G G Shapiro

Seattle Children's Hospital, Seattle, Washington, United States

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Publications (108)750.59 Total impact

  • Gail G. Shapiro, C. Warren Bierman
    Journal of Asthma 07/2009; 20(5). DOI:10.3109/02770908309077381 · 1.83 Impact Factor
  • Journal of Allergy and Clinical Immunology 07/2007; 119(6):1550-1. DOI:10.1016/j.jaci.2007.03.032 · 11.25 Impact Factor
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    ABSTRACT: The authors investigated the relation between ambient concentrations of five of the Environmental Protection Agency's criteria pollutants and asthma exacerbations (daily symptoms and use of rescue inhalers) among 990 children in eight North American cities during the 22-month prerandomization phase (November 1993-September 1995) of the Childhood Asthma Management Program. Short-term effects of carbon monoxide, nitrogen dioxide, particulate matter less than 10 mum in aerodynamic diameter (PM10), sulfur dioxide, and warm-season ozone were examined in both one-pollutant and two-pollutant models, using lags of up to 2 days. Lags in carbon monoxide and nitrogen dioxide were positively associated with both measures of asthma exacerbation, and the 3-day moving sum of sulfur dioxide levels was marginally related to asthma symptoms. PM10 and ozone were unrelated to exacerbations. The strongest effects tended to be seen with 2-day lags, where a 1-parts-per-million change in carbon monoxide and a 20-parts-per-billion change in nitrogen dioxide were associated with symptom odds ratios of 1.08 (95% confidence interval (CI): 1.02, 1.15) and 1.09 (95% CI: 1.03, 1.15), respectively, and with rate ratios for rescue inhaler use of 1.06 (95% CI: 1.01, 1.10) and 1.05 (95% CI: 1.01, 1.09), respectively. The authors believe that the observed carbon monoxide and nitrogen dioxide associations can probably be attributed to mobile-source emissions, though more research is required.
    American Journal of Epidemiology 10/2006; 164(6):505-17. DOI:10.1093/aje/kwj225 · 4.98 Impact Factor
  • Gail G Shapiro
    Journal of Allergy and Clinical Immunology 10/2006; 118(3):562-4. DOI:10.1016/j.jaci.2006.07.011 · 11.25 Impact Factor
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    ABSTRACT: Despite increasing awareness of the National Asthma Education and Prevention Program guidelines, the relative contribution of symptom frequency or pulmonary function to the recommended asthma severity levels remains poorly understood. To determine whether adding lung function measurements to clinical history substantially changes the asthma severity classification, thereby influencing treatment decisions. Baseline data were studied from children enrolled in 2 multicenter studies: phase 1 of the National Cooperative Inner-City Asthma Study (1992-1994) (cohort 1) and the Inner-City Asthma Study (1998-2001) (cohort 2). Fifteen (8 for cohort 1 and 7 for cohort 2) major metropolitan inner-city areas in the United States. Inner-city children aged 8 through 11 years with asthma. Proportion of children reclassified from less severe asthma categories based on symptom frequency into more severe categories because of lung function. Of children with symptoms of mild intermittent asthma, 22.8% in cohort 1 and 27.7% in cohort 2 would be reclassified as having either moderate or severe persistent asthma. Of children with symptoms of mild persistent asthma, 31.2% in cohort 1 and 33.3% in cohort 2 would be similarly reclassified. In 2 different studies of inner-city children with asthma, approximately one third of the participants were reclassified into higher National Asthma Education and Prevention Program asthma severity categories when pulmonary function was considered in addition to symptom frequency. This may have direct implications for the undertreatment of asthma.
