A. Scott Laney

Molecular Evidence of Sexual Transmission of Ebola Virus

A suspected case of sexual transmission from a male survivor of Ebola virus disease (EVD) to his female partner (the patient in this report) occurred in Liberia in March 2015. Ebola virus (EBOV) genomes assembled from blood samples from the patient and a semen sample from the survivor were consistent with direct transmission. The genomes shared three substitutions that were absent from all other Western African EBOV sequences and that were distinct from the last documented transmission chain in Liberia before this case. Combined with epidemiologic data, the genomic analysis provides evidence of sexual transmission of EBOV and evidence of the persistence of infective EBOV in semen for 179 days or more after the onset of EVD. (Funded by the Defense Threat Reduction Agency and others.).

Pneumoconiosis among underground bituminous coal miners in the United States: is silicosis becoming more frequent?

Objectives Epidemiological reports since 2000 have documented increased prevalence and rapid progression of pneumoconiosis among underground coal miners in the United States. To investigate a possible role of silica exposure in the increase, we examined chest x-rays (CXRs) for specific abnormalities (r-type small opacities) known to be associated with silicosis lung pathology. Methods Underground coal miners are offered CXRs every 5 years. Abnormalities consistent with pneumoconiosis are recorded by National Institute for Occupational Safety and Health (NIOSH) B Readers using the International Labour Organization Classification of Radiographs of Pneumoconioses. CXRs from 1980 to 2008 of 90 973 participating miners were studied, focussing on reporting of r-type opacities (small rounded opacities 3–10 mm in diameter). Log binomial regression was used to calculate prevalence ratios adjusted for miner age and profusion category. Results Among miners from Kentucky, Virginia and West Virginia, the proportion of radiographs showing r-type opacities increased during the 1990s (prevalence ratio (PR) 2.5; 95% CI 1.7 to 3.7) and after 1999 (PR 4.1; 95% CI 3.0 to 5.6), compared to the 1980s (adjusted for profusion category and miner age). The prevalence of progressive massive fibrosis in 2000–2008 was also elevated compared to the 1980s (PR 4.4; 95% CI 3.1 to 6.3) and 1990s (PR 3.8; 95% CI 2.1 to 6.8) in miners from Kentucky, Virginia and West Virginia. Conclusions The increasing prevalence of pneumoconiosis over the past decade and the change in the epidemiology and disease profile documented in this and other recent studies imply that US coal miners are being exposed to excessive amounts of respirable crystalline silica.

Human herpesvirus 8: Current issues

Although human herpesvirus 8 (HHV-8) is the etiologic agent of Kaposi sarcoma (KS), there are no formal guidelines for the clinical management of HHV-8 infection. In patients infected with human immunodeficiency virus (HIV), highly active antiretroviral therapy (HAART) is the best tool for the prevention of KS. In patients who have undergone transplantation, KS is often managed by curtailing immunosuppressive therapies, despite the potential adverse consequences for graft survival. Interventions related to HHV-8 infection might improve the management of KS in immunocompromised patients. However, knowledge from HHV-8 research cannot yet be translated into clinically useful interventions. Achieving clinical utility will require the commercial development of diagnostic tools currently available only in research settings and the evaluation of potential interventions. Such interventions might include the use of HHV-8 diagnostics to identify patients at high risk and to aid in the early detection of KS, prophylaxis with antiherpes drugs to prevent KS, treatment of KS with antiherpes drugs, and donor/recipient screening for organ transplantation.

Human herpesvirus 8 presence and viral load are associated with the progression of AIDS-associated Kaposi's sarcoma.

Objective:We present the largest longitudinal study to date that examines the association between Kaposis Sarcoma (KS) disease progression and the presence and viral load of human herpesvirus 8 (HHV-8). Methods:Ninety-six men were enrolled at HIV clinics in Atlanta, Georgia, who had KS (n = 47) or were without KS but seropositive for HHV-8. Visits occurred at 6-month intervals for 2 years at which the patients KS status was evaluated and oral fluid and blood were collected for quantification of HHV-8 DNA and antibodies. Results:The presence of HHV-8 DNA in blood was more common (P < 0.001) and the viral load higher (P < 0.001) in men with KS in comparison with men without KS. Mean HHV-8 viral loads in blood and oral fluids were associated with disease status, being highest among patients with progressing KS, intermediate among patients with stable KS, and lowest among patients with regressing KS. Consistent with our previous report high antibody titers to HHV-8 orf 65 were inversely associated with HHV-8 shedding in oral fluid. Conclusions:We observed a significant association between changes in KS disease severity and the presence and viral load of HHV-8. HHV-8 viral load in blood may provide useful information to clinicians for assessment of the risk of further disease progression in patients with KS.

