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5 Health Effects of Air Pollutants Detected at Joint Base Balad As discussed in Chapter 4, the committee found the air monitoring data gathered at Joint Base Balad (JBB) in 2007 and 2009 to be useful for identifying the major air pollutants and their sources in and around JBB. In Chapter 5, the committee begins its assessment of the potential long-term health effects associated with exposure to those air pollutants. To this end, the committee (1) reviews the health effects associated with the air pollutants identified in Chapter 4; (2) lists the health effects associated with exposure to the most frequently detected pol - lutants at JBB regardless of their source; and (3) provides a qualitative analysis of the assembled health effects data from a chemical mixture or cumulative risk perspective. The committee did not conduct a quantitative risk assessment. Exposure to both burn pit emissions and air pollutants from other sources in and around JBB will likely be of concern in future epidemiologic studies. RATIONALE AND DATA SOURCES The committee considers several of the air pollutants highlighted in Chapter 4 to be of concern because of their association with burn pit emissions (dioxins and dioxin-like compounds) and because some of the concentrations exceeded U.S. air quality standards (for example, particulate matter [PM]) or were in excess of concentrations found in polluted urban environments worldwide. Health effects associated with these pollutants are well docu - mented. The committee drew on previous expert panel reviews and selected research literature to summarize the health effects of the chemicals of concern. Typically, the hazard identification step of a risk assessment addresses what the chemicals of concern are as well as the specific health effects associated with exposure to them (see Figure 3-1) (NRC 1983, 2009). The screen- ing health risk assessments conducted by the U.S. Army Center for Health Promotion and Preventive Medicine (CHPPM, now the U.S. Army Public Health Command) and the U.S. Air Force Institute for Operational Health (AFIOH) focused on those chemicals detected in the air monitoring campaigns but restricted their review of associ - ated health effects to the broad categories of cancer and either to noncancer effects in general (Taylor et al. 2008), or to just the primary target organs for noncancer effects (CHPPM 2009, USAPHC 2010), and therefore specific health effects potentially related to exposure to air pollutants at JBB were not fully presented. The committee assembled specific health effects data (including all target organs) on the detected air pollutants as a step towards identifying the potential long-term effects of them. One step in the committee’s analysis of the air monitoring data was to evaluate how often a particular pollutant 47

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48 HEALTH CONSEQUENCES OF EXPOSURE TO BURN PITS was detected among the samples taken (see Chapter 4, Table 4-6). The pollutants listed in Table 5-1 were detected in at least 5% of the air monitoring samples collected at JBB in 2007 and 2009 (n = 47 chemicals). There are an additional four pollutants (1,2,4-trichlorobenzene, 1,3-dichlorobenzene, 1,3-butadiene, and 1,2-dichlorobenzene) that were detected at JBB although in fewer than 5% of the samples, but they were included in the committee’s assessment because they are expected to be present in burn pit emissions on the basis of burn barrel experiments (Lemieux et al. 2003, 2004; see also Chapter 4, Table 4-6). Health effects of particulate matter, dioxins (as rep - resented by 2,3,7,8-tetrachlorodibenzo-p-dioxin [TCDD]), and metals detected at JBB (lead, zinc, and antimony) are also described. In all, 56 pollutants are profiled in Table 5-1. When available, specific cancer and noncancer health effects data for the pollutants in Table 5-1 were obtained from the U.S. Environmental Protection Agency’s (EPA’s) Integrated Risk Information System (IRIS), Agency for Toxic Substances and Disease Registry (ATSDR) Toxicological Profiles, the National Institute of Occupational Safety and Health (NIOSH), or the National Library of Medicine’s (NLM’s) Hazardous Substance Data Bank. IRIS is the source of much of the toxicity information discussed in this chapter. The toxicity values and supporting documentation developed by the EPA and other agencies are the result of extensive review and synthesis of health effects literature and are designed for practical application in assessments of human health risks. The committee