    Archives of Pediatrics and Adolescent Medicine 09/2006; 160(8):844-50. DOI:10.1001/archpedi.160.8.844 · 4.25 Impact Factor
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    ABSTRACT: To determine whether increased exposure to particulate matter air pollution (PM), measured with personal, residential, or central site monitoring, was associated with pulmonary function decrements in either adults with COPD or children with asthma. We studied 57 adults with or without COPD and 17 children aged 6 to 13 years with physician-diagnosed asthma in Seattle during a 3-year panel study. Study design and measurements: Indoor and outdoor PM measurements were made at subjects' homes. The subjects wore personal exposure monitors for 10 consecutive 24-h periods, and PM was also measured at a central outdoor location. We assessed the within-subject effect of particulate exposure on FEV(1) and peak expiratory flow (PEF) in adults, and maximal midexpiratory flow (MMEF), PEF, FEV(1), and symptoms in children. FEV(1) decrements were associated with 1-day lagged central site PM </= 2.5 microm in diameter (PM(2.5)) in adult subjects with COPD. In children not receiving antiinflammatory medication, same day indoor, outdoor, and central site exposures to PM(2.5) were associated with decrements in MMEF, PEF, and FEV(1). Associations with PM(2.5) and lung function decrements were also observed for 1-day lagged indoor (MMEF, PEF, FEV(1)) and personal (PEF only) exposures. Antiinflammatory medication use in children significantly attenuated the PM effect on airflow rates and volumes. This study found consistent decrements in MMEF in children with asthma who were not receiving medications. It is notable that effects were observed even though PM exposures were low for an urban area. These findings suggest the need for future larger studies of PM effects in this susceptible population that repeatedly measure spirometry to include MMEF and potentially more sensitive markers of airway inflammation such as exhaled breath condensate and exhaled nitric oxide.
    Chest 06/2006; 129(6):1614-22. DOI:10.1378/chest.129.6.1614 · 7.13 Impact Factor
  • Ashley Jerath Tatum, Gail G Shapiro
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    ABSTRACT: Outdoor air pollution and environmental tobacco smoke adversely affect health in persons with asthma. Increased levels of ozone, particulate matter, and environmental tobacco smoke have been associated with increased asthma symptoms and health care use and with reduced lung function. These air contaminants have proinflammatory actions that can magnify existing lower airway inflammation in patients with asthma. Exposure to air contaminants can increase the risk of developing asthma in susceptible persons. Outdoor air pollution and environmental tobacco smoke may affect allergen-induced inflammation by initiating TH(2) responses to antigens or by exacerbating such inflammation in persons already sensitized.
    Immunology and Allergy Clinics of North America 03/2005; 25(1):15-30. DOI:10.1016/j.iac.2004.09.003 · 2.22 Impact Factor
  • Journal of Allergy and Clinical Immunology 04/2004; 113(3):558-60. DOI:10.1016/j.jaci.2003.11.015 · 11.25 Impact Factor
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    ABSTRACT: Exposure to air pollutants has been investigated as a possible cause of asthma attacks in children. To investigate the short-term effects of air pollutants on a panel of 133 children with asthma who enrolled in the Childhood Asthma Management Program. During screening, the children completed daily diary cards for an average of 58 days to indicate their medication use and asthma severity. We used ordinal logistic regression to compare the odds of a more serious relative to a less serious asthma attack, and we used a Poisson model to analyze medication use. In both analyses we accommodate dependence in the data and different periods of observation for study subjects. Our results indicate that a 10-microg/m3 increase in particulate matter less than or equal to 2.5 microm (PM2.5) lagged 1 day was associated with a 1.20 times increased odds of having a more serious asthma attack [95% confidence interval (CI), 1.05 to 1.37] and a 1.08-fold increase in medication use (95% CI, 1.01 to 1.15). A 10-microg/m3 increase in particulate matter less than or equal to 10 microm (PM10) increased the odds of a more serious asthma attack (odds ratio = 1.12; 95% CI, 1.04 to 1.22) and also increased medication use (relative risk = 1.05; 95% CI, 1.00 to 1.09). Increases in PM2.5 and PM10 are significantly associated with an increased risk of more severe asthma attacks and medication use in Seattle area children with asthma. We also found associations with carbon monoxide, but we believe that carbon monoxide is a marker for exposure to combustion byproducts.
