reported exposure. When exposure was classified as number of days with exposure at 65 μg/m3 or greater, the risk of asthma also increased. Both exposure metrics showed statistically significant associations with asthma when treated as continuous variables. Smoking appeared to modify the effect: the effect of oil-well-fire smoke exposure was observed among never-smokers and former smokers but not among current smokers. Study strengths include the objective exposure assessment and the use of physician-diagnosed asthma on the basis of clinical evaluations. Limitations include the lack of pulmonary function data and of specified criteria for the diagnosis of asthma and self-selection into the DOD registry, which could have introduced selection bias (for example, if the cohort was enriched with persons who both experienced exposure and had respiratory conditions, the risk estimate could be biased upward). Moreover, the study examined current 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 statistical association between modeled 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. (2002). Each veteran’s exposure was modeled on 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 aimed at assessing wheezing and chest tightness. Cases of bronchitis were assessed on the basis of 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. However, there was no statistical association between modeled exposure and the risk of asthma or bronchitis in models that controlled for sex, age, race, military rank, smoking history, military service, and level of preparedness. The correlation between self-reported exposure and modeled exposure was modest (0.40-0.48, p < 0.05). The authors ascribed the different results for self-reported and objective exposure measurement to recall bias. A study strength is the population-based sampling, which implies that findings can be generalized to all military personnel in the Persian Gulf. A limitation is that the study addressed the outcome of asthma symptoms rather than an asthma diagnosis. And, chronic bronchitis was not defined with the standard epidemiologic definition, so it was impossible to distinguish between acute and chronic symptoms.
In the postwar hospitalization study of 405,142 active-duty Gulf War veterans, Smith et al. (2002) examined the effect of oil-well-fire exposure. Exposure was estimated by using troop location data and estimated oil-smoke concentrations based on the same NOAA modeling used in the Cowan and Lange studies. There was no association between exposure to oil-well fires and the risk of hospitalization for asthma (RR 0.90, 95% CI 0.74-1.10), acute bronchitis (RR 1.09, 95% CI 0.62-1.90), or chronic bronchitis (RR 0.78, 95% CI 0.38-1.57). There was modest increase in the relative risk of emphysema from oil-well fire smoke (RR 1.36, 95% CI 0.62-2.98). Because most adults who have asthma or chronic bronchitis are never hospitalized for the condition, the study would not be expected to have captured most cases. No information was available on tobacco-smoking or other exposures that may be related to respiratory symptoms.
Several other studies on smoke from oil-well fires in the Persian Gulf are methodologically less robust. A cohort study of Gulf War veterans evaluated self-reported