Reduced evolutionary rate in reemerged Ebola virus transmission chains.

Surveillance of Ebola virus disease flare-ups uncovers a reduced rate of Ebola virus evolution during persistent infections. On 29 June 2015, Liberia’s respite from Ebola virus disease (EVD) was interrupted for the second time by a renewed outbreak (“flare-up”) of seven confirmed cases. We demonstrate that, similar to the March 2015 flare-up associated with sexual transmission, this new flare-up was a reemergence of a Liberian transmission chain originating from a persistently infected source rather than a reintroduction from a reservoir or a neighboring country with active transmission. Although distinct, Ebola virus (EBOV) genomes from both flare-ups exhibit significantly low genetic divergence, indicating a reduced rate of EBOV evolution during persistent infection. Using this rate of change as a signature, we identified two additional EVD clusters that possibly arose from persistently infected sources. These findings highlight the risk of EVD flare-ups even after an outbreak is declared over.

Resurgence of a Debilitating and Entirely Preventable Respiratory Disease among Working Coal Miners

To the Editor: For more than 40 years, the National Institute for Occupational Safety and Health (NIOSH) has monitored trends in coal workers’ pneumoconiosis, including progressive massive fibrosis (PMF). PMF is an advanced, debilitating, and lethal form of coal workers’ pneumoconiosis with limited, primarily palliative treatment options and no cure. As part of ongoing surveillance efforts, NIOSH administers the Coal Workers’ Health Surveillance Program (CWHSP), which offers underground coal miners periodic chest radiographs and confidentially informs them of their pneumoconiosis status (1). Just 15 years ago, PMF was virtually eradicated, with a prevalence of 0.08% among all CWHSP participants and 0.33% among active underground miners with at least 25 years of mining tenure. Since that time, the national prevalence of PMF identified through the CWHSP has increased; the rate of increase in the central Appalachian states of Kentucky, Virginia, and West Virginia has been especially pronounced (Figure 1). Excessive inhalation of coal mine dust is the sole cause of PMF in working coal miners, so this increase can only be the result of overexposures and/or increased toxicity stemming from changes in dust composition (2). During 1998 to 2012, NIOSH identified 154 cases of PMF among CWHSP participants, 125 of whom were long-tenured underground coal miners in central Appalachia. In 2012, the prevalence of PMF in this group of working miners reached 3.23% (5-year moving average), the highest level since the early 1970s. At the same time, NIOSH documented cases of PMF among surface coal miners with little or no underground mining tenure (3). Figure 1. Prevalence of progressive massive fibrosis among working underground coal miners with 25 or more years of underground mining tenure (1974–2012) in Kentucky, Virginia, and West Virginia, according to the Coal Workers’ Health Surveillance ... Each of these cases is a tragedy and represents a failure among all those responsible for preventing this severe disease. This year marks the 45th anniversary of the Federal Coal Mine Health and Safety Act. In that legislation, Congress enacted enforceable dust standards to reduce the incidence of coal workers’ pneumoconiosis and eliminate PMF among underground coal miners (4). Despite readily available dust control technology and best practices guidance (5), recent findings suggest dust exposures have not been adequately controlled and that a substantial portion of U.S. coal miners continue to develop PMF. On August 1, 2014, NIOSH issued an interim final rule modifying existing regulations to include surface coal miners in the CWHSP (6). In addition, the interim final rule expands medical surveillance beyond occupational history and chest radiography to include respiratory symptom assessment and spirometry testing for the recognition of undiagnosed chronic obstructive pulmonary disease among all working coal miners. We believe that expanded medical surveillance is an important part of ensuring success in efforts to protect U.S. coal miners from this deadly but entirely preventable disease.

Ebola and Its Control in Liberia, 2014–2015

Several factors explain the successful response to the outbreak in this country.

