Kristin J Cummings

Centers for Disease Control and Prevention, Атланта, Michigan, United States

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Publications (44)155.53 Total impact

  • Kristin J Cummings, Kathleen Kreiss
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    ABSTRACT: Occupational and environmental causes of bronchiolar disorders are recognized on the basis of case reports, case series, and, less commonly, epidemiologic investigations. Pathology may be limited to the bronchioles or also involve other components of the respiratory tract, including the alveoli. A range of clinical, functional, and radiographic findings, including symptomatic disease lacking abnormalities on noninvasive testing, poses a diagnostic challenge and highlights the value of surgical biopsy. Disease clusters in workplaces and communities have identified new etiologies, drawn attention to indolent disease that may otherwise have been categorized as idiopathic, and expanded the spectrum of histopathologic responses to an exposure. More sensitive noninvasive diagnostic tools, evidence-based therapies, and ongoing epidemiologic investigation of at-risk populations are needed to identify, treat, and prevent exposure-related bronchiolar disorders. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.
    Seminars in Respiratory and Critical Care Medicine 06/2015; 36(3):366-378. DOI:10.1055/s-0035-1549452 · 3.02 Impact Factor
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    ABSTRACT: Work-related asthma is asthma that is caused or exacerbated by exposure to specific substances in the workplace. Approximately 10%-16% of adult-onset asthma cases are attributable to occupational factors, and estimates of asthma exacerbated by work range from 13% to 58%. During 2008-2012, the Massachusetts Department of Public Health received nine reports of work-related asthma among workers at a facility that manufactured syntactic foam used for flotation in the offshore oil and gas industry. These reports and a request from facility employees led to a CDC health hazard evaluation during 2012-2013 in which CDC reviewed records, toured the facility, and administered a questionnaire to current employees. Investigators found that workers' risk for asthma increased substantially after hire, possibly because of known asthma triggers (i.e., asthmagens) used in production. The company has since initiated efforts to reduce employee exposures to these substances. This cluster of work-related asthma was identified through CDC-funded, state-based surveillance and demonstrates complementary state and federal investigations.
    MMWR. Morbidity and mortality weekly report 04/2015; 64(15):411-4.
  • PLoS ONE 04/2015; 10(4):e0124368. DOI:10.1371/journal.pone.0124368 · 3.53 Impact Factor
  • Nicotine & Tobacco Research 01/2015; DOI:10.1093/ntr/ntu338 · 2.81 Impact Factor
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    ABSTRACT: Rationale: Occupational exposure to indium compounds including indium-tin oxide (ITO) can result in potentially fatal indium lung disease. However, the early effects of exposure on the lungs are not well understood. Objectives: To determine the relationship between short-term occupational exposures to indium compounds and development of early lung abnormalities. Methods: Among ITO production and reclamation facility workers, we measured plasma indium, respiratory symptoms, pulmonary function, chest computed tomography, and serum biomarkers of lung disease. The relationships between plasma indium concentration and health outcome variables were evaluated using restricted cubic spline and linear regression models. Measurements and Main Results: Eighty-seven (93%) of 94 ITO facility workers (median tenure=2 years; median plasma indium=1.0 mcg/L) participated in the study. Spirometric abnormalities were not in excess and few had radiographic evidence of alveolar proteinosis (n=0), fibrosis (n=2), or emphysema (n=4). Compared to participants with plasma indium concentrations <1.0 mcg/L, those with values ≥1.0 mcg/L had more dyspnea, lower mean FEV1% and FVC%, and higher median serum KL-6 and SP-D levels. Spline regression demonstrated non-linear exposure-response, with significant differences occurring at plasma indium concentrations as low as 1.0 mcg/L for FEV1%, FVC%, KL-6, and SP-D compared to the reference. Associations between health outcomes and plasma indium were evident in linear regression models and not explained by age, smoking status, or facility tenure. Conclusions: In ITO facility workers with short-term, low-level exposure, plasma indium concentrations lower than previously reported were associated with lung symptoms, abnormal spirometry, and increased serum biomarkers of lung disease.