    Annals of allergy, asthma & immunology: official publication of the American College of Allergy, Asthma, & Immunology 11/2003; 91(4):346-53. DOI:10.1016/S1081-1206(10)61681-X · 2.75 Impact Factor
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    ABSTRACT: As part of a large panel study in Seattle, Washington, we measured levels of exhaled nitric oxide (eNO) in children's homes and fixed-site particulate matter with aerodynamic diameters of 2.5 micro m or less (PM(2.5)) outside and inside the homes as well as personal PM(2.5) during winter and spring sessions of 2000-2001. Nineteen subjects 6-13 years of age participated; 9 of the 19 were on inhaled corticosteroid (ICS) therapy. Exhaled breath measurements were collected offline into a Mylar balloon for up to 10 consecutive days. Mean eNO values were 19.1 (SD +/- 11.4) ppb in winter sessions and 12.5 +/- 6.6 ppb in spring sessions. Fixed-site PM(2.5) mean concentrations were 10.1 +/- 5.7 microg/m(3) outside homes and 13.3 +/- 1.4 inside homes; the personal PM(2.5) mean was 13.4 +/- 3.2 microg/m(3). We used a linear mixed-effects model with random intercept and an interaction term for medications to test for within-subject-within-session associations between eNO and various PM(2.5) values. We found a 10 microg/m(3) increase in PM(2.5) from the outdoor, indoor, personal, and central-site measurements that was associated with increases in eNO in all subjects at lag day zero. The effect was 4.3 ppb [95% confidence interval (CI), 1.4-7.29] with the outdoor monitor, 4.2 ppb (95% CI, 1.02-7.4) for the indoor monitor, 4.5 ppb (95% CI, 1.02-7.9) with the personal monitor, and 3.8 ppb (95% CI, 1.2-6.4) for the central monitors. The interaction term for medication category (ICS users vs. nonusers) was significant in all analyses. These findings suggest that eNO can be used as an assessment tool in epidemiologic studies of health effects of air pollution.
    Environmental Health Perspectives 11/2003; 111(13):1625-9. DOI:10.1289/ehp.6160 · 7.03 Impact Factor
  • Justin D Rothmier, Mary V Lasley, Gail G Shapiro
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    ABSTRACT: Although previous studies have looked at the motivation behind enrollment in clinical trials of adults and healthy subjects, little is known about the factors influencing parental consent in pediatric clinical studies where the subjects themselves do not provide consent. This study was conducted to define a group of factors that impact parental consent in the pediatric clinical trial. This may allow investigators to identify a subset of specific appealing aspects of clinical trials that will promote participation while also bringing ethical issues to light that may require further consideration. Forty-four parents or guardians of children currently participating in clinical asthma research completed questionnaires from July 1999 to September 1999 pertaining to motives for allowing their child to participate in clinical trials. The responses were then rated on a Likert numerical scale. The most important motive for parents is learning more about their child's illness. Next important was the motive of helping medical knowledge. Availability of free medication was negatively correlated with family income. Although altruistic motives are present in pediatric asthma research, most parents/guardians gave consent for their child to learn more about their child's asthma. Access to free medication was more important in families with lower incomes than in families with higher incomes.
