Beyond Original Intent – The Use of a Corporation’s Administrative Databases for Academic Research

Large corporations maintain a variety of administrative databases as part of their normal operations. These databases, created for distinct functions by separate organizational entities, are generally independent. For instance, a company’s Human Resources organization typically maintains a database containing information such as demographics, job and salary history, and employee status for all employees.. The environmental, health and safety department maintains information regarding work-place exposures and exposure levels for various agents within each job as well as injury and illness surveillance records. The medical department maintains occupational health information including audiometric and pulmonary function test results. As many large corporations are self-insured, they also have medical claims data available by employee that includes diagnosis codes, procedure codes, and prescription drug codes. Additional data maintained by corporations may include production output and quality information, employee contributions to retirement plans and health savings accounts, as well as workers compensation information. A synergistic partnership between industry and academia allows for linkage between company maintained databases to enable the conduct of research to examine associations between demographic, occupational and social factors not otherwise available to researchers, and the ability to define and test interventions to promote health and safety in the workplace. An almost 20 year relationship between Alcoa, Inc. and Yale University School of Medicine continues to facilitate investigation of root causes of disease and injury risk in a large manufacturing cohort. To date, over 50 peer-reviewed research papers have resulted from this joint venture

Individual-level and plant-level predictors of acute, traumatic occupational injuries in a manufacturing cohort

Objectives: Workplace and contextual factors that may affect risk for worker injury are not well described. This study used results from an employee job satisfaction survey to construct aggregate indicators of the work environment and estimate the relative contribution of those factors to injury rates in a manufacturing cohort. Methods: Principal components analysis was used to construct four plant-level factors from responses to a 32 question survey of the entire workforce, administered in 2006. Multilevel Poisson regression was used to evaluate the relationship between injury rate, individual-level and plant-level risk factors, unionisation and plant type. Results: Plant-level ‘work stress’ (incident rate ratio (IRR)=0.50, 95% CI 0.28 to 0.90) was significant in the multilevel model, indicating the rate of injury for an average individual in that plant was halved (conditional on plant) when job stress decreased by a tertile. ‘Overall satisfaction’, ‘work environment’ and ‘perception of supervisor’ showed the same trend but were not significant. Unionisation was protective (IRR=0.40, 95% CI 0.17 to 0.95) as was any plant type compared with smelter. Conclusions: We demonstrated utility of data from a human resources survey to construct indicators of the work environment. Our research suggests that aspects of the work environment, particularly work stress and unionisation, may have a significant effect on risk for occupational injury, emphasising the need for further multilevel studies. Our work would suggest monitoring of employee perceptions of job stress and the possible inclusion of stress management as a component of risk reduction programmes

Occupational noise exposure and risk of hypertension in an industrial workforce

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/140051/1/ajim22775_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/140051/2/ajim22775.pd

Phosphoinositide-dependent kinase 1 controls migration and malignant transformation but not cell growth and proliferation in PTEN-null lymphocytes

In normal T cell progenitors, phosphoinositide-dependent kinase l (PDK1)–mediated phosphorylation and activation of protein kinase B (PKB) is essential for the phosphorylation and inactivation of Foxo family transcription factors, and also controls T cell growth and proliferation. The current study has characterized the role of PDK1 in the pathology caused by deletion of the tumor suppressor phosphatase and tensin homologue deleted on chromosome 10 (PTEN). PDK1 is shown to be essential for lymphomagenesis caused by deletion of PTEN in T cell progenitors. However, PTEN deletion bypasses the normal PDK1-controlled signaling pathways that determine thymocyte growth and proliferation. PDK1 does have important functions in PTEN-null thymocytes, notably to control the PKB–Foxo signaling axis and to direct the repertoire of adhesion and chemokine receptors expressed by PTEN-null T cells. The results thus provide two novel insights concerning pathological signaling caused by PTEN loss in lymphocytes. First, PTEN deletion bypasses the normal PDK1-controlled metabolic checkpoints that determine cell growth and proliferation. Second, PDK1 determines the cohort of chemokine and adhesion receptors expressed by PTEN-null cells, thereby controlling their migratory capacity

β-Cells with Relative Low HIMP1 Overexpression Levels in a Transgenic Mouse Line Enhance Basal Insulin Production and Hypoxia/Hypoglycemia Tolerance

Rodent pancreatic β-cells that naturally lack hypoglycemia/hypoxia inducible mitochondrial protein 1 (HIMP1) are susceptible to hypoglycemia and hypoxia influences. A linkage between the hypoglycemia/hypoxia susceptibility and the lack of HIMP1 is suggested in a recent study using transformed β-cells lines. To further illuminate this linkage, we applied mouse insulin 1 gene promoter (MIP) to control HIMP1-a isoform cDNA and have generated three lines (L1 to L3) of heterozygous HIMP1 transgenic (Tg) mice by breeding of three founders with C57BL/6J mice. In HIMP1-Tg mice/islets, we performed quantitative polymerase chain reaction (PCR), immunoblot, histology, and physiology studies to investigate HIMP1 overexpression and its link to β-cell function/survival and body glucose homeostasis. We found that the HIMP1 level increased steadily in β-cells of L1 to L3 heterozygous HIMP1-Tg mice. HIMP1 overexpression at relatively lower levels in L1 heterozygotes results in a negligible decline in blood glucose concentrations and an insignificant elevation in blood insulin levels, while HIMP1 overexpression at higher levels are toxic, causing hyperglycemia in L2/3 heterozygotes. Follow-up studies in 5–30-week-old L1 heterozygous mice/islets found that HIMP1 overexpression at relatively lower levels in β-cells has enhanced basal insulin biosynthesis, basal insulin secretion, and tolerances to low oxygen/glucose influences. The findings enforced the linkage between the hypoglycemia/hypoxia susceptibility and the lack of HIMP1 in β-cells, and show a potential value of HIMP1 overexpression at relatively lower levels in modulating β-cell function and survival

Development of a job-exposure matrix for exposure to total and fine particulate matter in the aluminum industry

Increasing evidence indicates that exposure to particulate matter (PM) at environmental concentrations increases the risk of cardiovascular disease, particularly PM with an aerodynamic diameter of less than 2.5 μm (PM(2.5)). Despite this, the health impacts of higher occupational exposures to PM(2.5) have rarely been evaluated. In part, this research gap derives from the absence of information on PM(2.5) exposures in the workplace. To address this gap, we have developed a job-exposure matrix (JEM) to estimate exposure to two size fractions of PM in the aluminum industry. Measurements of total PM (TPM) and PM(2.5) were used to develop exposure metrics for an epidemiologic study. TPM exposures for distinct exposure groups (DEGs) in the JEM were calculated using 8385 personal TPM samples collected at 11 facilities (1980-2011). For eight of these facilities, simultaneous PM(2.5) and TPM personal monitoring was conducted from 2010 to 2011 to determine the percent of TPM that is composed of PM(2.5) (%PM(2.5)) in each DEG. The mean TPM from the JEM was then multiplied by %PM(2.5) to calculate PM(2.5) exposure concentrations in each DEG. Exposures in the smelters were substantially higher than in fabrication units; mean TPM concentrations in smelters and fabrication facilities were 3.86 and 0.76 mg/m(3), and the corresponding mean PM(2.5) concentrations were 2.03 and 0.40 mg/m(3). Observed occupational exposures in this study generally exceeded environmental PM(2.5) concentrations by an order of magnitude