    10/2014; DOI:10.1513/AnnalsATS.201407-346OC
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    ABSTRACT: Occupational exposure to indium compound particles has recently been associated with lung disease among workers in the indium-tin oxide (ITO) industry. Previous studies suggested that excessive alveolar surfactant and reactive oxygen species (ROS) may play a role in the development of pulmonary lesions following exposure to indium compounds. However, toxicity at the cellular level has not been comprehensively evaluated. Thus, the aim of this study was to assess which, if any, compounds encountered during ITO production are toxic to cultured cells and ultimately contribute to the pathogenesis of indium lung disease. The compounds used in this study were collected from eight different processing stages at an ITO production facility. Enhanced dark field imaging showed 5 of the compounds significantly associated with cells within 1 h, suggesting that cellular reactions to the compound particles may be occurring rapidly. To examine the potential cytotoxic effects of these associations, ROS generation, cell viability, and apoptosis were evaluated following exposures in RAW 264.7 mouse monocyte macrophage and BEAS-2B human bronchial epithelial cell lines. Both exhibited reduced viability with exposures, while apoptosis only occurred in RAW 264.7 cells. Our results suggested that excessive ROS production is likely not the predominant mechanism underlying indium-induced lung disease. However, the effects on cell viability reveal that several of the compounds are cytotoxic, and therefore, exposures need to be carefully monitored in the industrial setting.
    Journal of Toxicology and Environmental Health Part A 09/2014; 77(20):1193-209. DOI:10.1080/15287394.2014.920757 · 1.83 Impact Factor
  • Kathleen Kreiss, Kristin J Cummings
    American Journal of Industrial Medicine 08/2014; 57(8). DOI:10.1002/ajim.22358 · 1.59 Impact Factor
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    ABSTRACT: Objectives To better understand respiratory symptoms and lung function in flavouring manufacturing workers. Methods We offered a questionnaire and lung function testing to the current workforce of a flavouring manufacturing facility that had transitioned away from diacetyl and towards substitutes in recent years. We examined symptoms, spirometric parameters and diffusing capacity measurements by exposure variables, including facility tenure and time spent daily in production areas. We used linear and logistic regression to develop final models adjusted for age and smoking status. Results A total of 367 (93%) current workers participated. Shortness of breath was twice as common in those with tenure >= 7 years (OR 2.0, 95% CI 1.1 to 3.6). Other chest symptoms were associated with time spent daily in production. Participants who spent >= 1 h daily in production areas had twice the odds of any spirometric abnormality (OR 2.3; 95% CI 1.1 to 5.3) and three times the odds of low diffusing capacity (OR 2.8; 95% CI 0.9 to 9.4) than other participants. Mean spirometric parameters were significantly lower in those with tenure >= 7 years and those who spent >= 1 h daily in production. Mean diffusing capacity parameters were significantly lower in those with tenure >= 7 years. Differences in symptoms and lung function could not be explained by age, smoking status or employment at another flavouring plant. Conclusions Symptoms and lung function findings were consistent with undiagnosed or subclinical obliterative bronchiolitis and associated with workplace exposures. Further efforts to lower exposures to flavouring chemicals, including diacetyl substitutes, are warranted.
    Occupational and Environmental Medicine 06/2014; 71(8). DOI:10.1136/oemed-2013-101927 · 3.23 Impact Factor
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    The Journal of Infectious Diseases 03/2014; 210(3). DOI:10.1093/infdis/jiu127 · 5.78 Impact Factor
  • Kristin J Cummings, Anna-Binney McCague, Kathleen Kreiss
    Epidemiology (Cambridge, Mass.) 01/2014; 25(1):160-1. DOI:10.1097/EDE.0b013e3182a70b0f · 6.18 Impact Factor
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    ABSTRACT: To explore factors associated with fatal accidents among contractors and operators by using the Mine Safety and Health Administration database. Cross-sectional data on 157,410 miners employed by operators or contractors during 1998-2007 were analyzed using logistic regression and multiple imputation. Univariate odds of fatal versus nonfatal accident were 2.8 (95% confidence interval, 2.3 to 3.4) times higher for contractors than operators. In a multivariable model, fatality was associated with contractor, less experience at the current mine, and occurrence at more than 8 hours into the workday (P < 0.05 for each). Differences in odds of fatality by employment type were more pronounced in surface mines. Contractors had a higher proportion of fatal injuries. Fatality also varied by mine experience, the number of hours worked before injury, work location, and mine type.
    Journal of occupational and environmental medicine / American College of Occupational and Environmental Medicine 10/2013; 55(11). DOI:10.1097/JOM.0b013e3182a2a5a2 · 1.80 Impact Factor
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    American Journal of Industrial Medicine 05/2013; 56(5). DOI:10.1002/ajim.22131 · 1.59 Impact Factor
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    ABSTRACT: BACKGROUND: We evaluated the effectiveness of workplace changes to prevent indium lung disease, using 2002-2010 surveillance data collected by an indium-tin oxide production facility. METHODS: We assessed pulmonary function using lower limits of normal. Blood indium concentration and personal air sampling data were used to estimate exposure. RESULTS: Abnormalities were uncommon at hire. After hire, prevalence of spirometric restriction was 31% (n = 14/45), about fourfold higher than expected. Excessive decline in FEV1 was elevated at 29% (n = 12/41). Half (n = 21/42) had blood indium ≥5 µg/l. More recent hires had fewer abnormalities. There was a suggestion that abnormalities were more common among workers with blood indium ≥5 µg/l, but otherwise an exposure-response relationship was not evident. Peak dust concentrations were obscured by time averaging. CONCLUSIONS: Evolving lung function abnormalities consistent with subclinical indium lung disease appeared common and merit systematic investigation. Traditional measures of exposure and response were not illustrative, suggesting fresh approaches will be needed. Workplace changes seemed to have had a positive though incomplete impact; novel preventive interventions are warranted. Am. J. Ind. Med. Published 2012. This article is a U.S. Government work and is in the public domain in the USA.