recognizes there are concerns regarding IRIS (NRC 2009); nevertheless, IRIS and other agency databases provide the best readily available evaluation of health effects from exposure to toxic substances. HEALTH EFFECTS OF SELECTED AIR POLLUTANTS DETECTED AT JBB The evaluation of air monitoring data from JBB reported in Chapter 4 indicates that combustion products from burn pits were associated with low concentrations of dioxins and dioxin-like compounds but contributed a relatively small proportion of PM compared to local dust and other sources. The committee recognized that personnel at military bases similar to JBB were exposed to many hazardous agents associated with adverse health effects in addition to burn pits. These exposures may result from use of kerosene heaters, JP-8 fuel, and tobacco products in addition to the hazards and stress inflicted by war. Assessment of these additional exposures was outside the committee’s scope and thus focus was on only exposures related to burn pits. While not measured directly, first hand descriptions of the burn pits describe volumes of smoke resulting from the burn pit and use of JP-8 fuel to encourage combustion (see Chapter 2). Both smoke and JP-8 fuel are associated with adverse health effects as described below. JP-8 and similar fuels were used by the military to power aircraft, ground vehicles, tent heaters, and cooking stoves. These fuels were also used for less conventional purposes, such as suppressing sand, cleaning equipment, and burning trash. Military personnel serving in the Gulf War theater of operations could have been exposed to the uncombusted fuels, the combustion products from the burning of those fuels, or a combination of uncombusted and combusted materials (IOM 2005). Health effects of JP-8 are similar to those of kerosene, the primary com - ponent of JP-8, exposures generally causing nervous system effects. Large doses of inhaled JP-8 are known to cause headaches and fatigue, and affect concentration and coordination, while more chronic exposures can affect sleep, motivation, and cause dizziness, but not cancer (ATSDR 1998). As part of the IOM’s continuing series of Gulf War and Health reports, a previous IOM committee assessed the toxicological and epidemiological effects of these fuels and their combustion products. That committee did not find any association between exposure to uncombusted fuels and long-term health effects. Conversely, fuel combustion products were found to have suffi - cient evidence of an association with lung cancer; limited suggestive evidence of an association with several other cancers (nasal cavity, nasopharynx, oral cavity, laryngeal, and bladder cancers), reproductive effects, and incident asthma (IOM 2005). (See Chapter 6 for a description of the categories of association used for these combustion products and health effects.) While products of combustion vary greatly based on fuel composition and conditions of the burn, several health effects have been described consistently in association with exposure to smoke. Studies have examined health effects from exposure to ambient air pollution, exposure to wood smoke from indoor wood-burning stoves and fireplaces, and exposure to smoke from wildland or agricultural fires. Wood smoke has been associated with premature death, chronic obstructive pulmonary disease (COPD), tuberculosis, acute lower respiratory infections,

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49 HEALTH EFFECTS OF AIR POLLUTANTS 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 PM 10 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 devel - opmental 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, cardiomy - opathy, 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

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TABLE 5-1 Long-Term Health Effects for Chemicals of Interest Detected at JBB 50 Chemical Name and Inhalation Unit Risk Reference Concentration 1-yr Air MEG CAS Number Class Long-Term Health Effectsa (mg/m3) (mg/m3)c (mg/m3)d Acenaphthene PAH Increased liver weight, increased cholesterol, NA NA 1.40E-01 83-32-9 vascular disorders, and degeneration in the internal organs and central nervous system Acenaphthylene PAH NA NA NA 2.80E-02 208-96-8 Anthracene PAH No observed effects at highest dose NA NA 3.50E+01 120-12-7 Benz[a]anthracene PAH Probable carcinogen,b lung and liver cancers 1.1E-07 C NA 5.40E-02 56-55-3 Benzo[a]pyrene PAH Probable carcinogen,b stomach and 1.3E-06 C NA 5.40E-03 50-32-8 respiratory tract tumors Benzo[b]fluoranthene PAH Probable carcinogen,b lung and skin tumors, 1.1E-07 