5
RESPIRATORY OUTCOMES

This chapter focuses on several long-term respiratory conditions: asthma, chronic bronchitis, emphysema, and chronic obstructive pulmonary disease (COPD). The nature of respiratory symptoms and the reversibility of airway obstruction distinguish asthma from the other respiratory conditions listed above.

Asthma is marked by reversible airway obstruction and airway inflammation. People with asthma manifest symptoms—such as wheezing, coughing, and exertional dyspnea—that are accompanied by increased airflow obstruction. Chronic bronchitis is characterized by chronic cough and sputum production. Pulmonary emphysema (commonly referred to as emphysema) is a pathologic process involving air-space enlargement distal to the terminal bronchioles, accompanied by destruction of the bronchiolar walls. COPD includes chronic bronchitis and emphysema. The diagnosis of COPD requires objective evidence of airflow obstruction with spirometry according to GOLD1 criteria (Pauwels et al. 2001).

The epidemiologic literature covering environmental agents and respiratory conditions has used varying definitions as knowledge has evolved. Summaries of key studies used by the committee in drawing its conclusions include details of how respiratory conditions were defined. Because of the impracticality of spirometry for large-scale epidemiologic studies, researchers often asked respondents about “physician-diagnosed” respiratory conditions or about respiratory symptoms. The hallmark symptom of asthma is wheezing, and that of chronic bronchitis is persistent cough and phlegm production (usually lasting 3 months/year for more than 2 years). For the last half-century, epidemiologic studies have used standard questions about cough and phlegm or sputum to define chronic bronchitis. Definitive diagnosis of emphysema requires pathologic examination of lung tissue or high-resolution thoracic computed tomography, although it can be inferred from characteristic physiologic changes, such as reduction in diffusion capacity.

The present report focuses on induction rather than exacerbation of disease, so this chapter emphasizes incident cases rather than exacerbation of pre-existing disease (for example, Eisner et al. 2002; Hong et al. 1994). Studies of prevalent disease are also included because they cover both new cases and exacerbation of preexisting conditions. The committee excluded the numerous time-series studies as they examine episodes of daily morbidity or mortality. Time-

1  

World Health Organization Global Initiative for Chronic Obstructive Lung Disease (GOLD).



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Gulf War and Health: Fuels, Combustion Products, and Propellants - Volume 3 5 RESPIRATORY OUTCOMES This chapter focuses on several long-term respiratory conditions: asthma, chronic bronchitis, emphysema, and chronic obstructive pulmonary disease (COPD). The nature of respiratory symptoms and the reversibility of airway obstruction distinguish asthma from the other respiratory conditions listed above. Asthma is marked by reversible airway obstruction and airway inflammation. People with asthma manifest symptoms—such as wheezing, coughing, and exertional dyspnea—that are accompanied by increased airflow obstruction. Chronic bronchitis is characterized by chronic cough and sputum production. Pulmonary emphysema (commonly referred to as emphysema) is a pathologic process involving air-space enlargement distal to the terminal bronchioles, accompanied by destruction of the bronchiolar walls. COPD includes chronic bronchitis and emphysema. The diagnosis of COPD requires objective evidence of airflow obstruction with spirometry according to GOLD1 criteria (Pauwels et al. 2001). The epidemiologic literature covering environmental agents and respiratory conditions has used varying definitions as knowledge has evolved. Summaries of key studies used by the committee in drawing its conclusions include details of how respiratory conditions were defined. Because of the impracticality of spirometry for large-scale epidemiologic studies, researchers often asked respondents about “physician-diagnosed” respiratory conditions or about respiratory symptoms. The hallmark symptom of asthma is wheezing, and that of chronic bronchitis is persistent cough and phlegm production (usually lasting 3 months/year for more than 2 years). For the last half-century, epidemiologic studies have used standard questions about cough and phlegm or sputum to define chronic bronchitis. Definitive diagnosis of emphysema requires pathologic examination of lung tissue or high-resolution thoracic computed tomography, although it can be inferred from characteristic physiologic changes, such as reduction in diffusion capacity. The present report focuses on induction rather than exacerbation of disease, so this chapter emphasizes incident cases rather than exacerbation of pre-existing disease (for example, Eisner et al. 2002; Hong et al. 1994). Studies of prevalent disease are also included because they cover both new cases and exacerbation of preexisting conditions. The committee excluded the numerous time-series studies as they examine episodes of daily morbidity or mortality. Time- 1   World Health Organization Global Initiative for Chronic Obstructive Lung Disease (GOLD).

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Gulf War and Health: Fuels, Combustion Products, and Propellants - Volume 3 series studies do not consider pre-existing conditions and report on acute outcomes rather than long-term health effects. For relevance to Gulf War veterans, the committee focused on long-term respiratory effects that persist after exposure ceases (see Chapter 2). The first section of this chapter will discuss respiratory outcomes related to exposure to fuels, and the next section will discuss outcomes related to exposure to combustion products. The section on combustion products has the benefit of several large epidemiologic studies of Gulf War veterans who had objectively confirmed exposure to smoke from oil-well fires. FUELS AND RESPIRATORY OUTCOMES Most studies of fuel exposure reviewed by the committee were cohort-mortality studies. They included Australian petroleum-industry workers (Christie et al. 1987), Chevron petroleum-refinery workers (Dagg et al. 1992), Exxon refinery and chemical-plant workers (Hanis et al. 1985), US petroleum-refinery workers (Kaplan 1986), UK oil-refinery workers (Rushton and Alderson 1981), and petroleum-refinery workers in Beaumont, Texas (Wong et al. 2001a) and Torrance, California (Wong et al. 2001b). The occupational-cohort studies, which had multiple outcomes apart from respiratory disease, are described briefly in Appendix D. All the occupational studies examined mortality due to noncancer respiratory outcomes among petroleum workers. Generally, the studies failed to indicate specific respiratory outcomes, although some do examine asthma, bronchitis, emphysema, and pneumonia or influenza separately. Most studies group all respiratory outcomes under the broad heading of “diseases of the respiratory system or tract” or “non-malignant respiratory disease”. Nonmalignant Respiratory Disease The studies that examined nonmalignant respiratory disease (Christie et al. 1987; Dagg et al. 1992; Hanis et al. 1985; Kaplan 1986; Wong et al. 2001a, 2001b) included all respiratory disorders, such as acute infections, diseases of the upper respiratory tract, pneumonia and influenza, asthma, bronchitis, emphysema, COPD, pneumoconiosis and other diseases due to external agents (such as asbestos), and other respiratory diseases. In all of those studies, the standardized mortality ratios (SMRs) were below 1.0 when compared with the general population or those not employed in the petroleum industry; this indicates that persons involved in the petroleum industry are not at greater risk for dying from respiratory diseases than the general population. However, selection bias is a limitation of the studies cited above because of the “healthy-worker” effect. In addition to the retrospective mortality studies identified above, the committee reviewed a cross-sectional study of Norwegian cable-plant workers exposed to oil mist or kerosene vapors (Skyberg et al. 1986). Seven cases of pulmonary fibrosis were found in 25 workers compared with one case in the control group. In a followup study of those workers (Skyberg et al. 1992), the authors examined whether the progression of pulmonary fibrosis continued after exposure to oil mist and vapors ceased and found that 10 of the 25 workers had pulmonary fibrosis compared with one in the control group. Smoking and exposure to asbestos were possible confounders in both studies.