    American Journal of Industrial Medicine 03/2013; 56(3). DOI:10.1002/ajim.22125 · 1.59 Impact Factor
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    ABSTRACT: Vocal cord dysfunction (VCD) is the intermittent paradoxical adduction of the vocal cords during respiration, resulting in variable upper airway obstruction. Exposure to damp indoor environments is associated with adverse respiratory health outcomes, including asthma, but its role in the development of VCD is not well described. We describe the spectrum of respiratory illness in occupants of 2 water-damaged office buildings. The National Institute for Occupational Safety and Health conducted a health hazard evaluation that included interviews with managers, a maintenance officer, a remediation specialist who had evaluated the 2 buildings, employees, and consulting physicians. In addition, medical records and reports of building evaluations were reviewed. Diagnostic evaluations for VCD had been conducted at the Asthma and Allergy Center of the Medical College of Wisconsin. Two cases of VCD were temporally related to occupancy of water-damaged buildings. The patients experienced cough, chest tightness, dyspnea, wheezing, and hoarseness when in the buildings. Spirometry was normal. Methacholine challenge did not show bronchial hyperreactivity but did elicit symptoms of VCD and inspiratory flow-volume loop truncation. Direct laryngoscopy revealed vocal cord adduction during inspiration. Coworkers developed upper and lower respiratory symptoms; their diagnoses included sinusitis and asthma, consistent with recognized effects of exposure to indoor dampness. Building evaluations provided evidence of water damage and mold growth. VCD can occur with exposure to water-damaged buildings and should be considered in exposed patients with asthma-like symptoms.
    01/2013; 1(1):46-50. DOI:10.1016/j.jaip.2012.10.001
  • American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California; 05/2012
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    ABSTRACT: Reports of pulmonary fibrosis, emphysema, and, more recently, pulmonary alveolar proteinosis (PAP) in indium workers suggested that workplace exposure to indium compounds caused several different lung diseases. To better understand the pathogenesis and natural history of indium lung disease, a detailed, systematic, multidisciplinary analysis of clinical, histopathologic, radiologic, and epidemiologic data for all reported cases and workplaces was undertaken. Ten men (median age, 35 years) who produced, used, or reclaimed indium compounds were diagnosed with interstitial lung disease 4-13 years after first exposure (n = 7) or PAP 1-2 years after first exposure (n = 3). Common pulmonary histopathologic features in these patients included intraalveolar exudate typical of alveolar proteinosis (n = 9), cholesterol clefts and granulomas (n = 10), and fibrosis (n = 9). Two patients with interstitial lung disease had pneumothoraces. Lung disease progressed following cessation of exposure in most patients and was fatal in two. Radiographic data revealed that two patients with PAP subsequently developed fibrosis and one also developed emphysematous changes. Epidemiologic investigations demonstrated the potential for exposure to respirable particles and an excess of lung abnormalities among coworkers. Occupational exposure to indium compounds was associated with PAP, cholesterol ester crystals and granulomas, pulmonary fibrosis, emphysema, and pneumothoraces. The available evidence suggests exposure to indium compounds causes a novel lung disease that may begin with PAP and progress to include fibrosis and emphysema, and, in some cases, premature death. Prospective studies are needed to better define the natural history and prognosis of this emerging lung disease and identify effective prevention strategies.
