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Chronic Obstructive Pulmonary Disease (ICD-9 Codes 490-492, 494, 496)Chronic obstructive pulmonary disease (COPD) includes chronic bronchitis (ICD-9 codes 490-491), emphysema (bronchiectasis (ICD-9 code 494), and chronic airway obstruction (ICD-9 code 496). These diseases are commonirreversible airflow limitation. Some authorities include asthma (ICD-9 code 493) and hypersensitivity pneumonitin the COPD rubric, but these infrequent causes of death (see Table 1) are categorized separately in this atlas. COPD has become a major public health concern. In 1995, it ranked as the fourth leading cause of death in the Uaccounting for over 100,000 deaths--nearly twice as many as in 1980 [NCHS 1997]. In 1994, an estimated 16 miUnited States had the diagnosis of COPD, representing a 60 percent increase since 1982 [ALA 1996]. Although 80 to 90 percent of COPD cases are attributable to cigarette smoking [USDHHS 1984], the etiology of multifactorial. Additional risk factors include occupational exposures, air pollution, respiratory infection, and genrelationship of COPD to workplace exposure is well documented for several occupational agents (e.g., coal mine grain dust, etc.). More generally, estimates of the proportion of COPD attributable to occupational exposure basestudies conducted in the United States range as high as 14 percent and 28 percent [Becklake 1994]. InvestigationCOPD with exposure to particulates in the general environment suggest that nonoccupational exposure to airbornimportant cause of preventable morbidity and mortality [Dockery et al. 1993; Sunyer et al. 1993]. ReferencesALA (American Lung Association) [1996]. Trends in chronic bronchitis and emphysema: morbidity and mortality. New York, NY, pBecklake MR [1994]. The workrelatedness of airways dysfunction. In: Proceedings of the 9th international symposium in epidemiolo

health. DHHS(NIOSH) Publication No. 94-112, pp. 1-28.Dockery DW, Pope CA, Xiping X, et al. [1993]. An association between air pollution and mortality in six U.S. cities. N Engl J Med NCHS (National Center for Health Statistics) [1997]. Health United States 1996-97 and injury chartbook. DHHS Pub. No. (PHS) 97-1Sunyer J, Saez M, Murillo C, et al. [1993]. Air pollution and emergency room admissions for chronic obstructive pulmonary disease: Epidemiol 137:701-705.USDHHS (U.S. Department of Health and Human Services) [1984]. The health consequences of smoking: chronic obstructive lung disurgeon general. Washington, D.C.: U.S. Government Printing Office., pp. 5-9.
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Asthma (ICD-9 Code 493)Asthma (ICD-9 code 493) is a clinical condition characterized by variable airflow limitation and increased responstracheobronchial tree to a variety of stimuli [ATS 1987]. Asthma can be induced by occupational exposures to air[Chan-Yeung 1994]. Asthma can also be aggravated in individuals with underlying asthma who are exposed to airbronchoconstrictive agents in the workplace [Wagner and Wegman 1998]. Asthma has been estimated to affect approximately 5 to 7 percent of the United States population [Brooks 1992]. prevalence of occupational asthma in the United States is unknown, but occupational exposures may cause up to asthma [Blanc 1987], and 21-33 percent of adult asthma may be caused or significantly worsened by such exposur1998; Ng et al. 1994]. Asthma is the most frequently reported work-related respiratory disease in the United King1997].Little is known about the geographic variation of asthma mortality. In addition to possible differences in exposure agents that cause asthma, geographic variation in asthma mortality may be due to urban-rural differences, humidity conditions affecting both indoor and outdoor allergen exposures, ambient air pollution, nutrition, genetic predispoquality medical care, ethnic and socioeconomic factors [Sears 1997].  ReferencesATS (American Thoracic Society) [1987]. Standards for the diagnosis and care of patients with chronic obstructive pulmonary diseasAm Rev Respir Dis 136:225-244.Blanc P [1987]. Occupational asthma in a national disability survey. Chest 92:613-617.Brooks SM [1992]. Occupational and environmental asthma. In: Rom WN, ed. Environmental and occupational medicine. 2nd ed. Boand Company, pp. 393-446.Chan-Yeung M [1994]. Asthma. In: Rosenstock L, Cullen MR eds. Textbook of clinical occupational and environmental medicine. PSaunders Company, pp. 197-209Milton DK, Solomon GM, Rosiello RA, Herrick RF [1998]. Risk and incidence of asthma attributable to occupational exposure amonInd Med 33:1-10.Ng TP, Hong CY, Goh LG, Wong ML, Koh KT, Ling SL [1994]. Risks of asthma associated with occupations in a community-based Ind Med 25:709-718.Ross DJ, Keynes HL, McDonald JC [1997]. SWORD ‘96: surveillance of work-related and occupational respiratory disease in the UK381.Sears MR [1997]. Descriptive epidemiology of asthma. Lancet 350 (suppl II):1-27.Wagner GR, Wegman DH [1998]. Occupational asthma: prevention by definition. Am J Ind Med 33:427-429.
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Hypersensitivity Pneumonitis (ICD-9 Code 495)Hypersensitivity pneumonitis (HP), also referred to by the British as extrinsic allergic alveolitis (ICD-9 code 495), immunologically-mediated lung diseases caused by inhalation of a wide variety of antigenic materials [Schuyler 19induced by particulate organic antigens, but some reported cases have been caused by soluble antigens and low mreactive chemicals such as isocyanates and trimellitic anhydride. At the present time, farmer’s lung disease (causethermophilic actinomycetes growing on moldy hay), bird fancier’s disease (caused by bird proteins), HP associated bioaerosols in buildings (caused by microbes contaminating humidifiers, dehumidifiers, and heating, ventilation, asystems), and Japanese summer-type HP (caused by house dust contaminated with Trichosporon cutaneum) are th