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Gulf War and Health: Fuels, Combustion Products, and Propellants - Volume 3 Asthma Occupational factors are estimated to account for about 15% of the total burden of adult asthma (Balmes et al. 2003). Asthma is the most commonly reported occupational lung disease in most industrialized countries, and trends from long-standing surveillance in Finland and the UK show little change in incidence of occupational asthma over the last 10 years (Meyer et al. 2001; Reijula et al. 1996). Four cohort studies of refinery workers (Kaplan 1986); Rushton and Alderson 1981; Wong et al. 2001a, 2001b) did not find an increased risk of asthma compared with that in the general population, however, that may be due to the “healthy worker” effect which might involve self-selection against having asthma specifically. All the SMRs were below 1.0. The committee reviewed two case reports of asthma due to prolonged exposure to kerosene vapor from accidental domestic oil storage-tank spills (Todd and Buick 2000) and exposure to aviation fuel in an aircraft-engine mechanic (Makker and Ayres 1999). Six adults and three children were exposed to kerosene vapor, and one adult and the three children developed asthma that persisted for 3 years after the incident. A 42-year-old aircraft-engine mechanic reported being exposed to both high concentrations of aviation-fuel vapors and jet-stream emissions from aircraft engines. He developed symptoms almost immediately on beginning his job and was diagnosed with asthma within 4 years. The man reported that his symptoms improved when he was away from work for periods of at least 2 or 3 days. A review article by Rodriguez de 1a Vega et al. (1990) cites a study (Rodriguez de 1a Vega et al. 1981) in which 286 asthmatic patients who used kerosene for cooking were followed for 5 years. The authors found that 43.9% of those whose asthma did not improve continued to use kerosene as fuel for cooking; this suggests a relationship between exposure to kerosene and asthma. Chronic Bronchitis and Emphysema Rushton and Alderson (1981) and Wong et al. (2001a, 2001b) examined rates of bronchitis among refinery workers. Two of the three studies found no increased risk, however, one study found an SMR of 1.32, with a 95% confidence interval (CI) of 0.27–3.84 (Wong et al. 2001b). Three studies (Kaplan 1986; Wong et al. 2001a, 2001b) examined at emphysema and found SMRs of 1.0 or less, indicating no increased risk among refinery workers compared with the general population. The healthy-worker effect probably contributed to the results. Summary and Conclusion A fairly extensive literature describes results of cohort studies designed to examine mortality in workers in the petroleum industry (Table 5.1). Generally, those studies did not provide information about specific respiratory disease outcomes but rather provided SMRs for broad categories of diseases that are designated as “diseases of the respiratory system or tract” or “non-malignant respiratory disease.” The studies generally did not report exposure assessment, so it is difficult to reach a conclusion as to a relationship between respiratory disease outcomes and exposure to fuels. Most of the studies indicate a healthy-worker effect, which complicates interpretation of their results.

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Gulf War and Health: Fuels, Combustion Products, and Propellants - Volume 3 The committee concludes, from its assessment of the epidemiologic literature, that there is inadequate/insufficient evidence to determine whether an association exists between exposure to fuels and any specific, nonmalignant respiratory outcomes including asthma, bronchitis, and emphysema. COMBUSTION PRODUCTS AND RESPIRATORY OUTCOMES The committee divided the epidemiologic literature of respiratory effects and exposure to combustion products into four general types: studies of Gulf War veterans exposed to oil-well fires, community air pollution studies, occupational studies, and studies of biomass fuel, which is burned for heating or cooking primarily in developing countries. Each part of this section begins with the most robust primary studies (that is, studies with strong methods and exposure information), and continues with mortality studies and support studies that add weight to the primary evidence but are not as methodologically robust. Key primary studies used to draw conclusions are also depicted in tables (Tables 5.1 to 5.5). Most studies reported on more than one respiratory condition. TABLE 5.1 Selected Epidemiologic Studies—Fuel Exposure and Respiratory Outcomes Reference Population Exposed Cases Estimated Relative Risk (95% CI) Nonmalignant Respiratory Disease Cohort Studies—Mortality Christie et al. 1987 Australian petroleum workers (range of ICD-9 codes used) 0 0.00 (0.00–0.44) Dagg et al. 1992 Chevron petroleum-refinery workers (range of ICD-8 codes used)       Richmond Plant 118 0.69 (0.57–0.82) El Segundo Plant 59 0.59 (0.45–0.76) Total 177 0.65 (0.56–0.75) Hanis et al. 1985 Exxon refinery and chemical-plant workers (range of ICD-8 codes used)       Total 164 0.64 (0.55–0.75) Active employees 16 0.27 (0.15–0.44)a Employees hired before 1956 162 0.65 (0.55–0.75)a White men 150 0.64 (0.54–0.75)a Black men 14 0.82 (0.45–1.37)a Baton Rouge plant 66 0.71 (0.55–0.91) Baytown plant 48 0.70 (0.52–0.93) Bayway/Bayonne plant 50 0.54 (0.40–0.71) Kaplan 1986 US petroleum-refinery workers (range of ICD-8 codes used) 167 0.64 (0.54–0.74)

