Orleans. The study’s nearly 300 subjects made up a stratified random sample of 2,949 troops from Ft. Devens and 928 troops from New Orleans, both including active-duty, reserve, and National Guard troops. The response rate was 58–85% of those participating in an earlier study who could be contacted and located. The control group (n=50) was Gulf-era veterans deployed to Germany. Subjects were given symptom checklists (covering the previous 30 days), exposure questionnaires, and a neuropsychologic test battery; were interviewed about combat exposure; and underwent diagnostic interviews for posttraumatic stress disorder (PTSD). Each of the 52 symptoms on the symptom checklist was assigned by four independent judges to one of nine body systems, including one for “cardiac symptoms”, defined as irregular heartbeats (or “heart flutters”), chest pain, or racing heart. The exposure questionnaire, given only to Gulf War-deployed subjects, contained eight items, four of which were related to combustion products: “smoke from burning oil wells”, “vehicle exhaust”, “smoke from tent heaters”, “smoke from burning human waste”. In the Gulf War-deployed cohort, multiple regression adjusting for age, sex, education, and PTSD diagnosis was used to determine symptom-exposure relationships. Self-reported exposure to smoke from oil-well fires had no noteworthy associations, however, vehicle exhaust (p=0.026), smoke from burning human waste (p=0.001), and smoke from tent heaters (p<0.001) were associated with cardiac symptoms. But in a second set of multiple regression-analyses with exposures entered as independent variables, vehicle exhaust and smoke from burning human waste were no longer associated with those symptoms. The findings reported above were essentially unchanged when subjects who met criteria for PTSD were removed from analyses. The study limitations were self-reported symptoms and exposures, moderate to low response rate, and lack of representativeness of the entire Gulf War cohort.

Air-Pollution Studies

Respiratory mortality findings have been reported from several large, longitudinal cohorts with long-term exposures, usually more than 5 years—ACS (Pope et al. 1995), Six-Cities (Dockery et al. 1993), Netherlands Cohort Study on Diet and Cancer (Hoek et al. 2002), and Seventh-Day Adventists (SDAs) (Abbey et al. 1999). All but the SDA study relied on a broad mortality category—cardiopulmonary. Two further analyses, however, provided greater specificity regarding mortality in the ACS and Six-Cities cohorts.

For the ACS cohort, Pope et al. (2004) undertook a more diagnosis-specific analysis with the same methods as their previous report (Pope et al. 2002). The analysis expanded on earlier findings, including 7–16 years of followup of people enrolled in 1982. Exposures to particulate matter were assigned to each participant on the basis of his or her ZIP code at the time of enrollment. For cardiovascular-disease mortality as a composite category, the study found increased RR of 1.12 (95% CI 1.08–1.15) per increase of 10 μg/m3 in PM2.5.3 Within that category, deaths from ischemic heart disease (ICD-9 codes 410–414) were increased (RR 1.18, 95% CI 1.14–1.23) even after adjustment for smoking. Deaths from dysrhythmias, heart failure, and cardiac arrest (ICD-9 codes 420–429) were also increased (RR 1.13, 95% CI 1.05–1.21).

A reanalysis of the Six-Cities cohort by Krewski et al. (2003) found that cardiovascular mortality—instead of the less-specific “cardiopulmonary” mortality—was increased (RR 1.41, 95% CI 1.13–1.76 per increase of 18.6 μg/m3 in PM2.5). The vast majority of cardiovascular mortality was from ischemic heart disease. Nevertheless, although the Six-Cities and ACS findings have been robust to intense scrutiny and reanalysis, the exposure-assessment scheme is


PM2.5 is a notation for particulate matter less 2.5 μg in diameter.

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