We read with interest the article by Culver and colleagues (1), who describe the use of idiopathic pulmonary fibrosis (IPF) patient registries to capture clinically relevant data on the clinical course and impact of IPF. The authors summarize the attributes of IPF registries, including descriptions of current diagnostic and management practices and collection of biological specimens (1), but they do not discuss the role patient registries can play in the collection of occupational and environmental exposure data.

We read with interest the research letter by Fernández Pérez and colleagues (1) and agree that population-level mortality from hypersensitivity pneumonitis (HP) has not been well characterized in the United States. However, the role of occupation in the development and severity of HP is well established (2–4). Occupational exposures are responsible for a substantial portion of HP cases, and it is important to monitor trends in morbidity and mortality so that prevention activities can be prioritized. To that end, we conducted a similar analysis of HP mortality data from 2003 to 2017 (ICD-10 code J67.x) while also taking available employment history into account.

Silicosis is usually a disease of long latency affecting mostly older workers; therefore, silicosis deaths in young adults (aged 15-44 years) suggests acute or accelerated disease. To understand the circumstances surrounding silicosis deaths among young persons, CDC analyzed the underlying and contributing causes of death using multiple cause-of-death data (1999-2015) and industry and occupation information abstracted from death certificates (1999-2013). During 1999-2015, among 55 pneumoconiosis deaths of young adults with International Classification of Diseases, Tenth Revision (ICD-10) code J62 (pneumoconiosis due to dust containing silica), section sign 38 (69%) had code J62.8 (pneumoconiosis due to other dust containing silica), and 17 (31%) had code J62.0 (pneumoconiosis due to talc dust) listed on their death certificate. Decedents whose cause of death code was J62.8 most frequently worked in the manufacturing and construction industries and production occupations where silica exposure is known to occur. Among the 17 decedents who had death certificates listing code J62.0 as cause of death, 13 had certificates with an underlying or a contributing cause of death code listed that indicated multiple drug use or drug overdose. In addition, 13 of the 17 death certificates listing code J62.0 as cause of death had information on decedent's industry and occupation; among the 13 decedents, none worked in talc exposure-associated jobs, suggesting that their talc exposure was nonoccupational. Examining detailed information on causes of death (including external causes) and industry and occupation of decedents is essential for identifying silicosis deaths associated with occupational exposures and reducing misclassification of silicosis mortality.

Malignant mesothelioma is a neoplasm associated with occupational and environmental inhalation exposure to asbestos fibers and other elongate mineral particles (EMPs). Patients have a median survival of approximately 1 year from the time of diagnosis. The latency period from first causative exposure to malignant mesothelioma development typically ranges from 20 to 40 years but can be as long as 71 years. Hazardous occupational exposures to asbestos fibers and other EMPs have occurred in a variety of industrial operations, including mining and milling, manufacturing, shipbuilding and repair, and construction. Current exposures to commercial asbestos in the United States occur predominantly during maintenance operations and remediation of older buildings containing asbestos. To update information on malignant mesothelioma mortality (5), CDC analyzed annual multiple cause-of-death records for 1999-2015, the most recent years for which complete data are available. During 1999-2015, a total of 45,221 deaths with malignant mesothelioma mentioned on the death certificate as the underlying or contributing cause of death were reported in the United States, increasing from 2,479 deaths in 1999 to 2,597 in 2015 (in the same time period the age-adjusted death rates section sign decreased from 13.96 per million in 1999 to 10.93 in 2015). Malignant mesothelioma deaths increased for persons aged ≥85 years, both sexes, persons of white, black, and Asian or Pacific Islander race, and all ethnic groups. Despite regulatory actions and the decline in use of asbestos the annual number of malignant mesothelioma deaths remains substantial. The continuing occurrence of malignant mesothelioma deaths underscores the need for maintaining measures to prevent exposure to asbestos fibers and other causative EMPs and for ongoing surveillance to monitor temporal trends.