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Gulf War and Health: Fuels, Combustion Products, and Propellants - Volume 3 Reference Population Exposed Cases Estimated Relative Risk (95% CI) Wong et al. 2001a Beaumont, Texas, refinery workers (range of ICD-8 codes used)       Entire cohort 155 0.62 (0.52–0.72) (p<0.01) Female employees 1 0.16 (0.004–0.86) Male employees 154 0.63 (0.53–0.73) (p<0.01) Length of employment, <10 years 14 0.56 (p<0.05) Length of employment, 10–29 years 51 0.74 (p<0.05) Length of employment, 30+ years 89 0.59 (p<0.01) Time since employment, <20 years 4 0.33 (p<0.05) Time since employment, 20–39 years 51 0.74 (p<0.05) Time since employment, 40+ years 99 0.60 (p<0.01) Wong et al. 2001b Torrance, California, refinery workers (range of ICD-8 codes used)       Entire cohort 55 0.79 (0.60–1.03) Length of employment, <10 years 8 0.77 Length of employment, 10–29 years 34 0.79 Length of employment, 30+ years 13 0.86 Time since employment, <20 years 2 0.35 Time since employment, 20–39 years 21 0.77 Time since employment, 40+ years 32 0.90 Cohort Study—Incidence Tsai et al. 1992 Shell Deer Park refinery and petroleum workers (range of ICD-9 codes used) 725 1.05 (0.98–1.13)   Production employees, 1981–1988 646 1.08 (1.00–1.17)   Staff employees, 1981–1988 79 0.88 (0.69–1.09) Asthma Cohort Studies—Mortality Kaplan 1986 US petroleum-refinery workers (range of ICD-8 codes used) 5 0.79 (0.26–1.85) Rushton and Alderson 1981 UK oil-refinery workers (range of ICD-8 codes used) 15 0.80 (0.45–1.32)a Wong et al. 2001a Beaumont, Texas, refinery workers (range of ICD-8 codes used)       Entire cohort 3 0.78 (0.16–2.28)

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Gulf War and Health: Fuels, Combustion Products, and Propellants - Volume 3 Reference Population Exposed Cases Estimated Relative Risk (95% CI) Bronchitis Cohort Studies—Mortality Rushton and Alderson 1981 UK oil refinery-workers (range of ICD-8 codes used) 253 0.64 (0.57–0.73)a Wong et al. 2001a Beaumont, Texas, refinery workers (range of ICD-8 codes used)       Entire cohort 3 0.34 (0.07–0.99) Wong et al. 2001b Torrance, California, refinery workers (range of ICD-8 codes used)       Entire cohort 3 1.32 (0.27–3.84) Emphysema Cohort Studies—Mortality Kaplan 1986 US petroleum-refinery workers (range of ICD-8 codes used) 46 0.63 (0.46–0.84) Wong et al. 2001a Beaumont, Texas, refinery workers (range of ICD-8 codes used)       Entire cohort 42 1.03 (0.74–1.40) Wong et al. 2001b Torrance, California, refinery workers (range of ICD-8 codes used)       Entire cohort 9 0.82 (0.38–1.56) Pneumonia and Influenza Cohort Studies—Mortality Kaplan 1986 US petroleum-refinery workers—pneumonia (range of ICD-8 codes used) 45 0.51 (0.37–0.68) Rushton and Alderson 1981 UK oil-refinery workers (range of ICD-8 codes used)       Pneumonia 157 0.86 (0.73–1.00)a   Influenza 11 0.40 (0.20–0.72)a Wong et al. 2001a Beaumont, Texas, refinery workers (range of ICD-8 codes used)       Entire cohort 60 0.58 (0.44–0.75) Female employees 1 0.39 (0.01–2.18) Male employees 59 0.59 (0.45–0.76) Length of employment, <10 years 4 0.44 Length of employment, 10–29 years 16 0.54 Length of employment, 30+ years 39 0.63 Time since employment, <20 years 2 0.36

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Gulf War and Health: Fuels, Combustion Products, and Propellants - Volume 3 Reference Population Exposed Cases Estimated Relative Risk (95% CI)   Time since employment, 20–39 years 10 0.40 Time since employment, 40+ years 47 0.68 Wong et al. 2001b Torrance, California, refinery workers (range of ICD-8 codes used)       Entire cohort 15 0.59 (0.33–0.98) Length of employment, <10 years 0 0.00 (p<0.05) Length of employment, 10–29 years 12 0.75 Length of employment, 30+ years 3 0.59 Time since employment, <20 years 0 0.00 Time since employment, 20–39 years 5 0.59 Time since employment, 40+ years 10 0.71 Cohort Study—Incidence Tsai et al. 1992 Shell Deer Park refinery and petroleum workers (range of ICD-9 codes used)       Production employees 168 0.97 (0.83–1.13)   Staff employees 28 0.74 (0.49–1.08) NOTE: ICD, International Classification of Diseases. a95% CI calculated by committee with standard methods from observed and expected numbers presented in original study. Gulf War Studies In February 1991, retreating Iraqi forces set fire to more than 600 oil wells. Fires burned over a 10-month period, until November 1991, exposing thousands of US troops to combustion products. Several studies of US Gulf War veterans exposed to oil-well fires stand out from most other Gulf War studies by virtue of their focus on a narrow set of respiratory health outcomes and on a single type of exposure (smoke from oil-well fires) and their exposure validation on the basis of models of troop unit movements in relation to air-monitoring data. The vast majority of Gulf War health studies focused on multiple health outcomes, multiple exposures, and self-reporting of exposures without validation. The studies summarized below examined long-term respiratory effects as veterans were surveyed after their deployment to the Persian Gulf. The first indication of possible long-term effects was from an uncontrolled study conducted in Germany, four weeks after deployment, which found that Army veterans that had been stationed near the fires reported coughing more frequently than before the war (Petruccelli et al. 1999). All studies discussed below are summarized in Table 5.2. Cowan et al. (2002) conducted a case-control study to identify prevalent cases of physician-diagnosed asthma in the Department of Defense (DOD) registry (n=873) and controls without asthma (n=2,464). The DOD registry was established for active-duty Gulf War military who wished to receive a comprehensive physical examination. Cases of asthma were defined by physical examination conducted by military physicians (ICD-9-CM [Clinical Modification] codes 493 and 493.91). Exposure to smoke from oil-well fires was estimated by linking troop

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Gulf War and Health: Fuels, Combustion Products, and Propellants - Volume 3 locations with modeled oil-fire smoke exposure. National Oceanic and Atmospheric Administration (NOAA) researchers modeled exposure on the basis of meteorologic and ground-station air-monitoring data (Draxler et al. 1994; McQueen and Draxler 1994). DOD personnel records were used to ascertain each study subject’s unit and dates of service. Only Army personnel were included in the study because their location data were more precise. Two exposure measures were used: cumulative smoke exposure (the sum of the estimated concentration on all days when each subject was in the Gulf War theater) in milligrams per cubic meter per day (mg/m3 per day), with referent exposure less than 1.0 mg/m3 per day; and number of days when the subject was exposed at μg/m3 or higher.