C NA 5.40E-02 205-99-2 effects on liver Benzo[e]pyrene PAH NA NA NA NA 192-97-2 Benzo[g,h,i]perylene PAH NA NA NA NA 191-24-2 Benzo[k]fluoranthene PAH Probable carcinogen,b lung and skin tumors 1.1E-07 C NA 5.40E-01 207-08-9 Chrysene PAH Probable carcinogen,b carcinomas and 1.1E-08 C NA 5.50E+00 218-01-9 malignant lymphoma Dibenz[a,h]anthracene PAH Probable carcinogen,b stomach and 1.2E-06 C NA 5.40E-03 53-70-3 respiratory tract tumors Fluoranthene PAH Nephropathy, increased liver weights, NA NA 1.40E+00 206-44-0 hematological alterations Fluorene PAH Blood effects; increased liver, spleen, and NA NA 1.40E+00 86-73-7 kidney weights Indeno[1,2,3-cd]pyrene PAH Probable carcinogen,b lung and skin tumors 1.1E-07 C NA 5.40E-02 193-39-5 Naphthalene PAH Possible carcinogen,b respiratory tumors; 3.4E-08 C 3.0E-03 I 7.10E-02 91-20-3 decreased body weights Phenanthrene PAH NA NA NA 4.20E-02 85-01-8 Pyrene PAH Nephropathy and decreased kidney weight NA NA 1.05E-01 129-00-0 1,2-Dichlorobenzene VOC Increased liver and kidney weight, liver NA 2.0E-01 H 1.40E+00 95-50-1 necrosis, renal tubular degeneration

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1,2,4-Trimethylbenzene VOC Long term exposure in workers: defats NA 7.0E-03 P 3.06E+00 95-63-6 the skin, lungs may be affected, chronic bronchitis, CNS (impaired neurobehavioral test performance), hypochromic anemia (NLM 2011) 1,3,5-Trimethylbenzene VOC Long term exposure in workers: defats NA NA 3.06E+00 108-67-8 the skin, lungs may be affected, chronic bronchitis, CNS (impaired neurobehavioral test performance), hypochromic anemia (NLM 2011) 1,4-Dichlorobenzene VOC Increased liver and kidney weights, liver 1.1E-08 C 8.0E-01 I 1.70E+00 106-46-7 tumors 2-Butanone (MEK) VOC Maternal and developmental toxicity (e.g., NA 5.0E+00 I 1.44E+01 78-93-3 decreased weight gain in dams and decreased body weight and skeletal variations in pups) 4-Ethyltoluene VOC NA NA NA NA 622-96-8 Acetone VOC Eye and respiratory tract irritation, NA 3.1E+01 A 2.90E+01 67-64-1 neurobehavioral and neurological effects (e.g., reduced nerve conduction velocity, increased reaction time) Acrolein VOC Respiratory and inflammatory responses, NA 2.0E-05 I 1.40E-05 107-02-8 nasal lesions, increased heart and kidney weights, liver necrosis, decreased body weight gain Benzene VOC Known carcinogen,b leukemia and 7.8E-09 I 3.0E-02 I 3.90E-02 71-43-2 hematologic neoplasms; progressive deterioration of hematopoietic function with chronic exposure, suppression of circulating B-lymphocytes, menstrual disorders, limited evidence of reproductive toxicity and neurotoxicity 1,3-Butadiene VOC Probable carcinogen,b liver, lung, ovary, and 3.0E-08 I 2.0E-03 I 1.70E-02 106-99-0 mammary tumors; lymphohematopoietic cancers and leukemia; reproductive and developmental effects (e.g., ovarian and testicular atrophy, fetal skeletal variations, decreased fetal weight) Carbon disulfide VOC Peripheral nervous system dysfunction (e.g., NA 7.0E-01 I 4.80E-01 75-15-0 reduced nerve conduction velocity), possible CNS and ocular effects (e.g., blurred vision, memory difficulty) Chlorodifluoromethane VOC Increased kidney, adrenal and pituitary NA 5.0E+01 I 3.42E+00 75-45-6 weights 51 continued

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52 TABLE 5-1 Continued Chemical Name and Inhalation Unit Risk Reference Concentration 1-yr Air MEG CAS Number Class Long-Term Health Effectsa (mg/m3) (mg/m3)c (mg/m3)d Chloromethane VOC Cerebellar lesions, central nervous system NA 9.0E-02 I 2.70E+00 74-87-3 dysfunction Cyclohexane VOC Developmental and reproductive toxicity NA 6.0E+00 I NA 110-82-7 (reduced maternal and pup body weights), CNS depression Dichlorodifluoromethane VOC Cardiovascular system and peripheral NA 2.0E-01 H 9.90E+01 75-71-8 nervous system effects (CDC 2010) Ethylbenzene VOC Increased liver, kidney and spleen weights: 2.5E-06 C 1.0E+00 I 3.00E+00 100-41-4 developmental toxicity (e.g., skeletal variations) Hexane VOC Peripheral neuropathy NA 7.0E-01 I 4.30E+00 110-54-3 Isooctane VOC NA NA NA NA 540-84-1 Isopropyl alcohol VOC Eye and respiratory tract irritation: increased NA 7.0E+00 C NA 67-63-0 liver enzymes and relative liver weight: narcosis at highest exposures (CDC 2010; NLM 2011) Methyl tert-butyl ether VOC Increased absolute and relative liver and 2.67E-10 C 3.0E+00 I 2.10E+00 (MtBE) kidney weights and increased severity 1634-04-4 of spontaneous renal lesions (females), increased prostration (females), and swollen periocular tissue (males and females) Methylene chloride VOC Probable carcinogen,b liver, mammary gland, 4.7E-10 I 1.0E+00 A 2.10E+00 75-09-2 salivary gland, lung tumors; liver toxicity (e.g., fatty changes) n-Heptane VOC Skin, eye and respiratory irritant, and CNS NA NA NA 142-82-5 depression at high exposures (CDC 2010; NLM 2011) Octane VOC Skin, eye, and respiratory irritant, and CNS NA NA NA 111-65-9 depression at high exposures (CDC 2010; NLM 2011) Pentane VOC Skin, eye, and respiratory irritant, and CNS NA 1.0E+00 P NA 109-66-0 depression at high exposures (CDC 2010; NLM 2011)

