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Silicosis-Related Years of Potential Life Lost Before Age 65 Years – United States, 1968-2005

August 10, 2008

By Mazurek, JM Wood, JM

Occupational exposure to respirable crystalline silica occurs in construction, mining, manufacturing, and other industries and can result in silicosis and other lung diseases. Classic (chronic) silicosis results from exposure to relatively low concentrations of respirable crystalline silica for >/=10 years. Exposure to higher concentrations of silica for 5-10 years can cause accelerated silicosis, and symptoms of acute silicosis can sometimes develop within weeks of initial exposure to extreme concentrations of silica (I). Deaths in young adults from acute or accelerated silicosis generally reflect more recent and intense exposures (2). Silicosis is incurable, but preventable through effective control and elimination of exposure to respirable crystalline silica (1). To characterize recent trends in premature mortality attributed to silicosis in the United States, CDC analyzed annual mortality data from 1968-2005, the most recent years for which complete data were available.* Years of potential life lost before age 65 years (YPLL) and mean YPLL were calculated using standard methodology (3). During 1968-2005, total annual YPLL attributed to silicosis (17,130) declined 90.2%, from 1,441 (mean per decedent: 7-7 YPLL) to 141 (mean per decedent: 11.8), with an annual average of 8.6 YPLL per decedent for the period. However, the proportion of YPLL attributable to young silicosis decedents increased; an estimated 3,600-7,300 new silicosis cases occur annually (4). Hazard surveillance, workplace-specific interventions, and further silicosis prevention and elimination efforts, especially among young adults, are needed. For this analysis, decedents for whom the International Classification of Diseases (ICD) code for silicosis was listed as the underlying cause of death were identified from 1968-2005 mortality data. [dagger] Deaths with the ICD-10 underlying cause of death coded as J65 (pneumoconiosis associated with tuberculosis) were included if code J62 (silicosis) was listed on the entity axis. [section] Because silicosis primarily results from occupational exposure, only deaths of persons aged >/=15 years were considered. Young silicosis deaths were defined as those occurring in persons aged 15-44 years. Information on the usual industry and occupation (defined as the industry and occupation in which a person worked most of his or her life) of decedents was obtained from death certificates for a subset of decedents reported from 26 states[para] for some years during 1985-1999. Reporting the usual industry and occupation of decedents began in 1985 and ended in 1999. The number of states reporting data in a particular year during 1985-1999 ranged from 16 to 22, and the number of years of data availability for any one state varied from 2 to 15 years. Industry and occupation were coded using the 1980 and 1990 U.S. Census Bureau coding systems.

During 1968-2005, silicosis was coded as the underlying cause of death on 7,793 certificates. Of these, 1,997 (25-6%) were for decedents aged 15-64 years, accounting for 17,130 YPLL (mean per decedent: 8.6 YPLL). The majority of silicosis decedents aged 15-64 years were males (1,941; 97-2%) and whites (1,571; 78.6%), accounting for 16,390 (95-7%) and 12,289 (71.7%) YPLL, respectively (Table 1).

From 1968 to 2005, annual YPLL attributed to silicosis declined 90.2%, from 1,441 (mean per decedent: 7-7 YPLL) to 141 in 2005 (mean per decedent: 11.8); YPLL varied annually from a high of 1,441 (mean per decedent: 7-7) in 1968 to a low of 103 (mean per decedent: 6.4) in 1995 (Figure).

Of all silicosis decedents aged 15-64 years, 177 (8.9%) were considered young (aged 15-44 years), which accounted for 4,693 YPLL (mean per decedent: 26.5 YPLL), representing 27-4% of the total YPLL for the period. The YPLL attributed to young silicosis deaths declined 65-0%, from an average of 183-4 per year during 1968-1972 to 64.2 per year during 2001-2005. YPLL attributed to silicosis decedents aged 4564 years declined 88.0%, from an annual average of 898.4 during 1968-1972 to 108.2 during 2000-2005. The proportion of YPLL attributable to young silicosis decedents increased from 17.0% during 1968-1972 to 37.2% during 2000-2005 (Figure).