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Gulf War and Health: Fuels, Combustion Products, and Propellants - Volume 3 TABLE 5.2 Gulf War Veteran Health Studies of Oil-Well Fire Smoke Reference Type of Study and Population Exposure Determination Health Outcome and How Measured Results Adjusted OR (95% CI or p) Limitations Lange et al. 2002 Population-based cohort study of 1,560 Iowa veterans Self-reported exposure to “smoke from oil well fires” (5 years after war), duration 1–5, 6–30, or >30 days; exposure modeling via troop positions and air-monitoring data Self-reported symptoms of bronchitis and asthma (wheezing and coughing) vs control symptoms of major depression and injury Small correlation between self-reported and modeled exposures (r=0.40–0.48, p<0.05); no association between modeled exposure and symptoms of any type (ORs near 1.0, range 0.77–1.26); association found between self-reported exposure and asthma or bronchitis For modeled exposure, adjusted ORs for symptom groups, including control symptoms, near 1.0, range 0.77–1.26; for self-reported exposure, asthma, OR 1.77–2.83, bronchitis OR 2.14–4.78 Symptom-based case definitions of asthma and bronchitis Cowan et al. 2002 Case-control study of 873 cases of asthma vs 2,464 controls; DOD registry Army personnel only Exposure modeling via troop positions and air monitoring data: Cumulative exposure and number of days at high concentration (≥65 μg/m3) Physician-diagnosed asthma 3–6 years after war Asthma associated with both estimates of exposure, dose-response Cumulative exposure: OR 1.24 (95% CI 1.00–1.55) for intermediate exposure; 1.40 (95% CI 1.11–1.75) for high exposure; number of days at high levels: OR 1.22 (95% CI 0.99–1.51) for 1–5 days; 1.41 (95% CI 1.12–1.77) for 6–30 days Self-selected population, pre-exposure asthma status unknown, active-duty military (Army only) Smith et al. 2002 405,142 active-duty US military deployed to Gulf War Exposure modeling via troop positions and air-monitoring data used to create seven exposure levels based on average, daily exposure and length of exposure: no exposure; 1–260 μg/m3 for: 1–25 days, 26–50 days, >50 days; >260 μg/m3 for 1–25 days, 26–50 days, >50 days Hospitalizations (1991–1999) for any cause, major ICD-9-CM diagnoses and specific diagnoses related to oil-well fires (such as asthma, ischemic heart disease, and emphysema) With Cox modeling, three of 25 models showed increase in adjusted risk of hospitalization, but no dose-response relationship; when nonexposed and exposed, were compared, none of the adjusted risk ratio for postwar hospitalization   Limited to DOD hospitals, exposures unknown except for oil-well smoke, outpatient data not available

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Gulf War and Health: Fuels, Combustion Products, and Propellants - Volume 3 Reference Type of Study and Population Exposure Determination Health Outcome and How Measured Results Adjusted OR (95% CI or p) Limitations   due to diagnosis related to respiratory system was significant. The seven categories were collapsed into two (exposed and nonexposed) because of relatively small numbers   NOTE: CI=confidence interval; DOD=Department of Defense; ICD-9-CM=International Classification of Diseases, 9th Edition, Clinical Modification; OR=odds ratio.

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Gulf War and Health: Fuels, Combustion Products, and Propellants - Volume 3 Self-reported oil-well fire smoke exposure was associated with a higher risk of asthma (OR [odds ratio] 1.56, 95% CI 1.23–1.97). In addition, modeled cumulative smoke exposure was related to a greater risk of asthma (OR 1.21, 95% CI 0.97–1.51 for the intermediate-exposure group; OR 1.40, 95% CI 1.12–1.76 for the high-exposure group) after controlling for sex, age, race or ethnicity, rank, smoking history, and self-reported exposure. When exposure was classified as number of days with exposure over 65 μg/m3, the risk of asthma also increased. For both exposure metrics, there was evidence of a linear exposure-response trend. Smoking appeared to modify the effect—the effect of oil-well fire smoke exposure was observed among never and former smokers but not among current smokers. Study strengths include the objective exposure assessment and use of physician-diagnosed asthma on the basis of clinical evaluations. Limitations include the self-selection into the DOD registry, which could have introduced selection bias; for example, if the cohort was enriched in persons who both experienced exposure and have respiratory conditions, the risk estimate could be biased upward. Moreover, the study examined prevalent-asthma cases, so a higher incidence of asthma cannot be distinguished from exacerbation or recrudescence of pre-existing disease. The study did not ask about chronic bronchitis or other respiratory effects. In contrast, the population-based Iowa cohort of 1,560 Gulf War veterans found no association between oil-well fire exposure and the risk of asthma (Lange et al. 2002). Five years after the war, veterans were asked about their exposures and current symptoms. Exposure was modeled with an approach similar to that of Cowan et al. Each veteran’s exposure was modeled the basis of the identified unit and its location during the period of oil-well fires (February–October 1991). Cases of asthma were defined by questions assessing wheezing and chest tightness. Cases of bronchitis were assessed by self-reported cough and phlegm production. Both questions pertained to symptoms in the preceding month, so it is not possible to determine whether symptoms were chronic. Self-reported exposure to oil-well fires was associated with a greater risk of asthma and bronchitis. There was no statistical association, however, between modeled exposure and the risk of asthma or bronchitis, when sex, age, race, military rank, smoking history, military service, and level of preparedness for war were controlled for. The three higher exposure quartiles were associated with a similar risk of asthma and bronchitis compared with the lowest-exposure quartile (all ORs near 1.0 with a range of 0.77–1.26). The correlation between self-reported exposure and modeled exposure was moderate (range of 0.40–0.48, p<0.05). The authors ascribed the different results for self-reported vs objective exposure measurement to recall bias. Study strengths include the population-based sampling: findings probably can be generalized to all military personnel in the Persian Gulf; however, the study speaks to the outcome of asthma symptoms rather than an asthma diagnosis. Chronic bronchitis also was not defined with the standard epidemiologic definition, so it was impossible to distinguish between acute and chronic symptoms. Gray et al. (2000) conducted a study of hospitalizations (1991–1994) at DOD, Department of Veterans Affairs (VA), and used data from the California Office of Statewide Health Planning and Development. Because of the absence of denominator data, the authors compared proportional morbidity ratios (PMRs) of hospitalization discharge diagnoses (14 diagnostic categories from ICD-9) in Gulf War vs nondeployed veterans. PMRs of most disease categories were not increased; however, those of respiratory diseases were increased in veterans (PMR 1.19, 95% CI 1.10–1.29) but not in active-duty military or California residents. Among respiratory diseases, the authors reported increases in asthma, but no data were shown. The study was of hospitalizations, so no data were collected on individual self-reported exposures. The

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Gulf War and Health: Fuels, Combustion Products, and Propellants - Volume 3 Reference Type of Study and Population Exposure Determination Health Outcome and How Measured Results Adjusted OR (95% CI or p) Limitations   Health Survey (n=38,595), adults 60 years old or older fuels, cleaner fuels, or mix anyone [in the household] suffer from asthma?” use OR 1.24, CI 1.04–1.49 for mixed fuel vs clean fuel question NOTE: AOD=airway obstructive disease; CI=confidence interval; DOD=Department of Defense; OR=odds ratio; RR=relative risk; TSP=total suspended particles.