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Propylene VOC NA NA 3.0E+00 C NA 115-07-1 Styrene VOC Changes in red blood cells, reduced NA 1.0E+00 I 2.00E+00 100-42-5 red blood cell counts and hemoglobin; increased liver weight, liver, kidney and stomach lesions; neurological effects (e.g., increased reaction time, decreased memory, concentration); possibly carcinogenic in humans (IARC 2002) Tetrachloroethene (PCE) VOC Respiratory system, liver, kidney, and central 5.9E-09 C 2.7E-01 A 237 (8 hr MEG) 127-18-4 nervous system effects; potential carcinogen (liver) (CDC 2010) Toluene VOC Increased liver and kidney weight, NA 5.0E+00 I 4.60E+00 108-88-3 nephropathy, neurological effects (e.g., vision impairment, increased performance time) Trichloroethene (TCE) VOC Respiratory system, heart, liver, kidney, and 2.0E-09 NA 270 (8 hr MEG) 79-01-6 central nervous system effects; potential carcinogen (liver, kidney, non-Hodgkin’s lymphoma) (IARC 2010) Trichlorofluoromethane VOC Accelerated mortality, elevated incidences of NA 7.0E-01 H 4.80E+00 75-69-4 pleuritis and pericarditis Xylenes (Total) VOC Decreased body weight, increased mortality, NA 1.0E-01 I 1.06E+01 1330-20-7 eye and respiratory tract irritation, neurological effects (e.g., impaired learning and motor performance) (ATSDR 2007; EPA 2011) Antimony Metals Cardiovascular effects (altered NA NA NA 7440-36-0 electrocardiograph and myocardial damage), respiratory effects (focal and interstitial fibrosis, edema), limited evidence of reproductive and developmental toxicity Lead Metals Probable carcinogen, lung and kidney NA NA 1.5E-03 7439-92-1 tumors, neurotoxicity, developmental delays, hypertension, impaired hearing acuity, impaired hemoglobin synthesis, and male reproductive impairment Zinc Metals Inflammatory response in the lungs (ATSDR NA NA 7.2E-01 7440-66-6 2005) PM PM Cardiovascular and respiratory effects, NA NA 4.0E-02 for disease, and mortality; reproductive and PM2.5 developmental effects; lung cancer (EPA 7.0E-02 for 2009) PM10 53 continued

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TABLE 5-1 Continued 54 Chemical Name and Inhalation Unit Risk Reference Concentration 1-yr Air MEG CAS Number Class Long-Term Health Effectsa (mg/m3) (mg/m3)c (mg/m3)d 2,3,7,8-Tetrachlorodibenzo- Dioxin Likely carcinogen; cardiovascular 3.8E01 C 4.0E-08 C 1.1E-08 p-dioxin (TCDD) effects, diabetes, immunologic response, 1746-01-6 altered neurobehavior, reproductive and developmental effects, birth defects; changes to the endocrine system; wasting syndrome (EPA 2003a) NOTE: MEG = military exposure guideline; NA = not available. aHealth effects by any route of exposure as described in EPA IRIS chemical profiles are presented unless otherwise noted in text (EPA 2011); effects are based primarily on animal experi- ments. bCarcinogenicity determined by EPA IRIS as follows: Likely to be Carcinogenic to Humans : available tumor effects and other key data are adequate to demonstrate carcinogenic potential to humans, but does not reach the weight-of-evidence for the descriptor “carcinogenic to humans”; Suggestive Evidence of Carcinogenic Potential: evidence from human or animal data is suggestive of carcinogenicity, which raises a concern for carcinogenic effects but is judged not sufficient for a stronger conclusion; Inadequate Information to Assess Carcinogenic Potential: available data are judged inadequate to perform an assessment; Not Likely to be Carcinogenic to Humans: available data are considered robust for deciding that there is no basis for human hazard concern (EPA 2005). cData from EPA IRIS; EPA HEAST; EPA PPRTV; CalEPA; or ATSDR as noted : I = IRIS; P = PPRTV; A = ATSDR; C = Cal EPA; X = PPRTV; H = HEAST. (U.S. Environmental Protec- tion Agency Regions 3, 6, and 9. Regional Screening Levels for Chemical Contaminants at Superfund Sites; http://www.epa.gov/reg3hwmd/risk/human/rb-concentration_table/index.htm; accessed October 18, 2010). dFrom: USACHPPM Technical Guide 230, Chemical Exposure Guidelines for Deployed Military Personnel, Appendix C (http://www-nehc.med.navy.mil/downloads/prevmed/TG230.pdf; accessed October 17, 2010).

