asthma and respiratory symptoms, asthma related hospital admissions and emergency room visits, decreased lung function, and in some studies cardiac hospital admissions (Boman et al. 2003, 2006; Naeher et al. 2007). Asthma symptoms, asthma related hospital admissions, and cough are shown to be related to PM10 in five studies that specified wood smoke as a major contributor to ambient air pollution (Boman et al 2003).
Naeher et al. (2007) make the point that in addition to wood and biomass, tobacco, the most well-studied biomass smoke, is also important in determining and apportioning health effects from overall smoke exposure. Tobacco smoke provides another example of demonstrated adverse health effects from smoke and is especially relevant to military personnel because prevalence of smoking is elevated in military populations (IOM 2009). Tobacco smoke contains many environmental contaminants, including particulate matter, acrolein, polycyclic aromatic hydrocarbons, benzene, and metals. The 2004 Surgeon General’s report associated tobacco smoke with cancer, particularly of the lung and larynx, as well as the urinary tract and oral cavity; cardiovascular disease, including acute myocardial infarction, angina, stroke, and peripheral artery disease; pulmonary disease such as chronic bronchitis, emphysema, asthma, and increased susceptibility to pneumonia and other respiratory infections; gastrointestinal disease such as peptic ulcer and esophageal reflux; and reproductive effects, including low birth weight, spontaneous abortion, premature birth, and reduced fertility (U.S. Surgeon General 2004). Even exposure to secondhand smoke can result in long-term health effects, in particular, an increased risk for lung cancer (IARC 2004) and cardiovascular disease, including death and acute myocardial infarction (IOM 2010).
The committee acknowledges the many occupational and environmental exposures present at JBB; however, direct information on other exposures is lacking and outside the task of this report. Thus, the committee focused on the specific pollutants determined to be associated with burn pits—polycyclic aromatic hydrocarbons (PAHs), volatile organic compounds (VOCs), dioxins/furans, and PM—even though the proportion contributed by burn pits is thought to be relatively small, with the exception of dioxin.
Dioxins and Dioxin-Like Compounds
The dioxin TCDD is classified as carcinogenic to humans by the EPA (2003a) and by the International Agency for Research on Cancer (1997). In the 2003 draft report Exposure and Human Health Reassessment of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin and Related Compounds, the EPA focused on three epidemiologic cohort studies—Ott and Zober (1996); Becher et al. (1998); and Steenland et al. (2001)—that provided quantitative dose-response estimates that linked serum dioxin levels to cancer mortality (NRC 2006). The IARC also evaluated the study by Ott and Zober (1996) and additional studies by Fingerhut et al. (1991), Becher et al. (1996), Hooiveld et al. (1996), and Steenland et al. (2004). The cohort studies reviewed in these evaluations were used principally because they included subjects with serum dioxin levels higher than background and who were in industrial settings, which allowed for better characterization of exposure. The classification of dioxin as carcinogenic to humans addresses total cancer mortality and does not specify tumor type. The focus on total cancers is a result of the presumption that TCDD is not in itself genotoxic, but that rather it acts primarily as a promoter rather than an initiator of cancer (IARC 1997). The Veterans and Agent Orange: Update 2008 (VAO) from the Institute of Medicine (IOM) continued to support the association between exposure of Vietnam veterans to the TCDD-contaminated Agent Orange and soft-tissue sarcoma, non-Hodgkin’s lymphoma, Hodgkin’s disease, and chronic lymphocytic leukemia. The IOM report also broadened the categorization of sufficient evidence of an association between Agent Orange exposure and health effects to cover chronic lymphocytic leukemia, including hairy-cell leukemia and other chronic B-cell leukemias (IOM 2008).
In animal studies with oral administration, TCDD exposure has been associated with noncancer health effects. High exposures to TCDD affect many organs and can result in organ dysfunction and death. Other reported specific adverse health effects include diabetes; immunologic response; altered neurologic function; reproductive and developmental effects including birth defects; changes to the endocrine system; and wasting syndrome, which results in the loss of adipose and muscle tissues and severe weight loss (Mandal 2005; IOM 2008; White and Birnbaum 2009).
Rats and mice exposed to TCDD had increased incidence of degenerative cardiovascular lesions, cardiomyopathy, chronic active arteritis, increased heart weight, increased blood pressure, and severe atherosclerotic lesions (Humblet et al. 2008). The 2008 VAO update committee, after extensive deliberation regarding the strengths and