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Gulf War and Health: Fuels, Combustion Products, and Propellants - Volume 3 Chronic Bronchitis Chronic bronchitis is defined by symptoms of chronic cough and sputum production. A major prospective study of outdoor air pollution with more than a decade of exposure (Abbey et al. 1993b, 1995) and a cross-sectional study of biomass-fuel combustion (Albalak et al. 1999) revealed associations between long-term exposure to combustion products and chronic bronchitis (Table 5.5). Supporting findings were reported by five other studies (Dennis et al. 1996b; Garshick et al. 2003; Osterman et al. 1989a; Perez-Padilla et al. 1996; Raaschou-Nielsen et al. 1995). The study of Gulf War veterans in Iowa of Lange (2002) showed no relationship between exposure to oil-well fires and chronic bronchitis, but the standard epidemiologic definition of chronic bronchitis was not used, so acute and chronic bronchitis could not be distinguished. Although the studies reviewed by the committee indicate a probable relationship between long-term (over 1 year) exposure to combustion products and chronic bronchitis, a key unresolved issue is whether shorter-term exposures (less than 1 year) can cause the condition. The committee found inadequate published data that address the effect of shorter-term combustion-product exposures (less than 1 year) on the risk of developing chronic bronchitis. A related issue is the exposure-free period after combustion-product exposure. Will chronic bronchitis remit after exposure cessation? If so, how long does it take for symptoms to remit? Only one of the studies in this chapter examined people after an exposure-free period. Osterman et al. (1989a) examined silicon carbide workers with SO2 and dust exposure 6 months after cessation of exposure. They found strong symptom-SO2 associations after adjusting for the effects of dust exposure. The study suggests that chronic-bronchitis symptoms can persist for at least 6 months after cessation of combustion-product exposure, but there are no data from this study or others to indicate whether chronic-bronchitis symptoms might abate thereafter. It is instructive to examine the influence of smoking on the natural history of chronic bronchitis. Smoking is the dominant risk factor for chronic bronchitis. It is well known that chronic bronchitis, when defined as mucous hypersecretion, usually remits after smoking cessation (Fletcher 1976; Kanner et al. 1999; Willemse et al. 2004). In the Lung Health Study, most of the people who had COPD (defined by airway obstruction) and chronic cough had resolution of the cough by a year after sustained smoking cessation (Kanner et al. 1999). At 5-year followup, remission of symptoms persisted among the sustained quitters. Similarly, Fletcher (1976) showed that the most people who had chronic bronchitis had resolution of their symptoms after smoking cessation.

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Gulf War and Health: Fuels, Combustion Products, and Propellants - Volume 3 TABLE 5.5 Key Studies of Chronic Bronchitis Reference Type of Study and Population Exposure Determination Health Outcome and How Measured Results Adjusted OR (95% CI or p) Limitations Abbey et al. 1993b,c Prospective cohort n=3,310, 1977–1987 TSP, ozone, sulfates AOD, asthma, chronic bronchitis incidence via symptom questionnaire TSP and AOD, chronic bronchitis TSP>200 μg/m3 associated with new cases AOD (RR 1.36, CI 1.11–1.66), chronic bronchitis (RR 1.33, CI 1.07–1.65) with increase in average annual exceedance frequency of 1000 hr/yr Symptom questionnaire, varying specificity in measures of exposure Exceedance frequencies were expressed as average, hours exceeding TSP thresholds of 60, 75, 100, 150, 200 μg/m3 Abbey et al. 1995 Prospective cohort n=1,631, 1987 PM2.5 exposure estimated by regression of site, season-specific regression equations from paired PM2.5-visibility observations (1979–1986) and visibility data at nine airports throughout California; long-term averages of each subject’s estimated monthly PM2.5 mean concentrations and exceedance frequencies cumulated 1966–1977 according to ZIP code by monthly residence Same as above Onset of AOD and chronic bronchitis related to PM2.5 exposure, onset of asthma not noteworthy for increasing cutoffs of PM2.5, increased magnitudes of regression coefficients of AOD significant at all cutoffs, chronic bronchitis significant >20 μg/m3 Onset of chronic bronchitis RR 1.81 (0.98–3.25) per 45-μg/m3 increase in mean concentration Same as above Albalak 1999 Two villages in Bolivia (n=241), one with outdoor kitchens, other with indoor kitchens PM10 for kitchen and total daily integrated Chronic bronchitis via British Medical Research Council questionnaire Outdoor-kitchen village associated with lower risk of chronic bronchitis than indoor-kitchen village OR 0.4 (95% CI 0.2–0.8) with adjustment for age and sex and excluding smokers   NOTE: AOD=airway obstructive disease; CI=confidence interval; DOD=Department of Defense; OR=odds ratio; PM=particulate matter; RR=relative risk; TSP=total suspended particles.