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55 HEALTH EFFECTS OF AIR POLLUTANTS weaknesses of epidemiologic studies, concluded that there is limited or suggestive evidence of an association between TCDD exposure and hypertension and ischemic heart disease (IOM 2008). Humblet et al. (2008) con - ducted an exhaustive literature review to also evaluate the evidence for an association between TCDD exposure and cardiovascular disease morbidity or mortality. Acknowledging that confounders were not adjusted for in every study, they found a consistent association between TCDD exposure and increased risk of ischemic heart disease and to a lesser extent an increased risk of all-cardiovascular disease (Humblet et al. 2008). These reviews specifically evaluated TCDD, but laboratory animal data show that other 2,3,7,8 polychlo - rinated dibenzo dioxin and furan congeners act by similar mechanisms. It is thus generally presumed that 2,3,7,8-chlorinated congeners have similar effects; this has been demonstrated for some congeners and some health effects. These congeners are generally assessed by comparing their toxicity to that of TCDD using Toxicity Equivalence Factors (TEFs), the values of which have been estimated most recently by a World Health Organiza - tion committee (van den Berg et al. 2006). Particulate Matter PM air pollution includes smoke, fumes, soot, and other anthropogenic by-products, primarily from combus - tion sources, as well as particles from natural sources (dust, pollen, sea salt, forest fires) (Dockery 2009). PM measured at JBB would have included windblown dust and sand as well as combustion by-products. Although PM10 contains coarse particles with aerodynamic diameters between 2.5 mm and 10 mm, it also includes fine particles with aerodynamic diameters below 2.5 mm. PM10 does not include coarse particles with aerodynamic diameters greater than 10 mm, which in desert climes often constitute most of the airborne particle mass. Most of the long-term health risks that have been associated with PM10 in ambient air is now attributed to the PM2.5, part of PM10 (EPA 2009). Dust The Department of Defense (DoD) has been monitoring PM in the Middle East since 2001 with the begin - ning of the war in Afghanistan. In 2006, the DoD initiated its Enhanced Particulate Matter Surveillance Program (EPMSP) at 15 sites in the Middle East including Djibouti, Afghanistan, Qatar, United Arab Emirates, Iraq, and Kuwait to measure total suspended particles, PM10, and PM2.5. The EPMSP stated that PM dusts identified in the region were most likely from three sources—geologic dust, burn pits, and metal sources such as lead smelting and manufacturing—but the actual sources of the air pollution were not identified by the DoD (NRC 2010). The EPMSP reported that PM2.5 concentrations exceeded the CHPPM 1-year Military Exposure Guideline (MEG) concentration of 15 µg/m3. Other studies have also found that U.S. National Ambient Air Quality Standards (NAAQS) for PM are exceeded in Iraq and Afghanistan (Cahill 2011). A U.S. Navy researcher has found that dust collected in Iraq and Kuwait contains high concentrations of fine PM as well as chromium, nickel, aluminum, arsenic, and other metals; biological agents such as bacteria, viruses, and fungi were also detected (Lyles et al. 2011). Two epidemiologic studies conducted by CHPPM and the Navy failed to find an association between exposure to ambient PM and respiratory or cardiovascular outcomes in military personnel stationed at bases with burn pits, but these studies had substantial limitations including inadequate statistical power and short follow-up (AFHSC et al. 2010). The NRC review of the EPMSP found that exposure to ambient air pollution in the Middle East could plausibly be associated with chronic health effects but further research was needed to match air monitoring with deployment of military personnel and persistent health effects (NRC 2010). It has been suggested that high concentrations of PM from crustal sources may pose different risks for car - diovascular and respiratory effects than does PM from anthropogenic sources; nonetheless, studies have shown associations between windblown dust from the Mongolian desert and increased cardiac and respiratory morbidity in Taiwan and Korea (NRC 2010). Particular health outcomes were increased hospital admissions for COPD, cardiovascular disease, congestive heart failure, asthma, and pneumonia among others (although none of the asso -

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56 HEALTH CONSEQUENCES OF EXPOSURE TO BURN PITS ciations was statistically significant). Studies of coarse particle dust in North America, however, have not shown such health effect associations (NRC 2010). The EPA has established a NAAQS for fine particles of 35 µg/m3 averaged over 24 hours and 15 µg/m3 averaged over 1 year. For PM10, the NAAQS is 150 µg/m3 for 24 hours and there is no annual NAAQS for coarse particles because of a lack of long-term effects associated with these particles. The EPA also found a causal relationship between long-term exposure to PM2.5 and cardiovascular effects and mortality, and a likely causal relationship between exposure and respiratory effects. There was suggestive evidence of a causal association between long-term exposure to PM2.5 and reproductive and developmental effects, as well as cancer, mutagenicity, and genotoxicity (EPA 2009). Combustion-Related PM A large database of epidemiologic literature on the health effects of exposure to combustion-related PM has documented increased cardiovascular and respiratory morbidity and