    PEDIATRICS 06/2003; 111(5 Pt 1):1037-41. DOI:10.1542/peds.111.5.1037 · 5.30 Impact Factor
  • Gail G Shapiro
    Journal of Allergy and Clinical Immunology 05/2003; 111(4):695-6. DOI:10.1067/mai.2003.1410 · 11.25 Impact Factor
  • Gail G Shapiro, James W Stout
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    ABSTRACT: The prevalence and morbidity of asthma are growing problems that appear to affect urban populations and particularly impoverished centers disproportionately. Poor children are more likely to be hospitalized for asthma than nonpoor children, and are more likely to experience clinical and social dysfunction due to asthma. While guidelines exist for best care of childhood asthma, the neediest children are least likely to encounter the benefits of these recommendations. The relationship between host and environment in both primary causation and disease exacerbation is an area of research and debate. Allergen exposure in early life appears to correlate with sensitization and expression of atopy and asthma. Impoverished households are more likely to be reservoirs for dust mite and cockroach antigen in high concentrations than more affluent settings. Lifestyle factors, including diet and ambient air quality, may be disease modifiers. Suboptimal systems for delivery of healthcare to high-risk populations are obvious targets for blame. Poor children are more likely than nonpoor children to receive sick care in emergency rooms that lack a connection to chronic care providers. Besides the method of delivery, the quality of care is questionable, as poor children are less likely to receive the anti-inflammatory maintenance medications for asthma that evidence-based guidelines recommend. Efforts to correct these problems must take into account such issues as explaining the nature of the disease and the best intervention strategies to people who have a diverse array of cultural backgrounds, belief systems, and life stressors. Efforts to improve the status quo are underway in many communities. Environmental control measures to reduce dust mite and cockroach exposure have met with some success. Models to improve access to care and acceptance of care may improve community outreach maneuvers that connect the medical establishment with families and patients. Examination and assessment of new approaches to facilitate this sort of communication hold promise and are receiving attention as well as research dollars.
    Pediatric Pulmonology 01/2002; 33(1):47-55. DOI:10.1002/ppul.10029 · 2.30 Impact Factor
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    ABSTRACT: We observed a panel of 133 children (5-13 years of age) with asthma residing in the greater Seattle, Washington, area for an average of 58 days (range 28-112 days) during screening for enrollment in the Childhood Asthma Management Program (CAMP) study. Daily self-reports of asthma symptoms were obtained from study diaries and compared with ambient air pollution levels in marginal repeated measures logistic regression models. We defined days with asthma symptoms as any day a child reported at least one mild asthma episode. All analyses were controlled for subject-specific variables [age, race, sex, baseline height, and FEV(1) PC(20) concentration (methacholine provocative concentration required to produce a 20% decrease in forced expiratory volume in 1 sec)] and potential time-dependent confounders (day of week, season, and temperature). Because of variable observation periods for participants, we estimated both between- and within-subject air pollutant effects. Our primary interest was in the within-subject effects: the effect of air pollutant excursions from typical levels in each child's observation period on the odds of asthma symptoms. In single-pollutant models, the population average estimates indicated a 30% [95% confidence interval (CI), 11-52%] increase for a 1-ppm increment in carbon monoxide lagged 1 day, an 18% (95% CI, 5-33%) increase for a 10-microg/m(3) increment in same-day particulate matter < 1.0 microm (PM(1.0)), and an 11% (95% CI, 3-20%) increase for a 10-microg/m(3) increment in particulate matter < 10 microm (PM(10)) lagged 1 day. Conditional on the previous day's asthma symptoms, we estimated 25% (95% CI, 10-42%), 14% (95% CI, 4-26%), and 10% (95% CI, 3-16%) increases in the odds of asthma symptoms associated with increases in CO, PM(1.0), and PM(10), respectively. We did not find any association between sulfur dioxide (SO(2)) and the odds of asthma symptoms. In multipollutant models, the separate pollutant effects were smaller. The overall effect of an increase in both CO and PM(1. 0) was a 31% (95% CI, 11-55%) increase in the odds of symptoms of asthma. We conclude that there is an association between change in short-term air pollution levels, as indexed by PM and CO, and the occurrence of asthma symptoms among children in Seattle. Although PM effects on asthma have been found in other studies, it is likely that CO is a marker for vehicle exhaust and other combustion by-products that aggravate asthma.