Silicosis is a potentially fatal but preventable occupational lung disease caused by inhaling respirable crystalline silica (silica). Chronic silicosis, the most common form, occurs after exposure to relatively low silica concentrations for >10 years. Accelerated silicosis occurs after 5-10 years of exposure to higher silica levels, and acute silicosis can occur after only weeks or months of exposure to extremely high silica concentrations. New national mortality data for silicosis have become available since a previous report on silicosis surveillance was published earlier this year. CDC reviewed multiple cause-of-death mortality files from the National Center for Health Statistics to analyze deaths from silicosis (International Classification of Diseases, 10th Revision diagnosis code J62: a pneumoconiosis due to dust containing silica) reported during 1999-2013. Each record lists one underlying cause of death (the disease or injury that initiated the chain of events that led directly and inevitably to death), and up to 20 contributing causes of death (other significant conditions contributing to death but not resulting in underlying cause). Available death certificates from 35 states were reviewed for the period 2004-2006 to identify occupations associated with silicosis among decedents aged 15-44 years. Results indicate that despite substantial progress in eliminating silicosis, silicosis deaths continue to occur. Of particular concern are silicosis deaths in young adults (aged 15-44 years). These young deaths likely reflect higher exposures than those causing chronic silicosis mortality in older persons, some of sufficient magnitude to cause severe disease and death after relatively short periods of exposure. A total of 12 such deaths occurred during 2011-2013, with nine that had silicosis listed as the underlying cause of death.

Silicosis is a preventable occupational lung disease caused by the inhalation of respirable crystalline silica dust and can progress to respiratory failure and death. No effective specific treatment for silicosis is available; patients are provided supportive care, and some patients may be considered for lung transplantation. Chronic silicosis can develop or progress even after occupational exposure has ceased. The number of deaths from silicosis declined from 1,065 in 1968 to 165 in 2004. Hazardous occupational exposures to silica dust have long been known to occur in a variety of industrial operations, including mining, quarrying, sandblasting, rock drilling, road construction, pottery making, stone masonry, and tunneling operations. Recently, hazardous silica exposures have been newly documented during hydraulic fracturing of gas and oil wells and during fabrication and installation of engineered stone countertops. To describe temporal trends in silicosis mortality in the United States, CDC analyzed annual multiple cause-of-death data for 2001-2010 for decedents aged ≥15 years. During 2001-2010, a total of 1,437 decedents had silicosis coded as an underlying or contributing cause of death. The annual number of silicosis deaths declined from 164 (death ratedagger = 0.74 per 1 million population) in 2001 to 101 (0.39 per 1 million) in 2010 (p = 0.002). Because of new operations and tasks placing workers at risk for silicosis, efforts to limit workplace exposure to crystalline silica need to be maintained.

BACKGROUND: Although asbestos use has been restricted in recent decades, asbestos-associated deaths continue to occur in the United States. OBJECTIVES: We evaluated premature mortality and loss of potentially productive years of life attributable to asbestos-associated diseases. METHODS: Using 1999-2010 National Center for Health Statistics mortality data, we identified decedents aged ≥25 years whose death certificate listed asbestosis and malignant mesothelioma as the underlying cause of death. We computed years of potential life lost to life expectancy (YPLL) and to age 65 (YPLL65 ). RESULTS: During 1999-2010, a total of 427,005 YPLL and 55,184 YPLL65 were attributed to asbestosis (56,907 YPLL and 2,167 YPLL65 ), malignant mesothelioma (370,098 YPPL and 53,017 YPLL65 ). Overall and disease-specific asbestos-attributable total YPLL and YPLL65 and median YPLL and YPLL65 per decedent did not change significantly from 1999 to 2010. CONCLUSIONS: The continuing occurrence of asbestos-associated diseases and their substantial premature mortality burden underscore the need for maintaining prevention efforts and for ongoing surveillance to monitor temporal trends in these diseases.