mortality in the United States and internation - ally. In these studies, PM is characterized by its aerodynamic diameter; the most commonly studied particle sizes cutoffs are PM10 and PM2.5. The American Heart Association reviews of the epidemiologic literature on ambient PM and cardiovascular disease found strong evidence that short-term (hours to weeks) and long-term (months to years) exposure to ambient PM increases risk for cardiovascular disease-related mortality and ischemic heart disease (Brook et al. 2004; Brook and Rajagopalan 2010). There is strong evidence that short-term PM exposure increases risk for cardiovascular hospitalizations and moderate evidence for increased risk for heart failure and ischemic stroke (Brook and Rajagopalan 2010). Long-term exposure to PM2.5 has been associated with increased cardiopulmonary and lung cancer mortal - ity (Pope et al. 2002). Types of respiratory morbidity associated with PM exposure include increased respiratory symptoms such as cough and sneeze; increased susceptibility to infection; and exacerbation of asthma and COPD (Kelly and Fussell 2011). Other PM Constituents The EPMSP attempted to measure the elemental composition of the PM, including about 40 elements in the analyses (NRC 2010). The EPMSP report indicated that the average concentrations of the metals and other individual elements in the air at JBB were not likely to present a health hazard. The highest reported elemental concentrations were for soil-forming elements such as potassium, magnesium, aluminum, iron, calcium, silicon, and sulfur. Only three metals—lead, antimony, and zinc—found in all PM fractions at JBB, were reported at con - centrations above the claimed analytic method detection limit (see Chapter 4). Health effects for these latter three metals are summarized in Table 5-1. HEALTH EFFECTS OF OTHER AIR POLLUTANTS DETECTED AT JBB Table 5-1 summarizes the long-term health effects associated with exposure to the 47 air pollutants detected at JBB plus the four additional VOCs selected above. Although the route of exposure for most of the health effects reported in the table is inhalation, effects from ingestion and dermal contact are also reported if appropriate. The table is organized by chemical class with PAHs presented first, followed by VOCs and metals, with PM and dioxins at the end. Sufficiently high exposure to these air pollutants as single chemicals has been associated with a wide variety of health effects (generally based on animal studies) from functional changes to organ damage and cancer. Carcinogens Detected at JBB As is usual in most air sampling efforts, a number of carcinogens were detected during the JBB air sampling campaigns, including 1 known carcinogen (benzene), 13 probably carcinogens, and 1 possible human carcinogen. Health effects for these carcinogens are given in Table 5-1. One probably human carcinogen, 1,3-butadiene, was

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57 HEALTH EFFECTS OF AIR POLLUTANTS included in the list because while it was not detected in the air sampling at JBB, burn barrel experiments (see Chapter 4) indicate that it is a likely combustion product from the burning of household waste. Types or sites of cancers or neoplastic changes in test animals associated with one or more of these air pollutants include kidney, leukemia, liver, lung, lymphoma, mammary, ovary, salivary gland, skin, and stomach (see Table 5-1). Noncancer Health Effects A wide range of noncancer health effects has been observed primarily in animals following exposures by various routes to the air pollutants detected at JBB, including eye and throat irritation, organ weight changes, his - topathologic changes (e.g., lesions, hyperplasias), inflammation, and reduced or impaired function. These effects were found in many organs and organ systems including adrenal gland, blood, lungs, liver, kidney, stomach, spleen, and cardiovascular, respiratory, reproductive and central nervous systems. Increased or accelerated mortality was observed following exposure to trichlorofluoromethane (NCI 1978) and xylene (ATSDR 2007). Reproductive toxicity—for example, ovarian and testicular atrophy and decreased weight gain in rat dams—was observed follow- ing exposure to 2-butanone, benzene, and 1,3-butadiene. Developmental toxicity—for example, skeletal variations and decreased fetal weight—has been observed following exposure to 2-butanone, and 1,3-butadiene. Neurological and central nervous system effects include reduced nerve conduction velocity (acetone) and impaired learning and memory functions (acetone, carbon disulfide, styrene, toluene). CUMULATIVE RISK CONSIDERATIONS The screening risk assessments performed by the Army (Taylor et al. 2008; USAPHC 2010) indicate that the measured concentrations of all the individual chemicals are unlikely to cause health effects as they were below concentrations associated with an acceptable risk of health effects. However, health risks may be greater due to multiple pollutants, cumulative risk. Cumulative risk assessment can be used to characterize the effects of multiple exposures based on the dose and known effects of each pollutant. Since dose is dependent on several external (exposure magnitude, duration, frequency, and route) and internal (absorption, distribution, metabolism, and excre- tion) factors the committee could not conduct a formal cumulative risk assessment with available data, see Box 5-1. A simple way to evaluate possible effects of multiple contaminants or cumulative exposures is to consider target organs or specific effects that are shared by many of the