A primer for workers' compensation

Background contextA physician's role within a workers' compensation injury extends far beyond just evaluation and treatment with several socioeconomic and psychological factors at play compared with similar injuries occurring outside of the workplace. Although workers' compensation statutes vary among states, all have several basic features with the overall goal of returning the injured worker to maximal function in the shortest time period, with the least residual disability and shortest time away from work.PurposeTo help physicians unfamiliar with the workers' compensation process accomplish these goals.Study designReview.MethodsEducational review.ResultsThe streamlined review addresses the topics of why is workers' compensation necessary; what does workers' compensation cover; progression after work injury; impairment and maximum medical improvement, including how to use the sixth edition of American Medical Association's (AMA) Guides to the evaluation of permanent impairment (Guides); completion of work injury claim after impairment rating; independent medical evaluation; and causation.ConclusionsIn the “no-fault” workers' compensation system, physicians play a key role in progressing the claim along and, more importantly, getting the injured worker back to work as soon as safely possible. Physicians should remain familiar with the workers' compensation process, along with how to properly use the AMA Guides.     

Matrix metalloproteinase-7-dependent release of tumor necrosis factor-alpha in a model of herniated disc resorption

Herniated disc (HD), one of the major causes of low back pain, is often resolved spontaneously without surgical intervention. Resorption is associated with a marked increase in infiltrating macrophages, and the matrix metalloproteinases (MMP) MMP-3 and MMP-7 have been implicated in this phenomenon. We developed a murine organ culture model in which intact intervertebral discs were cocultured with peritoneal macrophages to investigate the role of MMPs in HD resorption. Using macrophages isolated from MMP-null mice, we report that macrophage-produced MMP-7 was required for proteoglycan degradation, loss of wet weight, and macrophage infiltration of cocultured discs. The inability of MMP-7-deficient macrophages to infiltrate discs could not be attributed to a defect in macrophage migration. MMP-7 was required for the release of the cytokine TNF-alpha from peritoneal macrophages. The generation of soluble TNF-alpha was essential for the induction of MMP-3 in disc cocultures, which in turn is required for the generation of a macrophage chemoattractant and subsequent macrophage infiltration. TNF-alpha release from macrophages was necessary but insufficient for disc resorption, which required macrophage infiltration. We conclude that there is extensive communication between macrophages and chondrocytes in HD resorption and that an essential component of this communication is the requirement for MMPs to release soluble bioactive factors.     

High frequency oscillation in newborn infants with respiratory failure

Objective: To report ventilation strategies, survival and complications in 39 outborn infants treated with high frequency oscillatory ventilation (HFOV).
Methodology Data were collected prospectively between 1 May 1992 and 31 December 1993 on all infants treated with HFOV who had severe respiratory failure despite optimal conventional ventilation.
Results Twenty-eight out of 39 (72%) survived. Of the 15 infants with birthweights <1500g, eight survived. Best survival rates were for infants with pulmonary interstitial emphysema with air leak (4/5) and for infants of birthweight >1500g with hyaline membrane disease (8/8), and meconium aspiration syndrome (7/7). Three infants deteriorated while on HFOV and required extracorporeal membrane oxygenation. Complications were: (i) development of pulmonary interstitial emphysema (1); (ii) recurrence of pneumothorax (3); (iii) hypotension (2); and (iv) bronchopulmonary dysplasia (9). One of the eight infants weighing <1500g who received HFOV in the first week of life developed periventricular haemorrhage.
Conclusion The initial results of HFOV for severe respiratory failure were encouraging although a learning curve was encountered with its introduction.     

The Harvard Southern California Chronic Ozone Exposure Study: assessing ozone exposure of grade-school-age children in two Southern California communities

The Harvard Southern California Chronic Ozone Exposure Study measured personal exposure to, and indoor and outdoor ozone concentrations of, approximately 200 elementary school children 6-12 years of age for 12 months (June 1995-May 1996). We selected two Southern California communities, Upland and several towns located in the San Bernardino mountains, because certain characteristics of those communities were believed to affect personal exposures. On 6 consecutive days during each study month, participant homes were monitored for indoor and outdoor ozone concentrations, and participating children wore a small passive ozone sampler to measure personal exposure. During each sampling period, the children recorded time-location-activity information in a diary. Ambient ozone concentration data were obtained from air quality monitoring stations in the study areas. We present ozone concentration data for the ozone season (June-September 1995 and May 1996) and the nonozone season (October 1995-April 1996). During the ozone season, outdoor and indoor concentrations and personal exposure averaged 48.2, 11.8, and 18.8 ppb in Upland and 60.1, 21.4, and 25.4 ppb in the mountain towns, respectively. During the nonozone season, outdoor and indoor concentrations and personal exposure averaged 21.1, 3.2, and 6.2 ppb in Upland, and 35.7, 2.8, and 5.7 ppb in the mountain towns, respectively. Personal exposure differed by community and sex, but not by age group.     