Overall, deaths reported from Pennsylvania (349; 2,343 YPLL), Ohio (197; 1,568), and Texas (94; 1,219) accounted for 32.0% of all deaths and 29-9% of the total YPLL during 1968-2005 (Table 1). Young silicosis deaths from eight states (Texas [19; 552 YPLL], Ohio [15; 362], California [11; 280], Pennsylvania [11; 228], Indiana [10; 242], Louisiana [10; 275], Michigan [9; 186], and Alabama [8; 229]) accounted for 52.5% of all young deaths and 51.4% of the YPLL contributed by young decedents.

Industry or occupation information was available for 148 (39-6%) of 374 decedents aged 15-64 years whose deaths were attributed to silicosis during 1985-1999 (Table 2). Of 46 industries reported, the greatest YPLL were in construction (263; mean per decedent: 10.1 YPLL); iron and steel foundries (131; mean per decedent: 10.9); and blast furnaces, steelworks, rolling and finishing mills (97; mean per decedent: 10.8). Among 53 occupations reported, the greatest YPLL were for miscellaneous metal and plastic processing machine operators (174; mean per decedent: 21.8 YPLL); laborers, except construction (120; mean per decedent: 12); and mining machine operators (113; mean per decedent: 5-4).**

Editorial Note: In 2005, CDC reported a decline in annual U.S. silicosis deaths, from 1,157 (8.91 per million persons aged >15 years) in 1968 to 148 (0.66) in 2002 (5). The decline was attributed to several factors, including enactment of national compliance standards for silica dust exposure in the early 1970s, general adoption of disease prevention measures, and changes over time in industrial activity (5). The findings in this report indicate that silicosis-attributable YPLL decreased substantially during 1968- 2005, but the decline became less pronounced during 1995-2005.

The decline in annual silicosis-attributable YPLL is mostly attributed to the decrease in deaths from silicosis among persons aged 45-64 years, indicating the effects of implementation of exposure standards and regulations, changes in industrial activity, and other factors. However, workers exposed to silica below permissible and recommended exposure limits are still at risk for developing radiographic evidence of silicosis (1). The decline among young adults aged 15-44 years is less marked, indicating that intense overexposures to respirable crystalline silica continue to occur despite the existence of legally enforceable limits. Overall, an average of 8.6 YPLL per decedent were attributed to silicosis during 1968-2005 (26.5 YPLL per decedent among young adults). Available data (for 148 decedents) indicated that the greatest YPLL values were associated with work in construction and manufacturing. Years of potential life lost before age 65 years is a measure of premature mortality (3) that emphasizes deaths occurring among younger persons, on the assumption that these are a person’s most productive years. YPLL is considered the best single indicator of the differences in the health status of populations and is a useful aid in allocating federal funding for core public health functions (6).

The findings in this report are subject to at least five limitations. First, this report used a death certificate-based definition of silicosis as the underlying cause of death. Because some deaths from silicosis might have been attributed to other causes (e.g., tuberculosis) instead of silicosis or pneumoconiosis, the findings in this report likely underestimate the effect of silicosis on mortality and YPLL in the United States (7). Second, because individual work histories are not listed on death certificates, the relevance of the reported usual industry and occupation to actual hazardous exposures could not be verified. Although no studies have examined the accuracy of the usual industry and occupation information on death certificates specifically for silicosis decedents, research suggests generally good agreement of this information on death certificates compared with that from other sources (8,9). Moreover, codes for usual industry and occupation were available only for 39-6% of silicosis decedents for some states and years. Thus, these data likely are not nationally representative and should be interpreted cautiously. Third, reports indicate that the state of residence at death is not always the state in which the decedent’s exposure occurred (9). Fourth, because no information on silica exposure intensity or duration is listed on death certificates, silica exposure-response associations could not be examined. Finally, YPLL does not account for the actual burden of silicosis and other chronic occupational illnesses. Persons with silicosis might live for years with severely limited lung function, few treatment options, and an inability to work.

Although the findings in this report indicate a decrease in annual silicosis-related YPLL for 1968-2005, the increased proportion of silicosis-related deaths among young adults underscores the need for targeted prevention programs, investigation of cases, and individual case follow-up of silicosis deaths occurring at younger ages, as recommended by the Council of State and Territorial Epidemiologists (10). Effective primary prevention is critical because chronic silicosis can develop or progress even after occupational exposure ends (2). Acknowledgments

This report is based, in part, on contributions from F Rice, MPH, and J Myers, PhD, National Institute for Occupational Safety and Health, CDC.