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Gulf War and Health: Fuels, Combustion Products, and Propellants - Volume 3 Consequently, even if it could be shown that long-term exposure to combustion products caused chronic bronchitis, it might be expected to remit after exposure cessation without long-term health consequences. The committee found inadequate published data to evaluate the natural history of chronic bronchitis after cessation of exposure to combustion products. The committee concludes, from its assessment of the epidemiologic literature, that there is inadequate/insufficient evidence of an association between short-term exposure (less than 1 year) to combustion products and chronic bronchitis. Emphysema Emphysema is a pathologic process involving air-space enlargement distal to the terminal bronchioles accompanied by destruction of the bronchiolar walls. Its major risk factor is cigarette-smoking. The ACS prospective study found that emphysema mortality was not considerably increased among workers exposed to diesel exhaust after adjustment for the effects of smoking (Boffetta et al. 1988). A study of veterans exposed to oil-well fires did not find a relationship with emphysema (Smith et al. 2002). Other studies that included emphysema in the analysis were methodologically inadequate. The committee concludes, from its assessment of the epidemiologic literature, that there is inadequate/insufficient evidence of an association between exposure to combustion products and the development of emphysema. Chronic Obstructive Pulmonary Disease (COPD) The committee did not identify any high-quality studies that evaluated the effect of exposure to combustion products on the risk of COPD, as defined by objective evidence of irreversible airflow obstruction with spirometry, for example, GOLD criteria (Pauwels et al. 2001). The study of Karakatsani (2003) used a clinical definition of COPD, but the 95% CI for FEV1 percent predicted among COPD cases ranged from 86 to 95%, which did not include values less than 80% of the predicted value. That range indicates that most subjects would not meet the GOLD criteria for airway obstruction, which require an FEV1 of less than 80% of predicted values (Pauwels et al. 2001). Several studies of biomass-smoke exposure used measures of airflow obstruction but had methodologic limitations that precluded clear conclusions about the connection between combustion exposure and COPD (Dennis et al. 1996a, 1996b; Dossing et al. 1994; Perez-Padilla et al. 1996). The committee concludes, from its assessment of the epidemiologic literature, that there is inadequate/insufficient evidence of an association between exposure to combustion products and the development of COPD as defined by irreversible airflow obstruction. Although some toxicologic studies do provide mechanistic insight as to how inhaled combustion products might act to bring about symptoms associated with asthma or COPD (for example, reviewed in Barnes 1995; Ichinose et al. 1998; MacNee and Donaldson 2003; Takano et al. 1998), the published toxicologic literature has a number of shortcomings that diminish its usefulness for extrapolation to either the human exposure scenario in general or the Gulf War experience specifically. Most controlled-exposure studies either are of short duration, fail to examine long-term residual effects, or use compromised animal models. In addition, the

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Gulf War and Health: Fuels, Combustion Products, and Propellants - Volume 3 endpoints selected for examination in those studies cannot be specifically linked to the pathogenesis of any particular respiratory disease. REFERENCES Abbey DE, Colome SD, Mills PK, Burchette R, Beeson WL, Tian Y. 1993a. Chronic disease associated with long-term concentrations of nitrogen dioxide. Journal of Exposure Analysis and Environmental Epidemiology 3(2):181–202. Abbey DE, Nishino N, McDonnell WF, Burchette RJ, Knutsen SF, Beeson WL, Yang JX. 1999. Long-term inhalable particles and other air pollutants related to mortality in nonsmokers. American Journal of Respiratory and Critical Care Medicine 159(2):373–382. Abbey DE, Ostro BE, Petersen F, Burchette RJ. 1995. Chronic respiratory symptoms associated with estimated long-term ambient concentrations of fine particulates less than 2.5 microns in aerodynamic diameter (PM2.5) and other air pollutants. Journal of Exposure Analysis and Environmental Epidemiology 5(2):137–159. Abbey DE, Petersen F, Mills PK, Beeson WL. 1993b. Long-term ambient concentrations of total suspended particulates, ozone, and sulfur dioxide and respiratory symptoms in a nonsmoking population. Archives of Environmental Health 48(1):33–46. Abbey DE, Petersen FF, Mills PK, Kittle L. 1993c. Chronic respiratory disease associated with long-term ambient concentrations of sulfates and other air pollutants. Journal of Exposure Analysis and Environmental Epidemiology 3(Suppl 1):99–115. Aditama TY. 2000. Impact of haze from forest fire to respiratory health: Indonesian experience. Respirology 5(2):169–174. Al-Khalaf B. 1998. Pilot study: The onset of asthma among the Kuwaiti population during the burning of oil wells after the Gulf War. Environment International 24(1–2):221–225. Albalak R, Frisancho AR, Keeler GJ. 1999. Domestic biomass fuel combustion and chronic bronchitis in two rural Bolivian villages. Thorax 54(11):1004–1008. Amoli K. 1998. Bronchopulmonary disease in Iranian housewives chronically exposed to indoor smoke. European Respiratory Journal 11(3):659–663. Aronson KJ, Tomlinson GA, Smith L. 1994. Mortality among fire fighters in metropolitan Toronto. American Journal of Industrial Medicine 26(1):89–101. Baldi I, Tessier JF, Kauffmann F, Jacqmin-Gadda H, Nejjari C, Salamon R. 1999. Prevalence of asthma and mean levels of air pollution: Results from the French PAARC survey. European Respiratory Journal 14(1):132–138. Balmes J, Becklake M, Blanc P, Henneberger P, Kreiss K, Mapp C, Milton D, Schwartz D, Toren K, Viegi G. 2003. American Thoracic Society Statement: Occupational contribution to the burden of airway disease. American Journal of Respiratory and Critical Care Medicine 167(5):787–797. Baris D, Garrity TJ, Telles JL, Heineman EF, Olshan A, Zahm SH. 2001. Cohort mortality study of Philadelphia firefighters. American Journal of Industrial Medicine 39(5):463–476. Barnes PJ. 1995. Air pollution and asthma: Molecular mechanisms. Molecular Medicine Today 1(3):149–155. Bates MN, Garrett N, Graham B, Read D. 1997. Air pollution and mortality in the Rotorua geothermal area. Australian and New Zealand Journal of Public Health 21(6):581–586. Bates MN, Garrett N, Graham B, Read D. 1998. Cancer incidence, morbidity and geothermal air pollution in Rotorua, New Zealand. International Journal of Epidemiology 27(1):10–14. Bates MN, Garrett N, Shoemack P. 2002. Investigation of health effects of hydrogen sulfide from a geothermal source. Archives of Environmental Health 57(5):405–411. Beaumont JJ, Chu GS, Jones JR, Schenker MB, Singleton JA, Piantanida LG, Reiterman M. 1991. An epidemiologic study of cancer and other causes of mortality in San Francisco firefighters. American Journal of Industrial Medicine 19(3):357–372.