    Environmental Health Perspectives 01/2001; 108(12):1209-14. DOI:10.2307/3434835 · 7.03 Impact Factor
  • M V Lasley, G G Shapiro
    Pediatrics in Review 03/2000; 21(2):39-43; quiz 43. DOI:10.1542/pir.21-2-39 · 0.82 Impact Factor
  • Mary V. Lasley, Gail G. Shapiro
    Immunology and Allergy Clinics of North America 05/1999; 19(2):437–452. DOI:10.1016/S0889-8561(05)70098-9 · 2.22 Impact Factor
  • Journal of Allergy and Clinical Immunology 12/1996; 98(6):1001–1011. DOI:10.1016/S0091-6749(96)80183-7 · 11.25 Impact Factor
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    ABSTRACT: Although both cromolyn (C) and inhaled corticosteroids are anti-inflammatory therapies for childhood asthma, there are few controlled comparisons of these medications for asthma therapy in children. None were conducted in the United States, and none specifically study triamcinolone acetonide (T) versus C. This 12-week evaluation followed 31 youths, aged 8 to 18 years, with moderate asthma who were assigned to receive C or T according to a prerandomized and blinded code. Patients were instructed to take two inhalations from the study metered-dose inhaler (active T or placebo) and to inhale the contents of one study-provided ampule (C, 20 mg, or placebo) from a compressor-driven home nebulizer three times per day. Patients also used albuterol, two inhalations from a metered-dose inhaler, three times a day (before study medication) and, additionally, if needed. Patients maintained a daily diary, recording extra medication use, adverse experiences, peak flow rates morning and night, and asthma symptom scores. Laboratory assessment of pulmonary function was done at 1, 4, 8, and 12 weeks. Cosyntropin challenge and methacholine bronchoprovocation challenge were performed at the beginning and end of the study. C and T provided similar, adequate asthma control. Symptoms of wheezing, cough, and chest tightness decreased, and daily peak expiratory flow rate increased with both regimens compared to during a 2-week baseline when patients received medication only as needed. There was no significant change in methacholine sensitivity and no change in endocrine function, as measured with fasting plasma control before and after administration of cosyntropin.(ABSTRACT TRUNCATED AT 250 WORDS)
    Journal of Allergy and Clinical Immunology 12/1991; 88(5):742-8. DOI:10.1016/0091-6749(91)90181-M · 11.25 Impact Factor
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    ABSTRACT: Sixty-one patients with chronic sinusitis who were referred for an allergy evaluation were evaluated for immunologic competence including assessment of quantitative serum immunoglobulin levels, IgG subclass levels, and response to pneumococcal and Haemophilus influenzae vaccines. In addition to chronic sinus disease, recurrent otitis media and asthma exacerbation were common problems in this group. Five patients had an elevated age-adjusted IgE level and 22 patients had positive prick tests to one or more environmental inhalants; these findings suggest an allergic component in this subgroup. Twelve additional patients had highly reactive intradermal tests to common environmental allergens, which also may be clinically significant for underlying atopy. Eleven patients had low immunoglobulin levels, 6 had low immunoglobulin levels and vaccine hyporesponsiveness, and 17 had poor vaccine response only. Thus, 34 of 61 patients with refractory sinusitis had abnormal results on immune studies, with depressed IgG3 levels and poor response to pneumococcal antigen 7 being most common. In addition to allergy, immunologic incompetence may be an important etiologic factor in patients with chronic, refractory sinusitis.
    Pediatrics 04/1991; 87(3):311-6. · 5.30 Impact Factor

Publication Stats

2k Citations
750.59 Total Impact Points

Institutions

  • 1985–2009
    • Seattle Children's Hospital
      • Division of Allergy
      Seattle, Washington, United States
  • 1976–2007
    • University of Washington Seattle
      • • Department of Pediatrics
      • • Department of Biostatistics
      • • Department of Medicine
      Seattle, Washington, United States
  • 2006
    • Vanderbilt University
      • Department of Biostatistics
      Nashville, MI, United States
  • 1999–2005
    • Northwest Asthma and Allergy Center
      Seattle, Washington, United States
  • 2003
    • University of California, Davis
      Davis, California, United States
  • 1984
    • Asthma UK
      Londinium, England, United Kingdom