* Since 1968, CDCs National Center for Health Statistics (NCHS) has compiled multiple cause of death data annually from death certificates in the United States. The National Institute for Occupational Safety and Health extracts information on deaths from occupationally related respiratory diseases and conditions from the NCHS data and stores the information in the National Occupational Respiratory Mortality System (NORMS), available at http:// webappa.cdc.gov/ords/norms.html.

[dagger] ICD-8 code 515.0 (silicosis) or code 010 (silicotuberculosis) for years 19681978, ICD-9 code 502 (pneumoconiosis due to other silica or silicates) for years 1979- 1998, and ICD-10 code J62 (pneumoconiosis due to dust containing silica [silicosis]) for years 1999-2005.

[section] Entity axis includes information on all of the diseases, injuries, or medical complications, as well as the location (part, line, and sequence) of the information recorded on each death certificate. “Detail Record Layout” available at http:// www.cdc.gov/nchs/about/major/dvs/mcd/1998mcd.htm.

[para] Alaska, Colorado, Georgia, Hawaii, Idaho, Indiana, Kansas, Kentucky, Maine, Missouri, Nebraska, Nevada, New Hampshire, New Jersey, New Mexico, North Carolina, Ohio, Oklahoma, Rhode Island, South Carolina, Tennessee, Utah, Vermont, Washington, West Virginia, and Wisconsin.

** Silicosis has been associated with sandblasting, exposure to cement dust, and other job activities that expose workers to respirable crystalline silica (1).

References

1. National Institute for Occupational Safety and Health. NIOSH hazard review. Health effects of occupational exposure to respirable crystalline silica. Washington, DC: US Department of Health and Human Services, CDC, National Institute for Occupational Safety and Health; 2002. DHHS (NIOSH) publication no. 2002-129. Available at http:// www.cdc.gov/niosh/02-129a.html.

2. CDC Silicosis deaths among young adults- United States, 1968- 1994. MMWR 1998;47:331-5.

3. Wise RP, Livengood JR, Berkelman RL, Goodman RA. Methodological alternatives for measuring premature mortality. Am J Prev Med 1988;4:268-73.

4. Rosenman KD, Reilly MJ, Henneberger PK. Estimating the total number of newly-recognized silicosis cases in the United States. Am J Ind Med 2003;44:14-7.

5. CDC. Silicosis mortality, prevention, and control-United States, 1968-2002. MMWR 2005;54:401-5.

6. US General Accounting Office. Public health: a health status indicator for targeting federal aid to states. Washington, DC: US General Accounting Office; 1996. GAO/HEHS-97-13. Available at http:/ / www. access, gpo.gov/cgi-bin/getdoc. cgi ?db name = gao &docid= fihe97013.txt.pdf.

7. Cottrell A, Schwartz E, Sokas R, Kofie V, Welch L. Surveillance of sentinel occupational mortality in the District of Columbia: 1980 to 1987. Am J Public Health 1992;82:117-9.

8. Gute DM, Fulton JP Agreement of occupation and industry data on Rhode Island death certificates with two alternative sources of information. Public Health Rep 1985;100:65-72.

9. Steenland K, Beaumont J. The accuracy of occupation and industry data on death certificates. J Occup Med 1984;26:288-96.

10. Council of State and Territorial Epidemiologists. Silicosis surveillance and case definition: position statement: 1999 ENV 4. Atlanta, GA: Council of State and Territorial Epidemiologists; 1999. Available at http://www.cste.org/ps/pssearch/9l9 9/19 99-env- 04.htm.

Reported by: JM Mazurek, MD, JM Wood, MS, Div Respiratory Disease Studies, National Institute for Occupational Safety and Health, CDC.

Copyright U.S. Center for Disease Control Jul 18, 2008

(c) 2008 MMWR. Morbidity and Mortality Weekly Report. Provided by ProQuest Information and Learning. All rights Reserved.




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