Quartz exposure can cause pneumoconiosis in coal workers

To the Editor: We read with interest the recent article by McCunney, Morfeld, and Payne entitled What Component of Coal Causes Coal Workers’ Pneumoconiosis (CWP)? The intent of the article was to identify the specific substance(s) in the underground coal mining environment that are directly responsible for causing CWP. In addressing this question, the authors use a substantial portion of their work to point out that exposure to silica does not likely contribute to CWP. The authors are not wrong in their assessment of the role of silica in the development of CWP when it occurs at low levels. Epidemiologic studies dating back to the early 1970s showed through modeling of quantitative exposure data that mixed coal mining dust was the primary factor relating to CWP development, whereas silica’s role was much smaller. Anthracite workers in many parts of the world have long been known to suffer high rates of CWP, although anthracite usually contains very low levels of silica. We believe that by downplaying silica in their desire to seek a more precise explanation for the cause of CWP, the authors have potentially done coal miners a great disservice. There is an important distinction that the authors fail to highlight in their report—silica may not be a major factor in the development of the clinical condition known as CWP, but silica does cause another form of pneumoconiosis among coal workers—silicosis. Silica remains a major risk factor for coal miners. This was amply demonstrated by the rapid development of pneumoconiosis among Scottish coal miners who had been engaged in cutting through a fault composed of sandstone rock. Weight for weight, silica is considerably more toxic than coal dust, and failure to control silica dust using a standard intended for coal dust can easily lead to massive overexposure to silica. In this, the approach to enforcing a silica standard in underground coal mines in the United States has been criticized as inadequate. As easily accessible coal seams are being depleted, attention is being paid increasingly to thin seams or to seams with rock intrusions that might not have been considered economically feasible to mine in the past. Mining these seams often requires cutting the adjacent rock, the roof, the floor, and intrusions, leading to exposures rich in silica dust. It is, therefore, critically important that the role of silica not be discounted when evaluating pneumoconiosis risk among coal miners. As surface and underground thin seam mining becomes more prominent the likelihood of increased silica exposure among miners, and the development of pneumoconiosis associated with those exposures becomes increasingly important. Situations where there is a risk of silica exposure must be identified, and silica dust levels controlled to the regulated level or lower. Only in this way will the potential future tragedy of an epidemic of silicosis in coal miners be averted. A. Scott Laney, PhD Michael D. Attfield, PhD Surveillance Branch, Division of Respiratory Disease Studies National Institute for Occupational Safety and Health Centers for Disease Control and Prevention Morgantown, WVa

Debilitating Lung Disease Among Surface Coal Miners With No Underground Mining Tenure

Objective: To characterize exposure histories and respiratory disease among surface coal miners identified with progressive massive fibrosis from a 2010 to 2011 pneumoconiosis survey. Methods: Job history, tenure, and radiograph interpretations were verified. Previous radiographs were reviewed when available. Telephone follow-up sought additional work and medical history information. Results: Among eight miners who worked as drill operators or blasters for most of their tenure (median, 35.5 years), two reported poor dust control practices, working in visible dust clouds as recently as 2012. Chest radiographs progressed to progressive massive fibrosis in as few as 11 years. One miners lung biopsy demonstrated fibrosis and interstitial accumulation of macrophages containing abundant silica, aluminum silicate, and titanium dust particles. Conclusions: Overexposure to respirable silica resulted in progressive massive fibrosis among current surface coal miners with no underground mining tenure. Inadequate dust control during drilling/blasting is likely an important etiologic factor.

Workshop summary: epidemiologic design strategies for studies of nanomaterial workers.

Objective: The potential health consequences of exposure to nanomaterials have yet to be elucidated though increasing evidence points to the potential for nanomaterials to cause adverse human health effects. This workshop addressed the feasibility of developing studies to measure health risks among nanomaterial workers. Methods: Breakout groups discussed different epidemiologic designs and methods to encourage companies to collect and retain exposure and health data. Results: Major challenges include defining and recruitment of appropriate study populations and obtaining adequate exposure data. Both prospective cohort studies and small cross-sectional panel studies utilizing biomarkers of exposure and effect offer approaches to study occupational groups. Conclusions: Potential exists to assemble cohorts to study the human health effects associated with nanomaterial exposure. Stakeholder partnerships are critical to the success of these studies and international partnerships hold great potential.