    Chest 12/2011; 141(6):1512-21. DOI:10.1378/chest.11-1880 · 7.13 Impact Factor
  • Kristin J. Cummings, Kathleen Kreiss, Victor L. Roggli
    American Journal of Respiratory and Critical Care Medicine 09/2011; 184(6):741-742. DOI:10.1164/ajrccm.184.6.741a · 11.99 Impact Factor
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    ABSTRACT: Exposure to soy antigens has been associated with asthma in community outbreaks and in some workplaces. Recently, 135 soy flake processing workers (SPWs) in a Tennessee facility were evaluated for immune reactivity to soy. Allergic sensitization to soy was common and was five times more prevalent than in health care worker controls (HCWs) with no known soy exposure. To characterize sensitization to soy allergens in SPWs. Sera that were positive to soy ImmunoCAP (n=27) were tested in IgE immunoblots. Wild-type (WT) and transgenic (TG) antigens were sequenced using nanoscale Ultra-Performance Liquid Chromatography Tandem Mass Spectrometry (nanoUPLC MS/MS). IgE reactivity towards 5-enolpyruvylshikimate-3-phosphate synthase (CP4-EPSP), a protein found in TG soy, was additionally investigated. De-identified sera from 50 HCWs were used as a control. Immunoblotting of WT and TG soy flake extracts revealed IgE against multiple soy antigens with reactivity towards 48, 54, and 62 kDa bands being the most common. The prominent proteins that bound SPW IgE were identified by nanoUPLC MS/MS analysis to be the high molecular weight soybean storage proteins, β-conglycinin (Gly m 5), and Glycinin (Gly m 6). No specific IgE reactivity could be detected to lower molecular weight soy allergens, Gly m 1 and Gly m 2, in soybean hull (SH) extracts. IgE reactivity was comparable between WT and TG extracts; however, IgE antibodies to CP4-EPSP could not be detected. SPWs with specific IgE to soy reacted most commonly with higher molecular weight soybean storage proteins compared with the lower molecular weight SH allergens identified in community asthma studies. IgE reactivity was comparable between WT and TG soy extracts, while no IgE reactivity to CP4-EPSP was observed. High molecular weight soybean storage allergens, Gly m 5 and Gly m 6, may be respiratory sensitizers in occupational exposed SPWs.
    Clinical & Experimental Allergy 07/2011; 41(7):1022-30. DOI:10.1111/j.1365-2222.2011.03756.x · 4.32 Impact Factor
  • American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado; 05/2011
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    ABSTRACT: In 2008, a company using multiple buttermilk flavorings in the production of dry bakery mixes replaced one liquid flavoring containing 15-20% diacetyl with a proprietary substitute meant to lower occupational risk for diacetyl-related bronchiolitis obliterans. Subsequently, the National Institute for Occupational Safety and Health (NIOSH) evaluated buttermilk flavoring-related exposures at this company's facility, with a focus on measuring ketones by several methods. Volatile organic compounds (VOCs) were evaluated in the headspaces of six bulk flavorings samples, including the substitute buttermilk flavoring. Ketones were evaluated in workplace air via area and personal samples collected during batch preparation of the substitute buttermilk flavoring and production of a bakery mix containing the same flavoring. Air samples were evaluated using five different methods: NIOSH 2549, Modified OSHA PV2118, OSHA 1013, NIOSH Draft Procedure SMP2, and evacuated canisters. Of five buttermilk flavorings from five different flavorings manufacturers, diacetyl was present in four, including the substitute flavoring; acetoin in two; 2,3-pentanedione in four; 2,3-hexanedione in one; and 2,3-heptanedione in three. Among material safety data sheets (MSDS) for four flavorings, only one listed a hazardous ingredient, which was acetoin. The predominant flavoring ingredient identified in the headspace of the substitute flavoring was 2,3-pentanedione; all other chemicals noted above were also present. Diacetyl and 2,3-pentanedione were measured in workplace air via evacuated canisters. In one area and one personal air sample, 2,3-pentanedione was measured by OSHA Method 1013 at concentrations of 78 and 91 ppb, respectively. Without their or the employer's knowledge, workers who used buttermilk flavorings were exposed to substitute ketones from many flavorings manufacturers. Because 2,3-pentanedione, 2,3-hexanedione, and 2,3-heptanedione all share the same functional α-diketone group as diacetyl, these compounds also may share diacetyl's mechanism of toxicity. Until more is known about 2,3-pentanedione and other α-diketone compounds, they should not be assumed to be safe. Companies using artificial buttermilk flavorings should use a precautionary approach that assumes these flavorings pose a health risk and limit exposures through engineering and administrative controls and use of personal protective equipment.
    Journal of Occupational and Environmental Hygiene 02/2011; 8(2):93-103. DOI:10.1080/15459624.2011.547148 · 1.21 Impact Factor

Publication Stats

281 Citations
155.53 Total Impact Points


  • 2006–2015
    • Centers for Disease Control and Prevention
      • • Division of Respiratory Disease Studies
      • • Health Effects Laboratory Division
      Атланта, Michigan, United States
  • 2009
    • Aga Khan University Hospital, Karachi
      • Department of Emergency Medicine
      Karachi, Sindh, Pakistan