chemicals of concern and dose (EPA 1989, 2000, 2003b). These effects may be more likely to occur when exposure is to multiple pollutants all individually capable of causing them, and more likely to occur as the cumulative dose of the pollutants increases. For example, although JBB personnel may be exposed to many pollutants that are liver toxicants, the dose of any specific liver toxicant is BOX 5-1 Factors Determining Exposure and Dose Magnitude—Toxicant concentration in contaminated medium Duration—Length of time exposed (minutes, hours, days, lifetime) Frequency—How often exposure occurs (e.g., daily, seasonally) Route—Inhalation, ingestion, or dermal exposure Absorption—Intake and uptake processes allowing substances to cross external and internal membranes and enter the bloodstream Distribution—Transport of absorbed material from point of absorption to tissues and fluids Metabolism—Biochemical processes by which chemicals are subjected to change by living organisms Excretion—Elimination of toxicants and other substances from the body

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58 HEALTH CONSEQUENCES OF EXPOSURE TO BURN PITS not great enough to impart an intolerable level of risk. However, exposure to multiple chemicals, all affecting liver function but not present at high doses individually, may cause liver damage collectively. To address the concerns of effects of multiple contaminants, the 2010 screening assessment (USAPHC 2010) attempted to screen for target organ effects, but accounted only for the primary target organ for each chemical (USAPHC 2010). The data sum - marized in Table 5-1 takes account of multiple potential target organs for each chemical, and includes 15 known, probable, or possible carcinogens affecting multiple tumor types or sites. There are also numerous pollutants with common target organs and systems, including central nervous system (15 pollutants), liver (15 pollutants), lungs/ respiratory (11 pollutants), kidney (12 pollutants), blood (7 pollutants), heart or vascular (7 pollutants), reproduc - tive (3 pollutants), developmental (5 pollutants), eye (8 pollutants), skin (5 pollutants) and spleen (1 pollutant). The presence of multiple pollutants in the air at JBB, many capable of causing similar health effects, suggests that there is likely an increased risk for such health effects from exposure to the ambient air. These organs or organ systems potentially affected by multiple chemicals constitute reasonable targets for epidemiologic monitoring. CONCLUSIONS The health effects of dioxin and PM are well characterized on the basis of toxicological, clinical, and obser- vational epidemiologic studies. The health effects from exposure to dioxin and dioxin-like compounds include cancer, diabetes, and other endocrine system effects, immunologic response, neurological effects, reproductive and developmental effects, birth defects, and wasting syndrome. The health effects of PM exposure include lung cancer mortality and other types of cardiovascular and respiratory morbidity and mortality. The data on the other pollutants reviewed here were compiled from a variety of summary sources that reviewed animal studies and less common epidemiologic investigations. The exposure conditions in many of these studies bear little resemblance to those experienced by military personnel at JBB or other locations. This hazard assess - ment identifies potential health effects that are biologically plausible but not definitively associated with human exposures in particular conditions. The data reviewed indicate that the potential long-term health effects associated with burn pit emissions could include any of the health effects discussed in this chapter. Numerous chemicals are associated with health effects in specific organs or organ systems. Health effects associated with five or more detected chemicals include: • Neurological, reduced CNS function; • Liver toxicity, reduced liver function; • Certain cancers (stomach, respiratory, skin, and leukemia, among others); • Respiratory toxicity and morbidity; • Kidney toxicity and reduced kidney function; • Blood effects (anemia, changes in various blood cell types); • Cardiovascular toxicity and morbidity; and • Reproductive and developmental toxicity. Evaluating the health effects associated with a particular pollutant yields hypotheses about potential health effects that may occur upon exposure to pollutant mixtures. These hypotheses can be investigated in two ways: • eview existing epidemiologic literature on health outcomes associated with exposures to burn pit emis- R sions (for example, recent studies on military populations) or to combustion sources similar to burn pit emissions (for example, firefighters and others) (see Chapter 6); or • Conduct new epidemiologic investigations (see Chapter 8). Chapter 5 has summarized health effects data from studies of exposures to particulate matter, dioxins, and 56 air pollutants detected in sampling at JBB. These data on single pollutant exposures have limited predictive value for deployed personnel at JBB or other burn pit locations because those personnel are known to have been exposed to complex combinations of the many pollutants identified in Chapter 4, but the exact combinations of pollutants,

