans implicates rare noncoding variants in asthma susceptibility. J Allergy Clin Immunol. 2009;124(6):1204–1209.e9. doi:10.1016/j.jaci.2009.09.013 [CrossRef]
  26. Sun X, Ma SF, Wade MS, Flores C, et al. Functional variants of the sphingosine-1-phosphate receptor 1 gene associate with asthma susceptibility. J Allergy Clin Immunol. 2010;126(2):241–249, 249.e1–e3. doi:10.1016/j.jaci.2010.04.036 [CrossRef]
  27. Salam MT, Gauderman WJ, McConnell R, Lin PC, Gilliland FD. Transforming growth factor-1 C-509T polymorphism, oxidant stress, and early-onset childhood asthma. Am J Respir Crit Care Med. 2007;176(12):1192–1199. doi:10.1164/rccm.200704-561OC [CrossRef]
  28. Choudhry S, Que LG, Yang Z, et al. GSNO reductase and beta2-adrenergic receptor genegene interaction: bronchodilator responsiveness to albuterol. Pharmacogenet Genomics. 2010;20(6):351–358. doi:10.1097/FPC.0b013e328337f992 [CrossRef]
  29. Corvol H, De Giacomo A, Eng C, et al. Genetics of Asthma in Latino Americans (GALA) StudyStudy of African-Americans, Asthma, Genes and Environments (SAGE) Investigators. Genetic ancestry modifies pharmacogenetic gene-gene interaction for asthma. Pharmacogenet Genomics. 2009;19(7):489–496. doi:10.1097/FPC.0b013e32832c440e [CrossRef]
  30. Moore PE, Ryckman KK, Williams SM, Patel N, Summar ML, Sheller JR. Genetic variants of GSNOR and ADRB2 influence response to albuterol in African-American children with severe asthma. Pediatr Pulmonol. 2009;44(7):649–654. doi:10.1002/ppul.21033 [CrossRef]
  31. Balmer DF, Schall JI, Stallings VA. Social disadvantage predicts growth outcomes in preadolescent children with cystic fibrosis. J Cyst Fibros. 2008;7(6):543–550. doi:10.1016/j.jcf.2008.06.004 [CrossRef]
  32. Ross LF. Newborn screening for cystic fibrosis: a lesson in public health disparities. J Pediatr. 2008;153(3):308–313. doi:10.1016/j.jpeds.2008.04.061 [CrossRef]
  33. Schechter MS, McColley SA, Silva S, Haselkorn T, Konstan MW, Wagener JSInvestigators and Coordinators of the Epidemiologic Study of Cystic FibrosisNorth American Scientific Advisory Group for ESCF. Association of socioeconomic status with the use of chronic therapies and healthcare utilization in children with cystic fibrosis. J Pediatr. 2009;155(5):634–639.e1–e4. doi:10.1016/j.jpeds.2009.04.059 [CrossRef]
  34. Quittner AL, Schechter MS, Rasouliyan L, Haselkorn T, Pasta DJ, Wagener JS. Impact of socioeconomic status, race, and ethnicity on quality of life in patients with cystic fibrosis in the United States. Chest. 2010;137(3):642–650. doi:10.1378/chest.09-0345 [CrossRef]
  35. O’Connor GT, Marshall B, Quinton H, et al. Public Reporting of Cystic Fibrosis Outomes: Methods for Case-Mix Adjustment [abstract]. Pediatric Pulmonology - Supplement. 2006;29S:119–120.
  36. Watts KD, Seshadri R, Sullivan C, McColley SA. Increased prevalence of risk factors for morbidity and mortality in the US Hispanic CF population. Pediatr Pulmonol. 2009;44(6):594–601. doi:10.1002/ppul.21037 [CrossRef]
  37. Goss CH, Newsom SA, Schildcrout JS, Sheppard L, Kaufman JD. Effect of ambient air pollution on pulmonary exacerbations and lung function in cystic fibrosis. Am J Respir Crit Care Med. 2004;169(7):816–821. doi:10.1164/rccm.200306-779OC [CrossRef]
  38. Collaco JM, Vanscoy L, Bremer L, et al. Interactions between secondhand smoke and genes that affect cystic fibrosis lung disease. JAMA. 2008Jan30;299(4):417–424. doi:10.1001/jama.299.4.417 [CrossRef]
  39. Drumm ML, Konstan MW, Schluchter MD, et al. Gene Modifier Study Group. Genetic modifiers of lung disease in cystic fibrosis [see comment]. N Engl J Med. 2005;353(14):1443–1453. doi:10.1056/NEJMoa051469 [CrossRef]
  40. Goss CH, Rubenfeld GD, Ramsey BW, Aitken ML. Clinical trial participants compared with nonparticipants in cystic fibrosis. Am J Respir Crit Care Med. 2006;173(1):98–104. doi:10.1164/rccm.200502-273OC [CrossRef]
Authors

Kimberly Danieli Watts, MD, MS, is Instructor, Pediatrics, Northwestern University Feinberg School of Medicine; and Attending, Pulmonary Medicine, Children’s Memorial Hospital, Chicago, IL. Michael S. Schechter, MD, MPH, is Associate Professor with Department of Pediatrics Children’s Healthcare of Atlanta, Division of Pulmonary, Allergy/Immunology, Cystic Fibrosis and Sleep, Emory University School of Medicine, Department of Environmental Health, Rollins School of Public Health.

Dr. Watts and Dr. Schechter have disclosed no relevant financial relationships.

Address correspondence to: Kimberly Danieli Watts, MD, MS, 2300 Children’s Plaza, Box #43, Chicago, IL 60614; fax: 773-880-6300; or e-mail: .kwatts@childrensmemorial.org

10.3928/00904481-20101116-10

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