Particulate matter and polycyclic aromatic hydrocarbon concentrations in indoor and outdoor microenvironments in Boston, Massachusetts

Estimating personal exposures to air pollution is a crucial component in identifying high-risk populations and determining efficient control strategies. Because of the difficulty of comprehensively measuring personal exposure, data on air pollution patterns in homogenous microenvironments linked with activity data are often used as surrogates. In this study, we focus on strengthening the available information about nonresidential microenvironmental exposures to particulate matter and other combustion pollutants. During the summer of 2000, we measured ultrafine particles, fine particulate matter (PM2.5), and particle-bound polycyclic aromatic hydrocarbons (PAHs) outdoors and in indoor microenvironments in Boston, Massachusetts. In indoor microenvironments averaged across sample days, mean ultrafine particle concentrations ranged from 3800 to 140,000 particles/cm(3), with 7-200 microg/m(3) of PM2.5 and 5-12 ng/m(3) of particle-bound PAH. PM2.5 indoor-outdoor ratios generally exceeded 1 in settings with high levels of human activity, with lower ratios for ultrafine particles. Cooking activities contributed significantly to elevated levels of all three pollutants. Using Linear Mixed Effects models with AR-1 autoregressive correlation structures, 10-min average outdoor concentrations were generally weak predictors of indoor levels, with stronger relationships in an apartment without mechanical ventilation than in air-conditioned nonresidential settings. Although further study would be needed to determine whether these patterns could be generalized beyond the monitored sites, these data support previous findings and enhance our knowledge about nonresidential exposure patterns.     

Future directions of environmental public health research: ATSDR's 2002-2010 agenda for six priority focus areas

Additional research on human exposures to hazardous substances in community settings and resultant adverse health effects is needed to fill an extensive number of information gaps. For example, information is needed to answer specific public health questions about the toxic effects of specific chemicals, who has been exposed, what the health risks might be, and what interventions are effective. The Agency for Toxic Substances and Disease Registry (ATSDR) is the principal federal agency responsible for addressing issues of public health concerning the human health risks associated with hazardous waste sites and unplanned releases of hazardous substances into the environment. Research is a critical component in how effectively the agency can identify persons exposed, determine health risks, and intervene to reduce exposures and adverse health outcomes. ATSDR has recently developed an agenda for public health environmental research for 2002-2010, divided into the following six research focus areas: exposure assessment; chemical mixtures; susceptible populations; community and tribal involvement; evaluation and surveillance of health effects; and health promotion and intervention. This article discusses the agenda's development, the research issues within each of the six focus areas, and preliminary implementation plans.     

International expert workshop on the analysis of the economic and public health impacts of air pollution: workshop summary

Forty-nine experts from 18 industrial and developing countries met on 6 September 2001 in Garmisch-Partenkirchen, Germany, to discuss the economic and public health impacts of air pollution, particularly with respect to assessing the public health benefits from technologies and policies that reduce greenhouse gas (GHG) emissions. Such measures would provide immediate public health benefits, such as reduced premature mortality and chronic morbidity, through improved local air quality. These mitigation strategies also allow long-term goals--for example, reducing the buildup of GHG emissions--to be achieved alongside short-term aims, such as immediate improvements in air quality, and therefore benefits to public health. The workshop aimed to foster research partnerships by improving collaboration and communication among various agencies and researchers; providing a forum for presentations by sponsoring agencies and researchers regarding research efforts and agency activities; identifying key issues, knowledge gaps, methodological shortcomings, and research needs; and recommending activities and initiatives for research, collaboration, and communication. This workshop summary briefly describes presentations made by workshop participants and the conclusions of three separate working groups: economics, benefits transfer, and policy; indoor air quality issues and susceptible populations; and development and transfer of dose-response relationships and exposure models in developing countries. Several common themes emerged from the working group sessions and subsequent discussion. Key recommendations include the need for improved communication and extended collaboration, guidance and support for researchers, advances in methods, and resource support for data collection, assessment, and research.     

Glucocorticoids induce neuroendocrine cell differentiation and increase expression of N-myc in N-type human neuroblastoma cells

Human neuroblastoma cell lines comprise cellular counterparts of normal differentiation phenotypes arising from the developing neural crest Three distinct cell types have been isolated from cell lines: N-type cells with properties of embryonic sympathoadrenoblasts, S-type cells resembling nonneuronal Schwannian/glial/melanoblastic precursors, and I-type stem cells that can differentiate into either N- or S-type cells. Sympathoadrenoblasts from the normal neural crest further differentiate into neuronal or neuroendocrine cells. In this study, we show that malignant N-type neuroblasts likewise can differentiate futher along these same pathways. Retinoic acid and forskolin induce a neuronalphenotype, denoted morphologically by cell aggregation and increased neurite formation and biochemically by increases in neurofilament proteins, tyrosine hydroxylase, and secretogranin II and decrease inchromogranin A. By contrast, dexamethasone, a synthetic glucocorticoid, induces a chromaffin cell phenotype characterized by increased cell flattening, loss of neuritic processes, increased chromogranin A and tyrosine hydroxylase proteins, and decreased amounts of secretogranin II and neurofilaments. N-myc gene expression is upregulated by glucocorticoids; dexamethasone-treated N-type cells show significant (2.3- to 7.8-fold) increases in N-myc mRNA and protein steady-state levels. This effect is specific for glucocorticosteroids, is blocked by addition of the steroid receptor antagonist RU486, and involves direct activation of the N-myc promoter. These findings are the first to show that glucocorticoids upregulate N-myc expression in human neuroblastoma cells.