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59 HEALTH EFFECTS OF AIR POLLUTANTS their magnitude, and the duration of exposure are unknown. Therefore, the findings presented in this chapter are preliminary at best. The committee’s recommendations on the potential long-term health effects of exposure to air pollutants at JBB, including burn pit emissions, will incorporate these data as well as the epidemiologic data review in the next chapter. REFERENCES AFHSC (U.S. Armed Forces Health Surveillance Center), Naval Health Research Center, and U.S. Army Public Health Com - mand. 2010. Epidemiological studies of health outcomes among troops deployed to burn pit sites . Silver Spring, MD: Defense Technical Information Center. ATSDR (Agency for Toxic Substances and Disease Registry). 1998. Toxicological profile for jet fuels JP-5 and JP-8. ToxPro- files. http://www.atsdr.cdc.gov/ToxProfiles/TP.asp?id=773&tid=150 (accessed July 9, 2010). ATSDR. 2005. Toxicological profile for zinc. ToxProfiles. http://www.atsdr.cdc.gov/ToxProfiles/tp60-c3.pdf (accessed July 9, 2010). ATSDR. 2007. Toxicological profile for xylenes. ToxProfiles. http://www.atsdr.cdc.gov/ToxProfiles/tp71-c3.pdf (accessed July 9, 2010). Becher, H., D. Flesch-Janys, T. Kauppinen, M. Kogevinas, K. Steindorf, A. Manz, and J. Wahrendorf. 1996. Cancer mortality in German male workers exposed to phenoxy herbicides and dioxins. Cancer Causes & Control 7(3):312-321. Becher, H., K. Steindorf, and D. Flesch-Janys. 1998. Quantitative cancer risk assessment for dioxins using an occupational cohort. Environmental Health Perspectives 106(Suppl 2):663-670. Boman, B. C., A. B. Forsberg, and B. G. Jarvholm. 2003. Adverse health effects from ambient air pollution in relation to residential wood combustion in modern society. Scandinavian Journal of Work, Environment and Health 29(4):251-260. Boman, B. C., A. B. Forsberg, and T. Sandstrom. 2006. Shedding new light on wood smoke: A risk factor for respiratory health. European Respiratory Journal 27(3):446-447. Brook, R. D., and S. Rajagopalan. 2010. Particulate matter air pollution and atherosclerosis. Current Atherosclerosis Reports 12(5):291-300. Brook, R. D., B. Franklin, W. Cascio, Y. Hong, G. Howard, M. Lipsett, R. Luepker, M. Mittleman, J. Samet, S. C. Smith, Jr., I. Tager. 2004. Air pollution and cardiovascular disease: A statement for healthcare professionals from the Expert Panel on Population and Prevention Science of the American Heart Association. Circulation 109(21):2655-2671. Cahill, C. F. 2011. UAF’s unique applied research capabilities: Unmanned aircraft and airborne contaminants. Fairbanks, AK: University of Alaska Fairbanks. CDC (Centers for Disease Control and Prevention). 2010. NIOSH pocket guide to chemical hazards. November 22, 2010. http:// www.cdc.gov/niosh/npg/ (accessed February 23, 2011). Dockery, D. W. 2009. Health effects of particulate air pollution. Annals of Epidemiology 19(4):257-63. EPA (U.S. Environmental Protection Agency). 1989. Risk assessment guidance for Superfund: Vol I. Human health evaluation manual (Part A). EPA/540/1-89/002. Washington, DC: Environmental Protection Agency. EPA. 2000. Supplementary guidance for conducting health risk assessment of chemical mixtures: Risk Assessment Forum Technical Panel. EPA/630/R-00/002. Washington, DC: U.S. Environmental Protection Agency. EPA. 2003a. Exposure and human health reassessment of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds National Academy of Sciences (NAS) review draft. EPA/600/P-00/001Cb. Washington, DC: U.S. Environmental Protec - tion Agency. December. EPA. 2003b. Framework for cumulative risk assessment. EPA/630/P-02/001F. Washington, DC: U.S. Environmental Protection Agency. EPA. 2005. Fact sheet: EPA’s guidelines for carcinogen risk assessment. EPA/630/P-03/001F. http://epa.gov/cancerguidelines/ cancer-guidelines-factsheet.htm (accessed October 12, 2010). EPA. 2009. Integrated science assessment for particulate matter (final report) . EPA/600/R-08/139F. Research Triangle Park, NC: U.S. Environmental Protection Agency. EPA. 2011. Integrated risk information system. http://www.epa.gov/IRIS/ (accessed March 8, 2011). Fingerhut, M. A., W. E. Halperin, D. A. Marlow, L. A. Piacitelli, P. A. Honchar, M. H. Sweeney, A. L. Greife, P. A. Dill, K. Steenland, and A. J. Suruda. 1991. Cancer mortality in workers exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin. New England Journal of Medicine 324(4):212-218. Hooiveld, M., D. Heederik, and H. B. de Mesquita. 1996. Preliminary results of the second follow-up of a Dutch cohort of workers occupationally exposed to phenoxy herbicides, chlorophenols and contaminants. Organohalogen Compounds 20:185-189.

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61 HEALTH EFFECTS OF AIR POLLUTANTS U.S. Surgeon General. 2004. The health consequences of smoking: A report of the Surgeon General . Washington, DC: U.S. Department of Health and Human Services, Public Health Service. USAPHC (U.S. Army Public Health Command). 2010. Screening health risk assessments, Joint Base Balad, Iraq, 11 May–19 June 2009. Aberdeen Proving Ground, MD: U.S. Army Center for Health Promotion and Preventive Medicine. Van den Berg M., L. S. Birnbaum, M. Denison, M. De Vito, W. Farland, M. Feeley, H. Fiedler, H. Hakansson, A. Hanberg, L. Haws, M. Rose, S. Safe, D. Schrenk, C. Tohyama, A. Tritscher, J. Tuomisto, M. Tysklind, N. Walker, and R. E. Peterson. 2006. The 2005 World Health Organization reevaluation of human and mammalian toxic equivalency factors for dioxins and dioxin-like compounds. Toxicological Sciences 093(2):223-241. White, S. S., and L. S. Birnbaum. 2009. An overview of the effects of dioxins and dioxin-like compounds on vertebrates, as documented in human and ecological epidemiology. Journal of Environmental Science and Health Part C-Environmental Carcinogenesis & Ecotoxicology Reviews 27(4):197-211.

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