Haemagglutination-inhibition (HI) and virus neutralisation (VN) assays are used to evaluate immunogenicity of pandemic H1N1 vaccines; however these bioassays are poorly standardised leading to inter-laboratory variation. A candidate International Standard (IS) for antibody to H1N1pdm virus (09/194) was prepared from pooled sera of subjects who had either recovered from H1N1pdm infection or who had been immunised with an adjuvanted subunit vaccine prepared from reassortant virus NYMC X-179A (derived from A/California/7/2009 virus). Ten laboratories from seven countries tested the candidate IS, 09/194 and a panel of human sera by HI and VN using the A/California/7/2009 virus (six laboratories) and/or the reassortant virus NYMC X-179A (ten laboratories). As expected, the inter-laboratory variability for HI and VN assay results was high. For results of antibody tests to NYMC X-179A, the % geometric coefficient of variation (%GCV) for 09/194 between laboratories was 83% for HI and 192% for VN. For tests of all sera, the median %GCV ranged from 95 to 345% for HI (80-fold variation) and 204 to 383% for VN (109-fold variation), but for the titres relative to 09/194 the median %GCV was much reduced (HI 34-231%; VN 44-214%). For tests of antibody to the A/California/7/2009 wild type virus there were similar reductions in %GCV when 09/194 was used. These results suggest that 09/194 will be of use to standardise assays of antibody to A/California/7/2009 vaccine and 09/194 has now been established by WHO as an IS for antibody to A/California/7/2009 with an assigned potency of 1300 IU per ml.

The presence of tuberculosis (TB) in patients with silicosis increases mortality risk. To characterize silicosis-respiratory TB comortality in the United States, the authors used 1968-2006 National Center for Health Statistics multiple cause-of-death data for decedents aged ≥25 years. The authors calculated proportionate mortality ratios (PMRs) using available information on decedents' industries and occupations reported from 26 states from 1985 through 1999. Among 16,648 silicosis deaths, 2,278 (13.7%) had respiratory TB listed on the death certificate. Of silicosis-respiratory TB deaths, 1,666 decedents (73.1%) were aged ≥65 years, 2,255 (99.0%) were male, and 1,893 (83.1%) were white. Silicosis-respiratory TB deaths declined 99.5% during the study period (P < 0.001 for time-related trend), from 239.8 per year during 1968-1972 to 1.2 per year during 2002-2006, with no reported deaths in 2006. Silicosis-respiratory TB deaths reported from Pennsylvania (n = 525; 1.29 per million population), Ohio (n = 258; 0.81 per million), and West Virginia (n = 146; 2.35 per million) accounted for 40.8% of all such deaths in the United States. The highest PMR for silicosis-respiratory TB death was associated with the "miscellaneous nonmetallic mineral and stone products" industry (PMR = 73.7, 95% confidence interval: 33.8, 139.8). In the United States, 2006 marked the first year since 1968 with no silicosis-respiratory TB deaths. The substantial decline in silicosis-respiratory TB comortality probably reflects prevention and control measures for both diseases.

Hemagglutination-inhibition (HI) and neutralization are used to evaluate vaccines against influenza virus A (H5N1); however, poor standardization leads to interlaboratory variation of results. A candidate antibody standard (07/150) was prepared from pooled plasma of persons given clade 1 A/Vietnam/1194/2004 vaccine. To test human and sheep antiserum, 15 laboratories used HI and neutralization and reassortant A/Vietnam/1194/2004, A/turkey/Turkey/1/2005 (clade 2.2), and A/Anhui/1/2005 (clade 2.3.4) viruses. Interlaboratory variation was observed for both assays, but when titers were expressed relative to 07/150, overall percentage geometric coefficient of variation for A/Vietnam/1194/2004 was reduced from 125% to 61% for HI and from 183% to 81% for neutralization. Lack of reduced variability to clade 2 antigens suggested the need for clade-specific standards. Sheep antiserum as a standard did not reliably reduce variability. The World Health Organization has established 07/150 as an international standard for antibody to clade 1 subtype H5 and has an assigned potency of 1,000 IU/ampoule.