recognized forms of HP. The disease is often occupationally-related, and new types of HP continue to be reporteagricultural and industrial practices lead to new types of antigenic exposures. For example, HP has recently been machinists exposed to aerosolized metal working fluids that are microbially-contaminated [Kreiss and Cox-Ganser HP has two different clinical presentations. In acute HP, shortness of breath, nonproductive cough, generalized aand malaise occur 2 to 9 hours after exposure. Chronic HP presents as progressively severe shortness of breath, nweight loss, and loss of appetite over a period of months to years. Chest radiographs show evidence of interstitial biopsies show chronic interstitial inflammation, usually with poorly formed nonnecrotizing granulomas; bronchiolipresent in 25-50 percent of cases. The prevalence of HP varies widely depending on the population studied and the method of case definition. Using definition, a large population-based study of over 1400 Wisconsin dairy farmers found disease prevalence to be 0.et al. 1981]. In contrast, a study of Scottish farmers estimated a prevalence rate of 2.3 percent to 8.6 percent baseexposure histories [Grant et al. 1972]. Unlike some other lung diseases, the risk of HP is substantially lower amonperhaps due to smoking effects on lung immunity [Schuyler 1998]. References

Grant IWB, Blyth W, Wardrop VE, Gordon RM, Pearson JC, Mair A [1972]. Prevalence of farmer’s lung disease in Scotland: a pilo1(799):530-534.Gruchow HW, Hoffmann RG, Marx JJ, Emanuel DA, Rimm AA [1981]. Precipitating antibodies to farmer’s lung antigens in a WiscAm Rev Respir Dis 124:411-415.Kreiss K, Cox-Ganser J [1997]. Metalworking fluid-associated hypersensitivity pneumonitis: a workshop summary. Am J Ind Med 3Schuyler M [1998]. Hypersensitivity pneumonitis. In: Fishman AP, Elias JA, Fishman JA, Grippi MA, Kaiser LR, Senior RM, eds. diseases and disorders. 3rd ed. New York, NY: McGraw-Hill, pp. 1085-1132.
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