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Gulf War and Health: Fuels, Combustion Products, and Propellants - Volume 3 Dunn CE, Woodhouse J, Bhopal RS, Acquilla SD. 1995. Asthma and factory emissions in northern England: Addressing public concern by combining geographical and epidemiological methods. Journal of Epidemiology and Community Health 49(4):395–400. Eisner MD, Yelin EH, Katz PP, Earnest G, Blanc PD. 2002. Exposure to indoor combustion and adult asthma outcomes: Environmental tobacco smoke, gas stoves, and woodsmoke. Thorax 57(11):973–978. Feuer E, Rosenman K. 1986. Mortality in police and firefighters in New Jersey. American Journal of Industrial Medicine 9(6):517–527. Fleming DM, Charlton JR. 2001. The prevalence of asthma and heart disease in transport workers: A practice-based study. British Journal of General Practice 51(469):638–643. Fletcher CM. 1976. The Natural History of Chronic Bronchitis and Emphysema: An Eight-year Study of Early Chronic Obstructive Lung Disease in Working Men in London. Oxford: Oxford University Press. Flodin U, Ziegler J, Jonsson P, Axelson O. 1996. Bronchial asthma and air pollution at workplaces. Scandinavian Journal of Work, Environment & Health 22(6):451–456. Gamble JF, Jones WG. 1983. Respiratory effects of diesel exhaust in salt miners. American Review of Respiratory Disease 128(3):389–394. Garshick E, Laden F, Hart JE, Caron A. 2003. Residence near a major road and respiratory symptoms in U.S. Veterans. Epidemiology 14(6):728–736. Goldstein IF, Weinstein AL. 1986. Air pollution and asthma: Effects of exposures to short-term sulfur dioxide peaks. Environmental Research 40(2):332–345. Golshan M, Faghihi M, Marandi MM. 2002. Indoor women jobs and pulmonary risks in rural areas of Isfahan, Iran, 2000. Respiratory Medicine 96(6):382–388. Gray GC, Smith TC, Kang HK, Knoke JD. 2000. Are Gulf War veterans suffering war-related illnesses? Federal and civilian hospitalizations examined, June 1991 to December 1994. American Journal of Epidemiology 151(1):63–71. Hanis NM, Shallenberger LG, Donaleski DL, Sales EA. 1985. A retrospective mortality study of workers in three major U.S. refineries and chemical plants. Part 1: Comparisons with U.S. population. Journal of Occupational Medicine 27(4):283–292. Hastings DL, Jardine S. 2002. The relationship between air particulate levels and upper respiratory disease in soldiers deployed to Bosnia (1997–1998). Military Medicine 167(4):296–303. Hoek G, Brunekreef B, Goldbohm S, Fischer P, Van den Brandt PA. 2002. Association between mortality and indicators of traffic-related air pollution in the Netherlands: A cohort study. Lancet 360(9341):1203–1209. Hong CY, Ng TP, Wong ML, Koh KTC, Goh LG, Ling SL. 1994. Lifestyle and behavioural risk factors associated with asthma morbidity in adults. Quarterly Journal of Medicine 87(10):639–645. Hunt TB, Holman CD. 1987. Asthma hospitalisation in relation to sulphur dioxide atmospheric contamination in the Kwinana industrial area of Western Australia. Community Health Studies 11(3):197–201. Ichinose T, Takano H, Miyabara Y, Sagai M. 1998. Long-term exposure to diesel exhaust enhances antigen-induced eosinophilic inflammation and epithelial damage in the murine airway. Toxicological Sciences 44(1):70–79. Jarvis D, Chinn S, Luczynska C, Burney P. 1996. Association of respiratory symptoms and lung function in young adults with use of domestic gas appliances. Lancet 347(8999):426–431. Jarvis D, Chinn S, Sterne J, Luczynska C, Burney P. 1998. The association of respiratory symptoms and lung function with the use of gas for cooking. European Community Respiratory Health Survey. European Respiratory Journal 11(3):651–658. Jindal SK, Gupta D, D’Souza GA, Kalra S. 1996. Bronchial responsiveness of non-smoking women exposed to environmental tobacco smoke or biomass fuel combustion. Indian Journal of Medical Research 104:359–364.

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Gulf War and Health: Fuels, Combustion Products, and Propellants - Volume 3 Kanner RE, Connett JE, Williams DE, Buist AS. 1999. Effects of randomized assignment to a smoking cessation intervention and changes in smoking habits on respiratory symptoms in smokers with early chronic obstructive pulmonary disease: The Lung Health Study. The American Journal of Medicine 106(4):410–416. Kaplan SD. 1986. Update of a mortality study of workers in petroleum refineries. Journal of Occupational Medicine 28(7):514–516. Karakatsani A, Andreadaki S, Katsouyanni K, Dimitroulis I, Trichopoulos D, Benetou V, Trichopoulou A. 2003. Air pollution in relation to manifestations of chronic pulmonary disease: A nested case-control study in Athens, Greece. European Journal of Epidemiology 18(1):45–53. Kilpelainen M, Koskenvuo M, Helenius H, Terho E. 2001. Wood stove heating, asthma and allergies. Respiratory Medicine 95(11):911–916. Kogevinas M, Anto JM, Sunyer J, Tobias A, Kromhout H, Burney P, Chinn S, Luczynska C, Jarvis D, Lai E, Abramson M, Kutin J, Vermeire P, Van Bastelaer F, Magnussen H, Nowak D, Wichmann HE, Heinrich J, Wjst M, Gialson T, Gislason D, Prichard J, Allwright S, MacLeod D, Bugiani M, Bucca C, Romano C, De Marco lo Cascio R, Campello C, Marinoni A, Cerveri I, Casali L, Crane J, D’Souza W, Pearce N, Barry D, Town I, Gulsvik A, Omenaas E, Bakke P, Soriano J, Roca J, Muniozguren N, Gonzalez JR, Capelastegui A, Martinez-Moratalla J, Almar E, Perez JM, Oereira A, Sanchez J, Quiros J, Huerta I, Boman G, Janson C, Bjornsson E, Rosenhall L, Norrman E, Lundback B, Lindholm N, Plaschke P, Burr M, Layzqll J, Hall R, Harrison B, Stark J, Buist S, Vollmer W, Osborne M. 1999. Occupational asthma in Europe and other industrialised areas: A population-based study. Lancet 353(9166):1750–1754. Kunii O, Kanagawa S, Yajima I, Hisamatsu Y, Yamamura S, Amagai T, Ismail IT. 2002. The 1997 haze disaster in Indonesia: its air quality and health effects. Archives of Environmental Health 57(1):16–22. Lange JL, Schwartz DA, Doebbeling BN, Heller JM, Thorne PS. 2002. Exposures to the Kuwait oil fires and their association with asthma and bronchitis among gulf war veterans. Environmental Health Perspectives 110(11):1141–1146. Liu D, Tager IB, Balmes JR, Harrison RJ. 1992. The effect of smoke inhalation on lung function and airway responsiveness in wildland fire fighters. American Review of Respiratory Disease 146(6):1469–1473. MacNee W, Donaldson K. 2003. Mechanism of lung injury caused by PM10 and ultrafine particles with special reference to COPD. European Respiratory Journal—Supplement 40:47s–51s. Maizlish N, Beaumont J, Singleton J. 1988. Mortality among California highway workers. American Journal of Industrial Medicine 13(3):363–379. Makker HK, Ayres JG. 1999. Work-related asthma in an aircraft engine mechanic. Respiratory Medicine 93(1):69–70. McQueen J, Draxler R. 1994. Evaluation of model back trajectories of the Kuwait oil fires smoke plume using digital satellite data. Atmospheric Environment 28:2159–2174. Meyer JD, Holt DL, Chen Y, Cherry NM, McDonald JC. 2001. SWORD ‘99: Surveillance of work-related and occupational respiratory disease in the UK. Occupational Medicine 51(3):204–208. Mishra V. 2003. Effect of indoor air pollution from biomass combustion on prevalence of asthma in the elderly. Environmental Health Perspectives 111(1):71–78. Musk A, Smith T, Peters J, McLaughlin E. 1979. Pulmonary function in firefighters: Acute changes in ventilatory capacity and their correlates. British Journal of Industrial Medicine 36(1):29–34. Musk AW, Peters JM, Bernstein L, Rubin C, Monroe CB. 1982. Pulmonary function in firefighters: A six-year follow-up in the Boston Fire Department. American Journal of Industrial Medicine 3(1):3–9. Ng TP, Hui KP, Tan WC. 1993. Respiratory symptoms and lung function effects of domestic exposure to tobacco smoke and cooking by gas in non-smoking women in Singapore. Journal of Epidemiology and Community Health 47(6):454–458. Osterman JW, Greaves IA, Smith TJ, Hammond SK, Robins JM, Theriault G. 1989a. Respiratory symptoms associated with low level sulphur dioxide exposure in silicon carbide production workers. British Journal of Industrial Medicine 46(9):629–635.

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Gulf War and Health: Fuels, Combustion Products, and Propellants - Volume 3 Osterman JW, Greaves IA, Smith TJ, Hammond SK, Robins JM, Theriault G. 1989b. Work related decrement in pulmonary function in silicon carbide production workers. British Journal of Industrial Medicine 46(10):708–716. Ostro BD, Lipsett MJ, Mann JK, Krupnick A, Harrington W. 1993. Air pollution and respiratory morbidity among adults in southern California. American Journal of Epidemiology 137(7):691–700. Pandey MR. 1984. Domestic smoke pollution and chronic bronchitis in a rural community of the Hill Region of Nepal. Thorax 39(5):337–339. Pandey MR, Regmi HN, Neupane RP, Gautam A, Bhandari DP. 1985. Domestic smoke pollution and respiratory function in rural Nepal. Tokai Journal of Experimental and Clinical Medicine 10(4):471–481. Papageorgiou N, Gaga M, Marossis C, Reppas Chr, Avarlis P, Kyriakou M, Tsipra S, Zeibecoglou K, Tracopoulos G. 1997. Prevalence of asthma and asthma-like symptoms in Athens, Greece. Respiratory Medicine 91(2):83–88. Pauwels RA, Buist AS, Calverley PM, Jenkins CR, Hurd SS. 2001. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease (GOLD) Workshop summary. American Journal of Respiratory and Critical Care Medicine 163(5):1256–1276. Perez-Padilla R, Regalado J, Vedal S, Pare P, Chapela R, Sansores R, Selman M. 1996. Exposure to biomass smoke and chronic airway disease in Mexican women. A case-control study. American Journal of Respiratory and Critical Care Medicine 154(3 Pt 1):701–706. Perez-Padilla R, Perez-Guzman C, Baez-Saldana R, Torres-Cruz A. 2001. Cooking with biomass stoves and tuberculosis: A case control study. International Journal of Tuberculosis and Lung Disease 5(5):441–447. Peters EJ, Esin RA, Immananagha KK, Siziya S, Osim EE. 1999. Lung function status of some Nigerian men and women chronically exposed to fish drying using burning firewood. Central African Journal of Medicine 45(5):119–124. Petruccelli BP, Goldenbaum M, Scott B, Lachiver R, Kanjarpane D, Elliott E, Francis M, McDiarmid MA, Deeter D. 1999. Health effects of the 1991 Kuwait oil fires: A survey of US army troops. Journal of Occupational and Environmental Medicine 41(6):433–439. Pope CA 3rd, Burnett RT, Thun MJ, Calle EE, Krewski D, Ito K, Thurston GD. 2002. Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. Journal of the American Medical Association 287(9):1132–1141. Pope CA 3rd, Burnett RT, Thurston GD, Thun MJ, Calle EE, Krewski D, Godleski JJ. 2004. Cardiovascular mortality and long-term exposure to particulate air pollution: Epidemiological evidence of general pathophysiological pathways of disease. Circulation 109(1):71–77. Pope CA 3rd, Thun MJ, Namboodiri MM, Dockery DW, Evans JS, Speizer FE, Heath CW Jr. 1995. Particulate air pollution as a predictor of mortality in a prospective study of U.S. adults. American Journal of Respiratory and Critical Care Medicine 151(3 Pt 1):669–674. Proctor SP, Heeren T, White RF, Wolfe J, Borgos MS, Davis JD, Pepper L, Clapp R, Sutker PB, Vasterling JJ, Ozonoff D. 1998. Health status of Persian Gulf War veterans: Self-reported symptoms, environmental exposures and the effect of stress. International Journal of Epidemiology 27(6): 1000–1010. Qureshi KA. 1994. Domestic smoke pollution and prevalence of chronic bronchitis/asthma in a rural area of Kashmir. Indian Journal of Chest Diseases & Allied Sciences 36(2):61–72. Raaschou-Nielsen O, Nielsen ML, Gehl J. 1995. Traffic-related air pollution: Exposure and health effects in Copenhagen street cleaners and cemetery workers. Archives of Environmental Health 50(3):207–213. Rafnsson V, Gunaarsdottir H. 1991. Mortality among professional drivers. Scandinavian Journal of Work, Environment & Health 17(5):312–317. Reger R, Hancock J, Hankinson J, Hearl F, Merchant J. 1982. Coal miners exposed to diesel exhaust emissions. Annals of Occupational Hygiene 26(1–4):799–815.

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